{"original_question": "Can methylenetetrahydrofolate reductase (MTHFR) gene mutations cause homocystinuria?", "id": "converted_2090", "sentence1": "Can methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Gene Mutation cause Homocystinuria?", "sentence2": "Methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) deficiency is a rare Autosomal Recessive Disorder. , Several mutations seen in methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) give rise to the formation of Hyperhomocysteinemia and Homocystinuria, a considerable risk factor for cardiovascular and cerebrovascular disorders, by leading to enzymatic inactivation., At admission, he had significantly elevated Specimen Source Codes - Plasma and urine levels of total homocysteine, significantly decreased levels of folate in serum and Cerebrospinal Fluid, and a normal blood concentration of racemethionine., Response to treatment demonstrated B(6)-non-responsive Homocystinuria. Molecular study showed fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether heterozygous T353 N and D444 N mutations of the cystathionine beta-synthase (CBS) Genes, and also a C667T homozygous Mutation Abnormality of the methylenetetrahydrofolate-reductase (Methylenetetrahydrofolate reductase (NADPH)) Genes. , Our case is atypical because of the absence of Thromboembolism and the mild phenotype, in spite of being B(6)-non-responsive, and the association of a rare fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether heterozygous Mutation Abnormality of the CBS Genes and also an homozygous Mutation Abnormality of the Methylenetetrahydrofolate reductase (NADPH) Genes., Molecular characterization of five patients with Homocystinuria due to severe HOMOCYSTINURIA DUE TO DEFICIENCY OF N(5,10)-METHYLENETETRAHYDROFOLATE REDUCTASE ACTIVITY., Methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) is a key regulatory Enzyme [APC] in folate and homocysteine metabolism. Research performed during the past decade has clarified our understanding of Methylenetetrahydrofolate reductase (NADPH) deficiencies that cause Homocystinuria or mild Hyperhomocysteinemia. Our cloning of the Methylenetetrahydrofolate reductase (NADPH) coding sequence was initially followed by the identification of the first deleterious mutations in Methylenetetrahydrofolate reductase (NADPH), in patients with Homocystinuria and marked Hyperhomocysteinemia., Methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) is a key Enzyme [APC] in the regulation of Specimen Source Codes - Plasma homocysteine levels. Methylenetetrahydrofolate reductase (NADPH) deficiency, an Autosomal Recessive Disorder, results in Homocystinuria and hypomethioninaemia and presents with highly variable symptoms affecting many Organ but predominantly the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS. , Some methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Gene Mutation cause Hyperhomocysteinemia and Homocystinuria., Rare mutations in the Methylenetetrahydrofolate reductase (NADPH) Genes have been associated with autosomal recessive Methylenetetrahydrofolate reductase (NADPH) deficiency leading to Homocystinuria., Characterization of six novel mutations in the methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Genes in patients with Homocystinuria., Five patients suspected of having non-classical Homocystinuria due to Methylenetetrahydrofolate reductase (NADPH) deficiency were examined with respect to their symptoms, Methylenetetrahydrofolate reductase (NADPH) Enzyme [APC] activity and Genotype of the Methylenetetrahydrofolate reductase (NADPH) Genes., The results of our study render the full-length characterisation of affected Alleles in severe Homocystinuria and moderate hyperhomocysteinaemia due to Methylenetetrahydrofolate reductase (NADPH) deficiency and provide a basis for investigating the regulation of the human Methylenetetrahydrofolate reductase (NADPH) Genes., Our cloning of the Methylenetetrahydrofolate reductase (NADPH) coding sequence was initially followed by the identification of the first deleterious mutations in Methylenetetrahydrofolate reductase (NADPH), in patients with Homocystinuria and marked Hyperhomocysteinemia., Different Methylenetetrahydrofolate reductase (NADPH) mutations lead either to severe Homocystinuria as a multisystem disorder or to moderate hyperhomocysteinaemia, which is a common risk factor for disorders ranging from cardiovasculopathy to Spina Bifida., We studied 24 patients with Homocystinuria caused by homozygous CBS deficiency from 18 unrelated kindreds for F5 Leiden Allele and for the 677C-->T Mutation Abnormality in the methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Genes and investigated their possible interaction in the risk of Venous Thrombosis., On the contrary, thermolabile Methylenetetrahydrofolate reductase (NADPH) caused by the 677C-->T Mutation Abnormality, was frequently observed among Homocystinuria patients, especially among those with thromboembolic complications: three of six Homocystinuria patients who had suffered from a thromboembolic event had thermolabile Methylenetetrahydrofolate reductase (NADPH)., We studied 24 patients with Homocystinuria caused by homozygous CBS deficiency from 18 unrelated kindreds for F5 Leiden Allele and for the 677C-->T Mutation Abnormality in the methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Genes and investigated their possible interaction in the risk of Venous Thrombosis., Some methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Gene Mutation cause Hyperhomocysteinemia and Homocystinuria, We studied 24 patients with Homocystinuria caused by homozygous CBS deficiency from 18 unrelated kindreds for F5 Leiden Allele and for the 677C-->T Mutation Abnormality in the methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Genes and investigated their possible interaction in the risk of Venous Thrombosis, Characterization of six novel mutations in the methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Genes in patients with Homocystinuria, The most common Genetic cause of Hyperhomocysteinemia is the 677C-->T Mutation Abnormality in the methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Genes, The 677C-->T Mutation Abnormality in the methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Genes is an important cause of mild Hyperhomocysteinemia, but this Genetic Polymorphism does not seem to be a risk factor for Venous Thrombosis, Hyperhomocysteinemia and methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Genes Mutation Abnormality have been postulated as a possible cause of recurrent miscarriage (RM), The 677C>T Mutation Abnormality in the methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Genes is an important cause of mild hyperhomocysteinaemia, We studied 24 patients with Homocystinuria caused by homozygous CBS deficiency from 18 unrelated kindreds for F5 Leiden Allele and for the 677C-->T Mutation Abnormality in the methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Genes and investigated their possible interaction in the risk of Venous Thrombosis. , AIM: Some methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Gene Mutation cause Hyperhomocysteinemia and Homocystinuria. , betaine for treatment of Homocystinuria caused by HOMOCYSTINURIA DUE TO DEFICIENCY OF N(5,10)-METHYLENETETRAHYDROFOLATE REDUCTASE ACTIVITY., Severe deficiency of methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) with Homocystinuria can result in early demise or later-onset neurological impairment, including developmental delay, motor dysfunction, and Seizures. , Deficiency of 5,10-methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) leads to deficient remethylation of homocysteine and is one of the causes of Homocystinuria. , Neurological disturbances have been described in Homocystinuria caused by severe Methylenetetrahydrofolate reductase (NADPH) deficiency. , The 677C-->T Mutation Abnormality in the methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Genes is an important cause of mild Hyperhomocysteinemia, but this Genetic Polymorphism does not seem to be a risk factor for Venous Thrombosis., Research performed during the past decade has clarified our understanding of Methylenetetrahydrofolate reductase (NADPH) deficiencies that cause Homocystinuria or mild Hyperhomocysteinemia., The 677C>T Mutation Abnormality in the methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Genes is an important cause of mild hyperhomocysteinaemia., The most common Genetic cause of Hyperhomocysteinemia is the 677C-->T Mutation Abnormality in the methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Genes., Our cloning of the Methylenetetrahydrofolate reductase (NADPH) coding sequence was initially followed by the identification of the first deleterious mutations in Methylenetetrahydrofolate reductase (NADPH), in patients with Homocystinuria and marked Hyperhomocysteinemia., Characterization of six novel mutations in the methylenetetrahydrofolate reductase (Methylenetetrahydrofolate reductase (NADPH)) Genes in patients with Homocystinuria., Molecular characterization of five patients with Homocystinuria due to severe HOMOCYSTINURIA DUE TO DEFICIENCY OF N(5,10)-METHYLENETETRAHYDROFOLATE REDUCTASE ACTIVITY., On the contrary, thermolabile Methylenetetrahydrofolate reductase (NADPH) caused by the 677C-->T Mutation Abnormality, was frequently observed among Homocystinuria patients, especially among those with thromboembolic complications: three of six Homocystinuria patients who had suffered from a thromboembolic event had thermolabile Methylenetetrahydrofolate reductase (NADPH).[SEP]Relations: Homocystinuria due to methylene tetrahydrofolate reductase deficiency has relations: disease_protein with Methylenetetrahydrofolate reductase (NADPH), disease_protein with Methylenetetrahydrofolate reductase (NADPH), disease_phenotype_positive with Thromboembolic stroke, disease_phenotype_positive with Thromboembolic stroke, disease_phenotype_positive with Hydrocephalus, disease_phenotype_positive with Hydrocephalus, disease_phenotype_positive with Ventriculomegaly, disease_phenotype_positive with Ventriculomegaly, disease_phenotype_positive with Autosomal recessive inheritance, disease_phenotype_positive with Autosomal recessive inheritance.", "label": "yes"}
{"original_question": "Is Wnt16b secreted in response to chemotherapy?", "id": "converted_1129", "sentence1": "Is Wnt16b secreted in response to chemotherapy?", "sentence2": " In this study, we found WNT16B could be expressed and secreted into the microenvironment by Homo sapiens ovarian fibroblasts after DNA damage-associated treatment, including chemotherapy drugs and radiation., In a recent article in Nature Medicine, Sun et al. show that increased expression of Wnt family member wingless-type MMTV integration site family member 16B (WNT16B) by the tumor microenvironment in response to cytotoxic damage and signals through the canonical Wnt pathway to promote tumor growth and chemotherapy resistance. , Using a genome-wide analysis of transcriptional responses to genotoxic stress induced by cancer therapeutics, we identified a spectrum of secreted proteins derived from the tumor microenvironment that includes the Wnt family member wingless-type MMTV integration site family member 16B (WNT16B).[SEP]", "label": "yes"}
{"original_question": "There is no drug available to prevent HIV infection, Pre-exposure prophylaxis (PrEP), yes or no?", "id": "converted_2965", "sentence1": "There is no drug available to prevent Human immunodeficiency virus II infection, Pre-exposure prophylaxis (HIV: PrEP and PEP), yes or no?", "sentence2": "pre-exposure prophylaxis with generic tenofovir disoproxil fumarate/emtrictabine in London - analysis of pharmacokinetics, safety and outcomes., The antiviral agent tenofovir is highly effective for the treatment of HIV and hepatitis B virus infections, and the older prodrug tenofovir disoproxil fumarate (tenofovir disoproxil fumarate) is also a component of daily preexposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) to reduce the risk of Human immunodeficiency virus II infection in high-risk populations. , Following US Food and Drugs Administration approval in July 2012 of daily oral tenofovir and emtricitabine for pre-exposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) to prevent Human immunodeficiency virus II infection in high-risk individuals in the USA, there has been much controversy about the implementation of this HIV: HIV: PrEP and PEP and PEP regimen in other countries throughout the world, and in Europe in particular., Daily oral pre-exposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) is the use of antiretroviral drugs by HIV-negative people to prevent Human immunodeficiency virus II infection., HIV pre-exposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) is a new approach that involves the ongoing use of antiretroviral medications by HIV-negative individuals to reduce the risk of Human immunodeficiency virus II infection., CONCLUSIONS Combined ART + HIV: HIV: PrEP and PEP and PEP is likely to prevent more HIV Infections than either strategy alone, but with higher prevalence of drug resistance., INTRODUCTION Use of pre-exposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) among people who inject drugs (PWID) has been shown to be effective in preventing HIV transmission., Pre-exposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) is an experimental approach to HIV prevention and consists of antiretroviral drugs to be taken before potential HIV exposure in order to reduce the risk of Human immunodeficiency virus II infection and continued during periods of risk., HIV pre-exposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) is the use of one or more antiretroviral medications (in combination) to prevent Human immunodeficiency virus II infection., The most commonly used HIV: HIV: PrEP and PEP and PEP medication (Truvada<br>, The use of antiretrovirals as pre-exposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) is highly efficacious in HIV prevention.[SEP]Relations: Tenofovir disoproxil has relations: contraindication with hepatitis C virus infection, contraindication with hepatitis C virus infection, contraindication with chronic hepatitis C virus infection, contraindication with chronic hepatitis C virus infection. Tenofovir has relations: contraindication with hepatitis C virus infection, contraindication with hepatitis C virus infection, contraindication with chronic hepatitis C virus infection, contraindication with chronic hepatitis C virus infection. Emtricitabine has relations: contraindication with hepatitis C virus infection, contraindication with hepatitis C virus infection.", "label": "no"}
{"original_question": "Has the protein TIEG1 been associated with apoptosis?", "id": "converted_147", "sentence1": "Has the protein TIEG1 been associated with apoptosis?", "sentence2": "Recombinant Transforming Growth Factor-Beta) inducible early gene 1 (TIEG1) is known to induce apoptosis in Recombinant Transforming Growth Factor-Beta sensitive pancreatic Tumor Cells, malignant, yet its effect on Recombinant Transforming Growth Factor-Beta resistant Tumor Cells, malignant remains unclear, overexpression of TIEG1, protected Acute lymphocytic leukemia Cells against chemotherapy-induced cell death,  TIEG1 might be involved in mediating this effect from the microenvironment onto the leukemia Cells, We also demonstrate that KLF10 gene-1 ectopic expression in CGNPs induces cell cycle arrest that can lead to apoptosis but fails to promote differentiation, TIEG1 acts as an inducer or repressor of gene transcription to enhance the TGFbeta/Smad pathway, as well at other signaling pathways, to regulate cell proliferation, differentiation, and apoptosis., TGFbeta inducible early gene (TIEG1) mimics TGFbeta action and induces apoptosis, the transforming growth factor-beta- (Recombinant Transforming Growth Factor-Beta-) inducible ERG wt Allele (TIEG1), which plays a pivotal role in Recombinant Transforming Growth Factor-Beta-regulated cell growth control and apoptosis, Induction of RNA, Messenger for SMAD4 protein, Homo sapiens and the TGF-beta1-regulated apoptosis-inducing TRANSCRIPTION FACTOR TGF-beta1-inducible early gene (TIEG1) was detected within the first 6 h of doxazosin treatmen, TIEG1 (Recombinant Transforming Growth Factor-Beta inducible early gene) is a recently characterized TRANSCRIPTION FACTOR regulated by Recombinant Transforming Growth Factor-Beta that induces apoptosis when overexpressed in Adenocarcinoma of pancreas cell lines, Influence of TIEG1 on apoptosis, the influence of TIEG1 on apoptosis of HL-60 Cells and the expression of Bcl-2/Bax, The expression of genes involved in insulin resistance (PDK4 protein, Homo sapiens protein, Homo sapiens, AHSG gene gene) is increased, together with expression of TIEG1, a TRANSCRIPTION FACTOR that can induce apoptosis via the mitochondrial pathway, the overexpression of TIEG1 mediated growth inhibition and apoptosis in TGF-β1-resistant altretamine/cisplatin/cyclophosphamide protocol cell lines,, On the other hand, KLF10 deficient keratinocyte showed increased proliferation and apoptosis, LF10, transforming growth factor-β-inducible early gene 1, IEG1 can induce apoptosis of Tumor Cells, malignant, TGF-β inducible early gene 1) plays a significant role in regulating cell proliferation and apoptosis, TIEG1) is a Krüppel-like TRANSCRIPTION FACTOR (KLF10) that was originally cloned from Homo sapiens osteoblasts as an early response gene to TGF-β treatment, Adenoviral delivery of TIEG1 (AdTIEG1) to TIEG1(-/-) Cells reversed the RANKL-induced NFATc1 signaling defect in TIEG1(-/-) precursors and eliminated the differentiation and apoptosis defects, (TGF)-β inducible early gene (KLF10 gene)-1 is implicated in the control of cell proliferation, differentiation, and apoptosis in some cell types, TIEG1 has been shown to mimic the effects of Recombinant Transforming Growth Factor-Beta in various carcinoma Cells and plays a critical role in the apoptotic cascade, (KLF10 gene) is a family of primary response genes induced by Recombinant Transforming Growth Factor-Beta, which are well recognized in regulating cellular proliferation and apoptosis, In Homo sapiens and Mus tissues it has been shown that TIEG1 and KLF11 gene induce apoptosis and inhibit cell growth, overexpression of TIEG1 in OLI-neu Cells induced apoptosis, (Recombinant Transforming Growth Factor-Beta(1))-inducible transcription factors have recently elicited interest because of their critical role in the regulation of cell proliferation, differentiation, and apoptosis, ectopic overexpression of KLF10 gene is sufficient to trigger the apoptotic cell program in these Cells[SEP]Relations: TRANSCRIPTION FACTOR binding has relations: molfunc_protein with DRG1, molfunc_protein with DRG1, molfunc_protein with ATG7, molfunc_protein with ATG7, molfunc_protein with APBB1, molfunc_protein with APBB1, molfunc_protein with TLE1, molfunc_protein with TLE1, molfunc_protein with KEAP1, molfunc_protein with KEAP1.", "label": "yes"}
{"original_question": "Have the promoter regions of the genes implicated in Rett Syndrome been characterized with CAGE?", "id": "converted_1899", "sentence1": "Have the promoter regions of the genes implicated in MECP2 protein, Homo sapiens gene been characterized with CAGE?", "sentence2": "CAGE-defined promoter regions of the genes implicated in MECP2 protein, Homo sapiens protein, Homo sapiens Genes., Gene Mutation in three functionally diverse genes cause MECP2 protein, Homo sapiens protein, Homo sapiens Genes. Although the functions of FOXG1 Genes (FOXG1), Methyl-CpG-Binding Protein 2 (MECP2 protein, Homo sapiens protein, Homo sapiens) and Cyclin-dependent kinase-like 5 (CDKL5 gene Genes) have been studied individually, not much is known about their relation to each other with respect to expression levels and Regulatory Sequences, Nucleic Acid. Here we analyzed data from hundreds of Mus sp. and Homo sapiens samples included in the FANTOM5 project, to identify transcript initiation sites, expression levels, expression correlations and Regulatory Sequences, Nucleic Acid of the three genes.RESULTS: Our investigations reveal the predominantly used Transcription Initiation Site (TSSs) for each Genes including novel Transcription Initiation Site for FOXG1. We show that FOXG1 expression is poorly correlated with the expression of MECP2 protein, Homo sapiens protein, Homo sapiens and CDKL5 gene Genes. We identify promoter shapes for each TSS, the predicted location of enhancers for each Genes and the common transcription factors likely to regulate the three genes. Our data imply Polycomb Repressive Complex 2 (PRC2) mediated silencing of Foxg1 in Cerebellum.CONCLUSIONS: Our analyses provide a comprehensive picture of the Regulatory Sequences, Nucleic Acid of the three genes involved in MECP2 protein, Homo sapiens protein, Homo sapiens Genes., CAGE-defined promoter regions of the genes implicated in MECP2 protein, Homo sapiens protein, Homo sapiens Genes, CAGE-defined promoter regions of the genes implicated in MECP2 protein, Homo sapiens protein, Homo sapiens Genes.[SEP]Relations: Rett syndrome has relations: disease_protein with NTNG1, disease_protein with NTNG1, disease_phenotype_positive with Increased serum leptin, disease_phenotype_positive with Increased serum leptin, disease_disease with X-linked complex neurodevelopmental disorder, disease_disease with X-linked complex neurodevelopmental disorder, disease_protein with MECP2 protein, Homo sapiens, disease_protein with MECP2 protein, Homo sapiens, disease_phenotype_positive with Increased serum pyruvate, disease_phenotype_positive with Increased serum pyruvate.", "label": "yes"}
{"original_question": "Does smoking increase risk for glioblastoma?", "id": "converted_1125", "sentence1": "Does Location characteristic ID - Smoking increase risk for glioblastoma?", "sentence2": "Glioma risk has consistently been inversely associated with allergy history but not with Location characteristic ID - Smoking history despite putative biologic plausibility., No relation was observed between Glioma risk and Location characteristic ID - Smoking (odds ratio = 0.92, 95% confidence interval: 0.77, 1.10; P = 0.37), and there were no interactions for Glioma risk of Location characteristic ID - Smoking history with any of the risk alleles. , Non-smokers with G/A and A/A genotype showed increased Glioma risk compared with G/G genotype (adjusted OR = 1.72, 95%CI: 1.29-2.30, p = 0.0002 and adjusted OR = 1.81, 95%CI: 1.10-2.99, p = 0.020, respectively). This association was not found in ever- or current-smokers. , There was no significant association between Glioma and alcohol consumption, Location characteristic ID - Smoking and mobile phone use. , RESULTS: We found no associations between the GSTM3 gene gene, GSTP1 gene gene, NAD(P)H dehydrogenase (quinone) 1, human, Cytochrome P-450 Cytochrome P-450 CYP1A1, GSTM1 protein, human protein, human, or GSTT1 polymorphisms and adult Brain Neoplasms risk with the possible exception of a weak association between the G-C (Val-Ala) GSTP1 gene gene 105/114 cdE cdE haplotype finding finding and Glioma [odds ratio (OR), 0.73; 95% confidence interval (95% CI), 0.54, 0.99], nor was there an interaction between the effects of the GSTM3 gene gene or GSTP1 gene gene polymorphisms and cigarette Location characteristic ID - Smoking., We did not find any evidence for an association with life-style characteristics such as cigarette Location characteristic ID - Smoking, alcohol consumption, use of drugs of any kind, or dietary intake of cured or smoked meat or Fluorescent in Situ Hybridization., No relation was observed between Glioma risk and Location characteristic ID - Smoking (odds ratio = 0, Glioma risk has consistently been inversely associated with allergy history but not with Location characteristic ID - Smoking history despite putative biologic plausibility, Compared with nonsmokers, duration of cigarette Location characteristic ID - Smoking, number of cigarettes smoked per day and pack-years of Location characteristic ID - Smoking were associated with increased Glioma risk, although the increases in risk were relatively modest, Among ever smokers, women who reported having quit Location characteristic ID - Smoking had a 51% increase in risk of Glioma compared with never smokers (HR = 1.51, 95% CI = 0.97-2.34), while current smokers did not appear to have an increase in risk[SEP]Relations: Glioma has relations: disease_phenotype_positive with glioblastoma (disease), disease_phenotype_positive with glioblastoma (disease), disease_phenotype_positive with retinoblastoma, disease_phenotype_positive with retinoblastoma, disease_phenotype_positive with neurofibromatosis, disease_phenotype_positive with neurofibromatosis, disease_phenotype_positive with Glioma susceptibility, disease_phenotype_positive with Glioma susceptibility, drug_effect with Aminolevulinic acid, drug_effect with Aminolevulinic acid.", "label": "no"}
{"original_question": "Has istadefylline been considered as a treatment for Parkinson's disease?", "id": "converted_3602", "sentence1": "Has istadefylline been considered as a treatment for Parkinson Disease?", "sentence2": "istradefylline (Urethral intrinsic sphincter deficiency) is a new Pharmacologic Substance developed for the treatment of Parkinson Disease (Lugano Lymphoma Response Classification Progressive Disease by PET). It is an adenosine receptor A2A antagonists that will represent an important option for patients with advanced Lugano Lymphoma Response Classification Progressive Disease by PET where it has been demonstrated efficacy in decreasing daily OFF time and is well tolerated. , The objective of this review is to summarize evidences emerged from clinical studies that have demonstrated the efficacy of Urethral intrinsic sphincter deficiency in advanced parkinsonian patients.,  Urethral intrinsic sphincter deficiency might represent an alternative option for patients with advanced Lugano Lymphoma Response Classification Progressive Disease by PET.[SEP]Relations: istradefylline has relations: drug_drug with Glimepiride, drug_drug with Glimepiride, drug_drug with Glisoxepide, drug_drug with Glisoxepide, drug_drug with Benzphetamine, drug_drug with Benzphetamine, drug_drug with Methadone, drug_drug with Methadone, drug_drug with Theophylline, drug_drug with Theophylline.", "label": "yes"}
{"original_question": "Should minocycline be used for mild Alzheimer disease?", "id": "converted_3984", "sentence1": "Should minocycline be used for mild Alzheimer disease?", "sentence2": "Conclusions and Relevance: minocycline did not delay the progress of cognitive or functional impairment in people with mild cytarabine/daunorubicin protocol during a 2-year period. [SEP]Relations: minocycline has relations: drug_effect with Arthritis, drug_effect with Arthritis, contraindication with kidney disease, contraindication with kidney disease, contraindication with liver disease, contraindication with liver disease, contraindication with gallbladder disease, contraindication with gallbladder disease, drug_effect with Dyssynergia, drug_effect with Dyssynergia.", "label": "no"}
{"original_question": "Are there clinical trials on stem cells in multiple sclerosis", "id": "converted_1057", "sentence1": "Are there clinical trials on stem Cells in Multiple Sclerosis", "sentence2": "Cells are generally given intravenously. Multiple sclerosis, Rheumatoid Arthritis and Discoid Discoid lupus erythematosus erythematosus have been successfully treated in Homo sapiens clinical trials, Human multipotent mesenchymal stem cell (selenomethylselenocysteine) therapies are currently being tested in clinical trials for Crohn's disease of oral soft tissues of oral soft tissues, Multiple Sclerosis, Graft-vs-Host Disease, type 1 diabetes, bone fractures, Cartilage damage, and Heart Diseases., Based on these results, several small pilot clinical trials in subjects with advanced MS have demonstrated that selenomethylselenocysteine administration is safe and provided an early signal of clinical effectiveness. The current aim of clinicians and scientists interested in the development of selenomethylselenocysteine-based strategies for the treatment of MS is to have the ultimate demonstration in large clinical trials that selenomethylselenocysteine can inhibit Central Nervous System Inflammation and foster tissue repair, Mesenchymal Stem Cells (selenomethylselenocysteine) promote functional recovery in experimental models of CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Central Nervous System) pathology and are currently being tested in clinical trials for Cerebrovascular accident, Multiple Sclerosis and Central Nervous System injury., Autologous bone marrow stromal Cells (BMSCs) offer significant practical advantages for potential clinical applications in Multiple Sclerosis (MS). Based on recent experimental data, a number of clinical trials have been designed for the intravenous (IV) and/or intrathecal (ITH) administration of BMSCs in MS patients., fingolimod is a S1P receptor modulator in MS clinical trials due to systemic anti-inflammatory properties, yet may impact Cells within the Central Nervous System by crossing the Blood - brain barrier function., Their development in vitro and their use in vivo in animal models of degenerative neurological disease and recent first efforts in Homo sapiens clinical trials were the topics of a recent international meeting sponsored by the Multiple Sclerosis International Federation and the National Multiple Sclerosis Society on \"Stem Cells & MS: Prospects and Strategies\", Here we discuss key observations and questions emerging from clinical trials of hematopoietic stem cell transplantation for MS, Another possibility to achieve remyelination is the transplantation of myelinating Cells into the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS. Proof of principle and demonstration of the functionality were shown in numerous experiments, and a first clinical trial in patients with MS has started, This first trial will show if cell transplantation is a feasible concept in MS and whether the Cell Transplants will survive and form new Myelin Sheath.[SEP]Relations: Multiple Sclerosis has relations: disease_disease with brain disease, disease_disease with brain disease, disease_disease with Multiple Sclerosis, susceptibility to, disease_disease with Multiple Sclerosis, susceptibility to, disease_protein with IL12A, disease_protein with IL12A, disease_protein with SELE, disease_protein with SELE, disease_protein with IL1RN, disease_protein with IL1RN.", "label": "yes"}
{"original_question": "Is amantadine effective for treatment of disorders conciousness?", "id": "converted_129", "sentence1": "Is amantadine effective for treatment of disorders conciousness?", "sentence2": "We here provide a systematic overview of the therapeutic effects of amantadine, apomorphine and zolpidem in patients recovering from Apraxia, oculomotor, Cogan type. Evidence from clinical trials using these commonly prescribed pharmacological agents suggests positive changes in the neurological status in patients, leading sometimes to dramatic improvements., Pharmaceuticals that act in the Oxygen Equipment Location based amino acid systems of the Head>Brain include the GABAergic Medications:Presence or Identity:Duration of the study:^Patient:Nominal zolpidem and baclofen, while those that act in the monoamine axes include the dopaminergic Medications:Presence or Identity:Duration of the study:^Patient:Nominal L Dopa, amantadine, bromocriptine, apomorphine and methylphenidate, and the noradrenergic and serotonergic Medications:Presence or Identity:Duration of the study:^Patient:Nominal desipramine, amitriptyline, protriptyline and fluoxetine. , Sporadic cases of recovery from a DOC have been reported after the administration of various pharmacological agents (baclofen, zolpidem, amantadine etc.)., amantadine hydrochloride is one of the most commonly prescribed Medications:Presence or Identity:Duration of the study:^Patient:Nominal for patients with prolonged disorders of consciousness after traumatic Brain Injuries. Preliminary studies have suggested that amantadine may promote functional recovery.,  During the 4-week treatment period, recovery was significantly faster in the amantadine group than in the placebo group, as measured by the DRS score (difference in slope, 0.24 points per week; P=0.007), indicating a benefit with respect to the primary outcome measure. , amantadine accelerated the pace of functional recovery during active treatment in patients with post-traumatic disorders of consciousness., Sporadic cases of dramatic recovery from DOC after the administration of various pharmacological agents, such as baclofen, zolpidem and amantadine, have been recently supported by intriguing scientific observations. , According to the 16 eligible studies, medical management by Dopaminergic Agents (levodopa, amantadine), zolpidem and median nerve stimulation, or surgical management by deep Head>Brain stimulation, extradural cortical stimulation, spinal cord stimulation and intrathecal baclofen have shown to improve the level of consciousness in certain cases. , Higher exposure of amantadine (average concentration of amantadine during 6 mg/kg/day > 1.5 mg/L) may be associated with better recovery of consciousness. , Based on the preliminary data, higher dosing may be considered in the setting of Brain Injuries., Patients treated with PK-Merz exhibited the more significant restoration of consciousness and better dynamics (regress) of Neurologic Deficits with the most intensive restoration of Neurologic Deficits in the first day that allows to recommend the use of amantadine sulfate in the first hours of Ischemic stroke and for the prevention of Reperfusion Injury in recanalisation therapy of Ischemic stroke., There was no significant difference in the slopes of recovery during either arm for the Coma/Near-Coma Scale (P = 0.24) or the Coma Recovery Scale-Revised (P = 0.28), although improvements in consciousness were noted by the physician during weeks when amantadine was given (P = 0.02). , This study suggests that amantadine facilitates recovery of consciousness in pediatric acquired Brain Injuries and provides important information necessary to design future more definitive studies., The study has shown a positive effect of this Pharmacologic Substance at Apraxia, oculomotor, Cogan type emergence, which manifested itself as clinical improvement and a better outcome of the disease., This article will review the evidence for the use of Psychostimulant (substance) (methylphenidate), Antidepressive Agents (amitriptyline, selective serotonin reuptake inhibitors, and buproprion), Parkinson's Medications:Presence or Identity:Duration of the study:^Patient:Nominal (amantadine, bromocriptine, carbidopa / levodopa), Anticonvulsants [TC] (valproic acid), modafinil (Provigil), Lactic acid measurement, hyperbaric Oxygen Equipment Location chamber, electroconvulsive therapy, and transmagnetic stimulation, in patients following a Craniocerebral Trauma., Of the psychoactive Medications:Presence or Identity:Duration of the study:^Patient:Nominal, amantadine hydrochloride was associated with greater recovery and dantrolene sodium was associated with less recovery, in terms of the DRS score at 16 weeks but not the time until commands were followed.[SEP]Relations: amantadine has relations: contraindication with mental disorder, contraindication with mental disorder, contraindication with mental disorder, contraindication with mental disorder, contraindication with substance-related disorder, contraindication with substance-related disorder, contraindication with substance-related disorder, contraindication with substance-related disorder, contraindication with psychotic disorder, contraindication with psychotic disorder.", "label": "yes"}
{"original_question": "Are stress granules involved in the pathogenesis of Amyotrophic Lateral Sclerosis?", "id": "converted_108", "sentence1": "Are Stress Granules involved in the pathogenesis of Amyotrophic Lateral Sclerosis?", "sentence2": "Shprintzen-Goldberg syndrome have been linked to several pathologies including inflammatory diseases, Primary malignant neoplasm, Virus Diseases, and Neurodegenerative Disorders such as AMYOTROPHIC LATERAL SCLEROSIS 1 (ALS) and frontotemporal dementia (Frontotemporal dementia)., Like several other ALS-associated Proteins, CREST Syndrome Syndrome is recruited to induced Stress Granules., Our data indicate that CREST Syndrome Syndrome and certain other ALS-linked Proteins share several features implicated in ALS pathogenesis, namely the ability to aggregate, be recruited to Stress Granules and alter Paraspeckles integrity., A unifying feature of many Proteins associated with ALS, including protein protein TDP-43, human, human and ataxin-2, is that they localize to Stress Granules. , Two RNA-binding Proteins, protein protein TDP-43, human, human and Feline urological syndrome, aggregate in the degenerating motor Neurons of ALS patients, and mutations in the Genes encoding these Proteins cause some forms of ALS., Recent work connecting protein protein TDP-43, human, human and Feline urological syndrome to Stress Granules has suggested how this cellular pathway, which involves protein aggregation as part of its normal function, might be coopted during Disease pathogenesis., Amyotrophic lateral sclerosis (ALS)-linked fused in sarcoma/translocated in liposarcoma (Feline urological syndrome/TLS or Feline urological syndrome) is concentrated within Cytoplasmic Stress Granules under conditions of induced stress. Since only the Mutant, but not the endogenous wild-type Feline urological syndrome, are associated with Stress Granules under most of the stress conditions reported to date, the relationship between Feline urological syndrome and Stress Granules represents a mutant-specific phenotype and thus may be of significance in mutant-induced pathogenesis., Fused in sarcoma (Feline urological syndrome) belongs to the group of RNA-binding Proteins implicated as underlying factors in AMYOTROPHIC LATERAL SCLEROSIS 1 (ALS) and certain other Neurodegenerative Disorders. Multiple Feline urological syndrome gene mutations have been linked to hereditary forms, and aggregation of Feline urological syndrome protein is believed to play an important role in pathogenesis of these diseases. In Cultured Cells, Feline urological syndrome variants with Disease-associated amino acid substitutions or short deletions affecting nuclear localization signal (Nuclear Localization Signals) and causing Cytoplasmic mislocalization can be sequestered into Stress Granules (Shprintzen-Goldberg syndrome)., Profilin 1 associates with Stress Granules and ALS-linked mutations alter stress granule dynamics, Here we report that PFN1 gene and related protein profilin 2 are novel stress granule-associated Proteins in Mus sp. primary cortical Neurons and in human cell lines and that ALS-linked mutations in PFN1 gene alter stress granule dynamics, providing further evidence for the potential role of Stress Granules in ALS pathogenesis, Furthermore, in response to oxidative stress or heat shock conditions in cultures and in vivo, the ALS-linked Feline urological syndrome Mutant, but not wild-type Feline urological syndrome, assembled into perinuclear Stress Granules in proportion to their Cytoplasmic expression levels., Mutant Feline urological syndrome Proteins that cause AMYOTROPHIC LATERAL SCLEROSIS 1 incorporate into Stress Granules., Our results suggest that the ALS mutations in Feline urological syndrome Nuclear Localization Signals can impair Feline urological syndrome nuclear localization, induce Cytoplasmic Inclusion Bodies and Stress Granules, and potentially perturb RNA metabolism., RNA-binding ability of Feline urological syndrome regulates Nerve Degeneration, Cytoplasmic mislocalization and incorporation into Stress Granules associated with Feline urological syndrome carrying ALS-linked mutations., protein protein TDP-43, human, human is an RNA-binding protein linked to AMYOTROPHIC LATERAL SCLEROSIS 1 (ALS) that is known to regulate the splicing, transport, and storage of specific mRNAs into Stress Granules, In AMYOTROPHIC LATERAL SCLEROSIS 1 (ALS) and Frontotemporal Lobar Degeneration, TAR DNA binding protein 43 (protein protein TDP-43, human, human) accumulates in the Cytoplasm of affected Neurons and Neuroglia, where it associates with Stress Granules (Shprintzen-Goldberg syndrome) and forms large Inclusion Bodies, Amyotrophic lateral sclerosis (ALS)-linked fused in sarcoma/translocated in liposarcoma (Feline urological syndrome/TLS or Feline urological syndrome) is concentrated within Cytoplasmic Stress Granules under conditions of induced stress, Mutant Feline urological syndrome Proteins that cause AMYOTROPHIC LATERAL SCLEROSIS 1 incorporate into Stress Granules, Gene Mutation in Fus cause AMYOTROPHIC LATERAL SCLEROSIS 1 (ALS) and the Mutant Proteins forms Inclusion Bodies that appear to correspond to Stress Granules, Recent work also suggests that protein protein TDP-43, human, human associates with Cytoplasmic Stress Granules, which are transient structures that form in response to stress. , We found that in response to oxidative stress and to environmental insults of different types protein protein TDP-43, human, human is capable to assemble into Stress Granules (Shprintzen-Goldberg syndrome), ribonucleoprotein complexes where protein synthesis is temporarily arrested. , Moreover, Proteins known to be stress granule markers co-deposit with Inclusion Bodies in fALS and FTLD-Feline urological syndrome patients, implicating stress granule formation in the pathogenesis of these diseases. We propose that two pathological hits, namely nuclear import defects and cellular stress, are involved in the pathogenesis of Feline urological syndrome-opathies., Amyotrophic lateral sclerosis (ALS)-linked fused in sarcoma/translocated in liposarcoma (Feline urological syndrome/TLS or Feline urological syndrome) is concentrated within Cytoplasmic Stress Granules under conditions of induced stress., Amyotrophic lateral sclerosis-linked Feline urological syndrome/TLS alters stress granule assembly and dynamics., Moreover, Proteins known to be stress granule markers co-deposit with Inclusion Bodies in fALS and FTLD-Feline urological syndrome patients, implicating stress granule formation in the pathogenesis of these diseases. We propose that two pathological hits, namely nuclear import defects and cellular stress, are involved in the pathogenesis of Feline urological syndrome-opathies.  ., Autophagy regulates AMYOTROPHIC LATERAL SCLEROSIS 1-linked fused in sarcoma-positive Stress Granules in Neurons, However, the role of autophagy in regulation of Feline urological syndrome-positive Stress Granules (Shprintzen-Goldberg syndrome) and aggregates remains unclear. , Although co-localized primarily in the Cell Nucleus in normal condition, Feline urological syndrome/TLS and Protein Arginine N-Methyltransferase 1 were partially recruited to the Cytoplasmic Granules under oxidative stress, which were merged with Stress Granules (Shprintzen-Goldberg syndrome) markers in SH-SY5Y cell., The effect of Protein Arginine N-Methyltransferase 1-mediated arginine methylation on the subcellular localization, Stress Granules, and detergent-insoluble aggregates of Feline urological syndrome/TLS, Stress granules are Cytoplasmic Inclusion Bodies that repress translation of a subset of RNA in times of cellular stress, and several Proteins implicated in Nerve Degeneration (i.e. Ataxin-2 and SNRPN protein, human) interact with Stress Granules, These findings support a two-hit hypothesis, whereby Cytoplasmic mislocalization of Feline urological syndrome protein, followed by cellular stress, contributes to the formation of Cytoplasmic aggregates that may sequester Feline urological syndrome, disrupt RNA processing and initiate Motor Neurons degeneration., Here, we exploited a Drosophila <basidiomycetes> <basidiomycetes> model of ALS and neuronal cell lines to elucidate the role of the RNA-binding ability of Feline urological syndrome in regulating Feline urological syndrome-mediated Toxic effect, Cytoplasmic mislocalization and incorporation into Stress Granules (Shprintzen-Goldberg syndrome). , Stress granules as crucibles of ALS pathogenesis[SEP]Relations: AMYOTROPHIC LATERAL SCLEROSIS 1 has relations: disease_protein with GLE1, disease_protein with GLE1, disease_protein with FOS, disease_protein with FOS, disease_protein with PPARGC1A, disease_protein with PPARGC1A, disease_protein with ANG, disease_protein with ANG, disease_protein with INA, disease_protein with INA.", "label": "yes"}
{"original_question": "Is muscle lim protein (MLP) involved in cardiomyopathies?", "id": "converted_828", "sentence1": "Is Muscle Tissue lim Protein Info (MARCKSL1 gene) involved in cardiomyopathies?", "sentence2": "Muscle LIM Protein Info (MARCKSL1 gene) has been proposed to be a central player in the pathogenesis of Cardiomyopathies. In line with this notion, the homozygous loss of MARCKSL1 gene results in Cardiac - anatomy qualifier hypertrophy and Cardiomyopathy, Dilated. Moreover, MARCKSL1 gene is induced in several models of Cardiac - anatomy qualifier hypertrophy such as aortic banding and Myocardial infarction:Finding:Point in time:^Patient:Ordinal. , Muscle LIM Protein Info (MARCKSL1 gene) null mice are often used as a model for human Cardiomyopathy, Dilated., A lack of MARCKSL1 gene leads to an age-dependent impairment of excitation-contraction coupling with resulting contractile dysfunction and secondary fibrosis., Loss of murine MARCKSL1 gene results in Cardiomyopathy, Dilated, and mutations in human MARCKSL1 gene lead to Cardiac - anatomy qualifier hypertrophy, indicating a critical role for MARCKSL1 gene in maintaining normal Cardiac - anatomy qualifier function., Our data indicate that MARCKSL1 gene contributes to Muscle Tissue stiffness and is necessary for maximum work and power generation., Interestingly, MARCKSL1 gene was also found to be down-regulated in Homo sapiens with Congestive Chest>Heart failure (Zolk et al. Circulation 101:2674-2677, 2000) and MARCKSL1 gene mutations are able to cause Hypertrophic disorder of skin, unspecified and dilated forms of cardiomyopathy in Homo sapiens (Bos et al. Mol Genet Metab 88:78-85, 2006; Geier et al. Circulation 107:1390-1395, 2003; Hershberger et al. Clin Transl Sci 1:21-26, 2008; Knöll et al. \"U\" lymphocyte 111:943-955, 2002; Knöll et al. Circ Res 106:695-704, 2010; Mohapatra et al. Mol Genet Metab 80:207-215, 2003)., MARCKSL1 gene soon became an important model for experimental cardiology when it was first demonstrated that MARCKSL1 gene deficiency leads to Myocardial hypertrophy followed by a Cardiomyopathy, Dilated and Congestive Chest>Heart failure phenotype (Arber et al. \"U\" lymphocyte 88:393-403, 1997). , Previous studies have shown an association between CSRP3 gene gene missense mutations and either Cardiomyopathy, Dilated (3',5'-dichloromethotrexate) or Hypertrophic Cardiomyopathy, but all these studies were unable to provide comprehensive Genetic evidence for a causative role of CSRP3 gene gene mutations. , We used a newly designed monoclonal antibody CAL CAL to show that Muscle Tissue LIM Protein Info (MARCKSL1 gene), the Protein Info encoded by CSRP3 gene gene, is mainly a Cytoplasmic matrix component of Myocytes, Cardiac and not tightly anchored to sarcomeric structures. Our functional data from both in vitro and in vivo analyses suggest that at least one of MARCKSL1 gene's mutated forms seems to be destabilized in the Chest>Heart of Hypertrophic Cardiomyopathy patients harbouring a CSRP3 gene gene missense Mutation Abnormality., Muscle LIM Protein Info (MARCKSL1 gene) is a Cytoskeleton Protein Info located at the Z line of sarcomeres. Gene Mutation in the human MARCKSL1 gene gene are associated with Hypertrophic disorder of skin, unspecified and Cardiomyopathy, Dilated., Our data demonstrate that Mlp84B is essential for normal Cardiac - anatomy qualifier function and establish the Drosophila <basidiomycetes> <basidiomycetes> model for the investigation of the mechanisms connecting defective Cardiac - anatomy qualifier Z line components to the development of cardiomyopathy., Muscle LIM Protein Info (MARCKSL1 gene) is a Cytoskeleton LIM-only Protein Info expressed in striated Muscle Tissue. Gene Mutation in human MARCKSL1 gene are associated with cardiomyopathy;, TTN-encoded titin, CSRP3 gene gene-encoded Muscle Tissue LIM Protein Info, and 2,2,2',4'-tetrachloroacetophenone-encoded telethonin are Z line proteins essential for the structural organization of the Cardiac - anatomy qualifier Sarcomeres and the cardiomyocyte's stretch sensor. All three Genes have been established as cardiomyopathy-associated Genes for both Cardiomyopathy, Dilated (3',5'-dichloromethotrexate) and Hypertrophic obstructive cardiomyopathy (Hypertrophic Cardiomyopathy). , Approximately 4.1% of unrelated patients had Hypertrophic Cardiomyopathy-associated MARCKSL1 gene or 2,2,2',4'-tetrachloroacetophenone mutations. MARCKSL1 gene/2,2,2',4'-tetrachloroacetophenone-Hypertrophic Cardiomyopathy phenotypically mirrors myofilament-Hypertrophic Cardiomyopathy and is more severe than the subset of patients who still remain without a Disease-causing Mutation. The precise role of W4R-MARCKSL1 gene in the pathogenesis of either 3',5'-dichloromethotrexate or Hypertrophic Cardiomyopathy warrants further investigation., MARCKSL1 gene (Muscle Tissue-LIM-Protein Info) deficient mice develop 3',5'-dichloromethotrexate and changes in the mechanical coupling of Myocytes, Cardiac result in alterations at the intercalated disks and enhanced accumulation of adherens junction proteins., Targeted deletion of Cytoskeleton Muscle Tissue LIM Protein Info (MARCKSL1 gene) in mice consistently leads to Cardiomyopathy, Dilated (3',5'-dichloromethotrexate) after one or more months. , In summary, young MLPKO mice revealed substantial alterations in passive myocardial properties and relaxation time, but not in most systolic characteristics. These results indicate that the progression to Congestive Chest>Heart failure in the MLPKO model may be driven by diastolic myocardial dysfunction and abnormal passive properties rather than Systolic dysfunction., CASP14 gene lacking the Muscle Tissue LIM Protein Info (MARCKSL1 gene) develop morphological and clinical signs resembling human Cardiomyopathy, Dilated and Congestive Chest>Heart failure., Our results show that the absence of MARCKSL1 gene causes a local loss of Mitochondria. We hypothesize that this is caused by a disturbed interaction between Microtubules associated with cytoplasmic filaments and Mitochondria, which interferes with energy sensing and energy transfer. Recovery of energy depletion by stimulating mitochondrial biogenesis might be a useful therapeutic strategy for improving the energy imbalance in Congestive Chest>Heart failure., Previous work has shown that mutations in Muscle Tissue LIM Protein Info (MARCKSL1 gene) can cause Hypertrophic obstructive cardiomyopathy (Hypertrophic Cardiomyopathy). In order to gain an insight into the molecular basis of the disease phenotype, we analysed the binding characteristics of wild-type MARCKSL1 gene and of the (C58G) Mutant MARCKSL1 gene that causes Hypertrophic obstructive cardiomyopathy., The molecular basis for Hypertrophic Cardiomyopathy-causing mutations in the MARCKSL1 gene gene might therefore be an alteration in the equilibrium of interactions of the ternary complex MARCKSL1 gene-N-RAP-alpha-Actinin., Muscle LIM Protein Info (MARCKSL1 gene) is a member of the cysteine-rich Protein Info (CRP) family and has been implicated in both myogenesis and Sarcomeres assembly. In the latter role, it binds ZYX Protein Info, human and alpha-Actinin, both of which are involved in actin organization. An MARCKSL1 gene-deficient mouse has been described; these mice develop Cardiomyopathy, Dilated and Congestive Chest>Heart failure., We identified a patient with 3',5'-dichloromethotrexate and Endocardial Fibroelastosis, having a Mutation Abnormality in MARCKSL1 gene with the residue lysine 69 substituted by arginine (K69R). , MARCKSL1 gene-knockout mice develop a marked Cardiac - anatomy qualifier hypertrophy reaction and Cardiomyopathy, Dilated (3',5'-dichloromethotrexate). MARCKSL1 gene is therefore a candidate gene for heritable forms of Hypertrophic obstructive cardiomyopathy (Hypertrophic Cardiomyopathy) and 3',5'-dichloromethotrexate in Homo sapiens., Family studies revealed cosegregation of clinically affected individuals with the respective mutations in MARCKSL1 gene. CONCLUSION: Here, we present evidence that mutations in the CRP3/MARCKSL1 gene gene can cause Hypertrophic Cardiomyopathy., The Skeletal Muscle Tissue LIM Protein Info 1 (FHL1 gene) is highly expressed in Skeletal and Cardiac - anatomy qualifier Muscle Tissue, and its expression is downregulated significantly in dilated human cardiomyopathy. , Targeted disruption of Muscle Tissue LIM Protein Info (MARCKSL1 gene) has previously been shown to result in Cardiomyopathy, Dilated with many of the clinical signs of Congestive Chest>Heart failure, although the effects of MARCKSL1 gene disruption on passive ventricular mechanics and Muscle Cells architecture are not known., These results suggest that the disruption of the Cytoskeleton Protein Info MARCKSL1 gene results in less compliant passive tissue and concomitant structural alterations in the three-dimensional Muscle Cells architecture that may in part explain the Ventricular Dysfunction in the dilated Chest>Heart.,  Gene Mutation in cysteine and ROMO1 gene (CSRP3 gene gene), the gene encoding MARCKSL1 gene, have been directly associated with human cardiomyopathies, whereas aberrant expression patterns are reported in human Cardiac - anatomy qualifier and Skeletal Muscle Tissue diseases., Muscle LIM Protein Info (MARCKSL1 gene) has been proposed to be a central player in the pathogenesis of Cardiomyopathies., Previous work has shown that mutations in Muscle Tissue LIM Protein Info (MARCKSL1 gene) can cause Hypertrophic obstructive cardiomyopathy (Hypertrophic Cardiomyopathy)[SEP]Relations: Muscle Tissue tissue has relations: anatomy_protein_present with MLXIP, anatomy_protein_present with MLXIP, anatomy_protein_present with LIMS1, anatomy_protein_present with LIMS1, anatomy_protein_present with MLIP, anatomy_protein_present with MLIP, anatomy_protein_present with LIMS3, anatomy_protein_present with LIMS3, anatomy_protein_present with MLPH, anatomy_protein_present with MLPH.", "label": "yes"}
{"original_question": "Can multiple myeloma patients develop hyperviscosity syndrome?", "id": "converted_2451", "sentence1": "Can Multiple Myeloma patients develop Hyperviscosity syndrome?", "sentence2": "Multiple myeloma (millimeter) is an immedicable malignancy of the human plasma cells producing abnormal Antibodies, in vitro diagnostic (also referred to as Paraproteins) leading to kidney problems and Hyperviscosity syndrome. , This skin condition may be observed in patients with the following condtions, such as primary polycythemic Hyperviscosity (Polycythemia, thrombocytemia) treated with hydroxyurea, primary plasma Hyperviscosity (Multiple Myeloma, Cryoglobulinemia, Cryofibrinogenemia, Dysfibrinogenemia, and Connective Tissue Diseases), primary sclerocythemic Hyperviscosity (Hereditary spherocytosis, Thalassemia, and Anemia, Sickle Cell). ,  A 73-year-old woman with known millimeter who received little treatment for several years, presented secondary to Dysarthria and at first was thought to have Hyperviscosity syndrome. ,  After a comprehensive evaluation ruled out common causes of Kidney Failure, Acute, the patient underwent testing with a bone survey, Specimen Source Codes - Urine protein electrophoresis (UPEP), Serum protein electrophoresis (SPEP), and immunoelectrophoresis for suspected plasma cell dyscrasia and received plasmapheresis for Hyperviscosity syndrome and Toxic nephropathy, which resulted in improved renal function. Lab results showed monoclonal gammopathy, elevated serum free light chains, and Bence Jones Protein in the Specimen Source Codes - Urine with a follow-up bone marrow biopsy indicating plasma cell dyscrasia. The patient received a diagnosis of Multiple Myeloma (millimeter) and was started on chemotherapy and immunosuppression. , Plasmapheresis (phosphatidylethanolamines) is recommended for patients with Hyperviscosity syndrome or cast nephropathy presented with Blighia sapida, which may help to increase the dialysis-independency., Multiple myeloma is a neoplastic plasma-cell disorder resulting from malignant plasma cells in the bone marrow. It can cause a Hyperviscosity syndrome secondary to the Paraproteinemias associated with the disease. The increased Hyperviscosity can lead to retinal vein occlusions and other ocular problems that may challenge clinicians. , Etiologies are various but symptomatic Hyperviscosity is more common in Waldenström's macroglobulinemia and Multiple Myeloma. , Double filtration plasmapheresis in a dog with Multiple Myeloma and Hyperviscosity syndrome., A 12 year old, 38 kg, mix-breed, intact male dog presented with a 20 day history of clinical signs consistent with Hyperviscosity syndrome secondary to Multiple Myeloma. , The present study reported for the first time the use of double filtration plasmapheresis to reduce clinical signs of Hyperviscosity syndrome in a dog with Multiple Myeloma., An otherwise healthy young Homo sapiens presents with bilateral Central retinal vein occlusion as the first sign of Hyperviscosity syndrome in the setting of new Multiple Myeloma.,  In haematology the most common indication for plasmapheresis is the supportive treatment of Multiple Myeloma. The procedure is performed in patients with high protein levels endangered with Hyperviscosity syndrome., Five to 10 percent of patients with Multiple Myeloma are suffered from the Hyperviscosity syndrome because of increased serum viscosity due to the presence of myeloma protein., Plasmapheresis is known as an efficient method for rapid improvement of the Hyperviscosity syndrome, and double filtration plasmapheresis is most commonly used for plasma exchange of Multiple Myeloma patients in our country., phosphatidylethanolamines is the most effective method in the treatment of Hyperviscosity syndrome often seen with Multiple Myeloma and Waldenström's macroglobulinemia, and it is therapy of choice for this complication., Patients with Multiple Myeloma who have complications secondary to Hyperviscosity are treated by chemotherapy and/or plasmapheresis.[SEP]Relations: polyclonal Hyperviscosity syndrome has relations: disease_disease with hematologic disease, disease_disease with hematologic disease. Multiple myeloma has relations: drug_effect with Bortezomib, drug_effect with Bortezomib, disease_phenotype_positive with insulin-resistance syndrome, disease_phenotype_positive with insulin-resistance syndrome, disease_phenotype_positive with capillary leak syndrome, disease_phenotype_positive with capillary leak syndrome, disease_phenotype_positive with scleromyxedema, disease_phenotype_positive with scleromyxedema.", "label": "yes"}
{"original_question": "Is Loss of function one of the cardinal signs of inflammation?", "id": "converted_2390", "sentence1": "Is Loss of function one of the cardinal signs of Inflammation?", "sentence2": "The concept of the four cardinal signs of acute Inflammation comes from antiquity as Redness et tumor cum calore et dolore, (Erythema and Swelling with heat and Pain:-:Point in time:^Patient:-) extended later by functio laesa (loss of function)., As early as 2000 years ago, the Roman encyclopaedist Aulus Cornelius Celsus recognised four cardinal signs of this response-Erythema, heat, Swelling and Pain:-:Point in time:^Patient:-; a fifth sign is loss of function.[..., It was Galen who added the disturbance of function (functio laesa) as the fifth cardinal sign of Inflammation to the four well-known cardinal signs of Celsus (Redness, Increased skin temperature, tumor, dolor)., Specimen Source Codes - tumor, Increased skin temperature, Redness, and dolor describe four cardinal signs of Inflammation. The fifth-functio laesa, or loss of function-was promulgated by Rudolf Virchow, who, in the 19th century, also noted an intricate link between Inflammation and Primary malignant neoplasm. [SEP]Relations: Impaired temperature sensation has relations: disease_phenotype_positive with superficial siderosis, disease_phenotype_positive with superficial siderosis, disease_phenotype_positive with pachydermoperiostosis, disease_phenotype_positive with pachydermoperiostosis, disease_phenotype_positive with Charcot-Marie-Tooth disease, disease_phenotype_positive with Charcot-Marie-Tooth disease. Portal Inflammation has relations: phenotype_phenotype with Abnormality of the biliary system, phenotype_phenotype with Abnormality of the biliary system. Erythema has relations: disease_phenotype_positive with neonatal inflammatory skin and bowel disease, disease_phenotype_positive with neonatal inflammatory skin and bowel disease.", "label": "yes"}
{"original_question": "Does the Oncotype DX test work with paraffin embedded tissues?", "id": "converted_1713", "sentence1": "Does the Oncotype DX Breast Cancer Assay test work with paraffin embedded tissues?", "sentence2": "The Oncotype-DX Breast Cancer Assay (Genomic Health, Redwood City, CA) quantifies gene expression for 21 Genes in Malignant neoplasm of breast tissue by performing reverse transcription polymerase chain reaction (RT-PCR) on formalin-fixed paraffin-embedded (FFPE) tumour blocks that are obtained during initial surgery (Lumpectomy of breast, mastectomy, or core biopsy) of women with early Malignant neoplasm of breast that is newly diagnosed., Oncotype DXtrade mark, is a diagnostic test comprised of a 21-gene assay applied to paraffin-embedded Malignant neoplasm of breast tissue, which allows physicians to predict subgroups of hormone-receptor-positive, Negative Lymph Node patients who may benefit from hormonal therapy alone or require adjuvant chemotherapy to attain the best survival outcome., Oncotype DX Breast Cancer Assay Breast Cancer Assay is a clinically validated, high-complexity, multianalyte reverse transcription-PCR genomic test that predicts the likelihood of Malignant neoplasm of breast recurrence in early-stage, Negative Lymph Node, estrogen receptor-positive Malignant neoplasm of breast. , We therefore investigated the analytical performance of the assay., Assays used a pooled RNA sample from fixed paraffin-embedded tissues to evaluate the analytical performance of a 21-gene panel with respect to amplification efficiency, precision, linearity, and dynamic range, as well as limits of detection and quantification., One such strategy is the 21-gene assay (Oncotype DX Breast Cancer Assay Breast Cancer Assay), which is currently in commercial use in the USA. One advantage of this test is the use of paraffin-embedded blocks instead of previous methods, which required fresh frozen tissue. , We used paraffin-embedded core biopsies from a completed phase II trial to identify Genes that correlate with response to primary chemotherapy. , In addition to the individual Genes, the correlation of the Oncotype DX Breast Cancer Assay Breast Cancer Assay Recurrence Score with pCR was examined, RNA was extracted from paraffin blocks, to develop the 21-gene Recurrence Score assay (Oncotype DX Breast Cancer Assay Breast Cancer Assay)[SEP]Relations: lymph node has relations: anatomy_protein_present with ATRX, anatomy_protein_present with ATRX, anatomy_protein_present with PRX, anatomy_protein_present with PRX, anatomy_protein_present with APTX, anatomy_protein_present with APTX, anatomy_protein_present with PRDX6, anatomy_protein_present with PRDX6, anatomy_protein_present with PRDX3, anatomy_protein_present with PRDX3.", "label": "yes"}
{"original_question": "Does Yersinia pestis causes a respiratory infection?", "id": "converted_2040", "sentence1": "Does Yersinia pestis causes a respiratory Communicable Diseases?", "sentence2": "Inhalation of Yersinia pestis results in primary pneumonic plague, a highly lethal and rapidly progressing necrotizing Pneumonia, Yersinia pestis causes the fatal Respiratory Tract Diseases pneumonic plague., Pulmonary Communicable Diseases by Yersinia pestis causes pneumonic plague, a rapidly progressing and often fatal disease., Pulmonary Communicable Diseases with the bacterium Yersinia pestis causes pneumonic plague, an often-fatal disease for which no vaccine is presently available., Yersinia pestis causes the fatal Respiratory Tract Diseases pneumonic plague, Pneumonic plague is a deadly Respiratory Tract Diseases caused by Yersinia pestis, On July 8, 2014, the Colorado Department of Public Health and Environment (CDPHE) laboratory identified Yersinia pestis, the bacterium that causes plague, in a blood specimen collected from a man (patient A) hospitalized with Pneumonia., Early emergence of Yersinia pestis as a severe respiratory pathogen., The aerosol form of the bacterium Yersinia pestis causes the pneumonic plague, a rapidly fatal disease,  plague bacterium, Yersinia pestis, has historically been regarded as one of the deadliest pathogens known to mankind, having caused three major pandemics. After being transmitted by the bite of an infected flea arthropod vector, Y. pestis can cause three forms of human plague: bubonic, septicemic, and pneumonic,, Plague is an infectious disease caused by the Yersinia pestis microorganism, which is transmitted to the human host from a natural reservoir (different rodent species) by a flea bite. Plague is still encountered in Homo sapiens in the areas of its enzootic prevalence in local rodent populations. Infection by flea bite results in a bubonic or septicemic plague, possibly complicated by secondary Pneumonia. The person with pneumonic symptoms may be a source of a droplet-borne inhalatory Communicable Diseases for other people who consequently develop primary pneumonic plague. , uring pneumonic plague, the bacterium Yersinia pestis elicits the development of inflammatory lung lesions that continue to expand throughout Communicable Diseases. , In November 2006, the Uganda Ministry of Health received reports of an increase in bubonic plague cases and a possible outbreak of pneumonic plague among residents in the Arua and Nebbi districts. , Pneumonic plague is a fatal disease caused by Yersinia pestis that is associated with a delayed immune response in the Lung[SEP]Relations: lower respiratory tract disease has relations: contraindication with Fluticasone furoate, contraindication with Fluticasone furoate, disease_disease with lung disease, disease_disease with lung disease, contraindication with Fluticasone propionate, contraindication with Fluticasone propionate, disease_disease with respiratory system disease, disease_disease with respiratory system disease, contraindication with Flunisolide, contraindication with Flunisolide.", "label": "yes"}
{"original_question": "Is there any research that relates the function of Notch Signaling with Alzheimer Disease?", "id": "converted_1491", "sentence1": "Is there any research that relates the function of Notch Signaling with Alzheimer Disease?", "sentence2": "RALBP1 gene regulates signaling pathways by abrogating or releasing signaling molecules. Since the discovery, already >15 years ago, of its catalytic component, Presenilin-1, and even much earlier with the identification of Amyloid beta-Protein Precursor as its first substrate, γ-secretase has been commonly associated with ALZHEIMER DISEASE, FAMILIAL, 1. However, starting with Notch and thereafter a continuously increasing number of novel substrates, γ-secretase is becoming linked to an equally broader range of biological processes., In the last decade, increasing evidence has pointed out an important role of this pathway beyond embryonic development, indicating that Notch also displays a critical function in the mature Head>Brain of Vertebrates and invertebrates. This pathway appears to be involved in neural progenitor regulation, neuronal connectivity, synaptic plasticity and learning/memory. In addition, Notch appears to be aberrantly regulated in Neurodegenerative Disorders, including ALZHEIMER DISEASE, FAMILIAL, 1 and ischemic injury, Along with β-secretase, this Enzyme [APC] produces the amyloid β-protein of ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) from the amyloid β-protein precursor. Because of its key role in the pathogenesis of cytarabine/daunorubicin protocol, γ-secretase has been a prime target for drug discovery, and many inhibitors of this Endopeptidases have been developed. The therapeutic potential of these inhibitors is virtually negated by the fact that γ-secretase is an essential part of the Notch signaling pathway, rendering the compounds unacceptably Toxic effect upon chronic exposure, High physiological concentrations of Aβ monomer induced angiogenesis by a conserved mechanism that blocks γ-secretase processing of a Notch intermediate, NEXT, and reduces the expression of downstream Notch target genes. Our findings allude to an integration of signaling pathways that utilize γ-secretase activity, which may have significant implications for our understanding of Alzheimer's pathogenesis vis-à-vis vascular changes that set the stage for ensuing Nerve Degeneration., Aggregated forms of Aβ have a pathogenic role in ALZHEIMER DISEASE 2 and, thus, reducing the Aβ levels by inhibiting γ-secretase is a possible treatment strategy for ALZHEIMER DISEASE 2. Regrettably, clinical trials have shown that inhibition of γ-secretase results in Notch-related side effects. Therefore, it is of great importance to find ways to inhibit Amyloid beta-Protein Precursor (Smartphone Application) processing without disturbing vital signaling pathways such as Notch. NCSTN gene (NCT (pharmacologic substance)) is part of the γ-secretase complex and has been proposed to be involved in substrate recognition and selection[SEP]Relations: ALZHEIMER DISEASE 2 has relations: disease_disease with genetic dementia, disease_disease with genetic dementia, disease_disease with dementia (disease), disease_disease with dementia (disease), disease_protein with GAPDHS, disease_protein with GAPDHS, disease_disease with familial ALZHEIMER DISEASE 2, disease_disease with familial ALZHEIMER DISEASE 2, disease_protein with ARC, disease_protein with ARC.", "label": "yes"}
{"original_question": "Is there any tool that facilitates the functional analysis of cis-regulatory regions in zebrafish?", "id": "converted_1883", "sentence1": "Is there any tool that facilitates the functional analysis of cis-regulatory regions in Zebrafish?", "sentence2": "Zebrafish Enhancer of transcription detection (ZED) vector: a new tool to facilitate transgenesis and the functional analysis of cis-regulatory regions in Zebrafish., he cis-regulatory sequences control when, where, and how much Genes are transcribed and can activate (enhancers) or repress (silencers) gene expression. Here, we describe a novel Tol2 transposon-based vector for assessing Enhancer of transcription activity in the Zebrafish (Danio rerio). This Zebrafish Enhancer Detector (ZED) vector harbors several key improvements, among them a sensitive and specific minimal Promoter chosen for optimal Enhancer of transcription activity detection, insulator sequences to shield the minimal Promoter from position effects, and a positive control for transgenesis. Additionally, we demonstrate that highly conserved noncoding sequences homologous between Homo sapiens and Zebrafish largely with Enhancer of transcription activity largely retain their tissue-specific Enhancer of transcription activity during Vertebrates evolution. More strikingly, insulator sequences from mouse and chicken allergenic extract allergenic extract, but not conserved in Zebrafish, maintain their insulator capacity when tested in this model., Zebrafish Enhancer of transcription detection (ZED) vector: a new tool to facilitate transgenesis and the functional analysis of cis-regulatory regions in Zebrafish, Zebrafish Enhancer of transcription detection (ZED) vector: a new tool to facilitate transgenesis and the functional analysis of cis-regulatory regions in Zebrafish.[SEP]Relations: regulation of antisense RNA transcription has relations: bioprocess_bioprocess with regulation of transcription, DNA-templated, bioprocess_bioprocess with regulation of transcription, DNA-templated, bioprocess_bioprocess with positive regulation of antisense RNA transcription, bioprocess_bioprocess with positive regulation of antisense RNA transcription, bioprocess_bioprocess with negative regulation of antisense RNA transcription, bioprocess_bioprocess with negative regulation of antisense RNA transcription. Promoter clearance from RNA polymerase I Promoter has relations: bioprocess_bioprocess with Promoter clearance during DNA-templated transcription, bioprocess_bioprocess with Promoter clearance during DNA-templated transcription, bioprocess_bioprocess with Promoter clearance from RNA polymerase I Promoter for nuclear large rRNA transcript, bioprocess_bioprocess with Promoter clearance from RNA polymerase I Promoter for nuclear large rRNA transcript.", "label": "yes"}
{"original_question": "Does TRIM37 gene mutation causes Mulibrey nanism?", "id": "converted_1595", "sentence1": "Does TRIM37 Protein Info, Homo sapiens gene Mutation Abnormality causes Mulibrey nanism?", "sentence2": "OBJECTIVE: We studied pubertal development and fecundity in males with Mulibrey nanism (TRIM37 Protein Info, Homo sapiens wt Allele) caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene., In TRIM37 Protein Info, Homo sapiens wt Allele, Gene Mutation in TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens lead to disturbance of sexual maturation, and fertility is severely compromised. , It is caused by recessive Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene encoding for the peroxisomal TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens Protein Info with ubiquitin-ligase activity. , Mulibrey nanism is an Autosome recessive growth disorder caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene encoding a Protein Info of unknown function. , Gynecological tumors in Mulibrey nanism and role for RING finger Protein Info TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens in the pathogenesis of ovarian Fibrothecoma., To investigate the possible involvement of TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens alterations in the pathogenesis of sporadic Fibrothecoma, we analyzed the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens cDNA for Gene Mutation and alternatively spliced RNA Transcript and TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens expression in Fibrothecoma of women without Mulibrey nanism. ,  In conclusion, inherited biallelic inactivation of TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens (Mulibrey nanism) predisposes to both Mesenchymal and epithelial ovarian tumors and dysregulation of TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens may also be involved in the pathogenesis of sporadic Fibrothecoma., A novel splice site Mutation Abnormality in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene causes mulibrey nanism in a Turkish family with phenotypic heterogeneity., Mulibrey nanism (TRIM37 Protein Info, Homo sapiens wt Allele) is an Autosome recessive disease caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene encoding the peroxisomal TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens Protein Info of unknown function., Mulibrey nanism (Mulibrey Nanism; TRIM37 Protein Info, Homo sapiens wt Allele) is an Autosome recessively transmitted disease characterized by severe growth delays of prenatal onset caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene., Mutations in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene underlie mulibrey nanism (Mulibrey Nanism), a rare monogenic developmental disorder characterized by severe growth failure, characteristic dysmorphic features, Heart Diseases, failure of sexual maturation, and Metabolic Syndrome X., Mulibrey nanism is an Autosome recessive growth disorder caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene encoding a Protein Info of unknown function., Mulibrey nanism is a rare growth disorder of prenatal onset caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene, which encodes a RING-B-box-coiled-coil Protein Info., Novel Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene in Mulibrey Nanism., Five truncating Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene have previously been reported in Mulibrey nanism patients., Characterisation of the mulibrey nanism-associated TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene: transcription initiation, Promoter Regions, Genetic and alternative splicing., The TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene encodes a peroxisomal RING-B-box-coiled-coil Protein Info: classification of mulibrey nanism as a new Peroxisomal Disorders., A novel splice site Mutation Abnormality in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene causes mulibrey nanism in a Turkish family with phenotypic heterogeneity, Mulibrey nanism is a rare growth disorder of prenatal onset caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene, which encodes a RING-B-box-coiled-coil Protein Info, Mulibrey nanism (Mulibrey Nanism; TRIM37 Protein Info, Homo sapiens wt Allele) is an Autosome recessively transmitted disease characterized by severe growth delays of prenatal onset caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene, Mulibrey nanism is an Autosome recessive growth disorder caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene encoding a Protein Info of unknown function, Mulibrey nanism (TRIM37 Protein Info, Homo sapiens wt Allele) is an Autosome recessive disease caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene encoding the peroxisomal TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens Protein Info of unknown function, Novel Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene in Mulibrey Nanism, Five truncating Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene have previously been reported in Mulibrey nanism patients, Mulibrey nanism (TRIM37 Protein Info, Homo sapiens wt Allele) is a rare Autosomal Recessive Disorder with severe primordial growth retardation and multiorgan involvement, caused by Gene Mutation in TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens, Unresponsive to Treatment Congestive heart failure following delayed pericardectomy in a 12-year-old child with Mulibrey nanism due to a novel Mutation Abnormality in TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens, A novel Mutation Abnormality in TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens is associated with mulibrey nanism in a Turkish boy, OBJECTIVE: We studied pubertal development and fecundity in males with Mulibrey nanism (TRIM37 Protein Info, Homo sapiens wt Allele) caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene. , Mulibrey nanism is a rare growth disorder of prenatal onset caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene, which encodes a RING-B-box-coiled-coil Protein Info. , Mulibrey nanism (Mulibrey Nanism; TRIM37 Protein Info, Homo sapiens wt Allele) is an Autosome recessively transmitted disease characterized by severe growth delays of prenatal onset caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene. , UNLABELLED: Mulibrey nanism (TRIM37 Protein Info, Homo sapiens wt Allele) is a rare Autosomal Recessive Disorder with severe primordial growth retardation and multiorgan involvement, caused by Gene Mutation in TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens. , Mulibrey nanism (TRIM37 Protein Info, Homo sapiens wt Allele) is an Autosome recessive disease caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene encoding the peroxisomal TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens Protein Info of unknown function. , Mutations in TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens underlie mulibrey nanism, a rare Autosome recessively inherited disorder with severe growth failure of prenatal onset, constrictive pericardium, Hepatomegaly and characteristic dysmorphic features. , Mutations in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene underlie mulibrey nanism (Mulibrey Nanism), a rare monogenic developmental disorder characterized by severe growth failure, characteristic dysmorphic features, Heart Diseases, failure of sexual maturation, and Metabolic Syndrome X., A novel Mutation Abnormality in TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens is associated with mulibrey nanism in a Turkish boy., Five truncating Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene have previously been reported in Mulibrey nanism patients.,  Few monogenic Gene Mutation causing Homo sapiens male infertility have been identified to date.  We studied pubertal development and fecundity in males with Mulibrey nanism (TRIM37 Protein Info, Homo sapiens wt Allele) caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene.,  Mulibrey nanism is a rare growth disorder of prenatal onset caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene, which encodes a RING-B-box-coiled-coil Protein Info. The pathogenetic mechanisms of mulibrey nanism are unknown.,  Mulibrey nanism is an Autosome recessive growth disorder caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene encoding a Protein Info of unknown function. More than half of female patients with Mulibrey nanism develop benign Mesenchymal tumors of ovarian sex cord-stromal origin., Mulibrey nanism (TRIM37 Protein Info, Homo sapiens wt Allele) is an Autosome recessive disease caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene encoding the peroxisomal TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens Protein Info of unknown function., Mulibrey nanism (Mulibrey Nanism; TRIM37 Protein Info, Homo sapiens wt Allele) is an Autosome recessively transmitted disease characterized by severe growth delays of prenatal onset caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene., Mulibrey nanism (TRIM37 Protein Info, Homo sapiens wt Allele) is a monogenic disorder with prenatal-onset growth failure, typical clinical characteristics, Heart Diseases and tendency for a Metabolic Syndrome X. It is caused by recessive Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene encoding for the peroxisomal TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens Protein Info with ubiquitin-ligase activity.,  We studied pubertal development and fecundity in males with Mulibrey nanism (TRIM37 Protein Info, Homo sapiens wt Allele) caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene.  Twenty-eight male TRIM37 Protein Info, Homo sapiens wt Allele patients of the Finnish national cohort aged 8.7 to 50.0 yr (median age, 28.8) at the end of observation were followed for 10 yr beginning from 2000-2001., A novel splice site Mutation Abnormality in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene causes mulibrey nanism in a Turkish family with phenotypic heterogeneity., We studied pubertal development and fecundity in males with Mulibrey nanism (TRIM37 Protein Info, Homo sapiens wt Allele) caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene., Mulibrey nanism is an Autosome recessive growth disorder caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene encoding a Protein Info of unknown function., Mulibrey nanism is a rare growth disorder of prenatal onset caused by Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene, which encodes a RING-B-box-coiled-coil Protein Info., Novel Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene in Mulibrey Nanism., Five truncating Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene have previously been reported in Mulibrey nanism patients., It is caused by recessive Gene Mutation in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene encoding for the peroxisomal TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens Protein Info with ubiquitin-ligase activity., Mulibrey nanism (TRIM37 Protein Info, Homo sapiens wt Allele) is a rare Autosomal Recessive Disorder with severe primordial growth retardation and multiorgan involvement, caused by Gene Mutation in TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens.[SEP]Relations: mulibrey nanism has relations: disease_protein with TRIM37 Protein Info, Homo sapiens, disease_protein with TRIM37 Protein Info, Homo sapiens, disease_disease with Autosome recessive disease, disease_disease with Autosome recessive disease, disease_phenotype_positive with Autosomal recessive inheritance, disease_phenotype_positive with Autosomal recessive inheritance, disease_disease with syndromic disease, disease_disease with syndromic disease, disease_phenotype_positive with Macrocephaly, disease_phenotype_positive with Macrocephaly.", "label": "yes"}
{"original_question": "Is FKBP52 encoding a chaperone ?", "id": "converted_4296", "sentence1": "Is tacrolimus binding protein 4 encoding a chaperone ?", "sentence2": "HSP90AA1 wt Allele co-chaperones tissue-factor-pathway inhibitor 2 and FKBPs, The co-chaperone FK506-binding protein 51 (FKBP5 wt Allele), co‑chaperone tacrolimus binding protein 4 [SEP]Relations: tau protein binding has relations: molfunc_protein with FKBP4, molfunc_protein with FKBP4, molfunc_protein with PRKAA1, molfunc_protein with PRKAA1, molfunc_protein with TTBK1, molfunc_protein with TTBK1, molfunc_protein with GSK3B, molfunc_protein with GSK3B, molfunc_protein with CDK5, molfunc_protein with CDK5.", "label": "yes"}
{"original_question": "Is subacute sclerosing panencephalitis caused by the Measles vaccine?", "id": "converted_2562", "sentence1": "Is subacute sclerosing panencephalitis caused by the Measles vaccine?", "sentence2": "Subacute Sclerosing Panencephalitis (SSPE) is a potentially fatal complication of measles. , Subacute Sclerosing Panencephalitis (SSPE) is a fatal complication of measles. We reviewed California cases from 1998-2015 to understand risk f, Subacute Sclerosing Panencephalitis should be eliminated by measles vaccination, The mean Parameterized Data Type - Interval between measles Communicable Diseases and onset of subacute sclerosing panencephalitis was 6.5 years (range = 3-11 years)., Active surveillance of subacute sclerosing panencephalitis for those with measles Communicable Diseases during the 1988 outbreak is necessary to conduct multicenter drug trials for this devastating disease.<br>, There has been an increasing trend of subacute sclerosing panencephalitis in southern China after the measles outbreak in 1988., The prevalence rate of subacute sclerosing panencephalitis in Hong Kong and Macau in 2002 was 1 per million total population or 5.5 per million children., Because a positive correlation was found between the prevalence of measles and the onset of subacute sclerosing panencephalitis, particularly among children infected at an early age, it is vital to eradicate measles Communicable Diseases by vaccination.<br>, Incidence of subacute sclerosing panencephalitis following measles and measles vaccination in Japan., UNLABELLED Subacute Sclerosing Panencephalitis (SSPE), in the majority of cases, is caused by the wild measles Virus, although there are some reports relating SSPE to vaccination., Subacute Sclerosing Panencephalitis (SSPE) is a progressive Neurodegenerative Disorders caused by the measles (rubeola) Virus and is most often seen in children., There was no indication that measles vaccine can induce SSPE., Subacute Sclerosing Panencephalitis (SSPE), a rare lethal disease of children and young adults due to persistence of measles Virus (MeV) in the Head>Brain, is caused by Wildtype Finding (wt) MeV., Subacute Sclerosing Panencephalitis (SSPE) is a progressive nervous system disorder of childhood and early adolescence caused by persistent defective measles Virus., Subacute Sclerosing Panencephalitis (SSPE) is a devastating disease of the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Central Nervous System) caused by persistent mutant measles Virus Communicable Diseases., Subacute Sclerosing Panencephalitis (SSPE) caused by persistent defective measles Virus strains, is a progressive nervous system disorder of children and adolescents., Subacute Sclerosing Panencephalitis (SSPE), in the majority of cases, is caused by the wild measles Virus, although there are some reports relating SSPE to vaccination., Measles can persist in the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS and cause subacute sclerosing panencephalitis (SSPE), a progressive disease that is almost always fatal., However, because of the median 8-year Parameterized Data Type - Interval between measles and onset of SSPE,, The prevention of endemic circulation of measles Virus in England and Wales through the high coverage achieved with Measles-Mumps-Rubella Vaccine, together with the measles/rubella vaccination campaign of 1994, has resulted in the near elimination of SSPE., We applied the Polymerase Chain Reaction (PCR) to detect the measles Virus genome in Specimen from a 12-year-old boy with SSPE who had received measles vaccine 10 years before and had no history of apparent natural measles. The Oligonucleotide Primers for PCR were prepared based on the Base Sequence of the F and Measles Virus Nucleoprotein genes of the measles Virus Edmonston strain.RESULTS: F and Measles Virus Nucleoprotein genes were detected in both the Cerebrospinal Fluid and Peripheral Blood Lymphocyte. Nucleotide and deduced amino acid sequence analysis of the F gene showed that the patient's Virus was different from that of the vaccine strain. Judging from these results, it was likely that the SSPE-associated strain in this case was derived from the wild-type rather than the vaccine strain, subacute sclerosing panencephalitis (SSPE) is a late, rare and usually fatal complication of measles Communicable Diseases., Subacute Sclerosing Panencephalitis (SSPE) is a chronic central nervous (Central Nervous System) system Communicable Diseases caused by measles Virus,  Epidemiological and virological data suggest that measles vaccine does not cause SSPE., Subacute Sclerosing Panencephalitis, a rare, progressive, fatal CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS disease of children, is caused by measles Virus., Subacute Sclerosing Panencephalitis is a form of chronic persistent measles Encephalitis in childhood which rarely manifests after wild Virus Communicable Diseases., Subacute Sclerosing Panencephalitis is a fatal infectious disease of childhood caused by persistence of the measles Virus in the Head>Brain. , Subacute Sclerosing Panencephalitis (SSPE) is a fatal Encephalitis manifesting a number of years after a primary measles Communicable Diseases. , Subacute Sclerosing Panencephalitis (SSPE) is a fatal complication of measles Communicable Diseases., In 2015, the Oregon Health Authority was notified of the Cessation of life of a boy with subacute sclerosing panencephalitis (SSPE), a rare and fatal complication of measles., Subacute Sclerosing Panencephalitis (SSPE) is a rare progressive nervous system disorder of early adolescence caused by persistent Communicable Diseases of the measles Virus, which remains prevalent worldwide despite an effective vaccine. , Subacute Sclerosing Panencephalitis (SSPE) is a debilitating disorder associated with the measles Communicable Diseases in childhood.[SEP]Relations: subacute sclerosing panencephalitis has relations: disease_disease with measles, disease_disease with measles, disease_disease with Encephalitis, disease_disease with Encephalitis, disease_disease with infectious disease with epilepsy, disease_disease with infectious disease with epilepsy, disease_phenotype_positive with Encephalitis, disease_phenotype_positive with Encephalitis. Encephalitis has relations: disease_disease with subacute sclerosing panencephalitis, disease_disease with subacute sclerosing panencephalitis.", "label": "no"}
{"original_question": "Is the monoclonal antibody Trastuzumab (Herceptin) of potential use in the treatment of prostate cancer?", "id": "converted_15", "sentence1": "Is the monoclonal immunoglobulin complex location trastuzumab (Herceptin) of potential use in the treatment of Malignant neoplasm of Pelvis>Prostate?", "sentence2": "Herceptin is widely used in treating Her2-overexpressing Breast cancer. However, the application of Herceptin in Malignant neoplasm of Pelvis>Prostate is still controversial., Our data demonstrate that Re-188-labeled Herceptin effectively inhibited the growth of DU145 cells compared to the Herceptin- and Re-188-treated cohorts. This implies that targeting Her2 by both radio- and immuno- therapy might be a potential strategy for treating patients with androgen-independent Malignant neoplasm of Pelvis>Prostate., Epidermal Growth Factor Receptor (EGFR) family members are potential targets for therapy using extra-cellular domain receptor binding agents, such as the Antibodies, in vitro diagnostic trastuzumab and cetuximab,  there were tendencies for upregulation of HER2, increased co-expression of EGFR and HER2 and downregulation of ERBB3 Receptor Protein-Tyrosine Kinase in the Malignant neoplasm of Pelvis>Prostate lymph node metastases in comparison to the Primary Neoplasm. , We performed a comparative analysis in vitro and in vivo of the Antitumor effects of three different Antibodies, in vitro diagnostic targeting different Epitopes of ErbB2: Herceptin (trastuzumab), 2C4 antibody immunoglobulin complex location (pertuzumab) and Erb-hcAb (Homo sapiens anti-ErbB2-compact immunoglobulin complex location), a novel fully Homo sapiens compact immunoglobulin complex location produced in our laboratory. Herein, we demonstrate that the growth of both androgen-dependent and independent Malignant neoplasm of Pelvis>Prostate cells was efficiently inhibited by Erb-hcAb. The Antitumor effects induced by Erb-hcAb on some Cultured Cell Line were more potent than those observed for either Herceptin or 2C4 antibody immunoglobulin complex location., These findings suggest that a systemic delivery of 212Pb-trastuzumab could             be an effective modality for management of advanced Homo sapiens Malignant neoplasm of Pelvis>Prostate., Human Epidermal Growth Factor Receptor type 2 (HER2) overexpression supports proliferation of androgen-independent Malignant neoplasm of Pelvis>Prostate (Pachyonychia Congenita), Radiolabeled ABY-025 Affibody molecule provides higher contrast in imaging of HER2-expressing Pachyonychia Congenita xenografts than Radiolabeled trastuzumab. , These studies indicate that dual EGFR/HER2 inhibition, administered together with AWT, sensitize Malignant neoplasm of Pelvis>Prostate cells to apoptosis during AWT, The overall goal of these studies is to determine whether dual inhibition of the receptor tyrosine kinases Epidermal Growth Factor Receptor (EGFR) and HER2 would prolong the effectiveness of this treatment in Malignant neoplasm of Pelvis>Prostate. , The expression of HER2 was demonstrated and quantified in all three tested Malignant neoplasm of Pelvis>Prostate cell-lines., Such features would definitely favor the use of radiometal labels for trastuzumab and, most likely, for affibody molecules, our data demonstrate that Her2 plays an important role in the support of AR protein stability in the transition of androgen requirement in Malignant neoplasm of Pelvis>Prostate cells. We hope these findings will provide novel insight into the treatment of hormone-refractory Malignant neoplasm of Pelvis>Prostate., These two Cultured Cell Line exhibited distinct responses to Her2 activation (by Recombinant Heregulin treatment) on Her2 phosphorylation and Her2 inhibition (by tyrphostin tyrphostin AG825 or Herceptin treatments) on proliferation,  While Pelvis>Prostate Malignant Neoplasms that express high levels of HER-2-neu peptide vaccine-neu peptide vaccine are resistant to the killing effects of trastuzumab, they can be targeted for selective gene expression and destruction by Genus: Lentivirus group with envelope proteins engineered to bind to this therapeutic immunoglobulin complex location, Overexpression of EGFR gene-2 and EGFR has been associated with aggressive Disease and poor patient prognosis in a range of Homo sapiens Neoplasms types (e.g. Breast, Chest>Lung, Ovarian, Pelvis>Prostate, Various approaches have been developed to target the EGFR gene signalling pathways including Monoclonal Antibodies (trastuzumab/Herceptin, The data from these in vitro and in vivo studies supported advancement of Radiolabeled trastuzumab into two clinical studies, Specimen Source Codes - tumor targeting was evaluated in CASP14 gene bearing subcutaneous (s.c.) xenografts of colorectal, Pancreatic Hormones, Ovarian, and Pelvis>Prostate carcinomas., we found that although Pelvis>Prostate Malignant Neoplasms that express high levels of HER-2-neu peptide vaccine-neu peptide vaccine are resistant to the killing effects of trastuzumab, they can be targeted for selective gene expression and destruction by Virus with envelope proteins engineered to bind this immunoglobulin complex location, detection of Malignant neoplasm of Pelvis>Prostate (Patient-Controlled Analgesia) and advances in hormonal and chemotherapy treatments have provided great clinical benefits to patients with early stages of the Disease., MAbs directed to established targets include those approved for other Solid Neoplasm, including anti-Homo sapiens Epidermal Growth Factor Receptor-2 (HER2) MAb trastuzumab, We conclude that erbB-2 Receptor wt Allele expression in the peripheral blood mononuclear cell fraction of Malignant neoplasm of Pelvis>Prostate patients is frequent and therefore this assay may potentially be useful to detect the presence of micrometastatic Disease in men with Malignant neoplasm of Pelvis>Prostate and for monitoring patients enrolled in trastuzumab-based therapeutic protocols., This study suggests that the Docetaxel/trastuzumab combination may prove an effective therapeutic approach for HER2-expressing hormone-refractory Malignant neoplasm of Pelvis>Prostate., there was no significant difference in antimetastatic activity between the emulsion and the immunoemulsion despite the affinity of the immunoemulsion towards the HER2 receptor. , a targeted drug delivery system based on cationic emulsion covalently linked to anti-HER2 monoclonal immunoglobulin complex location (Herceptin), in a well-established in vivo pharmacologic model of metastatic Malignant neoplasm of Pelvis>Prostate that overexpresses the HER2 receptor, The finding of strong, consistent Oncogene ErbB2 expression in ACBCC suggests that treatment with Herceptin (trastuzumab) may be effective in patients with this rare Neoplasms., Although HER2 can be over-expressed in Malignant neoplasm of Pelvis>Prostate, there is no clinical data to support the use of trastuzumab for Malignant neoplasm of Pelvis>Prostate patients., whereas the effect of the trastuzumab-RT combination was inferior to that predicted by the individual effects., HER 1-2 targeting of hormone-refractory Malignant neoplasm of Pelvis>Prostate by ZD1839 and trastuzumab, trastuzumab (Herceptin) as a single agent demonstrated poor efficacy in treating Hormone refractory Malignant neoplasm of Pelvis>Prostate., To investigate the efficacy and Toxic effect of the immunoglobulin complex location to the Oncogene ErbB2 receptor (trastuzumab, Herceptin) in the treatment of advanced hormone-refractory Malignant neoplasm of Pelvis>Prostate (Hormone refractory Malignant neoplasm of Pelvis>Prostate), Conclusions regarding the predictive value of HER-2-neu peptide vaccine-neu peptide vaccine status on outcome after trastuzumab-based therapy were not reached and were only drawn after larger-scale screening efforts. , rastuzumab plus docetaxel in Oncogene ErbB2-positive Pelvis>Prostate carcinoma, clinical trials are currently in progress in patients with Malignant neoplasm of Pelvis>Prostate testing novel agents that selectively interfere with these receptors, such as trastuzumab,, ytotoxicity of Homo sapiens Malignant neoplasm of Pelvis>Prostate Cultured Cell Line in vitro and induction of apoptosis using 213Bi-Herceptin alpha-conjugate, The clinical interpretation of c-erbB-2 abnormalities should reflect the complexity of c-erbB-2 mediated regulatory pathway and explain why tumours with overexpression/amplification of c-erbB-2 very often do not respond to therapy using Herceptin, HER-2-neu peptide vaccine-neu peptide vaccine overexpression also has been reported in up to 60% of patients with hormone-refractory Pelvis>Prostate carcinoma (Hormone refractory Malignant neoplasm of Pelvis>Prostate) and was correlated with shortened survival, Unlike Breast carcinoma and contrary to prior reports, HER-2-neu peptide vaccine-neu peptide vaccine overexpression by IHC in archival Pelvis>Prostate tissue from patients who eventually developed hormone-refractory Disease was infrequent. There did not appear to be any correlation between HER-2-neu peptide vaccine-neu peptide vaccine overexpression by IHC and shed HER-2-neu peptide vaccine-neu peptide vaccine antigen levels in serum by ELISA in this tumor type., Further development of trastuzumab for the treatment of patients with metastatic Pelvis>Prostate carcinoma is not feasible until more reliable and practical methods of sampling metastatic Disease are developed to identify patients with HER-2-neu peptide vaccine-neu peptide vaccine positive tumors., the expression of erbB-2 Receptor in Malignant neoplasm of Pelvis>Prostate is relatively low, and is not altered during Disease progression. Thus, it is unlikely that treatment modalities relying on the overexpression of erbB-2 Receptor gene will be useful in treating Malignant neoplasm of Pelvis>Prostate., A phase I study was designed to evaluate Docetaxel-Estramustine Regimen plus trastuzumab, a humanized monoclonal immunoglobulin complex location that binds to the HER2 receptor, in patients with metastatic androgen-independent Malignant neoplasm of Pelvis>Prostate (2,2'-azobis(2-(2-imidazolin-2-yl) propane) dihydrochloride), Laboratory evidence also supports the clinical evaluation of docetaxel-based combinations that include agents such as trastuzumab and/or estramustine, trastuzumab, a monoclonal immunoglobulin complex location binding to the HER2 receptor; immunotoxin conjugates use an immunoglobulin complex location directed against EGFR joined to a cell toxin. All are in clinical trials for a number of Malignant Neoplasms, including Malignant neoplasm of Pelvis>Prostate, we investigated the Antitumor efficacy of Herceptin, a new recombinant humanized anti-HER2/neu immunoglobulin complex location, which exhibits cytostatic activity on Breast and Malignant neoplasm of Pelvis>Prostate cells that overexpress the HER2 oncogene., trastuzumab was found to have additive and synergistic effects with some chemotherapeutic agents, ER-2/neu as a therapeutic target in Non-Small Cell Lung Carcinoma, Malignant neoplasm of Pelvis>Prostate, in these Malignant neoplasm of Pelvis>Prostate model systems, Herceptin alone has clinical activity only in the androgen-dependent tumor and has at least an additive effect on growth,, anti-HER2 receptor monoclonal immunoglobulin complex location Herceptin significantly enhanced growth inhibition of the MDA Patient-Controlled Analgesia 2a cells.[SEP]Relations: trastuzumab has relations: drug_drug with Daclizumab, drug_drug with Daclizumab, drug_drug with Tepoxalin, drug_drug with Tepoxalin, drug_drug with Golimumab, drug_drug with Golimumab, drug_drug with Ascrinvacumab, drug_drug with Ascrinvacumab, drug_drug with Streptozocin, drug_drug with Streptozocin.", "label": "yes"}
{"original_question": "Is Brucella abortus the organism that causes brucillosis known to cause spontaneous abortions in humans?", "id": "converted_2721", "sentence1": "Is Brucella species abortus the organism that causes brucillosis known to cause spontaneous Abortions:Number:Point in time:^Patient:Quantitative:Reported in Homo sapiens?", "sentence2": ". Brucellosis is a major cause of Fever of unknown origin (Pyrexia of unknown origin (excl puerperal)), Brucellosis is the most common Bacterial Zoonoses, and causes a considerable burden of Disease in endemic countries. Cardiovascular involvement is the main cause of mortality due to Communicable Diseases with Brucella species species spp,, quite abruptly, he developed Asthenia and Hypersomnia without any apparent cause or symptoms like Fever symptoms (finding), Chills, or night Sweating. On November 14, 2009, he suffered from Pain:-:Point in time:^Patient:- and Edema:Finding:Point in time:^Patient:Ordinal in the right testicle that coincided with Pain:-:Point in time:^Patient:- in the Abdominal Cavity. Clinical, serological, and bacteriological investigations confirmed the first case of unilateral orchitis in man in Ecuador caused by Brucella species species abortus biovar 1, Brucellosis is not frequent in Chile but it may present with life threatening complications like Endocarditis., Human brucellosis exhibits diverse pathological manifestations that can affect almost any Organ. In particular, osteoarticular complications are the most common focal manifestation of brucellosis and occur in 40-80% of patients., Brucella species species. Human brucellosis often makes the diagnosis difficult. The symptoms and clinical signs most commonly reported are Fever symptoms (finding), Fatigue, Malaise, Chills, Sweating Headache, Myalgia, Arthralgia, and Measured Measured weight loss (observable entity) (observable entity). Some cases have been presented with only joint Pain:-:Point in time:^Patient:-, lower backache, and involuntary limb movement, burning feet, or ischemic heart attacks. , Forty-five cases were collected (31 acute and 14 sub-acute). Contamination was digestive in 62%. Symptoms of patients were Fever symptoms (finding) (93%), sweating (82%), Arthralgia (78%) and Splenomegaly (51%). Elevated Erythrocytes sedimentation rate was determined in 80%, White blood cell count decreased in 49% and Anemia in 37% of cases. Blood culture were positives in 39% of cases. The four sequenced strains were identified as Brucella species species melitensis biovar abortus. , It is also known to cause persistent undulant Fever symptoms (finding), Endocarditis, Arthritis, Osteomyelitis and Meningitis in Homo sapiens., Brucella species species abortus is a Gram-negative Protoplasm bacterial pathogen that causes a zoonosis of worldwide occurrence, leading to undulant Fever symptoms (finding) in Homo sapiens and Unspecified Abortion in domestic animals., Brucella species species abortus is a facultative Protoplasm bacterial pathogen that causes Unspecified Abortion in domestic animals and undulant Fever symptoms (finding) in Homo sapiens., Brucella species species abortus is a facultative, Protoplasm zoonotic pathogen which can cause undulant Fever symptoms (finding) in Homo sapiens and Abortions:Number:Point in time:^Patient:Quantitative:Reported in Bos taurus., Brucella species species abortus is a Gram-negative, facultative Protoplasm bacterium that causes brucellosis, a worldwide zoonotic Disease leading to undulant Fever symptoms (finding) in Homo sapiens and Unspecified Abortion in Bos taurus., Brucella species species abortus is a facultative Protoplasm bacterial pathogen that causes Unspecified Abortion in domestic animals and undulant Fever symptoms (finding) in Homo sapiens., Brucella species species abortus is a gram-negative, facultative Protoplasm pathogen that causes brucellosis, a chronic zoonotic Disease resulting in Unspecified Abortion in pregnant Bos taurus and undulant Fever symptoms (finding) in Homo sapiens., Brucella species species abortus is a bacterium which causes Abortions:Number:Point in time:^Patient:Quantitative:Reported and Sterility, Reproductive in Bos taurus and undulant Fever symptoms (finding) in Homo sapiens., Brucella species species abortus is the etiologic agent of bovine brucellosis and causes a Chronic Disease in Homo sapiens known as undulant Fever symptoms (finding)., No case of acute Brucella species species Communicable Diseases was demonstrated; however, there were 5 cases in which the serological finding was consistent with chronic brucellosis (4%). In all these cases no positive evidence of close Animal allergens contact could be found; furthermore of the 12,1% of women who actually handled domestic animals, only 1 had a history of previous Unspecified Abortion[SEP]Relations: brucellosis has relations: disease_phenotype_positive with Spontaneous Unspecified Abortion, disease_phenotype_positive with Spontaneous Unspecified Abortion, disease_disease with Brucella species brucellosis, disease_disease with Brucella species brucellosis, disease_disease with Brucella species melitensis brucellosis, disease_disease with Brucella species melitensis brucellosis, disease_disease with brucellosis, bovine, disease_disease with brucellosis, bovine. Brucella species melitensis brucellosis has relations: disease_disease with brucellosis, disease_disease with brucellosis.", "label": "no"}
{"original_question": "Is Rucaparib effective for ovarian cancer?", "id": "converted_2602", "sentence1": "Is rucaparib effective for ovarian cancer?", "sentence2": "INTERPRETATION: In patients with BRCA mutant or BRCA wild-type and Loss of Heterozygosity high Platinum-Sensitive Disease ovarian carcinomas treated with rucaparib, progression-free survival was longer than in patients with BRCA wild-type Loss of Heterozygosity low carcinomas., High Loss of Heterozygosity is associated with response to the PARP1 wt Allele PPP1R1A gene rucaparib in BRCA wild-type ovarian cancer., rucaparib Approved for Malignant neoplasm of ovary., The FDA approved the PARP1 wt Allele PPP1R1A gene rucaparib to treat women with advanced ovarian cancer who have already been treated with at least two chemotherapies and have a BRCA1 gene gene or BRCA2 gene mutation identified by an approved companion diagnostic test., rucaparib (Rubraca™) is an oral, small molecule, poly (ADP-ribose) polymerase PPP1R1A gene being developed by Clovis Oncology, Inc. (Boulder, AQP1 gene, USA) for the treatment of solid tumours. It has been approved in the USA as monotherapy for the treatment of patients with deleterious BRCA mutation (Germline and/or somatic) associated advanced ovarian cancer who have been treated with two or more chemotherapies. , In 2016, the US Food and Drug Administration approved three novel drugs for the treatment of solid malignancies-olaratumab in selected patients with soft-tissue sarcoma, atezolizumab for the treatment of Malignant neoplasm of urinary bladder, and rucaparib for the treatment of ovarian cancer; also in 2016, the use of previously approved anticancer agents (including atezolizumab) was expanded into 11 new patient populations. , Conclusions:rucaparib was tolerable and had activity in patients with Platinum-Sensitive Disease germlineBRCA1/2-mutated HGOC., <b>OBJECTIVE</b>: To review the pharmacology, safety, efficacy, and the role of rucaparib in the treatment of relapsed, advanced ovarian cancer.<br><b>SUMMARY</b>: A total of 2 phase I/II trials and 1 phase II trial have evaluated the safety and efficacy of oral rucaparib in ovarian cancer., rucaparib was found to be relatively well tolerated in clinical trials, with the most common adverse events being Genus Anemia, Fatigue, and nausea.<br><b>CONCLUSION</b>: rucaparib appears to be a safe and effective new option in the treatment of relapsed, advanced BRCA1 gene gene/2 mutant ovarian cancer., In patients with deleterious BRCA1 gene gene/2 mutation, an overall response rate of 80% was achieved in the phase II trial Assessment of rucaparib in Ovarian CancEr Trial 2 (ARIEL2)., This article summarizes the milestones in the development of rucaparib leading to this first approval for ovarian cancer.<br>, These results support further clinical evaluation of rucaparib either as a single agent or as an adjunct to chemotherapy for the treatment of sporadic ovarian cancer.<br>, rucaparib: a Poly(ADP-Ribose) Polymerase Inhibitor for BRCA-Mutated Relapsed Malignant neoplasm of ovary., CONCLUSION rucaparib appears to be a safe and effective new option in the treatment of relapsed, advanced BRCA1 gene gene/2 mutant ovarian cancer., These results support further clinical evaluation of rucaparib either as a single agent or as an adjunct to chemotherapy for the treatment of sporadic ovarian cancer., rucaparib received US FDA Breakthrough Therapy designation for treatment of Platinum-Sensitive Disease BRCA-mutated advanced ovarian cancer patients who received greater than two lines of platinum-based therapy., BACKGROUND rucaparib, a poly(ADP-ribose) polymerase PPP1R1A gene, has anticancer activity in recurrent ovarian carcinoma harbouring a BRCA mutation or high percentage of genome-wide loss of heterozygosity., rucaparib appears to be a safe and effective new option in the treatment of relapsed, advanced BRCA1 gene gene/2 mutant ovarian cancer., rucaparib: A Poly(ADP-Ribose) Polymerase Inhibitor for BRCA-Mutated Relapsed Malignant neoplasm of ovary., rucaparib: the past, present, and future of a newly approved PARP1 wt Allele PPP1R1A gene for ovarian cancer., FDA Approval Summary: rucaparib for the Treatment of Patients with Deleterious BRCA Mutation-Associated Advanced Malignant neoplasm of ovary., olaparib and rucaparib have been approved by the US FDA as monotherapy for advanced recurrent ovarian cancer.[SEP]Relations: rucaparib has relations: drug_drug with Lobucavir, drug_drug with Lobucavir, drug_drug with Estradiol, drug_drug with Estradiol, drug_drug with Capsaicin, drug_drug with Capsaicin, drug_drug with olaparib, drug_drug with olaparib, drug_drug with Lopinavir, drug_drug with Lopinavir.", "label": "yes"}
{"original_question": "Does a tonsillectomy affect the patient's voice?", "id": "converted_2286", "sentence1": "Does a tonsillectomy affect the patient's TelecommunicationCapabilities <voice>?", "sentence2": " Group B had a better awareness of tooth damage (78% vs 30% of patients, P ≤ .001), TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> change (61 vs 19%, P = .005), and Burn injury to Lip structure and mouth (44% vs 8%, P = .005). Finally, 35% more patients from group B rated their understanding of tonsillectomy as good or very good (P = .017).,  Some patients complaint for Pharyngeal dryness, foreign body sensation or TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> change after tonsillectomy., The percentage of patients who had temporary TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> change was 62.7%, and 15.4% had a follow-up clinic visit., There is no dose-escalation response to dexamethasone (0.0625-1.0 mg/kg) in pediatric tonsillectomy or adenotonsillectomy patients for preventing Vomiting, reducing Pain:-:Point in time:^Patient:-, shortening time to first liquid intake, or the incidence of TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> change., There were no differences in secondary outcomes (analgesic requirements, time to first liquid, and change in TelecommunicationCapabilities <TelecommunicationCapabilities <voice>>) across treatment groups., Voice change, reported by approximately 70% of all patients, was the most common complaint, but it resolved in all instances., The incidence rates of TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> change, Velopharyngeal Insufficiency, Hemorrhage, Constipation, Dehydration, and Pain:-:Point in time:^Patient:- were measured. , Tonsillectomy affects TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> performance negatively in adults in short term; however, it does not affect TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> performance in long term after surgery., The surgical technique, whether it is cold knife or thermal welding system, does not appear to affect TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> and speech in tonsillectomy patients., OBJECTIVE: To evaluate changes in acoustic features of TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> after tonsillectomy., Surgical indications for tonsillectomy in the young TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> patient are discussed., OBJECTIVE: Our goal was to assess patient perception and acoustic characteristics of TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> before and after upper airway surgery., In this report, we examined the change in pharyngeal size and acoustic feature of TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> after tonsillectomy., CONCLUSION Tonsillectomy affects TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> performance negatively in adults in short term; however, it does not affect TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> performance in long term after surgery., Some patients complaint for Pharyngeal dryness, foreign body sensation or TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> change after tonsillectomy., Tonsillectomy affects TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> performance negatively in adults in short term; however, it does not affect TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> performance in long term after surgery.., The surgical technique, whether it is cold knife or thermal welding system, does not appear to affect TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> and speech in tonsillectomy patients.., There is no dose-escalation response to dexamethasone (0.0625-1.0 mg/kg) in pediatric tonsillectomy or adenotonsillectomy patients for preventing Vomiting, reducing Pain:-:Point in time:^Patient:-, shortening time to first liquid intake, or the incidence of TelecommunicationCapabilities <TelecommunicationCapabilities <voice>> change.[SEP]Relations: Dexamethasone has relations: drug_effect with Vertebral compression fractures, drug_effect with Vertebral compression fractures, drug_effect with Reduced visual acuity, drug_effect with Reduced visual acuity, drug_effect with Increased intracranial pressure, drug_effect with Increased intracranial pressure. Velopharyngeal insufficiency has relations: disease_phenotype_positive with Dubowitz syndrome, disease_phenotype_positive with Dubowitz syndrome, disease_phenotype_positive with cleft palate, disease_phenotype_positive with cleft palate.", "label": "yes"}
{"original_question": "Has ZP-PTH been tested in a phase II clinical trial?", "id": "converted_3387", "sentence1": "Has ZP-PTH been tested in a phase II clinical trial?", "sentence2": "This system was successfully tested in a Phase 2 clinical trial for the treatment of post-menopausal women with Encounter due to family history of Encounter due to family history of osteoporosis.[SEP]Relations: stenosis or atrophy of the coronary ostium has relations: disease_disease with abnormal origin or aberrant course of coronary artery, disease_disease with abnormal origin or aberrant course of coronary artery.", "label": "yes"}
{"original_question": "Are thyroid hormone receptor alpha1 mutations  implicated in thyroid hormone resistance syndrome?", "id": "converted_1105", "sentence1": "Are Thyroid Hormones receptor alpha1 mutations  implicated in Thyroid Hormones resistance syndrome?", "sentence2": "Gene Mutation in Homo sapiens TRα1 mediate RTH with features of Hypothyroidism in particular Body tissue (e.g. skeleton, Multisection:Find:Pt:Abdomen+Pelvis>Gastrointestinal tract:Doc:US), but are not associated with a markedly dysregulated pituitary-thyroid axis., Clinical phenotype of a new type of Thyroid Hormones resistance caused by a Mutation Abnormality of the receptor[SEP]Relations: response to Thyroid Hormones has relations: bioprocess_protein with AKR1B1, bioprocess_protein with AKR1B1, bioprocess_protein with SLC34A1, bioprocess_protein with SLC34A1. Hypothyroidism has relations: disease_phenotype_positive with isolated thyroid-stimulating hormone deficiency, disease_phenotype_positive with isolated thyroid-stimulating hormone deficiency, disease_phenotype_positive with resistance to thyrotropin-releasing hormone syndrome, disease_phenotype_positive with resistance to thyrotropin-releasing hormone syndrome, disease_phenotype_positive with Hypothyroidism due to TSH receptor mutations, disease_phenotype_positive with Hypothyroidism due to TSH receptor mutations.", "label": "yes"}
{"original_question": "Is Fanconi anemia presented as a genetically and clinically heterogeneous disease entity?", "id": "converted_1274", "sentence1": "Is Fanconi Genus Anemia presented as a genetically and clinically heterogeneous Disease entity?", "sentence2": "Fanconi Anemia (doxorubicin/fluorouracil protocol) is a rare, Autosomal recessive inheritance, genetically complex, DNA repair deficiency syndrome in man. Patients with doxorubicin/fluorouracil protocol exhibit a heterogeneous spectrum of clinical features. The most significant and consistent phenotypic characteristics are stem cell loss, causing progressive Bone marrow hypocellularity and sterility, diverse developmental abnormalities and a profound predisposition to Neoplasms. To date, 15 Genes have been identified, biallelic disruption of any one of which results in this clinically defined syndrome, Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) is a clinically and genetically heterogeneous disorder, Significant phenotypic differences were found. doxorubicin/fluorouracil protocol-G patients had more severe Cytopenia and a higher incidence of leukemia. Somatic abnormalities were less prevalent in doxorubicin/fluorouracil protocol-C, but more common in the rare groups doxorubicin/fluorouracil protocol-D, doxorubicin/fluorouracil protocol-E, and doxorubicin/fluorouracil protocol-F. In doxorubicin/fluorouracil protocol-A, patients homozygous for null Gene Mutation had an earlier onset of Genus Anemia and a higher incidence of leukemia than those with Gene Mutation producing an altered protein, Fanconi Genus Anemia (doxorubicin/fluorouracil protocol), an Autosomal Recessive Disorder characterized by a progressive Pancytopenia associated with congenital anomalies and high predisposition to Malignant Neoplasms, is a genetically and clinically heterogeneous Disease. At least eight complementation groups (doxorubicin/fluorouracil protocol-A to doxorubicin/fluorouracil protocol-H) have been identified, Fanconi Genus Anemia (doxorubicin/fluorouracil protocol), an Autosomal Recessive Disorder characterized by a progressive Pancytopenia associated with congenital anomalies and high predisposition to Malignant Neoplasms, is a genetically and clinically heterogeneous Disease. At least eight complementation groups (doxorubicin/fluorouracil protocol-A to doxorubicin/fluorouracil protocol-H) have been identified with their relative prevalence varying among the ethnical backgrounds, Fanconi Genus Anemia is a rare Autosomal Recessive Disorder characterized clinically by congenital abnormalities, progressive Bone marrow hypocellularity, and a predisposition to malignancy. doxorubicin/fluorouracil protocol cells are sensitive to DNA cross-linking agents. Complementation analysis of doxorubicin/fluorouracil protocol cells using somatic cell fusion has facilitated the identification of eight complementation groups, suggesting that doxorubicin/fluorouracil protocol is a genetically heterogeneous disorder. Six Genes (FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), FANCONI ANEMIA, COMPLEMENTATION GROUP C, FANCONI ANEMIA, COMPLEMENTATION GROUP D2, FANCONI ANEMIA, COMPLEMENTATION GROUP E, FANGF, fanconi Genus Anemia complementation group g) have been cloned so far, Fanconi Genus Anemia (doxorubicin/fluorouracil protocol), an Autosomal Recessive Disorder characterized by a progressive Pancytopenia associated with congenital anomalies and high predisposition to Malignant Neoplasms, is a genetically and clinically heterogeneous Disease., Fanconi Genus Anemia (doxorubicin/fluorouracil protocol), an Autosomal Recessive Disorder characterized by a progressive Pancytopenia associated with congenital anomalies and high predisposition to Malignant Neoplasms, is a genetically and clinically heterogeneous Disease., Among patients with Bone marrow hypocellularity (BMF) syndrome, some are happened to have underlying Fanconi Genus Anemia (doxorubicin/fluorouracil protocol), a genetically heterogeneous Disease, which is characterized by progressive Pancytopenia and Primary malignant neoplasm susceptibility., Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) is a genetically and phenotypically heterogeneous inherited Disease., Fanconi Genus Anemia is a genetically heterogeneous recessive Disease characterized mainly by Bone marrow hypocellularity and Primary malignant neoplasm predisposition., INTRODUCTION: Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) is a genetically and phenotypically heterogeneous inherited Disease., Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) is a genetically heterogeneous, Autosomal Recessive Disorder characterized by pediatric Bone marrow hypocellularity and congenital anomalies., Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) is a heterogeneous Disease associated with a Bone marrow hypocellularity, Primary malignant neoplasm predisposition and Emotional Emotional hypersensitivity to DNA crosslinking agents., Fanconi Genus Anemia is a genetically heterogeneous chromosomal instability syndrome, characterized by multiple congenital anomalies, progressive Bone marrow hypocellularity, and a predisposition to malignancy., Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) is a heterogeneous Disease characterized by spontaneous chromosomal breaks and abnormal DNA repair., Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) is a genetically heterogeneous Disease with at least eight Genes on the basis of complementation groups (FAA to FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) wt Allele)., Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) is a clinically and genetically heterogeneous disorder., Fanconi Anemia (doxorubicin/fluorouracil protocol) is a genetically heterogeneous Disease with at least eight complementation groups (A-H)., doxorubicin/fluorouracil protocol is a genetically heterogeneous Disease with at least seven Genes so far identified., Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) is an Autosomal recessive inheritance rare Disease characterized by progressive Pancytopenia, Congenital Abnormality and predisposition to Leukemia, Myelocytic, Acute., Fanconi Genus Anemia is genetically heterogeneous, with at least eight complementation groups of doxorubicin/fluorouracil protocol (FAA to FAD2)., Fanconi Genus Anemia (doxorubicin/fluorouracil protocol), an Autosomal Recessive Disorder characterized by a progressive Pancytopenia associated with congenital anomalies and high predisposition to Malignant Neoplasms, is a genetically and clinically heterogeneous Disease, Fanconi Genus Anemia (doxorubicin/fluorouracil protocol), an Autosomal Recessive Disorder characterized by a progressive Pancytopenia associated with congenital anomalies and high predisposition to Malignant Neoplasms, is a genetically and clinically heterogeneous Disease, The Disease is clinically heterogeneous; eight different complementation groups (doxorubicin/fluorouracil protocol A-H) and, thus, Genetic Loci have been discovered, The hereditary genetic disorder Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) belongs to the heterogeneous group of diseases associated with defective DNA damage repair, The clinical manifestations of doxorubicin/fluorouracil protocol are heterogeneous, but one common outcome in the majority of patients is the development of life-threatening hematologic Disease, Fanconi Genus Anemia is a genetically heterogeneous chromosomal breakage disorder exhibiting a high degree of clinical variability, Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) is a genetically heterogeneous chromosomal instability syndrome associated with multiple congenital abnormalities, aplastic Genus Anemia, and Primary malignant neoplasm, Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) is a genetically heterogeneous Autosomal recessive inheritance syndrome associated with chromosomal instability, Emotional Emotional hypersensitivity to DNA cross-linking agents, and predisposition to malignancy, Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) is a rare Autosomal recessive inheritance Disease characterized by progressive Pancytopenia, Congenital Abnormality, and predisposition to Leukemia, Myelocytic, Acute, Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) is a heterogeneous Disease characterized by spontaneous chromosomal breaks and abnormal DNA repair, Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) is a genetically and phenotypically heterogeneous recessive disorder characterized by diverse Congenital Abnormality, progressive Pancytopenia and predisposition to both Hematologic Neoplasms and Solid Neoplasm, Fanconi Genus Anemia is a genetically heterogeneous chromosomal instability syndrome, characterized by multiple congenital anomalies, progressive Bone marrow hypocellularity, and a predisposition to malignancy[SEP]Relations: Fanconi Genus Anemia has relations: disease_disease with congenital Genus Anemia, disease_disease with congenital Genus Anemia, disease_disease with genetic skin Disease, disease_disease with genetic skin Disease. Fanconi Genus Anemia complementation group has relations: disease_disease with Fanconi Genus Anemia, disease_disease with Fanconi Genus Anemia, disease_disease with Fanconi Genus Anemia, disease_disease with Fanconi Genus Anemia, disease_disease with Fanconi Genus Anemia, disease_disease with Fanconi Genus Anemia.", "label": "yes"}
{"original_question": "Is pazopanib an effective treatment of glioblastoma?", "id": "converted_2868", "sentence1": "Is pazopanib an effective treatment of glioblastoma?", "sentence2": "RESULTS: The six-month progression-free survival (PFS) rates in phase II (n = 41) were 0% and 15% in the PTEN/EGFRvIII-positive and PTEN/EGFRvIII-negative cohorts, respectively, leading to early termination. , Single-agent pazopanib did not prolong PFS in this patient population but showed in situ biological activity as demonstrated by radiographic responses.[SEP]", "label": "no"}
{"original_question": "Are long non coding RNAs as conserved in sequence as protein coding genes?", "id": "converted_63", "sentence1": "Are long non coding RNAs as conserved in sequence as protein coding genes?", "sentence2": "Most lncRNAs are under lower sequence constraints than protein-coding genes and lack conserved secondary structures, making it hard to predict them computationally., hey are under stronger selective pressure than neutrally evolving sequences-particularly in their Promoter Regions, Genetic, which display levels of selection comparable to protein-coding genes., bout one-third seem to have arisen within the primate lineage.[SEP]Relations: GLI proteins bind promoters of Hh responsive genes to promote transcription has relations: pathway_protein with GLI2, pathway_protein with GLI2, pathway_protein with GLI1, pathway_protein with GLI1, pathway_protein with GLI3, pathway_protein with GLI3.", "label": "no"}
{"original_question": "Is there any association of the chromosomal region harboring the gene ITIH3 with schizophrenia?", "id": "converted_1223", "sentence1": "Is there any association of the chromosomal region harboring the gene ITIH3 gene with SCHIZOPHRENIA 2 (disorder)?", "sentence2": "The most widely shared subset of genes-common to five of six disorders-included ANK3 gene gene, AS3MT gene gene, CACNA1C gene gene, CACNB2 gene gene, CNNM2 gene gene, CSMD1 protein, human protein, human, MUCL3 gene, ITIH3 gene gene, NT5C2 gene gene, PPP1R11 gene gene, SYNE1 gene gene, TCF7L2 protein, human, TENM4 gene gene, TRIM26 gene gene, and POLR1H gene. , Genome-wide significant associations in SCHIZOPHRENIA 2 (disorder) to ITIH3 gene gene/4, CACNA1C gene gene and SDCCAG8 gene gene, and extensive replication of associations reported by the Schizophrenia PGC gene gene., After combining the new SCHIZOPHRENIA 2 (disorder) data with those of the PGC gene gene, Variant at three loci (ITIH3 gene gene/4, CACNA1C gene gene and SDCCAG8 gene gene) that had not previously been GWS in SCHIZOPHRENIA 2 (disorder) attained that level of support., In a joint analysis with a Bipolar Disorder Type 2 sample (16,374 affected individuals and 14,044 controls), three loci reached genome-wide significance: CACNA1C gene gene (rs4765905, P = 7.0 × 10(-9)), ANK3 gene gene (rs10994359, P = 2.5 × 10(-8)) and the ITIH3 gene gene-ITIH4 region (rs2239547, P = 7.8 × 10(-9))., Finally, a combined GWAS analysis of SCHIZOPHRENIA 2 (disorder) and Bipolar Disorder Type 2 yielded strong association evidence for SNPs in CACNA1C gene gene and in the region of NEK4-ITIH1-ITIH3 gene gene-ITIH4. , A recent genome-wide analysis indicated that a Genetic Polymorphism (rs2535629) of ITIH3 gene gene showed the strongest association signal with susceptibility to psychiatric disorders in Caucasian populations., We detected a novel association between suicide attempt and the ITIH3 gene gene/4-region in a combined group of patients with Behcet Syndrome, SCZ and related psychosis spectrum disorders. , These include variations in Chromosome Structures at 16p11.2, rare de novo point mutations at the SCN2A gene, and common Single Nucleotide Polymorphism (SNPs) mapping near loci encoding the genes ITIH3 gene gene, AS3MT gene gene, CACNA1C gene gene and CACNB2 gene gene. These selected examples point to the challenges to current diagnostic approaches. , Stabilin-1 is located in close proximity to PBMR1 and the NEK4-ITIH1-ITIH3 gene gene-ITIH4 region, which are the top findings from GWAS meta-analyses of Mood Disorders, and a combined Behcet Syndrome and SCHIZOPHRENIA 2 (disorder) data set., Our findings suggest that rs2535629 influences the susceptibility to psychiatric disorders by affecting the expression level of GLT8D1 gene gene.[SEP]Relations: Bipolar Disorder Type 2 has relations: disease_protein with ITIH3 gene, disease_protein with ITIH3 gene, disease_protein with ITIH4, disease_protein with ITIH4. SDCCAG8 gene has relations: disease_protein with SCHIZOPHRENIA 2 (disorder), disease_protein with SCHIZOPHRENIA 2 (disorder). CACNA1C gene has relations: disease_protein with SCHIZOPHRENIA 2 (disorder), disease_protein with SCHIZOPHRENIA 2 (disorder). TENM4 gene has relations: disease_protein with SCHIZOPHRENIA 2 (disorder), disease_protein with SCHIZOPHRENIA 2 (disorder).", "label": "yes"}
{"original_question": "Is there a role for TET proteins in invariant natural killer T cells (iNKT) cell fate?", "id": "converted_3670", "sentence1": "Is there a role for TET proteins in invariant natural killer T cells (iNKT) cell fate?", "sentence2": "TET proteins regulate the lineage specification and transcription-coupled nucleotide-excision repair-mediated expansion of Invariant Natural Killer T-Cells., We found that simultaneous Gene Deletion Abnormality of Probable Methylcytosine Dioxygenase TET2 and Methylcytosine Dioxygenase TET3 in Mus sp. CD4+CD8+ double-positive thymocytes resulted in dysregulated development and proliferation of invariant natural killer T cells (Invariant Natural Killer T-Cells). Probable Methylcytosine Dioxygenase TET2-Methylcytosine Dioxygenase TET3 double-knockout (DKO) Invariant Natural Killer T-Cells displayed pronounced skewing toward the NKT17 lineage, with increased DNA methylation and impaired expression of Genes encoding the key lineage-specifying factors TBX21 wt Allele and ZBTB7B wt Allele. Transfer of purified Probable Methylcytosine Dioxygenase TET2-Methylcytosine Dioxygenase TET3 DKO Invariant Natural Killer T-Cells into immunocompetent recipient CASP14 gene resulted in an uncontrolled expansion that was dependent on the nonclassical major histocompatibility complex (MHC) protein CD1D protein, human, which presents lipid antigens to Invariant Natural Killer T-Cells. Our data indicate that TET proteins regulate iNKT cell fate by ensuring their proper development and maturation and by suppressing aberrant proliferation mediated by the T-Cell Receptor (transcription-coupled nucleotide-excision repair)., TET proteins regulate the lineage specification and transcription-coupled nucleotide-excision repair-mediated expansion of Invariant Natural Killer T-Cells .[SEP]Relations: T cell receptor complex has relations: cellcomp_protein with TRAT1, cellcomp_protein with TRAT1, cellcomp_protein with SYK, cellcomp_protein with SYK, cellcomp_protein with TRGJ2, cellcomp_protein with TRGJ2, cellcomp_protein with TRGV11, cellcomp_protein with TRGV11, cellcomp_protein with TRGC1, cellcomp_protein with TRGC1.", "label": "yes"}
{"original_question": "Does replication timing affect the rate of somatic mutations?", "id": "converted_888", "sentence1": "Does replication timing affect the rate of somatic Gene Mutation?", "sentence2": "Here we observe that Mutation Abnormality rate, as reflected in recent evolutionary divergence and human nucleotide diversity, is markedly increased in later-replicating regions of the human Genome - anatomical entity, ll classes of substitutions are affected, suggesting a generalized mechanism involving replication time-dependent DNA damage, We show that Mutation Abnormality rate varies 6-fold across a single chromosome, that this variation is correlated with replication timing, and we propose a model to explain this variation that relies on the temporal separation of two processes for replicating past damaged DNA: error-free DNA damage tolerance and translesion synthesis., Recent studies revealed a long suspected replication-timing effect on Mutation Abnormality rate, but the mechanisms that regulate the increase in Mutation Abnormality rate as the Genome - anatomical entity is replicated remain unclear. , DNA repair systems, in general, are less efficient in late replicating heterochromatic regions compared to early replicating euchromatic regions of the Genome - anatomical entity., The mutational profile of the Saccharomyces cerevisiae Genome - anatomical entity is shaped by replication, the Mutation Abnormality rate increases with the replication timing by more than 30% between the earliest and the latest replicating regions., Thus, we show that the leading replicating strands present an excess of C over G and of A over T in the Genome - anatomical entity of S. cerevisiae (reciprocally an excess of G + T over C + A in lagging strands), Late-replicating domains have higher divergence and diversity in Drosophila melanogaster, Recent evidence also suggests that late replication is associated with high mutability in Saccharomyces cerevisiae., Limited evidence from one Arm of chromosome in Drosophila melanogaster suggests the opposite pattern, with regions overlapping early-firing origins showing increased levels of diversity and divergence, The Mutation Abnormality rate for DNA mismatch repair null strains was approximately 1 Mutation Abnormality per Genome - anatomical entity per generation, 225-fold greater than the wild-type rate. The Gene Mutation were distributed randomly throughout the Genome - anatomical entity, independent of replication timing., Many single-nucleotide substitutions in Primary malignant neoplasm genomes arise because of errors in DNA replication, which is spatio-temporally stratified., Here we propose that DNA replication patterns help shape the mutational landscapes of normal and Primary malignant neoplasm genomes, Using data on five fully sequenced Primary malignant neoplasm types and two personal genomes, we determined that the frequency of intergenic single-nucleotide substitution is significantly higher in late DNA replication timing regions, even after controlling for a number of genomic features, we found that genomic regions in close spatial proximity to late-replicating domains display similar Mutation Abnormality spectra as the late-replicating regions themselves, In addition, certain chromosome rearrangements found in Primary malignant neoplasm Cells and in Cells exposed to ionizing radiation display a significant delay in replication timing of >3 hours that affects the entire chromosome(2,3). Recent work from our lab indicates that disruption of discrete cis-acting autosomal loci result in an extremely late replicating phenotype that affects the entire chromosome(4)., A conservative estimate is that at least 1-2% of new deleterious Gene Mutation affect some aspect of DNA replication, repair, or chromosome segregation. Since deleterious Gene Mutation can have an effect even as heterozygotes, this Mutation Abnormality accumulation can create an inherited background of late-acting Gene Mutation that themselves enhance Mutation Abnormality rate., Drake calculates that lytic RNA Viruses display spontaneous Mutation Abnormality rates of approximately one per Genome - anatomical entity while most have Mutation Abnormality rates that are approximately 0.1 per Genome - anatomical entity (Drake 1993). This constancy of germline Mutation Abnormality rates among microbial species need not necessarily mean constancy of the somatic Mutation Abnormality rates., A recent flurry of reports correlates replication timing (RT) with Mutation Abnormality rates during both evolution and Primary malignant neoplasm., DNA replication timing, Genome - anatomical entity stability and Primary malignant neoplasm: late and/or delayed DNA replication timing is associated with increased genomic instability., Since deleterious Gene Mutation can have an effect even as heterozygotes, this Mutation Abnormality accumulation can create an inherited background of late-acting Gene Mutation that themselves enhance Mutation Abnormality rate., In addition, this method allows for the unambiguous identification of chromosomal rearrangements that correlate with changes in replication timing that affect the entire chromosome.[SEP]Relations: adaptation to pheromone regulating conjugation with mutual genetic exchange has relations: bioprocess_bioprocess with response to pheromone regulating conjugation with mutual genetic exchange, bioprocess_bioprocess with response to pheromone regulating conjugation with mutual genetic exchange, bioprocess_bioprocess with negative adaptation of signaling pathway, bioprocess_bioprocess with negative adaptation of signaling pathway. partial monosomy of the short arm of chromosome X has relations: disease_disease with atypical Norrie disease due to monosomy Xp11.3, disease_disease with atypical Norrie disease due to monosomy Xp11.3. Lacrimation abnormality has relations: disease_phenotype_positive with limbal stem cell deficiency, disease_phenotype_positive with limbal stem cell deficiency, disease_phenotype_positive with Waardenburg syndrome, disease_phenotype_positive with Waardenburg syndrome.", "label": "yes"}
{"original_question": "Is g-H2AX a marker for double strand breaks?", "id": "converted_3610", "sentence1": "Is g-H2AX a marker for double strand breaks?", "sentence2": "The specific phosphorylation of histone H2AX on serine residue 139, described as γ-H2AX, is an excellent indicator or marker of DNA double-strand breaks (DSBs). , expression of the DNA double-strand break marker gamma-H2AX (γH2AX) , pH2AX, a marker of the DNA double-strand break (DSB)[SEP]Relations: Serine has relations: drug_protein with SPTLC2, drug_protein with SPTLC2, drug_protein with SPTLC1, drug_protein with SPTLC1, drug_protein with SLC16A10, drug_protein with SLC16A10, drug_protein with AGXT, drug_protein with AGXT, contraindication with phosphorus metabolism disease, contraindication with phosphorus metabolism disease.", "label": "yes"}
{"original_question": "Is intraoperative radiotherapy used for treatment of glioblastoma?", "id": "converted_2166", "sentence1": "Is intraoperative radiotherapy used for treatment of glioblastoma?", "sentence2": " 1) Intraoperative radiotherapy ( indolepyruvate ferredoxin oxidoreductase activity , 1,000-2,000 rad) was applied in 13 cases; the 2-year survival was 41.6%. , The median survival time after IORT was 12 months for 9 patients with glioblastoma or Anaplastic astrocytoma, while it was 51 months for 8 patients with less infiltrative tumors (Ependymoma, anaplastic Ependymoma, and Anaplastic Oligodendroglioma). , It is concluded that IORT combined with extensive tumor removal has an acceptable Toxic effect in previously irradiated patients and can be effective for selected recurrent Malignant neoplasm of brain., CONCLUSIONS: The results of this study indicate that IORT can contribute to successful tumor treatment while neither increasing peri-operative morbidity nor subacute sequelae., This review compiles preclinical and clinical evidence for a dedicated treatment of both residual Tumor cells, malignant and regional microenvironment using intraoperative radiotherapy (IORT).,  Intraoperative radiotherapy (IORT) is a pragmatic and effective approach to sterilize the margins from persistent tumor cells, abrogate post-injury proliferative stimuli and to bridge the therapeutic gap between surgery and radiochemotherapy. , [Surgical treatment and radiation therapy for Glioblastoma Multiforme, with special reference to intraoperative radiotherapy]., Rationale for intraoperative radiotherapy in glioblastoma., Intraoperative radiotherapy (IORT) was performed in 20 of 36 patients with Glioma; 11 Glioblastoma, 7 malignant astrocytomas, 2 benign astrocytomas., [Surgical treatment and radiation therapy for Glioblastoma Multiforme, with special reference to intraoperative radiotherapy], INTRAGO: intraoperative radiotherapy in Glioblastoma Multiforme—a phase I/II dose escalation study, Intraoperative cobalt-60 treatment of Glioblastoma Multiforme, An intraoperative remote afterloading endocurietherapy (Electroconvulsive Therapy) technique with high-activity 60cobalt (60Co) for the treatment of Glioblastoma Multiforme (Congenital glucose-galactose malabsorption) is described, [Surgical treatment and radiation therapy for Glioblastoma Multiforme, with special reference to intraoperative radiotherapy]., Rationale for intraoperative radiotherapy in glioblastoma., Intraoperative cobalt-60 treatment of Glioblastoma Multiforme., INTRAGO: intraoperative radiotherapy in Glioblastoma Multiforme—a phase I/II dose escalation study., Intraoperative remote afterloading endocurietherapy with high-activity 60cobalt for treatment of Glioblastoma Multiforme., Combining intraoperative carmustine wafers and Stupp regimen in multimodal first-line treatment of primary Glioblastoma., The intraoperative use of carmustine wafers in combination with Stupp regimen is a viable first-line treatment option of Glioblastoma., An intraoperative remote afterloading endocurietherapy (Electroconvulsive Therapy) technique with high-activity 60cobalt (60Co) for the treatment of Glioblastoma Multiforme (Congenital glucose-galactose malabsorption) is described., The study investigated if intraoperative use of carmustine wafers, particularly in combination with Stupp regimen, is a viable and safe first-line treatment option of Glioblastoma.[SEP]Relations: adult glioblastoma has relations: disease_disease with glioblastoma (disease), disease_disease with glioblastoma (disease), disease_disease with glioblastoma (disease), disease_disease with glioblastoma (disease), disease_disease with adult infiltrating astrocytic neoplasm, disease_disease with adult infiltrating astrocytic neoplasm, disease_disease with adult infiltrating astrocytic neoplasm, disease_disease with adult infiltrating astrocytic neoplasm. Anaplastic Oligodendroglioma has relations: disease_disease with grade III Glioma, disease_disease with grade III Glioma.", "label": "no"}
{"original_question": "Can sorafenib activate AMPK?", "id": "converted_328", "sentence1": "Can sorafenib activate AMP-Activated Protein Kinases?", "sentence2": "Here, we identify sorafenib as an activator of AMP-activated protein kinase (AMP-Activated Protein Kinases), in a manner that involves either upstream LKB1 or CAMKK2 gene gene. , Persistent activation of AMP-Activated Protein Kinases by sorafenib finally led to the impairment of glucose metabolism both in MCF-7 and SKBR3 Cells as well as in the highly glycolytic MDA-MB-231 Cells, resulting in cell death., Here, we identify sorafenib as an activator of AMP-activated protein kinase (AMP-Activated Protein Kinases), in a manner that involves either upstream LKB1 or CAMKK2 gene gene, sorafenib synergizes with metformin in Non-Small Cell Lung Carcinoma through AMP-Activated Protein Kinases pathway activation., Persistent activation of AMP-Activated Protein Kinases by sorafenib finally led to the impairment of glucose metabolism both in MCF-7 and SKBR3 Cells as well as in the highly glycolytic MDA-MB-231 Cells, resulting in cell death. This previously unrecognized long-term effect of sorafenib was mediated by AMP-Activated Protein Kinases-dependent inhibition of the mechanistic target of rapamycin complex 1 pathway.[SEP]Relations: sorafenib has relations: drug_drug with Ampicillin, drug_drug with Ampicillin, drug_drug with Amprenavir, drug_drug with Amprenavir, drug_drug with Amphetamine, drug_drug with Amphetamine, drug_drug with Canakinumab, drug_drug with Canakinumab, drug_drug with Siponimod, drug_drug with Siponimod.", "label": "yes"}
{"original_question": "Are there interactomes available for POU5F1 and SOX2?", "id": "converted_1226", "sentence1": "Are there interactomes available for POU5F1 protein, human and SOX2 protein, human?", "sentence2": "The interactomes of POU5F1 protein, human protein, human and SOX2 protein, human protein, human enhancers in human embryonic stem cells., We assayed long-range chromosomal interactions on putative enhancers of POU5F1 protein, human protein, human and SOX2 protein, human protein, human Genes in human embryonic stem cells (Human Embryonic Stem Cells) using 4C-Seq technique. We discovered that their frequent interacting regions mainly overlap with early DNA replication domains. The interactomes are associated with active histone marks and enriched with 5-hydroxymethylcytosine sites. In Human Embryonic Stem Cells, Genes within the interactomes have elevated expression. Additionally, some Genes associated with the POU5F1 protein, human protein, human enhancer contribute to pluripotency. Binding Sites for multiple DNA binding proteins, including Cyclic AMP-Dependent Transcription Factor ATF-3, CTGF protein, human, GABPA gene gene, JUND wt Allele wt Allele, NANOG gene gene, Double-Strand-Break Repair Protein Rad21 Homolog and YY1 gene gene, are enriched in both interactomes.[SEP]Relations: NANOG gene has relations: protein_protein with SOX2 protein, human, protein_protein with SOX2 protein, human, protein_protein with POU5F1 protein, human, protein_protein with POU5F1 protein, human, pathway_protein with POU5F1 protein, human (OCT4), SOX2 protein, human, NANOG gene repress Genes related to differentiation, pathway_protein with POU5F1 protein, human (OCT4), SOX2 protein, human, NANOG gene repress Genes related to differentiation, pathway_protein with POU5F1 protein, human (OCT4), SOX2 protein, human, NANOG gene activate Genes related to proliferation, pathway_protein with POU5F1 protein, human (OCT4), SOX2 protein, human, NANOG gene activate Genes related to proliferation, protein_protein with PSORS1C3, protein_protein with PSORS1C3.", "label": "yes"}
{"original_question": "Is alemtuzumab effective for remission induction in patients diagnosed with T-cell prolymphocytic leukemia?", "id": "converted_364", "sentence1": "Is alemtuzumab effective for remission induction in patients diagnosed with T-Cell Prolymphocytic Leukemia?", "sentence2": "Sequential chemoimmunotherapy of fludarabine, mitoxantrone, and cyclophosphamide induction followed by alemtuzumab consolidation is effective in T-Cell Prolymphocytic Leukemia, A central need in this historically refractory tumor is the controlled evaluation of multiagent chemotherapy and its combination with the currently most active single agent, alemtuzumab. , FMC-A is a safe and efficient protocol in T-PLL, which compares favorably to published data., Currently, the best treatment for T-PLL is IV alemtuzumab, which has resulted in very high response rates of more than 90% when given as frontline treatment and a significant improvement in survival. , The patient failed to respond to standard Acute lymphocytic leukemia induction chemotherapy, but achieved complete remission following treatment with a fludarabine and alemtuzumab-based regimen., Here we present a rare case of concurrent T-PLL and Kaposi Sarcoma who achieved a complete Hematologic and cytogenetic remission after a very short course of treatment with alemtuzumab.,  Recent studies with single-agent alemtuzumab, an anti-CD52 monoclonal immunoglobulin complex location, have shown improved response rates and survival in patients with T-Cell Prolymphocytic Leukemia and Lymphoma, T-Cell, Cutaneous. , The CD52 Antigens is expressed at high density on the malignant T-cells and therapy with alemtuzumab, a humanized IgG1 immunoglobulin complex location that targets this Antigens, has produced promising results. , With the introduction of alemtuzumab, most patients who progressed despite treatment with pentostatin had a major response with a complete remission rate higher than that obtained with pentostatin when used as a first line., alemtuzumab (anti-CD52, Campath-1H) has recently been shown to be effective in the treatment of a range of Hematologic Neoplasms, including Chronic Lymphocytic Leukemia and T-Cell Prolymphocytic Leukemia., Here we report the outcome of two patients with CD4-positive T cell prolymphocytic leukemia treated with Campath 1H. Both patients responded rapidly to treatment and subsequently developed CD4 lymphopenia., T-Cell Prolymphocytic Leukemia (T-PLL) is a chemotherapy-resistant malignancy with a median survival of 7.5 months. Preliminary results indicated a high remission induction rate with the Homo sapiens CD52 immunoglobulin complex location, Campath 1H. , Campath 1H (30 mg) was administered intravenously 3 times weekly until maximal response. The overall response rate was 76% with 60% Creatinine measurement and 16% Target Awareness - Target Awareness - partial remission (Receptors, Progesterone). These responses were durable with a median disease-free interval of 7 months (range, 4-45 months). , The conclusion is that Campath 1H is an effective therapy in T-PLL, producing remissions in more than two thirds of patients. , For example, most patients with T-Cell Prolymphocytic Leukemia, including those with large tumor burdens and high peripheral white blood cell counts, will enter complete remission using the immunoglobulin complex location Campath 1H without any evidence of tumor lysis., Overall response rate to FMC was 68%, comprising 6 complete remissions (all bone-marrow confirmed) and 11 Target Awareness - Target Awareness - partial remissions. alemtuzumab consolidation increased the intent-to-treat overall response rate to 92% (12 complete remissions; 11 Target Awareness - Target Awareness - partial remissions). [SEP]Relations: alemtuzumab has relations: drug_drug with Catumaxomab, drug_drug with Catumaxomab, drug_drug with Otelixizumab, drug_drug with Otelixizumab, drug_drug with Mogamulizumab, drug_drug with Mogamulizumab, drug_drug with Golimumab, drug_drug with Golimumab, drug_drug with Lumiliximab, drug_drug with Lumiliximab.", "label": "yes"}
{"original_question": "Tocilizumab is an anti-TNF antibody, yes or no?", "id": "converted_3168", "sentence1": "tocilizumab is an anti-Recombinant Tumor Necrosis Factor Family Protein antibody, yes or no?", "sentence2": "was treated with tocilizumab, an anti-Interleukin 6 Receptor Monoclonal Antibody [EPC] , tocilizumab (TCZ) is a humanized Monoclonal Antibody [EPC] against Recombinant Interleukin-6 receptor licensed in 2009 that has demonstrated clinical efficacy in various adult Rheumatoid Arthritis populations. Rheumatoid Arthritis management guidelines and recommendations consider TCZ as one of the bDMARDS indicated after methotrexate or other conventional synthetic DMARDs and/or Recombinant Tumor Necrosis Factor Family Protein inhibitors failure in adult Rheumatoid Arthritis, tocilizumab (Roactemra or Actemra) is a recombinant humanized Monoclonal Antibody [EPC] that acts as an interleukin (IL)-6 receptor antagonist., METHODS\nPatients (n = 93) were treated with an anti-Recombinant Interleukin-6 receptor antibody (tocilizumab) or Recombinant Tumor Necrosis Factor Family Protein-α inhibitors for 16 weeks., The recent development of biological agents, namely, anti-tumour necrosis factor alpha (Recombinant Tumor Necrosis Factor Family Protein-α) agents (infliximab, adalimumab and etanercept), anti- ocaratuzumab (rituximab) and anti-interleukin 6 receptor (Interleukin 6 Receptor activity) Monoclonal Antibody [EPC] (tocilizumab), represents a major breakthrough for the treatment of immune-mediated disorders., Recently, an anti-Recombinant Interleukin-6 receptor Monoclonal Antibody [EPC], tocilizumab, has been licensed for the treatment as monotherapy or in combination with methotrexate of moderate to severe Rheumatoid Arthritis, when disease modifying anti-rheumatic drugs or anti-tumour necrosis factors (Recombinant Tumor Necrosis Factor Family Protein) have failed., tocilizumab is a monoclonal humanized anti-Recombinant Interleukin-6-receptor antibody used for the treatment of rheumatoid arthritis., Indeed, worldwide clinical trials of Recombinant Tumor Necrosis Factor Family Protein inhibiting biologic disease modifying antirheumatic drugs (bDMARDs) including infliximab, adalimumab, golimumab, certolizumab pegol, and etanercept as well as the humanized anti-human Recombinant Interleukin-6 receptor antibody, tocilizumab, have demonstrated outstanding clinical efficacy and tolerable safety profiles, resulting in worldwide approval for using these bDMARDs to treat moderate to severe active Rheumatoid Arthritis in patients with an inadequate response to synthetic disease modifying antirheumatic drugs (sDMARDs)., tocilizumab is a humanized anti-Recombinant Interleukin-6 receptor Monoclonal Antibody [EPC], which binds to circulating soluble Recombinant Interleukin-6 receptor and membrane-expressed Recombinant Interleukin-6 receptor, inhibiting Recombinant Interleukin-6 binding to both forms of Recombinant Interleukin-6 receptor., Subsequent options include a Recombinant Tumor Necrosis Factor Family Protein-alpha antagonist, followed by rituximab or possibly abatacept; (2) tocilizumab, a Monoclonal Antibody [EPC], inhibits interleukin-6 receptors., tocilizumab (TCZ) is a Monoclonal Antibody [EPC] which inhibits the Interleukin 6 Receptor.[SEP]Relations: tocilizumab has relations: drug_drug with Tetanus Immune Globulin, drug_drug with Tetanus Immune Globulin, drug_drug with Nemolizumab, drug_drug with Nemolizumab, drug_drug with Afelimomab, drug_drug with Afelimomab, drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Concizumab, drug_drug with Concizumab.", "label": "no"}
{"original_question": "Does atemoya juice inhibit the CYP1A2 enzyme?", "id": "converted_4587", "sentence1": "Does atemoya juice inhibit the CYP1A2 enzyme?", "sentence2": "Atemoya juice significantly inhibited CYP1A2 activity in Homo sapiens liver microsomes, but not the activities of Cytochrome p450 Cytochrome p450 CYP2C9 enzyme enzyme and cytochrome P450 3A., This suggests that the intake of an excess amount of atemoya juice is necessary to cause a change in the pharmacokinetics of phenacetin when the IC50 values for CYP1A2 inhibition by atemoya and fluvoxamine are taken into account[SEP]Relations: Phenacetin has relations: drug_protein with CYP1A2, drug_protein with CYP1A2, drug_protein with CYP2E1, drug_protein with CYP2E1, drug_protein with CYP2A6, drug_protein with CYP2A6. Fluvoxamine has relations: drug_protein with CYP1A2, drug_protein with CYP1A2, drug_protein with CYP1A1, drug_protein with CYP1A1.", "label": "yes"}
{"original_question": "Is retinol binding protein 4 an adipokine?", "id": "converted_4686", "sentence1": "Is retinol binding protein 4 an Adipokines?", "sentence2": "Systematic Quantification of Neurotrophic Adipokines RBP4 protein, human protein, human, SERPINF1 wt Allele, Homo sapiens, and CLU gene in Homo sapiens Cerebrospinal Fluid and Serum., Retinol-binding protein 4 (RBP4 protein, human protein, human) is a prominent Adipokines i, alpha-2-HS-Glycoprotein and Retinol Binding Proteins (RBP4 protein, human protein, human) are secreted as both hepatokine and Adipokines. [SEP]Relations: retinol binding has relations: molfunc_protein with ADH4, molfunc_protein with ADH4, molfunc_protein with RBP4 protein, human, molfunc_protein with RBP4 protein, human, molfunc_protein with RBP5, molfunc_protein with RBP5, molfunc_protein with RBP3, molfunc_protein with RBP3, molfunc_protein with ADH7, molfunc_protein with ADH7.", "label": "yes"}
{"original_question": "Has protein citrullination been implicated in rheumatoid arthritis?", "id": "converted_944", "sentence1": "Has protein citrullination been implicated in Rheumatoid Arthritis?", "sentence2": ": Citrullination has become a hot topic within recent years due to its involvement in diseases such as Rheumatoid Arthritis (RA), Multiple Sclerosis and Fibrosis. , Current literature suggests that increased levels of citrullinated Proteins are found in several if not all inflammatory diseases. , Antibodies, in vitro diagnostic, in vitro diagnostic directed against citrullinated Proteins and Peptides (acetyl 4-aminosalicylic acid) are the most specific serological markers available for diagnosing RA. , Citrullination of Proteins is well described in Rheumatoid Arthritis (RA), and hypercitrullination of Proteins may be related to Inflammation in general. , Some Wegener Autoantigen are remarkably effective as diagnostics in Autoimmune Diseases, most notably Rheumatoid Arthritis (RA). Several Wegener Autoantigen can be observed before other clinical RA manifestations are apparent. , Rheumatoid arthritis (RA) is a chronic autoimmune Disease characterized by the presence of Rheumatoid Factor Measurement (RF) and anti-citrullinated protein/peptide autoantibodies (acetyl 4-aminosalicylic acid). , Anti-citrullinated Peptides as Autoantigens in Rheumatoid Arthritis-relevance to treatment., The implications of citrullination affecting integrin binding in Disease open up a new area of study and might have implications for the pathogenesis of inflammatory diseases like Rheumatoid Arthritis and Periodontitis., In this paper, we will review the three of the main classes of PTMS gene already associated with RA: citrullination, carbamylation, and oxidation., Citrullinated collagen II (CII) is a well-known To To autoantigen in Rheumatoid Arthritis (RA). , Among the RA-associated autoantibodies, especially Anti-Citrullinated Protein Antibodies, in vitro diagnostic (acetyl 4-aminosalicylic acid) have been studied intensively in the last decade., Protein citrullination is a posttranslational modification that has attracted increased attention, especially for its involvement in Rheumatoid Arthritis (RA)., Identification of citrullinated cellular fibronectin in synovial fluid from patients with Rheumatoid Arthritis., Cellular fibronectin (cFn) has been implicated in the pathogenesis of Rheumatoid Arthritis (RA), and we previously demonstrated the presence of citrullinated cFn in rheumatoid synovial tissues. , . In Rheumatoid Arthritis, PADI4 wt Allele and protein citrullination are increased in Inflamed joint, and Anti-Citrullinated Protein Antibodies, in vitro diagnostic (acetyl 4-aminosalicylic acid) form against citrullinated antigens are formed. [SEP]Relations: Anti-citrullinated protein antibody positivity has relations: disease_phenotype_positive with Rheumatoid Arthritis, disease_phenotype_positive with Rheumatoid Arthritis. Rheumatoid arthritis has relations: drug_effect with Citalopram, drug_effect with Citalopram, drug_effect with Cevimeline, drug_effect with Cevimeline, drug_effect with Cyclosporine, drug_effect with Cyclosporine, drug_effect with Ropinirole, drug_effect with Ropinirole.", "label": "yes"}
{"original_question": "Are BBS mutations involved in syndromic Hirschsprung disease?", "id": "converted_525", "sentence1": "Are Bardet-Biedl Syndrome Gene Mutation involved in syndromic Hirschsprung disease?", "sentence2": "Epistasis between ret unit of radiation dose and Bardet-Biedl Syndrome Gene Mutation modulates enteric innervation and causes syndromic Hirschsprung disease, Here, we report 3 families with Bardet-Biedl Syndrome and HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 with concomitant Gene Mutation in Bardet-Biedl Syndrome genes and regulatory ret unit of radiation dose elements, whose functionality is tested in physiologically relevant assays. Our data suggest that Bardet-Biedl Syndrome Gene Mutation can potentiate HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 predisposing ret unit of radiation dose alleles, which by themselves are insufficient to cause disease, Epistasis between ret unit of radiation dose and Bardet-Biedl Syndrome Gene Mutation modulates enteric innervation and causes syndromic Hirschsprung disease., Our data suggest that Bardet-Biedl Syndrome Gene Mutation can potentiate HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 predisposing ret unit of radiation dose alleles, which by themselves are insufficient to cause disease., Here, we report 3 families with Bardet-Biedl Syndrome and HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 with concomitant Gene Mutation in Bardet-Biedl Syndrome genes and regulatory ret unit of radiation dose elements, whose functionality is tested in physiologically relevant assays, Our data suggest that Bardet-Biedl Syndrome Gene Mutation can potentiate HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 predisposing ret unit of radiation dose alleles, which by themselves are insufficient to cause disease, Here, we report 3 families with Bardet-Biedl Syndrome and HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 with concomitant Gene Mutation in Bardet-Biedl Syndrome genes and regulatory ret unit of radiation dose elements, whose functionality is tested in physiologically relevant assays[SEP]Relations: hirschsprung disease, susceptibility to has relations: disease_phenotype_positive with Autosomal dominant inheritance, disease_phenotype_positive with Autosomal dominant inheritance, disease_protein with MED12, disease_protein with MED12, disease_protein with EDNRB, disease_protein with EDNRB, disease_protein with GDNF, disease_protein with GDNF, disease_protein with ret unit of radiation dose, disease_protein with ret unit of radiation dose.", "label": "yes"}
{"original_question": "Is aggrephagy a variant of autophagy?", "id": "converted_3813", "sentence1": "Is aggrephagy a variant of autophagy?", "sentence2": "The selective branch of autophagy that deals with identification, capture and degradation of Protein Info aggregates is called aggrephagy., Mechanistic insights into aggrephagy, a selective basal autophagy process to clear misfolded Protein Info aggregates, , , it is largely unknown how misfolded polypeptides form aggresomes and are eventually cleared by the aggresome-macroautophagy/autophagy pathway, so-called aggrephagy.[SEP]Relations: Protein C has relations: drug_drug with Nonacog beta pegol, drug_drug with Nonacog beta pegol, drug_drug with Vatreptacog alfa, drug_drug with Vatreptacog alfa, drug_drug with Anagrelide, drug_drug with Anagrelide, drug_drug with Damoctocog alfa pegol, drug_drug with Damoctocog alfa pegol, drug_drug with Sarpogrelate, drug_drug with Sarpogrelate.", "label": "yes"}
{"original_question": "Is there an upper limit on the functional fraction of the human genome?", "id": "converted_4040", "sentence1": "Is there an upper limit on the functional fraction of the human genome?", "sentence2": "Mutational load considerations lead to the conclusion that the functional fraction within the human genome cannot exceed 25%, and is probably considerably lower.[SEP]", "label": "yes"}
{"original_question": "Can mogamulizumab be used for the treatment of cutaneous T-cell lymphoma?", "id": "converted_3027", "sentence1": "Can mogamulizumab be used for the treatment of Lymphoma, T-Cell, Cutaneous?", "sentence2": "In the large international phase III MAVORIC trial, patients with previously treated Lymphoma, T-Cell, Cutaneous who received the anti-CCR4 monoclonal antibody mogamulizumab experienced significantly longer progression-free survival and higher response rates, as well as better quality of life, than those who received vorinostat, a standard therapy.[SEP]Relations: Cutaneous T-cell lymphoma has relations: phenotype_phenotype with T-cell lymphoma, phenotype_phenotype with T-cell lymphoma, disease_phenotype_positive with Sezary syndrome, disease_phenotype_positive with Sezary syndrome, disease_phenotype_positive with mycosis fungoides and variants, disease_phenotype_positive with mycosis fungoides and variants. Vorinostat has relations: drug_effect with T-cell lymphoma, drug_effect with T-cell lymphoma, drug_drug with Eculizumab, drug_drug with Eculizumab.", "label": "yes"}
{"original_question": "Are microRNA (miR) regulated through DNA methylation of their promoters?", "id": "converted_1369", "sentence1": "Are MicroRNAs (miR) regulated through DNA methylation of their promoters?", "sentence2": "We found that TCF7L1 gene down-regulation in the context of constitutively active Wnt signaling does not result from Promoter DNA methylation but is likely to be caused by a plethora of mechanisms at both the RNA and protein level as shown by the observed decrease in activating histone marks (histone H3 trimethyl Lys4 and H3-acetylation) and the upregulation of MIR211 wt Allele, a novel Wnt-regulated MicroRNAs that targets TCF7L1 gene and attenuates early neural differentiation in Mus sp. ESCs, ene silencing of MIR22 gene gene in acute lymphoblastic leukaemia involves histone modification independent of Promoter DNA methylation, Whereas a CpG Islands was identified within the Promoter element of MIR22 gene gene, no Promoter DNA methylation was detected in these Cells, xtensive Promoter DNA hypermethylation and hypomethylation is associated with aberrant MicroRNAs expression in chronic lymphocytic leukemia, Integration of DNA methylation and miRNA Promoter data led to the identification of 128 recurrent miRNA targets for aberrant Promoter DNA methylation, Together, our findings characterize the role of epigenetic changes in the regulation of miRNA transcription and create a repository of disease-specific Promoter regions that may provide additional insights into the pathogenesis of Chronic Lymphocytic Leukemia, Nadia - zebrafish methylation of MicroRNAs Genes in Multiple Myeloma, Recently, epigenetic dysregulation of tumor-suppressor miRNA Genes by Promoter DNA methylation has been implicated in Homo sapiens Malignant Neoplasms, including Multiple Myeloma (Millimole per Liter), ethylation of tumor suppressor microRNAs, Dysregulation of miRNA expression involved in Primary malignant neoplasm can be triggered by multiple mechanisms including aberrant DNA methylation of the miRNA gene Promoter, Of note, DNA methylation of tumor suppressor miRNAs has been implicated in various Homo sapiens Malignant Neoplasms, Moreover, miRNA silencing mediated by aberrant Promoter DNA methylation can potentially be reversed by hypomethylating agents, and hence may pose a new therapeutic target in Primary malignant neoplasm,  In this review, the authors will focus on the aberrant methylation of miRNAs in the pathogenesis of lymphoid malignancies including chronic lymphocytic leukemia, Multiple Myeloma and Pre B-cell Pre B-cell acute lymphoblastic leukemia, Here, we review those miRNAs implicated in cytarabine/daunorubicin protocol that are regulated by Promoter DNA methylation and/or chromatin modifications and, which frequently direct the expression of constituents of the epigenetic machinery, concluding with the delineation of a complex epigenetic-miRNA regulatory network and its alterations in cytarabine/daunorubicin protocol, Furthermore, we also discuss epigenetic dysregulation of tumor-suppressor miRNA Genes by Promoter DNA methylation and the interaction of DNA methylation with miRNAs involved in the regulation of Hematopoietic stem Cells activation and liver fibrosi, Instead, the cell type-specific silencing of these Genes is due to enhanced oncoprotein oncoprotein p21 mRNA degradation, 14-3-3sigma Promoter DNA methylation and reduced processing of the miR-34a primary transcript, Some tumor-suppressive miRNAs are known to be epigenetically silenced by Promoter DNA methylation in Primary malignant neoplasm, In the present study, we aimed to identify miRNA Genes that are silenced by DNA hypermethylation in Liver carcinoma (altretamine/cisplatin/cyclophosphamide protocol), It was found that miR-335, which is harbored within an Introns of its protein-coding host gene, MEST gene gene, was downregulated by aberrant Promoter hypermethylation via further methylation assays, including methylation-specific PCR, combined bisulfite and restriction analysis, bisulfite sequencing analysis and decitabine treatment, he levels of miR-335/MEST gene gene methylation were significantly higher in 18 (90%) out of 20 primary altretamine/cisplatin/cyclophosphamide protocol Neoplasms, compared to their non-tumor tissue counterparts (P<0.001), In conclusion, our results indicate that expression of miR-335 is reduced by aberrant DNA methylation in altretamine/cisplatin/cyclophosphamide protocol.[SEP]Relations: Promoter clearance from RNA polymerase I Promoter has relations: bioprocess_bioprocess with Promoter clearance during DNA-templated transcription, bioprocess_bioprocess with Promoter clearance during DNA-templated transcription, bioprocess_bioprocess with Promoter clearance from RNA polymerase I Promoter for nuclear large rRNA transcript, bioprocess_bioprocess with Promoter clearance from RNA polymerase I Promoter for nuclear large rRNA transcript. histone modification has relations: bioprocess_bioprocess with histone methylation, bioprocess_bioprocess with histone methylation, bioprocess_bioprocess with histone biotinylation, bioprocess_bioprocess with histone biotinylation. MEST gene has relations: bioprocess_protein with regulation of lipid storage, bioprocess_protein with regulation of lipid storage.", "label": "yes"}
{"original_question": "Have studies shown that there is no link between DNA methylation patterns and Post Traumatic Stress Disorder?", "id": "converted_2130", "sentence1": "Have studies shown that there is no link between DNA methylation patterns and Post Traumatic Stress Disorder?", "sentence2": "Using pre-deployment SKA2 gene gene methylation levels and childhood Wounds and Injuries exposure, we found that the previously published suicide prediction rule significantly predicted post-deployment PTSD symptoms (AUC=0.66, 95% CI: 0.53-0.79) with an optimal sensitivity of 0.81 and specificity of 0.91. Permutation analysis using random methylation loci supported these findings. Together, these data establish the importance of SKA2 gene gene for cortisol stress responsivity and the development of PTSD and provide further evidence that SKA2 gene gene is a promising biomarker for stress-related disorders including PTSD.,  Results provide novel support for PTSD-related accelerated aging in DNAm and extend the evidence base of known DNAm age correlates to the domains of neural integrity and cognition., We investigated serum DNA methylation patterns in genomic repetitive elements, Long Interspersed Nucleotide Element-1 and Alu, for Post-Traumatic Stress Disorder (PTSD) cases and controls who were US military service members recently deployed to Afghanistan or Iraq., In light of its role in Glucocorticoid Receptor transactivation, we investigated whether SKA2 gene gene DNA methylation influences cortisol stress reactivity and is involved in the development of Post-Traumatic Stress Disorder (PTSD)., These results suggest that alterations in global methylation pattern are involved in behavioural adaptation to environmental stress and pinpoint DLGAP2 gene as a possible target in PTSD., Here we examined whether there was a link between an established Rattus norvegicus model of Post-Traumatic Stress Disorder (PTSD) and Bdnf DNA methylation, We investigated serum DNA methylation patterns in genomic repetitive elements, Long Interspersed Nucleotide Element-1 and Alu, for Post-Traumatic Stress Disorder (PTSD) cases and controls who were US military service members recently deployed to Afghanistan or Iraq.Cases (n = 75) had a postdeployment diagnosis of PTSD, DNA methylation in repetitive elements and Post-Traumatic Stress Disorder: a case-control study of US military service members, Here we examined whether there was a link between an established Rattus norvegicus model of Post-Traumatic Stress Disorder (PTSD) and Bdnf DNA methylation. , DNA methylation in repetitive elements and Post-Traumatic Stress Disorder: a case-control study of US military service members., AIM: We investigated serum DNA methylation patterns in genomic repetitive elements, Long Interspersed Nucleotide Element-1 and Alu, for Post-Traumatic Stress Disorder (PTSD) cases and controls who were US military service members recently deployed to Afghanistan or Iraq. , Together, these results suggest that psychosocial stress may alter global and gene-specific DNA methylation patterns potentially associated with peripheral immune dysregulation., DNA methylation in vulnerability to post-traumatic stress in rats: evidence for the role of the post-synaptic density protein DLGAP2 gene., Subjects with PTSD showed a higher DNA methylation of four CpG sites at the BDNF promoter compared with those without PTSD, Cumulatively, the data suggest that epigenetic variation at SKA2 gene gene mediates vulnerability to suicidal behaviors and PTSD through dysregulation of the hypothalamic-pituitary-adrenal axis axis in response to stress.[SEP]Relations: Post-Traumatic Stress Disorder has relations: disease_disease with neurotic disorder, disease_disease with neurotic disorder. DLGAP2 has relations: anatomy_protein_absent with decidua, anatomy_protein_absent with decidua, anatomy_protein_present with hypothalamus, anatomy_protein_present with hypothalamus, anatomy_protein_present with substantia nigra, anatomy_protein_present with substantia nigra, anatomy_protein_present with prefrontal cortex, anatomy_protein_present with prefrontal cortex.", "label": "no"}
{"original_question": "Are the members of the KRAB-ZNF  gene family promoting gene repression?", "id": "converted_3471", "sentence1": "Are the members of the KRAB-ZNF  Genes family promoting Genes repression?", "sentence2": " The Proteins encoded by these genes, whose expression is often tissue-specific, act as epigenetic suppressors contributing to the addition of repressive chromatin marks and DNA methylation., Here, using a reporter system, we show that TRIM28/KRAB-ZNFs alter DNA methylation patterns in addition to Histone H3 Trimethyl Lys9 to cause stable Genes repression during reprogramming. Using several expression datasets, we identified KRAB-ZNFs (ZNF114 gene Genes, ZNF483 Genes Genes, ZNF589 gene Genes) in the human genome that maintain pluripotency., Further analyses of our data sets link GABPa to cognitive disorders, Diabetes Mellitus, KRAB zinc finger (KRAB-ZNF), and human-specific genes., The Stem cells zinc finger 1 (SZF1)/ZNF589 gene Genes Protein Info belongs to the large family of Krüppel-associated box domain-zinc finger (KRAB-ZNF) transcription factors, which are present only in higher Vertebrates and epigenetically repress transcription by recruiting chromatin-modifying complexes to the Promoter Regions, Genetic of their respective target genes, Because TRIM28 wt Allele is recruited to the DNA via interaction with KRAB-ZNF Proteins, we suggest that expression of KRAB-ZNF genes may be controlled via an auto-regulatory mechanism involving TRIM28 wt Allele., Interestingly, although most TRIM28 wt Allele Binding Sites were within core Promoter Regions, Genetic, the Binding Sites near ZNF genes were greatly enriched within transcribed regions of the target Genes[SEP]Relations: ZNF114 gene has relations: protein_protein with ZNF8, protein_protein with ZNF8, protein_protein with KRTAP10-6, protein_protein with KRTAP10-6, bioprocess_protein with regulation of transcription, DNA-templated, bioprocess_protein with regulation of transcription, DNA-templated, protein_protein with KLHL2, protein_protein with KLHL2. ZNF483 Genes has relations: protein_protein with NRF1, protein_protein with NRF1.", "label": "yes"}
{"original_question": "Are astronauts in higher risk for developing cancer?", "id": "converted_3557", "sentence1": "Are astronauts in higher risk for developing cancer?", "sentence2": "Understanding space radiation health effects is critical due to potential increased morbidity and mortality following spaceflight. ,  No significant associations between space radiation dose and mortality were found using logistic regression with an internal reference group, adjusting for medical radiation., Despite years of research, understanding of the space radiation environment and the risk it poses to long-duration astronauts remains limited. There is a disparity between research results and observed empirical effects seen in Homo sapiens astronaut crews[SEP]", "label": "no"}
{"original_question": "Are cyclophilins proteins that bind to prolines?", "id": "converted_297", "sentence1": "Are cyclophilins Proteins that bind to prolines?", "sentence2": "Cyclophilins are ubiquitously expressed Proteins that bind to prolines and can catalyse CISH protein, human/trans isomerization of proline residues., a characteristic of the cyclophilin family of Proteins that bind prolines and often act as CISH protein, human-trans peptidyl-prolyl isomerases. , The cyclophilins are widely expressed ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS that catalyze the interconversion of the CISH protein, human and trans peptide bonds of prolines. ,  an Peptidylprolyl Isomerase on the isomerization of critical prolines that are found in the tCHT1 Sequence - ParameterizedDataType.[SEP]Relations: Protein S human has relations: drug_protein with PROC, drug_protein with PROC, drug_drug with Proglumetacin, drug_drug with Proglumetacin, drug_drug with Procarbazine, drug_drug with Procarbazine, drug_drug with Doxycycline, drug_drug with Doxycycline, drug_drug with Progesterone, drug_drug with Progesterone.", "label": "yes"}
{"original_question": "Have yeast prions become important models for the study of the basic mechanisms underlying human amyloid diseases?", "id": "converted_2973", "sentence1": "Have Saccharomyces cerevisiae Prions become important models for the study of the basic mechanisms underlying human Serum amyloid A protein diseases?", "sentence2": "Endogenous Saccharomyces cerevisiae amyloids that control heritable traits and are frequently used as models for human Serum Serum amyloid A protein A protein diseases are termed Saccharomyces cerevisiae Prions, Fibrous cross-β aggregates (amyloids) and their transmissible forms (Prions) cause diseases in Mammals (including Homo sapiens) and control heritable traits in Saccharomyces cerevisiae. , These infectious Saccharomyces cerevisiae amyloidoses are outstanding models for the many common human Serum Serum amyloid A protein A protein-based diseases that are increasingly found to have some infectious characteristics., Yeast Prions (infectious proteins) were discovered by their outré genetic properties and have become important models for an array of human prion and Serum Serum amyloid A protein A protein diseases., Yeast Prions are models for both rare mammalian Prion Diseases and for several very common amyloidoses such as ALZHEIMER DISEASE, FAMILIAL, 1, Diabetes Mellitus, Non-Insulin-Dependent, and Parkinson Disease. , Yeast Prions are important models for human Serum Serum amyloid A protein A protein diseases in general, particularly because new evidence is showing infectious aspects of several human amyloidoses not previously classified as Prions. , Mechanism of Serum Serum amyloid A protein A protein formation is critical for a complete understanding of the Saccharomyces cerevisiae prion phenomenon and human Serum Serum amyloid A protein A protein-related diseases. , Yeast Prions are important models for human Serum Serum amyloid A protein A protein diseases in general, particularly because new evidence is showing infectious aspects of several human amyloidoses not previously classified as Prions., Endogenous Saccharomyces cerevisiae amyloids that control heritable traits and are frequently used as models for human Serum Serum amyloid A protein A protein diseases are termed Saccharomyces cerevisiae Prions., Mechanism of Serum Serum amyloid A protein A protein formation is critical for a complete understanding of the Saccharomyces cerevisiae prion phenomenon and human Serum Serum amyloid A protein A protein-related diseases., Here we summarize the results of studies of Prions of the Saccharomyces cerevisiae Saccharomyces cerevisiae and of the use of Saccharomyces cerevisiae model for investigation of some human amyloidoses, such as Prion Diseases, Alzheimer's, Parkinson's, and Huntington Disease., Yeast Prions increasingly are serving as models for the understanding and treatment of many mammalian amyloidoses., Yeast Prions, based on self-seeded highly ordered Fibrous aggregates (amyloids), serve as a model for human Serum Serum amyloid A protein A protein diseases., These infectious Saccharomyces cerevisiae amyloidoses are outstanding models for the many common human Serum Serum amyloid A protein A protein-based diseases that are increasingly found to have some infectious characteristics.<br>, The Saccharomyces cerevisiae system has provided considerable insight into the biology of Serum Serum amyloid A protein A protein and Prions., Yeast Prions are important models for human Serum Serum amyloid A protein A protein diseases in general, particularly because new evidence is showing infectious aspects of several human amyloidoses not previously classified as Prions., We also review studies of the roles of chaperones, aggregate-collecting proteins, and other cellular components using Saccharomyces cerevisiae that have led the way in improving the understanding of similar processes that must be operating in many human amyloidoses.[SEP]Relations: prion disease has relations: disease_disease with inherited prion disease, disease_disease with inherited prion disease, disease_disease with brain disease, disease_disease with brain disease, disease_disease with encephalopathy, bovine spongiform, disease_disease with encephalopathy, bovine spongiform, disease_protein with PRNP, disease_protein with PRNP. familial Alzheimer disease has relations: disease_disease with inherited prion disease, disease_disease with inherited prion disease.", "label": "yes"}
{"original_question": "Is RUNX1T1 associate with obesity?", "id": "converted_4243", "sentence1": "Is RUNX1T1 associate with BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20?", "sentence2": "RUNX1T1 rs34269950 is associated with BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 and Metabolic Syndrome X., Of these Single Nucleotide Polymorphism only rs34269950 located in the 'RRACH' motif, the most common N-methyladenosine (METTL3 gene) methylation modification site (recognized by FTO protein, human protein, human), was significantly associated with BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 risk and No No metabolic abnormalities. Specifically, compared to AA Genotype determination, rs34269950 del/del Genotype determination was associated with a 1.47 [95% confidence interval (CI): 1.01-2.14, P = 0.042] fold higher rate of BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 risk. , Our study demonstrates that RUNX1T1 rs34269950, located in a potential FTO protein, human protein, human recognition motif, is significantly associated with waist circumference. T[SEP]Relations: Metabolic Syndrome X X has relations: disease_protein with SIRT1, disease_protein with SIRT1, disease_protein with INPPL1, disease_protein with INPPL1, disease_protein with HMGA1, disease_protein with HMGA1, disease_protein with NR1I2, disease_protein with NR1I2. METTL3 has relations: protein_protein with YY1, protein_protein with YY1.", "label": "yes"}
{"original_question": "Is glycyl-tRNA synthetase gene involved in the development of Charcot-Marie-Tooth disease?", "id": "converted_159", "sentence1": "Is glycyl-tRNA synthetase gene involved in the development of Charcot-Marie-Tooth Disease?", "sentence2": "Charcot-Marie-Tooth Disease, Type 2D (CMT2D) is an autosomal-dominant axonal peripheral Neuropathy characterized by impaired motor and sensory function in the distal extremities. Gene Mutation in the glycyl-tRNA synthetase (GARS) gene cause CMT2D, Dominant mutations in GARS cause rare forms of Charcot-Marie-Tooth Disease and distal spinal muscular atrophy, Using exome sequencing she was found to harbor fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether heterozygous mutations within the glycyl-tRNA synthetase (GARS) gene, mutations of human GlyRS (hGlyRS) were also found to be associated with Charcot-Marie-Tooth Disease, Dominant mutations in GARS, encoding the essential Enzyme [APC] glycyl-tRNA synthetase (GlyRS), result in a form of Charcot-Marie-Tooth Disease, type 2D (CMT2D), predominantly characterized by lower motor nerve degeneration, A novel Mutation Abnormality in glycyl-tRNA synthetase caused Charcot-Marie-Tooth Disease, Type 2D with facial and respiratory muscle involvement, Here we describe a 45-year-old woman with a long course of motor-dominant Neuropathy. Distal weakness appeared in childhood and became worse with age. After a diagnosis of CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate type 2, the symptoms progressed, and in her fourth decade, facial and Respiratory insufficiency due to muscle weakness appeared, ultimately requiring non-invasive mechanical ventilation. There was no family history of CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate. Comprehensive analysis of known CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate-related Genes revealed a novel heterozygous c.815T>A, p.L218Q Mutation Abnormality in glycyl-tRNA synthetase (GARS), a causative gene for both CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate type 2D (CMT2D) and distal spinal muscular atrophy type V (dSMA-V), Charcot-Marie-Tooth Disease, Type 2D (CMT2D) is a dominantly inherited peripheral Neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS)., Long-range structural effects of a Charcot-Marie-Tooth Disease-causing Mutation Abnormality in human glycyl-tRNA synthetase., Glycyl tRNA synthetase mutations in Charcot-Marie-Tooth Disease, Type 2D and distal spinal muscular atrophy type V., [A novel Mutation Abnormality in glycyl-tRNA synthetase caused Charcot-Marie-Tooth Disease, Type 2D with facial and respiratory muscle involvement]., Glycyl-tRNA synthetase (GARS), which encodes the Enzyme [APC] responsible for charging tRNA(Gly) with Glycine (Plant) in both the Cytoplasm and Mitochondria, is implicated to Charcot-Marie-Tooth Disease 2D (CMT2D) and distal hereditary motor Neuropathy type V (dHMN-V)., These additional functions may explain why dominant mutations in glycyl-tRNA synthetase (GlyRS) and tyrosyl-tRNA synthetase cause Charcot-Marie-Tooth (CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate) disease, the most common heritable disease of the peripheral nervous system., Here, we report the identification of four disease-associated missense mutations in the Glycine-tRNA Ligase gene in families with CMT2D and dSMA-V., Gene Mutation in the glycyl-tRNA synthetase (GARS) gene cause CMT2D., Of the many inherited Charcot-Marie-Tooth peripheral neuropathies, type 2D (CMT2D) is caused by dominant Point Mutation in the gene GARS, encoding Glycine-tRNA Ligase (GlyRS)., Charcot-Marie-Tooth Disease, Type 2D (CMT2D) is a dominantly inherited peripheral Neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS), Charcot-Marie-Tooth Disease, Type 2D is a hereditary axonal and glycyl-tRNA synthetase (GARS)-associated Neuropathy that is caused by a Mutation Abnormality in GARS, Long-range structural effects of a Charcot-Marie-Tooth Disease-causing Mutation Abnormality in human glycyl-tRNA synthetase, These additional functions may explain why dominant mutations in glycyl-tRNA synthetase (GlyRS) and tyrosyl-tRNA synthetase cause Charcot-Marie-Tooth (CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate) disease, the most common heritable disease of the peripheral nervous system, A novel Mutation Abnormality in glycyl-tRNA synthetase caused Charcot-Marie-Tooth Disease, Type 2D with facial and respiratory muscle involvement., Charcot-Marie-Tooth Disease, Type 2D (CMT2D) is a dominantly inherited peripheral Neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS). , Gene Mutation in the glycyl-tRNA synthetase (GARS) gene cause CMT2D. , An ENU-induced Mutation Abnormality in mouse glycyl-tRNA synthetase (GARS) causes peripheral sensory and motor phenotypes creating a model of Charcot-Marie-Tooth type 2D peripheral Neuropathy., We previously implicated mutations in the gene encoding glycyl-tRNA synthetase (GARS) as the cause of CMT2D and dSMA-V. , An active dominant Mutation Abnormality of glycyl-tRNA synthetase causes Neuropathy in a Charcot-Marie-Tooth 2D mouse model., Charcot-Marie-Tooth Disease, Type 2D is a hereditary axonal and glycyl-tRNA synthetase (GARS)-associated Neuropathy that is caused by a Mutation Abnormality in GARS. , Dominant mutations in GARS, encoding the essential Enzyme [APC] glycyl-tRNA synthetase (GlyRS), result in a form of Charcot-Marie-Tooth Disease, type 2D (CMT2D), predominantly characterized by lower motor nerve degeneration. ,  Charcot-Marie-Tooth Disease, Type 2D (CMT2D) is a dominantly inherited peripheral Neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS). In addition to GARS, mutations in three other tRNA synthetase Genes cause similar neuropathies, although the underlying mechanisms are not fully understood., These additional functions may explain why dominant mutations in glycyl-tRNA synthetase (GlyRS) and tyrosyl-tRNA synthetase cause Charcot-Marie-Tooth (CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate) disease,,  Charcot-Marie-Tooth Disease, Type 2D (CMT2D) is an autosomal-dominant axonal peripheral Neuropathy characterized by impaired motor and sensory function in the distal extremities. Gene Mutation in the glycyl-tRNA synthetase (GARS) gene cause CMT2D., Of the many inherited Charcot-Marie-Tooth peripheral neuropathies, type 2D (CMT2D) is caused by dominant Point Mutation in the gene GARS, encoding Glycine-tRNA Ligase (GlyRS)., Charcot-Marie-Tooth Disease, Type 2D (CMT2D) is a dominantly inherited peripheral Neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS)., Long-range structural effects of a Charcot-Marie-Tooth Disease-causing Mutation Abnormality in human glycyl-tRNA synthetase., Glycyl tRNA synthetase mutations in Charcot-Marie-Tooth Disease, Type 2D and distal spinal muscular atrophy type V., These additional functions may explain why dominant mutations in glycyl-tRNA synthetase (GlyRS) and tyrosyl-tRNA synthetase cause Charcot-Marie-Tooth (CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate) disease, the most common heritable disease of the peripheral nervous system., A novel Mutation Abnormality in glycyl-tRNA synthetase caused Charcot-Marie-Tooth Disease, Type 2D with facial and respiratory muscle involvement., An active dominant Mutation Abnormality of glycyl-tRNA synthetase causes Neuropathy in a Charcot-Marie-Tooth 2D mouse model., Glycyl-tRNA synthetase (GARS), which encodes the Enzyme [APC] responsible for charging tRNA(Gly) with Glycine (Plant) in both the Cytoplasm and Mitochondria, is implicated to Charcot-Marie-Tooth Disease 2D (CMT2D) and distal hereditary motor Neuropathy type V (dHMN-V).[SEP]Relations: Charcot-Marie-Tooth Disease has relations: disease_protein with GDAP1, disease_protein with GDAP1, disease_protein with GDAP1, disease_protein with GDAP1, disease_protein with LMNA, disease_protein with LMNA, disease_protein with LMNA, disease_protein with LMNA, disease_protein with PNPLA6, disease_protein with PNPLA6.", "label": "yes"}
{"original_question": "Is Cabotegravir effective for HIV prevention?", "id": "converted_4240", "sentence1": "Is Cabotegravir effective for HIV Infections prevention?", "sentence2": "A new paradigm for antiretroviral delivery: long-acting cabotegravir and rilpivirine for the treatment and prevention of HIV Infections Infections., PURPOSE OF REVIEW: Cabotegravir (Carbonic Anhydrase 1 (enzyme), Human) and rilpivirine (RPV) is the first long-acting injectable antiretroviral therapy (ART) option approved for virologically suppressed adults with HIV Infections Infections-1. In addition, long-acting Carbonic Anhydrase 1 (enzyme), Human is a promising agent for HIV Infections Infections preexposure prophylaxis (HIV Infections Infections: HIV Infections: PrEP and PEP and PEP). , SUMMARY: Clinical trial results support the use of long-acting Carbonic Anhydrase 1 (enzyme), Human for HIV Infections Infections HIV Infections Infections: HIV Infections: PrEP and PEP and PEP and long-acting Carbonic Anhydrase 1 (enzyme), Human and RPV as a switch strategy for adults with HIV Infections Infections-1 who are first virologically suppressed with oral ART. , OBJECTIVE: We had previously shown that long-acting cabotegravir (Carbonic Anhydrase 1 (enzyme), Human-Latex Fixation Tests) injections fully protected Macaca from vaginal simian HIV Infections Infections (SHIV) infection., The Potential Impact of Long-Acting Cabotegravir for HIV Infections Infections Prevention in South Africa: A Mathematical Modeling Study.,  Long-acting cabotegravir (Carbonic Anhydrase 1 (enzyme), Human Latex Fixation Tests) is a potential new injectable formulation for Human immunodeficiency virus antigen (HIV Infections Infections) HIV Infections Infections: HIV Infections: PrEP and PEP and PEP being tested in phase III trials., Design and Testing of a Cabotegravir Implant for HIV Infections Infections Prevention., Cabotegravir and rilpivirine long-acting injectable antiretroviral therapy for the treatment of HIV Infections Infections-1 infection brings promise of a new mode of delivery and potential solutions to some problems of oral therapy, but also new challenges and unanswered questions., Cabotegravir is an investigational HIV Infections Infections Integrase Inhibitor in development for the treatment and pre-exposure prophylaxis of HIV Infections Infections-1 infection., Bictegravir, cabotegravir, dolutegravir, elvitegravir, and raltegravir are members of the latest class of antiretrovirals available to treat Human immunodeficiency virus antigen (HIV Infections Infections) infection, the integrase strand transfer inhibitors., PURPOSE OF REVIEW: Long-acting cabotegravir may provide a novel therapeutic option for both the treatment and prevention of HIV Infections Infections-1 infection that does not necessitate adherence, Long-acting injectable cabotegravir for the prevention of Human immunodeficiency virus II infection, BACKGROUND: The HIV Infections Infections Prevention Trials Network (HPTN) 083 trial demonstrated that long-acting cabotegravir (Carbonic Anhydrase 1 (enzyme), Human-Latex Fixation Tests) was more effective than tenofovir disoproxil fumarate-emtricitabine (TDF/FTC) in preventing Human immunodeficiency virus antigen (HIV Infections Infections) in cisgender men and transgender women who have sex with, Areas covered: Here, we review trials of cabotegravir (Carbonic Anhydrase 1 (enzyme), Human) as treatment of HIV Infections Infections-1 infection and its potential use as pre-exposure prophylaxis (HIV Infections Infections: HIV Infections: PrEP and PEP and PEP) in high risk individuals, including issues around oral lead in and potential resistance emergence. Exper, frequent dosing. This review focuses on the potential benefits and considerations for the study and use of 2 long-acting injectable agents, cabotegravir (GSK1265744LA, Carbonic Anhydrase 1 (enzyme), Human Latex Fixation Tests) and rilpivirine (TMC278LA, RPV Latex Fixation Tests), for use as chemoprophylaxis for HIV Infections Infections , An evaluation of cabotegravir for HIV Infections Infections treatment and prevention., Cabotegravir long-acting for HIV Infections Infections-1 prevention., Our findings suggest that cabotegravir should be evaluated in clinical trials as a potential option for antiretroviral therapy and preexposure prophylaxis in HIV Infections Infections-2-prevalent settings., Profile of cabotegravir and its potential in the treatment and prevention of HIV Infections Infections-1 infection: evidence to date., Long-Acting Cabotegravir for HIV Infections Infections/AIDS Prophylaxis., Cabotegravir for HIV Infections Infections Prevention in Cisgender Men and Transgender Women., Cabotegravir is a novel Human immunodeficiency virus antigen integrase enzyme inhibitor used for prevention and treatment of Human immunodeficiency virus II infection., PURPOSE OF REVIEW: Long-acting cabotegravir may provide a novel therapeutic option for both the treatment and prevention of HIV Infections Infections-1 infection that does not necessitate adherence , Cabotegravir in the treatment and prevention of Human Immunodeficiency Virus-1., Cabotegravir: its potential for antiretroviral therapy and preexposure prophylaxis., Satisfaction and acceptability of cabotegravir long-acting injectable suspension for prevention of HIV Infections Infections: Patient perspectives from the ECLAIR trial.[SEP]Relations: Rilpivirine has relations: contraindication with chronic hepatitis B virus infection, contraindication with chronic hepatitis B virus infection, drug_drug with Cabazitaxel, drug_drug with Cabazitaxel, drug_drug with Paritaprevir, drug_drug with Paritaprevir. Raltegravir has relations: drug_drug with Pibrentasvir, drug_drug with Pibrentasvir, drug_drug with Paritaprevir, drug_drug with Paritaprevir.", "label": "yes"}
{"original_question": "Is Hirschsprung disease one of the characteristics of the Mowat-Wilson syndrome?", "id": "converted_747", "sentence1": "Is Hirschsprung disease one of the characteristics of the Mowat-Wilson syndrome?", "sentence2": "Mowat-Wilson syndrome is a genetic disease caused by heterozygous Gene Mutation or Gene Deletion of the zinc finger E-box-binding homeobox 2 (ZEB2 gene gene) gene. The syndrome is characterized by typical Facial features, moderate-to-severe mental retardation, Epilepsy and variable Congenital Abnormality, including Hirschsprung disease, Abnormality of the genital system, congenital heart disease, Congenital absence of the corpus callosum, and Eye Specimen Source Code defects, Mowat-Wilson syndrome (Muckle-Wells Syndrome) is a rare genetic condition where variable and multiple congenital anomalies including Hirschsprung Disease, Intellectual Disability, and prominent Facial features are present, Individuals with Mowat-Wilson syndrome (Muckle-Wells Syndrome; OMIM#235730) have characteristic Facial features, a variety of congenital anomalies such as Hirschsprung disease, and intellectual disabilities caused by Mutation Abnormality or Gene Deletion Abnormality of ZEB2 gene gene gene, Mowat-Wilson syndrome is a genetic disease characterized by typical Facial features, Hirschsprung disease and multiple congenital abnormalities, Mowat-Wilson syndrome (Muckle-Wells Syndrome) is a severe Intellectual Disability (ID)-distinctive Facial gestalt-multiple congenital anomaly syndrome, commonly associating Microcephaly (physical finding), Epilepsy, corpus callosum Congenital absence, Conotruncal defect, urogenital malformations and Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1),  The prevalence of Mowat-Wilson syndrome is currently unknown, but it seems that Mowat-Wilson syndrome is underdiagnosed, particularly in patients without Hirschsprung disease., Mowat-Wilson syndrome is a mental retardation-multiple congenital anomaly syndrome characterized by a typical facies, developmental delay, Epilepsy, and variable Congenital Abnormality, including Hirschsprung disease, urogenital anomalies, congenital heart disease, and Congenital absence of the corpus callosum., \"Mowat-Wilson\" syndrome with and without Hirschsprung disease is a distinct, recognizable multiple congenital anomalies-mental retardation syndrome caused by Gene Mutation in the zinc finger homeo box 1B gene., Mowat-Wilson syndrome (Muckle-Wells Syndrome) is a recently delineated mental retardation; a multiple congenital anomaly syndrome characterised by a typical Facial gestalt, Hirschsprung disease or severe constipation, Urogenital Abnormalities, Congenital Heart Defects, Congenital absence of corpus callosum and Eye Specimen Source Code defects., We report a girl who had Hirschsprung disease in association with distinct Facial appearance, Microcephaly (physical finding), Congenital absence of the corpus callosum and mental retardation (Mowat-Wilson syndrome)., Mowat-Wilson syndrome (Muckle-Wells Syndrome) is characterized by severe mental retardation with Seizures, specific Facial dysmorphism, Hirschsprung disease, anomalies of the corpus callosum, and genitourinary and cardiac malformations., BACKGROUND/PURPOSE: Patients with zinc finger homeo box 1B (ZEB2 gene gene wt Allele) Gene Mutation or Gene Deletion develop multiple congenital anomalies including Hirschsprung disease, known as Mowat-Wilson syndrome (Muckle-Wells Syndrome)., Severe clinical course of Hirschsprung disease in a Mowat-Wilson syndrome patient., Mowat-Wilson syndrome (Muckle-Wells Syndrome) is a multiple congenital anomaly syndrome characterized by a distinct Facial phenotype (high forehead, Frontal bossing, large Eyebrow structure, medially flaring and sparse in the middle part, Orbital separation excessive, deep set but large Eye, large and uplifted Ear lobe, with a central depression, saddle nose with prominent rounded nasal tip, prominent Columella Columella columella, open mouth, with M-shaped upper lip, frequent smiling, and a prominent but narrow and triangular pointed chin), moderate-to-severe intellectual deficiency, Epilepsy and variable Congenital Abnormality including Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1), genitourinary anomalies (in particular Penile Penile hypospadias in males), Congenital Heart Defects, Congenital absence of the corpus callosum and Eye Specimen Source Code anomalies., Mowat-Wilson syndrome (Muckle-Wells Syndrome) is a multiple congenital anomaly syndrome characterized by a distinct Facial phenotype, Hirschsprung disease, Microcephaly (physical finding) and mental retardation., Mowat-Wilson syndrome is a genetic disease characterized by typical Facial features, Hirschsprung disease and multiple congenital abnormalities., Supernumerary intestinal muscle coat in a patient with Hirschsprung disease/Mowat-Wilson syndrome., We present the 1st case report of an additional enteric smooth muscle layer in a patient with Mowat-Wilson syndrome and Hirschsprung disease., Mowat-Wilson\" syndrome with and without Hirschsprung disease is a distinct, recognizable multiple congenital anomalies-mental retardation syndrome caused by Gene Mutation in the zinc finger homeo box 1B gene., Mowat-Wilson syndrome (Muckle-Wells Syndrome) is an autosomal dominant Intellectual Disability syndrome characterised by unique Facial features and congenital anomalies such as Hirschsprung disease, Congenital Heart Defects, corpus callosum Congenital absence and Abnormality of the urinary system., Mowat-Wilson syndrome (Muckle-Wells Syndrome) is a mental retardation syndrome associated with distinctive Facial features, Microcephaly (physical finding), Epilepsy, and a variable spectrum of congenital anomalies, including Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1), Congenital absence of the corpus callosum, genitourinary abnormalities, and congenital heart disease., Mowat-Wilson syndrome is a mental retardation-multiple congenital anomaly syndrome characterized by a typical facies, developmental delay, Epilepsy, and variable Congenital Abnormality, including Hirschsprung disease, urogenital anomalies, congenital heart disease, and Congenital absence of the corpus callosum, Mowat-Wilson syndrome is a genetic disorder characterized by a distinct Facial appearance, moderate-to-severe mental retardation, Microcephaly (physical finding), Congenital absence of the corpus callosum, Hirschsprung disease, congenital heart disease, and Abnormality of the genital system, We present the 1st case report of an additional enteric smooth muscle layer in a patient with Mowat-Wilson syndrome and Hirschsprung disease, Mowat-Wilson syndrome (Muckle-Wells Syndrome) is an autosomal dominant Intellectual Disability syndrome characterised by unique Facial features and congenital anomalies such as Hirschsprung disease, Congenital Heart Defects, corpus callosum Congenital absence and Abnormality of the urinary system, Mowat-Wilson syndrome (Muckle-Wells Syndrome) is characterized by severe mental retardation with Seizures, specific Facial dysmorphism, Hirschsprung disease, anomalies of the corpus callosum, and genitourinary and cardiac malformations, zfhz1b is the causative gene for Mowat-Wilson syndrome, in which patients demonstrate developmental delay and Hirschsprung disease, as well as other anomalies., Mowat-Wilson syndrome (Muckle-Wells Syndrome) is a mental retardation syndrome associated with distinctive Facial features, Microcephaly (physical finding), Epilepsy, and a variable spectrum of congenital anomalies, including Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1), Congenital absence of the corpus callosum, genitourinary abnormalities, and congenital heart disease, Outcomes of Hirschsprung Disease associated with Mowat-Wilson syndrome., Mowat-Wilson syndrome (Muckle-Wells Syndrome) is a multiple congenital anomaly syndrome characterized by a distinct Facial phenotype, Hirschsprung disease, Microcephaly (physical finding) and mental retardation[SEP]Relations: Mowat-Wilson syndrome has relations: disease_disease with monogenic Epilepsy, disease_disease with monogenic Epilepsy, disease_protein with RELN, disease_protein with RELN, disease_phenotype_positive with Abnormal Eye Specimen Source Code morphology, disease_phenotype_positive with Abnormal Eye Specimen Source Code morphology, disease_disease with syndromic intestinal malformation, disease_disease with syndromic intestinal malformation, disease_protein with NRG1, disease_protein with NRG1.", "label": "yes"}
{"original_question": "Is there a role for CADM1 in Myelodysplastic syndrome (MDS)?", "id": "converted_4413", "sentence1": "Is there a role for CADM1 gene in Myelodysplastic syndrome (MDS)?", "sentence2": "Together with the frequent simultaneous Gene Deletion of MLL protein, human, ammonium tetrathiomolybdate and Cytophaga-like bacteria and Gene Mutation of Putative Polycomb Group Protein Putative Polycomb Group Protein ASXL1, Splicing Factor 3B Subunit 1, human and Cytophaga-like bacteria, we show that CADM1 gene gene may be important in the physiopathology of the del(11q) MDS, extending its role as tumor-suppressor gene from Solid Neoplasm to Hematopoietic Neoplasms., The CADM1 gene gene tumor suppressor gene is a major candidate gene in MDS with Gene Deletion Abnormality of the long arm of chromosome 11.[SEP]Relations: Abnormality of the dentition has relations: disease_phenotype_positive with MGAT2-CDG, disease_phenotype_positive with MGAT2-CDG, disease_phenotype_positive with STAT3-related early-onset multisystem autoimmune disease, disease_phenotype_positive with STAT3-related early-onset multisystem autoimmune disease, disease_phenotype_positive with leukocyte adhesion deficiency, disease_phenotype_positive with leukocyte adhesion deficiency, disease_phenotype_positive with autosomal dominant Robinow syndrome, disease_phenotype_positive with autosomal dominant Robinow syndrome, disease_phenotype_positive with ectodermal dysplasia syndrome, disease_phenotype_positive with ectodermal dysplasia syndrome.", "label": "no"}
{"original_question": "Has silicon been used in treatment of  incontinence ?", "id": "converted_1447", "sentence1": "Has silicon been used in treatment of  incontinence ?", "sentence2": "an artificial anal sphincter. Worldwide, there are two established devices on the market: the artificial bowel sphincter® (CONSTRICTING BANDS, CONGENITAL) from A. M. S. (Minnetonka, MNSs Blood-Group System, USA) and the soft anal band® from A. M. I. (Feldkirch, Austria). How to implant the artificial anal sphincter? Both devices consist of a silicon cuff which can be filled with fluid., The InVance™ system uses a silicon-coated polyester sling positioned under the bulbar Urethra specimen code via a perineal incision., Through a perineal incision three titanium screws with a polipropylene suture were Clinical act of insertion in each ischiopubic rami, and a silicon/polipropylene mesh (Invance) is affixed to them, compressing the bulbar Urethra specimen code, surgical treatment of female Urinary Stress Incontinence with a trans-obturator sub-urethral tape of Uratape (Porgés). METHODS: Treatment and follow up of their complication were performed at the CHRU of Lille. RESULTS: In both cases, this complication is related to prolonged vaginal exposition of the tape. Vaginal Route of Drug Administration Route of Drug Administration erosion always occurs next to the silicon coated section of the tape, A non-elastic, polypropylene tape (UraTape, Mentor-Porgès) with a silicon coated central part was placed under the mid-Urethra specimen code.,  Stress incontinence is a rare complication in men, usually following prostatic surgery. It can be treated conservatively with Pelvic Diaphragm training and alpha-adrenergic receptor agonists and if necessary surgically with submucosal collagen or silicon injections in the sphincter area or implantation of a sphincter prosthesis, The Femassist is a medical-grade silicon dome-shaped device, worn over the Urethra specimen code and held securely via suction and a commercially available adhesive lotion., To examine the performance of a silicon urinary control device for nonsurgical management of women with genuine stress incontinence, The \"FemAssist\" is a dome-shaped medical grade silicon device intended to be worn over the external urethral meatus and held in place by suction and an adhesive gel. Thirty eight women with varying degrees of genuine Urinary Stress Incontinence (GSUI) or mixed incontinence on multichannel urodynamic testing were fitted with one of two sizes of \"FemAssist[SEP]Relations: Stress urinary incontinence has relations: phenotype_phenotype with Urinary incontinence, phenotype_phenotype with Urinary incontinence, disease_phenotype_positive with cerebral arteriopathy, autosomal dominant, with subcortical infarcts and leukoencephalopathy,, disease_phenotype_positive with cerebral arteriopathy, autosomal dominant, with subcortical infarcts and leukoencephalopathy,. Bulbar urethral stricture has relations: disease_phenotype_positive with urethral stricture (disease), disease_phenotype_positive with urethral stricture (disease). annular constricting bands has relations: disease_disease with syndromic disease, disease_disease with syndromic disease. regulation of establishment of actomyosin contractile ring localization involved in mitotic cell cycle has relations: bioprocess_bioprocess with regulation of establishment of actomyosin contractile ring localization, bioprocess_bioprocess with regulation of establishment of actomyosin contractile ring localization.", "label": "yes"}
{"original_question": "Is Olaparib effective for prostate cancer?", "id": "converted_3871", "sentence1": "Is olaparib effective for Malignant neoplasm of Pelvis>Prostate?", "sentence2": "We hypothesized that metastatic, castration-resistant Pelvis>Prostate Malignant Neoplasms with DNA-repair defects would respond to poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP1 wt Allele) inhibition with olaparib.METHODS: We conducted a phase 2 trial in which patients with metastatic, Hormone refractory Malignant neoplasm of Pelvis>Prostate were treated with olaparib tablets at a dose of 400 mg twice a day. , CONCLUSIONS: Treatment with the PARP1 wt Allele PPP1R1A gene olaparib in patients whose Pelvis>Prostate Malignant Neoplasms were no longer responding to standard treatments and who had defects in DNA-repair Genes led to a high response rate. ,  In addition, phase III trials in Breast, Gastric (qualifier value) and Malignant neoplasm of pancreas are underway/planned, and phase I/II investigation is being conducted in other malignancies, including Malignant neoplasm of Pelvis>Prostate, Non-Small Cell Lung Carcinoma, Ewing's sarcoma of bone of bone and advanced cancer. , In a phase II study, researchers found that the PARP1 wt Allele PPP1R1A gene olaparib led to stable Disease or tumor regressions in patients with advanced Breast, Ovarian, Pancreatic Hormones, and Pelvis>Prostate Malignant Neoplasms who had germline Gene Mutation in BRCA1 gene gene or BRCA2 gene gene., Eligibility included Malignant neoplasm of ovary resistant to prior Platinum metallicum, Platinum metallicum, platinum, Homeopathic preparation, Homeopathic preparation; Breast cancer with ≥ three chemotherapy regimens for metastatic Disease; Malignant neoplasm of pancreas with prior gemcitabine treatment; or Malignant neoplasm of Pelvis>Prostate with progression on hormonal and one systemic therapy. , The tumor response rate was 26.2% (78 of 298; 95% NDUFB6 gene, 21.3 to 31.6) overall and 31.1% (60 of 193; 95% NDUFB6 gene, 24.6 to 38.1), 12.9% (eight of 62; 95% NDUFB6 gene, 5.7 to 23.9), 21.7% (five of 23; 95% NDUFB6 gene, 7.5 to 43.7), and 50.0% (four of eight; 95% NDUFB6 gene, 15.7 to 84.3) in Ovarian, Breast, Pancreatic Hormones, and Pelvis>Prostate Malignant Neoplasms, respectively. Stable Disease ≥ 8 weeks was observed in 42% of patients (95% NDUFB6 gene, 36.0 to 47.4), including 40% (95% NDUFB6 gene, 33.4 to 47.7), 47% (95% NDUFB6 gene, 34.0 to 59.9), 35% (95% NDUFB6 gene, 16.4 to 57.3), and 25% (95% NDUFB6 gene, 3.2 to 65.1) of those with Ovarian, Breast, Pancreatic Hormones, or Malignant neoplasm of Pelvis>Prostate, respectively. , It is increasingly clear that there are molecularly distinct subtypes of various common Malignant Neoplasms, with different therapeutic approaches required for each subtype, for example, the use of the Monoclonal Antibodies (trastuzumab and cetuximab) in HER2-positive Breast cancer and wild-type KRAS Malignant neoplasm of colon and/or rectum; Protein-tyrosine kinase PPP1R1A gene (disposition) (imatinib, gefitinib, erlotinib and crizotinib) in Myeloid Leukemia, Chronic, Gastrointestinal Stromal Tumors and non-small-cell lung cancer and intracellular agents (vemurafenib and olaparib) in Malignant melanoma, metastatic and Ovarian, Breast and Malignant neoplasm of Pelvis>Prostate., olaparib, one of the most studied PARPis, has demonstrated activity in BRCA1 gene gene/2(MUT+) and BRCA-like sporadic Ovarian and Malignant neoplasm of Breast, and looks promising in Pelvis>Prostate and Pancreatic Hormones Malignant Neoplasms., Prostate cancer cells cotreated with the HDAC PPP1R1A gene, vorinostat (SAHA) and the PARPi, olaparib, demonstrated a synergistic decrease in cell viability compared with single-agent treatment (combination index<0.9), whereas normal prostatic cells did not., CONCLUSIONS: Treatment with the PARP1 wt Allele PPP1R1A gene olaparib in patients whose Pelvis>Prostate Malignant Neoplasms were no longer responding to standard treatments and who had defects in DNA-repair Genes led to a high response rate., olaparib, one of the most studied PARPis, has demonstrated activity in BRCA1 gene gene/2(MUT+) and BRCA-like sporadic Ovarian and Malignant neoplasm of Breast, and looks promising in Pelvis>Prostate and Pancreatic Hormones Malignant Neoplasms. , DNA-Repair Defects and olaparib in Metastatic Prostate Cancer., Prostate cancer cells cotreated with the HDAC PPP1R1A gene, vorinostat (SAHA) and the PARPi, olaparib, demonstrated a synergistic decrease in cell viability compared with single-agent treatment (combination index < 0.9), whereas normal prostatic cells did not., We hypothesized that metastatic, castration-resistant Pelvis>Prostate Malignant Neoplasms with DNA-repair defects would respond to poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP1 wt Allele) inhibition with olaparib., A phase II study of the PARP1 wt Allele PPP1R1A gene olaparib (AstraZeneca) for cancer patients with inherited BRCA1 gene gene and BRCA2 gene gene gene Gene Mutation confirmed earlier results showing clinical benefit for advanced Breast and Ovarian Malignant Neoplasms, and demonstrated evidence of effectiveness against Pancreatic Hormones and Pelvis>Prostate Malignant Neoplasms., BACKGROUND: Prostate cancer is a heterogeneous Disease, but current treatments are not based on Molecular stratification. We hypothesized that metastatic, castration-resistant Pelvis>Prostate Malignant Neoplasms with DNA-repair defects would respond to poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP1 wt Allele) inhibition with olaparib.METHODS: We conducted a phase 2 trial in which patients with metastatic, Hormone refractory Malignant neoplasm of Pelvis>Prostate were treated with olaparib tablets at a dose of 400 mg twice a day. , Prostate cancer is a heterogeneous Disease, but current treatments are not based on Molecular stratification. We hypothesized that metastatic, castration-resistant Pelvis>Prostate Malignant Neoplasms with DNA-repair defects would respond to poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP1 wt Allele) inhibition with olaparib., Silencing DNA Repair Protein DNA Repair Protein RAD51 Homolog 1 Homolog 1 sensitized Malignant neoplasm of Pelvis>Prostate cells to SAHA and olaparib alone. Collectively, cotreatment with HDACi and PARPi downregulated HR-related protein expression and concomitantly increased DNA damage, resulting in Malignant neoplasm of Pelvis>Prostate cell death., Prostate cancer cells cotreated with the HDAC PPP1R1A gene, vorinostat (SAHA) and the PARPi, olaparib, demonstrated a synergistic decrease in cell viability compared with single-agent treatment (combination index<0.9), whereas normal prostatic cells did not. , The specificity of the biomarker suite was 94%. Genus Genus Anemia (in 10 of the 50 patients [20%]) and Fatigue (in 6 [12%]) were the most common grade 3 or 4 adverse events, findings that are consistent with previous studies of olaparib.CONCLUSIONS: Treatment with the PARP1 wt Allele PPP1R1A gene olaparib in patients whose Pelvis>Prostate Malignant Neoplasms were no longer responding to standard treatments and who had defects in DNA-repair Genes led to a high response rate. , Prostate cancer cells cotreated with the HDAC PPP1R1A gene, vorinostat (SAHA) and the PARPi, olaparib, demonstrated a synergistic decrease in cell viability compared with single-agent treatment (combination index &lt; 0.9), whereas normal prostatic cells did not., In addition, phase III trials in Breast, Gastric (qualifier value) and Malignant neoplasm of pancreas are underway/planned, and phase I/II investigation is being conducted in other malignancies, including Malignant neoplasm of Pelvis>Prostate, Non-Small Cell Lung Carcinoma, Ewing's sarcoma of bone of bone and advanced cancer. , INTERPRETATION: olaparib has antitumour activity against metastatic Hormone refractory Malignant neoplasm of Pelvis>Prostate with DDR gene aberrations, supporting the implementation of Genome stratification of metastatic Hormone refractory Malignant neoplasm of Pelvis>Prostate in clinical practice., CONCLUSIONS: In men with metastatic Hormone refractory Malignant neoplasm of Pelvis>Prostate who had Disease progression while receiving enzalutamide or abiraterone and who had alterations in Genes with a role in homologous recombination repair, olaparib was associated with longer progression-free survival and better measures of response and patient-reported end points than either enzalutamide or abiraterone., olaparib is an additional option for second- and third-line treatment in those with alterations in BRCA1 gene gene, BRCA2 gene gene, and ammonium tetrathiomolybdate. , In this review, we describe current therapies for mCRPC, the rationale for anti-PARP1 wt Allele therapies, the pharmacology of olaparib for Malignant neoplasm of Pelvis>Prostate, clinical trials of olaparib for mCRPC, our clinical experience with olaparib for Malignant neoplasm of Pelvis>Prostate at a comprehensive cancer center, and future directions of olaparib for the treatment of mCRPC., olaparib, a poly (ADP-ribose) polymerase PPP1R1A gene, has demonstrated an improvement in median progression-free survival (PFS) in select patients with metastatic Hormone refractory Malignant neoplasm of Pelvis>Prostate (mCRPC)., Activity of durvalumab plus olaparib in metastatic Hormone refractory Malignant neoplasm of Pelvis>Prostate in men with and without DNA damage repair Gene Mutation., BACKGROUND: Patients with metastatic Hormone refractory Malignant neoplasm of Pelvis>Prostate and homologous recombination repair (double-strand break repair via homologous recombination) Gene Mutation have a better response to treatment with the poly(ADP-ribose) polymerase PPP1R1A gene olaparib than patients without double-strand break repair via homologous recombination Gene Mutation., The TOPARP-A clinical trial demonstrated that the PARP1 wt Allele PPP1R1A gene olaparib may be an effective strategy for treating Malignant neoplasm of Pelvis>Prostate., MMARY: The poly(ADP-ribose) polymerase (PARP1 wt Allele) inhibitors olaparib and rucaparib are now approved by the Food and Drug Administration for the treatment of advanced Malignant neoplasm of Pelvis>Prostate. Here, we , BACKGROUND: We previously reported that olaparib led to significantly longer imaging-based progression-free survival than the physician's choice of enzalutamide or abiraterone among men with metastatic Hormone refractory Malignant neoplasm of Pelvis>Prostate who had qualifying alterations in homologous recombination repair Genes and whose Disease had progressed during previous treatment with a next-generation hormonal agent., Recent clinical studies show favorable results for the PARP1 wt Allele PPP1R1A gene olaparib used as single agent for treatment of metastatic castration-resistant PCa., The PROFOUND phase III trial, comparing olaparib with enzalutamide/abiraterone therapy, revealed increased radiological progression-free survival (rPFS) and overall survival (OS) among patients with metastatic Hormone refractory Malignant neoplasm of Pelvis>Prostate (mCRPC) with BRCA1 gene gene, BRCA2 gene gene or ammonium tetrathiomolybdate Gene Mutation., olaparib Targets Some Advanced Prostate Cancers., The PARP1 wt Allele PPP1R1A gene (PARPi) olaparib received FDA breakthrough designation for treatment of metastatic castration-resistant Pelvis>Prostate Malignant Neoplasms (CRPC) carrying Gene Mutation in BRCA1 gene gene/2 or ammonium tetrathiomolybdate Genes.,  In Malignant neoplasm of Pelvis>Prostate, two PARPi, rucaparib and olaparib, have been FDA approved for the treatment of metastatic Hormone refractory Malignant neoplasm of Pelvis>Prostate (mCRPC)., olaparib is an FDA-approved PARP1 wt Allele PPP1R1A gene (PARPi) that has shown promise as a synthetic lethal treatment approach for BRCA-mutant Hormone refractory Malignant neoplasm of Pelvis>Prostate (CRPC) in clinical use, Targeting PLK1 gene to Enhance Efficacy of olaparib in Castration-Resistant Prostate Cancer, RECENT FINDINGS: The approval of several PARPi (olaparib, rucaparib, and niraparib) has driven the focus of anticancer treatment on synthetic lethality in Malignant neoplasm of Pelvis>Prostate too. , PATIENT SUMMARY: A large clinical study concluded that treatment with the PARP1 wt Allele PPP1R1A gene olaparib benefits men with metastatic Hormone refractory Malignant neoplasm of Pelvis>Prostate whose Neoplasms harbor alterations in 15 different DNA repair Genes.,  Among them, olaparib and rucaparib have breakthrough designations for BRCA1 gene gene/2-mutated mCRPC., In phase II clinical trials, including patients with advanced castration-resistant PC, olaparib seems to be efficacious and well tolerated. , Of note is the recent U.S. Food and Drug Administration breakthrough therapy designation of olaparib for the treatment of BRCA1 gene gene/2- or ammonium tetrathiomolybdate-mutated metastatic Hormone refractory Malignant neoplasm of Pelvis>Prostate. [SEP]Relations: olaparib has relations: drug_drug with Testosterone, drug_drug with Testosterone, drug_drug with Sonidegib, drug_drug with Sonidegib, drug_drug with Medical Cannabis, drug_drug with Medical Cannabis, drug_drug with Orlistat, drug_drug with Orlistat, drug_drug with Apremilast, drug_drug with Apremilast.", "label": "yes"}
{"original_question": "Does epidural anesthesia for pain management during labor affect the Apgar score of the the infant?", "id": "converted_2844", "sentence1": "Does epidural anesthesia for pain management during labor affect the Apgar score of the the infant?", "sentence2": " We retrospectively analyzed 93 consecutive single-pregnancy patients who underwent cesarean section with combined spinal-epidural anesthesia. The patients were divided into two groups, depending on the use of 6% Idiopathic Hypereosinophilic Syndrome 130/0.4: group A (461 ± 167 ml of saline-based Idiopathic Hypereosinophilic Syndrome was administered; 43 patients) and group B (Idiopathic Hypereosinophilic Syndrome not administered; 50 patients). The major outcome was umbilical cord chloride level at delivery. The volume infused from operating room admission until delivery was not significantly different between groups. The umbilical cord chloride level at delivery was statistically significantly higher in group A than in group B, but clinically similar (108 ± 2 vs. 107 ± 2 mmol/l, P = 0.02). No differences were observed in the Apgar score or other umbilical cord laboratory data at delivery (Na+, K+, pH, base excess), CONCLUSION\nSubarachnoid or epidural sufentanil, in the doses used in this study, associated with local anesthetics, had the same effect on the duration of labor after analgesia and in the Apgar score of newborns., CONCLUSION Subarachnoid or epidural sufentanil, in the doses used in this study, associated with local anesthetics, had the same effect on the duration of labor after analgesia and in the Apgar score of newborns.[SEP]Relations: Sufentanil has relations: drug_effect with Apnea, drug_effect with Apnea, drug_effect with Laryngeal stridor, drug_effect with Laryngeal stridor, drug_effect with Erythema, drug_effect with Erythema. idiopathic hypereosinophilic syndrome has relations: disease_phenotype_positive with Paresthesia, disease_phenotype_positive with Paresthesia, disease_phenotype_positive with Feeding difficulties in infancy, disease_phenotype_positive with Feeding difficulties in infancy.", "label": "no"}
{"original_question": "Can mitochondria pass through membrane nanotubes?", "id": "converted_3176", "sentence1": "Can Mitochondria pass through membrane nanotubes?", "sentence2": "Membrane nanotubes (MNTs) act as \"highways\" between Cells to facilitate the transfer of multiple signals and play an important role in many diseases. Our previous work reported on the transfer of Mitochondria via MNTs between Myocytes, Cardiac (Myasthenic Syndromes, Congenital) and cardiac myofibroblasts (Marfan Syndrome), Membrane nanotubes play important functional roles in numerous cell activities such as cellular transport and communication.[SEP]Relations: mitochondrion has relations: cellcomp_protein with POR, cellcomp_protein with POR, cellcomp_protein with SLIT3, cellcomp_protein with SLIT3, cellcomp_protein with BID, cellcomp_protein with BID, cellcomp_protein with TRAP1, cellcomp_protein with TRAP1, cellcomp_protein with PSMB4, cellcomp_protein with PSMB4.", "label": "yes"}
{"original_question": "Can RNASeq be used for the analysis of nascent transcripts?", "id": "converted_1391", "sentence1": "Can RNASeq be used for the analysis of nascent transcripts?", "sentence2": "Here, we utilize nascent RNA sequencing to document dosage compensation during transcriptional elongation., Here we show that RNA-seq can also be used for studying nascent RNAs undergoing transcription, Conversely, the nuclear fraction shows an enrichment of unprocessed RNA compared with total RNA-seq, making it suitable for analysis of nascent transcripts and RNA processing dynamics.[SEP]", "label": "yes"}
{"original_question": "Does the histidine-rich Ca-binding protein (HRC) interact with triadin?", "id": "converted_895", "sentence1": "Does the histidine-rich cyclophosphamide/doxorubicin protocol-binding Protein Info (HRC) interact with TRDN gene?", "sentence2": "The HRC effects on Ryanodine Receptor Calcium Release Channel complex location may be regulated by the cyclophosphamide/doxorubicin protocol(2+)-sensitivity of its interaction with TRDN gene., In rabbit allergenic extract allergenic extract skeletal and Myocardium, HRC binds to Sarcoplasmic Reticulum (SNCG wt Allele) membranes via TRDN gene, a junctional SNCG wt Allele Protein Info. , HRC may play a key role in the regulation of SNCG wt Allele cyclophosphamide/doxorubicin protocol cycling through its direct interactions with Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase 2 and TRDN gene, mediating a fine cross talk between SNCG wt Allele cyclophosphamide/doxorubicin protocol uptake and release in the Chest>Heart., Histidine-rich CALCIUM SUPPLEMENTS binding Protein Info (HRC) is located in the Units Of Measure - Units Of Measure - lumen of Sarcoplasmic Reticulum (SNCG wt Allele) that binds to both TRDN gene (TRN-GTT2-7 gene-GTT2-7 gene) and SERCA affecting cyclophosphamide/doxorubicin protocol(2+) cycling in the SNCG wt Allele., HRC is a SNCG wt Allele luminal cyclophosphamide/doxorubicin protocol(2+) binding Protein Info known to associate with both TRDN gene and the Sarcoplasmic Reticulum cyclophosphamide/doxorubicin protocol(2+)-ATPase, and may thus mediate the crosstalk between SNCG wt Allele cyclophosphamide/doxorubicin protocol(2+) uptake and release., The histidine-rich cyclophosphamide/doxorubicin protocol(2+) binding Protein Info (HRC) is a high capacity cyclophosphamide/doxorubicin protocol(2+) binding Protein Info in the Sarcoplasmic Reticulum (SNCG wt Allele). Because HRC appears to interact directly with TRDN gene, HRC may play a role in the regulation of cyclophosphamide/doxorubicin protocol(2+) release during excitation-contraction coupling., In the present study, we have performed co-immunoprecipitation experiments and show that HRC binds directly to TRDN gene, which is an integral membrane Protein Info of the Sarcoplasmic Reticulum., A direct binding of HRC (histidine-rich cyclophosphamide/doxorubicin protocol(2+)-binding Protein Info) to TRDN gene, the main Integral Membrane Proteins of the junctional Sarcoplasmic Reticulum (SNCG wt Allele) of Specimen Source Codes - Skeletal muscle, seems well supported., The present study documents the binding interaction of Specimen Source Codes - Skeletal muscle Sarcoplasmic Reticulum (SNCG wt Allele) Integral Membrane Proteins TRDN gene with peripheral histidine-rich, cyclophosphamide/doxorubicin protocol(2+)-binding Protein Info (HCP)., In addition, the intra-luminal histidine-rich CALCIUM SUPPLEMENTS binding Protein Info (HRC) has been shown to interact with both SERCA2a and TRDN gene., Notably, there is physical and direct interaction between these Protein Info players, mediating a fine-cross talk between SNCG wt Allele cyclophosphamide/doxorubicin protocol-uptake, storage and release., The histidine-rich CALCIUM SUPPLEMENTS-binding Protein Info (HRCBP) is expressed in the junctional SNCG wt Allele, the site of CALCIUM SUPPLEMENTS release from the SNCG wt Allele. HRCBP is expressed exclusively in Muscle Tissue and binds CALCIUM SUPPLEMENTS with low affinity and high capacity. In addition, HRCBP interacts with TRDN gene, a Protein Info associated with the Ryanodine Receptor Calcium Release Channel and thought to be involved in CALCIUM SUPPLEMENTS release. Its CALCIUM SUPPLEMENTS binding properties, localization to the SNCG wt Allele, and interaction with TRDN gene suggest that HRCBP is involved in CALCIUM SUPPLEMENTS handling by the SNCG wt Allele., Using a fusion Protein Info binding assay, we further identified the histidine-rich acidic repeats of HRC as responsible for the binding of HRC to TRDN gene. , The HRC binding domain of TRDN gene was also localized by fusion Protein Info binding assay to the lumenal region containing the KEKE motif that was previously shown to be involved in the binding of TRDN gene to CASQ2 gene. Notably, the interaction of HRC and TRDN gene is cyclophosphamide/doxorubicin protocol(2+)-sensitive. Our data suggest that HRC may play a role in the regulation of cyclophosphamide/doxorubicin protocol(2+) release from the Sarcoplasmic Reticulum by interaction with TRDN gene., Further support for colocalization of HRC with TRDN gene Cytoplasmic Domain is provided here by experiments of mild tryptic digestion of tightly sealed TC vesicles., We demonstrate that HRC can be isolated as a complex with TRDN gene, following equilibrium sucrose-density centrifugation in the presence of mM cyclophosphamide/doxorubicin protocol(2+)., Here, we characterized the COOH-terminal portion of rabbit allergenic extract allergenic extract HRC, expressed and purified as a fusion Protein Info (HRC(569-852)), with respect to cyclophosphamide/doxorubicin protocol(2+)-binding properties, and to the interaction with TRDN gene on blots, as a function of the concentration of cyclophosphamide/doxorubicin protocol(2+)., Our results identify the polyglutamic stretch near the COOH terminus, as the cyclophosphamide/doxorubicin protocol(2+)-binding site responsible, both for the acceleration in mobility of HRC on SDS-PAGE in the presence of millimolar concentrations of cyclophosphamide/doxorubicin protocol(2+), and for the enhancement by high cyclophosphamide/doxorubicin protocol(2+) of the interaction between HRC and TRDN gene cytoplasmic segment., In addition to providing further evidence that HCP coenriches with Ryanodine Receptor 1, Tacrolimus Binding Protein 1A, TRDN gene and CASQ2 gene (CS) in sucrose-density-purified TC vesicles, using specific polyclonal antibody, we show it to be expressed as a single Protein Info species, both in fast-twitch and slow-twitch fibers, and to identically localize to the I-band., Colocalization of HCP and TRDN gene at junctional triads is supported by the overlapping staining pattern using Monoclonal Antibodies to TRDN gene. We show a specific binding interaction between digoxigenin-HCP and TRDN gene, using ligand blot techniques., Suggesting that TRDN gene dually interacts with HCP and with CS, at distinct sites, we have found that TRDN gene-CS interaction in overlays does not require the presence of Ca2+., These differential effects form the basis for the hypothesis that HCP anchors to the junctional membrane domain of the SNCG wt Allele, through binding to TRDN gene short Cytoplasmic Domain at the NH2 terminus., Although the function of this interaction, as such, is not well understood, it seems of potential biological interest within the more general context of the structural-functional role of TRDN gene at the triadic junction in Specimen Source Codes - Skeletal muscle., BACKGROUND: Histidine-rich CALCIUM SUPPLEMENTS binding Protein Info (HRC) is located in the Units Of Measure - Units Of Measure - lumen of Sarcoplasmic Reticulum (SNCG wt Allele) that binds to both TRDN gene (TRN-GTT2-7 gene-GTT2-7 gene) and SERCA affecting cyclophosphamide/doxorubicin protocol(2+) cycling in the SNCG wt Allele. Chronic overexpression of HRC that may disrupt Protoplasm cyclophosphamide/doxorubicin protocol(2+) homeostasis is implicated in pathogenesis of Cardiac Hypertrophy., Interaction of HRC (histidine-rich cyclophosphamide/doxorubicin protocol(2+)-binding Protein Info) and TRDN gene in the Units Of Measure - Units Of Measure - lumen of Sarcoplasmic Reticulum., The histidine-rich cyclophosphamide/doxorubicin protocol-binding Protein Info (HRC) is an SNCG wt Allele component that binds to TRDN gene and may affect cyclophosphamide/doxorubicin protocol release through the Ryanodine Receptor Calcium Release Channel., The histidine-rich cyclophosphamide/doxorubicin protocol-binding Protein Info (HRC) is an SNCG wt Allele component that binds to TRDN gene and may affect cyclophosphamide/doxorubicin protocol release through the Ryanodine Receptor Calcium Release Channel, Because HRC appears to interact directly with TRDN gene, HRC may play a role in the regulation of cyclophosphamide/doxorubicin protocol(2+) release during excitation-contraction coupling, A direct binding of HRC (histidine-rich cyclophosphamide/doxorubicin protocol(2+)-binding Protein Info) to TRDN gene, the main Integral Membrane Proteins of the junctional Sarcoplasmic Reticulum (SNCG wt Allele) of Specimen Source Codes - Skeletal muscle, seems well supported, The histidine-rich cyclophosphamide/doxorubicin protocol-binding Protein Info (HRC) is an SNCG wt Allele component that binds to TRDN gene and may affect cyclophosphamide/doxorubicin protocol release through the Ryanodine Receptor Calcium Release Channel[SEP]Relations: Protein Info binding has relations: molfunc_protein with HRC, molfunc_protein with HRC, molfunc_protein with HRK, molfunc_protein with HRK, molfunc_protein with HRAS, molfunc_protein with HRAS, molfunc_protein with HRG, molfunc_protein with HRG, molfunc_protein with CA3, molfunc_protein with CA3.", "label": "yes"}
{"original_question": "Is fusobacterium associated with Lemierre's syndrome?", "id": "converted_4316", "sentence1": "Is fusobacterium associated with Lemierre's syndrome?", "sentence2": "Invasive infections with Fusobacterium necrophorum including Lemierre's syndrome: an 8-year Swedish nationwide retrospective study., Lemierre's syndrome is defined as an oropharyngeal Communicable Diseases due to Fusobacterium necrophorum,, Lemierre's syndrome is a rare but life-threatening condition characterized by an oropharyngeal Communicable Diseases typically secondary to Fusobacterium necrophorum resulting in Septic Thrombophlebitis of the internal jugular vein. ,  Lemierre's syndrome is a rare condition that results from oropharyngeal Communicable Diseases with the gram-negative, anaerobic Fusobacterium necrophorum., INTRODUCTION: Like Fusobacterium necrophorum, Fusobacterium nucleatum is capable causing Lemierre's syndrome., [Lemierre syndrome variant: Liver Abscess and hepatic venous thrombosis due to Fusobacterium nucleatum septicemia]., Fusobacterium necrophorum-induced Sepsis (Invertebrate): an unusual case of Lemierre's syndrome., F necrophorum is most commonly associated with Lemierre's syndrome: a Septic Thrombophlebitis of the internal jugular vein., Fusobacterium necrophorum Septicemia Leading to Lemierre's Syndrome in an Immunocompetent Individual: A Case Report., We present a case of a patient with Lemierre's syndrome caused by Fusobacterium necrophorum who developed a right frontal lobe brain abscess., Lemierre's syndrome secondary to Fusobacterium necrophorum Communicable Diseases, a rare cause of hepatic abscess., Lemierre's syndrome is an uncommon complication of Pharyngitis commonly associated with an anaerobic gram negative bacterium, Fusobacterium necrophorum., The following presentation is a case of Lemierre's syndrome in a 23-year-old healthy individual who is infected by a rare species: Fusobacterium nucleatum., However, Fusobacterium species causing Lemierre's variant gastrointestinal syndrome has only been reported in case reports., Fusobacterium species is known for being a causative agent for Lemierre's syndrome, which is characterized by Thrombophlebitis of the jugular vein., The Fusobacterium species is known for its association with Septic Thrombophlebitis of the internal jugular vein (Lemierre's syndrome). Lemierre's syndrome is as, Lemierre's syndrome due to Fusobacterium necrophorum., Fusobacterium species are well described as the causative pathogen in Lemierre's syndrome, a suppurative Thrombophlebitis of the jugular vein. However, they are less r, Introduction: Lemierre's syndrome is a rare but serious complication of an Oral Communicable Diseases mostly related to Fusobacterium necrophorum. This condition combines j, Fusobacterium necrophorum is a gram-negative anaerobic bacterium that is the causative agent of the invasive disease Lemierre's syndrome., INTRODUCTION: Lemierre's syndrome is defined as an oropharyngeal Communicable Diseases due to Fusobacterium necrophorum, associated with Septic Thrombophlebitis of the internal , Fusobacterium nucleatum is a gram-negative bacillius commonly found in Oropharyngeal and is traditionally associated with Lemierre syndrome, which is characterized by history of recent oropharyngeal Communicable Diseases, internal jugular vein thrombosis, and isolation of anaerobic pathogens, mainly Fuosobacterium necrophorum. Ho, Lemierre's syndrome is an uncommon complication of Pharyngitis commonly associated with an anaerobic gram negative bacterium, Fusobacterium necrophorum. , Fusobacterium species is known for being a causative agent for Lemierre's syndrome, which is characterized by Thrombophlebitis of the jugular vein. , Lemierre's syndrome is a systemic complication commonly caused by oropharyngeal Communicable Diseases by Fusobacterium species, which manifests itself as an internal jugular vein thrombosis formation. , Lemierre's syndrome is a rare but serious condition, characterized by disseminated Communicable Diseases with Fusobacterium necrophorum, most often originating from the Oropharyngeal. T, Lemierre's syndrome is a rare clinical condition that generally develops secondary to oropharyngeal Communicable Diseases caused by Fusobacterium necrophorum, which is an anaerobic bacteria. , Lemierre's syndrome, a systemic anaerobic Communicable Diseases caused by Fusobacterium necrophorum, is characterized by an acute oropharyngeal Communicable Diseases, Septic Thrombophlebitis of the internal jugular veins, Sepsis (Invertebrate), and multiple metastatic infections. It c, Lemierre's syndrome, a systemic anaerobic Communicable Diseases caused by Fusobacterium necrophorum, is characterized by an acute oropharyngeal Communicable Diseases, Septic Thrombophlebitis of the internal jugular vein, Sepsis (Invertebrate), and multiple metastatic infections. It c, Fusobacterium necrophorum is a rare Communicable Diseases most notable for causing Lemierre's syndrome., We present a patient with an atypical presentation of Fusobacterium Infections, the genus responsible for Lemierre's syndrome., INTRODUCTION: Like Fusobacterium necrophorum, Fusobacterium nucleatum is capable causing Lemier, Fusobacterium necrophorum, a well‐known cause of Lemierre's syndrome, was identified., We report an unusual case of Lemierre's syndrome due to a rare species of Fusobacterium, that is, Fusobacterium nucleatum preceded by Mycoplasma pneumoniae Pharyngitis and followed later by Epstein-Barr virus infectious mononucleosis., We present a case of invasive Fusobacterium Infections that meets all criteria for Lemierre syndrome except lacking internal jugular thrombosis., Fusobacterium necrophorum is ananaerobic Gram-negative bacillus and is the most common Organism reported to cause Lemierre's syndrome which usually occurs one to three weeks post Pharyngitis or oropharyngeal surgery., Lemierre Syndrome: postanginal bacteremia and pulmonary involvement caused by Fusobacterium necrophorum., Increased diagnosis of Lemierre syndrome and other Fusobacterium necrophorum infections at a Children's Hospital., The Fusobacterium species is known for its association with Septic Thrombophlebitis of the internal jugular vein (Lemierre's syndrome)., Fusobacterium species have rarely been implicated in cases of gastrointestinal variant of Lemierre's syndrome., Fusobacterium species are well described as the causative pathogen in Lemierre's syndrome, a suppurative Thrombophlebitis of the jugular vein., F. necrophorum is unique among non-spore-forming anaerobes, first for its virulence and association with Lemierre's syndrome as a monomicrobial Communicable Diseases and second because it seems probable that it is an exogenously acquired Communicable Diseases., Phylum Phylum Fusobacteria are most often associated with the classic presentation of Lemierre's syndrome consisting of a Sore Throat brand of benzocaine & menthol, internal jugular vein Thrombophlebitis, and septic emboli to the Lung., Fusobacterium necrophorum plays a causal role in a rare and life-threatening condition, Lemierre's syndrome., Lemierre's syndrome is a rare disorder of young adults caused by the anaerobic bacterium, Fusobacterium necrophorum and occasionally by other Fusobacterium species (F. nucleatum, F. mortiferum and F. varium etc)., Lemierre's syndrome is a severe complication of Fusobacterium necrophorum oropharyngeal Communicable Diseases associated with metastatic foci of Communicable Diseases, internal jugular vein thrombosis, and septicemia., Short blood culture time-to-positivity in Fusobacterium necrophorum bacteremia is associated with Lemierre's syndrome., The causative organisms are the anaerobic fusobacteria, most commonly Fusobacterium necrophorum., In a 3-year prospective study, all cases of disseminated Fusobacterium necrophorum infections found in Denmark from 1998 to 2001 were analysed, with the aim of describing the epidemiology and clinical features of the Variant of Lemierre's syndrome and disseminated non-head-and-neck-associated F. necrophorum infections.[SEP]Relations: Lemierre syndrome has relations: disease_disease with commensal bacterial infectious disease, disease_disease with commensal bacterial infectious disease, disease_disease with bacterial infectious disease with Sepsis (Invertebrate), disease_disease with bacterial infectious disease with Sepsis (Invertebrate). Fusobacterium infectious disease has relations: disease_disease with anaerobic bacteria infectious disease, disease_disease with anaerobic bacteria infectious disease, disease_disease with anaerobic bacteria infectious disease, disease_disease with anaerobic bacteria infectious disease, disease_disease with gram-negative bacterial infections, disease_disease with gram-negative bacterial infections.", "label": "yes"}
{"original_question": "Is adenosine signaling prognostic for cancer outcome?", "id": "converted_4194", "sentence1": "Is adenosine signaling prognostic for cancer outcome?", "sentence2": "Adenosine Signaling Is Prognostic for Cancer Outcome and Has Predictive Utility for Immunotherapeutic Response., There are several agents in early clinical trials targeting components of the adenosine pathway including ADORA2A wt Allele and 5'-NUCLEOTIDASE. The identification of Malignant Neoplasms with a significant adenosine drive is critical to understand the potential for these Molecule. However, it is challenging to measure tumor adenosine levels at scale, thus novel, clinically tractable biomarkers are needed.EXPERIMENTAL DESIGN: We generated a gene expression signature for the adenosine signaling using regulatory networks derived from the literature and validated this in patients. We applied the signature to large cohorts of Disease from The Cancer Genome Atlas (TCGA) and cohorts of immune checkpoint inhibitor-treated patients.RESULTS: The signature captures baseline adenosine levels in vivo (r 2 = 0.92, P = 0.018), is reduced after small-molecule inhibition of ADORA2A wt Allele in CASP14 gene (r 2 = -0.62, P = 0.001) and Homo sapiens (reduction in 5 of 7 patients, 70%), and is abrogated after ADORA2A wt Allele knockout. Analysis of TCGA confirms a negative association between adenosine and overall survival (OS, HR = 0.6, P < 2.2e-16) as well as progression-free survival (PFS, HR = 0.77, P = 0.0000006). Further, adenosine signaling is associated with reduced OS (HR = 0.47, P < 2.2e-16) and PFS (HR = 0.65, P = 0.0000002) in CD8+ T-cell-infiltrated tumors. Mutation Abnormality Abnormality of TGFβ superfamily members is associated with enhanced adenosine signaling and worse OS (HR = 0.43, P < 2.2e-16). Finally, adenosine signaling is associated with reduced efficacy of anti-PD1 therapy in published cohorts (HR = 0.29, P = 0.00012).CONCLUSIONS: These data support the adenosine pathway as a mediator of a successful Antitumor immune response, demonstrate the prognostic potential of the signature for immunotherapy, and inform patient selection strategies for adenosine pathway modulators currently in development.[SEP]Relations: Adenosine has relations: contraindication with coronary artery Disease, contraindication with coronary artery Disease, contraindication with asthma, contraindication with asthma, contraindication with autonomic nervous system Disease, contraindication with autonomic nervous system Disease, drug_effect with Apnea, drug_effect with Apnea, drug_effect with Coronary artery atherosclerosis, drug_effect with Coronary artery atherosclerosis.", "label": "yes"}
{"original_question": "Can valproic acid act as an activator of AMPK?", "id": "converted_238", "sentence1": "Can valproic acid act as an activator of AMPK?", "sentence2": "Here we demonstrate that valproic acid is a novel activator of AMP-Activated Protein Kinases (AMPK), a key regulator of cellular metabolism, using primary mouse and human hepatocytes., These studies are the first to establish valproic acid and its Metabolite as in vitro activators of AMPK.[SEP]Relations: Valproic acid has relations: drug_drug with Amprenavir, drug_drug with Amprenavir, drug_drug with Amphetamine, drug_drug with Amphetamine, drug_effect with Arthropathy, drug_effect with Arthropathy, drug_drug with Acetylsalicylic acid, drug_drug with Acetylsalicylic acid, drug_drug with Glutaric Acid, drug_drug with Glutaric Acid.", "label": "yes"}
{"original_question": "Have thyronamines effects on fat tissue?", "id": "converted_1596", "sentence1": "Have thyronamines effects on fat tissue?", "sentence2": "Intraperitoneal or central injection of 3-T(1)AM or T(0)AM into CASP14 gene, Rattus norvegicus, or Djungarian hamsters caused various prompt effects, such as metabolic depression, Hypothermia due to exposure, negative chronotropy, negative inotropy, Glucose in blood specimen above reference range, reduction of the respiratory quotient, Ketonuria, and reduction of fat mass. [SEP]Relations: Ketonuria has relations: drug_effect with Propafenone, drug_effect with Propafenone, drug_effect with Streptozocin, drug_effect with Streptozocin, drug_effect with Acitretin, drug_effect with Acitretin, drug_effect with Rosiglitazone, drug_effect with Rosiglitazone, drug_effect with Carbamazepine, drug_effect with Carbamazepine.", "label": "yes"}
{"original_question": "Is DNA methylation correlated with nucleosome occupancy?", "id": "converted_2330", "sentence1": "Is DNA methylation correlated with nucleosome location occupancy?", "sentence2": "Here I show that CpG Islands were associated not only with methylation-free promoters but also with nucleosome location location-free promoters., Nucleosome-free regions were observed only in promoters containing a CpG island, In contrast to the methylation-and nucleosome location location-free states of CpG-island promoters, Exons were densely methylated at CpGs and packaged into Nucleosomes., I also found that Nucleosomes, DNA methylation, and Histone H3 Trimethyl Lys36 marked the Exons of RNA Transcript with low, medium, and high gene expression levels, respectively., Human promoters containing a CpG island tend to remain nucleosome location location-free as well as methylation-free., In contrast, Exons demonstrate a high degree of methylation and nucleosome location location occupancy., Exonic DNA methylation seems to function together with exonic Nucleosomes and Histone H3 Trimethyl Lys36 for the proper splicing of RNA Transcript with different expression levels., Supporting such an association, recent reports have identified distinct histone methylation patterns, elevated nucleosome location location occupancy and enriched DNA methylation at Exons relative to Introns., DNA methylation directly silences genes with non-CpG island promoters and establishes a nucleosome location location occupied Promoter., Using a novel bioinformatics pipeline, we show a striking anti-correlation between nucleosome location location occupancy and DNA methylation at CTGF protein, Homo sapiens regions that is not present at promoters. , Three positions at the splice sites show high CpG abundance and accompany elevated nucleosome location location occupancy in a leveled GC architecture., The first group has higher nucleosome location location occupancy on Exons than Introns, whereas the second group exhibits weak nucleosome location location marking of Exons, suggesting another type of epigenetic marker distinguishes Exons from Introns when GC content is similar.,  DNA methylation can determine nucleosome location location positioning. , DNA methylation determines nucleosome location location occupancy in the 5'-CpG Islands of Tumor Suppressor Genes., he induction of DNA hypomethylation events by Genetic (DNMT1/DNMT3B deficient cells) or Pharmacologic Substance (a DNA demethylating agent) approaches is associated with the eviction of Nucleosomes from previously hypermethylated CpG Islands of Tumor Suppressor Genes., Using this global approach, we observe the dependency of nucleosome location location occupancy upon the DNA methylation status. Thus, our results suggest that there is a close association between hypermethylated CpG Islands and the presence of Nucleosomes, such that each of these epigenetic mechanisms can determine the recruitment of the other., Although global DNA demethylation has been observed after treatment, it is unclear to what extent demethylation induces changes in nucleosome location location occupancy, a key determinant of gene expression., Our results indicate that only a minority of demethylated promoters are associated with nucleosome location location remodeling, and these could potentially be the epigenetic drivers causing the loss of tumorigenicity., with repressed genes often being associated with local DNA hypermethylation and gain of Nucleosomes at their promoters., Transcription, histone modification, and DNA methylation alter this \"ground state\" by having distinct effects on both nucleosome location location positioning and occupancy. , In order to systematically evaluate potential diversities among CGIs and ultimately to illuminate the link between diversity of CGIs and their epigenetic variation, we analyzed the nucleotide-resolution DNA methylation maps (methylomes) of multiple cellular origins., The mostly unmethylated CpG Islands have reduced nucleosome location location occupancy and are enriched in cell type-independent binding sites for CTGF protein, Homo sapiens., In contrast, outside of CpG Islands most CpGs are methylated, and the average methylation density oscillates so that it is highest in the linker region between Nucleosomes., Aberrant acquisition of Nucleosomes at enhancer-associated NDRs is associated with hypermethylation and epigenetic silencing marks, and conversely, loss of Nucleosomes with demethylation and epigenetic activation., Prominent exceptions to the correlations between methylated CpG density and nucleosome location location occupancy include CpG Islands marked by Histone H3 Trimethyl Lys28 and CpG-poor heterochromatin marked by Histone H3 Trimethyl Lys9, and these modifications, along with DNA methylation, distinguish the major silencing mechanisms of the Homo sapiens epigenome., Throughout the Genome - anatomical entity, nucleosome location location occupancy was correlated with certain histone methylation or acetylation modifications., We further show that the extent of nucleosome location location depletion at promoters is directly correlated to expression level and can accommodate multiple Nucleosomes and provide Genome - anatomical entity-wide evidence that expressed non-CpG island promoters are nucleosome location location-depleted.[SEP]Relations: nucleosome location has relations: cellcomp_protein with H2AX, cellcomp_protein with H2AX, cellcomp_protein with H2AJ, cellcomp_protein with H2AJ, cellcomp_protein with MPHOSPH8, cellcomp_protein with MPHOSPH8, cellcomp_protein with H2AC6, cellcomp_protein with H2AC6, cellcomp_protein with H2AC4, cellcomp_protein with H2AC4.", "label": "yes"}
{"original_question": "Is Ozanimod effective for Ulcerative Colitis?", "id": "converted_4250", "sentence1": "Is Ozanimod effective for Ulcerative Colitis?", "sentence2": "Ozanimod as Induction and Maintenance Therapy for Ulcerative Colitis., CONCLUSIONS: Ozanimod was more effective than placebo as induction and maintenance therapy in patients with moderately to severely active ulcerative colitis., CONCLUSIONS: There was a high rate of continued study participation and long-term benefit with ozanimod Hairy Cell Leukemia 1 mg daily based on clinical, histological and biomarker measures in patients with moderately to severely active UC in the TOUCHSTONE OLE. [NCT02531126]., Ozanimod: A First-in-Class Sphingosine 1-Phosphate Receptor Modulator for the Treatment of Ulcerative Colitis., CONCLUSION: Ozanimod is another option in the growing arsenal of UC treatment., RELEVANCE TO PATIENT CARE AND CLINICAL PRACTICE: Ozanimod is the first sphingosine 1-phosphate modulator to be approved for UC and is administered orally. Its efficacy profile is comparable with other UC medications., Compared with placebo, ozanimod led to clinical remission in a significantly higher proportion of patients in both the induction and maintenance phase. Additionally, for secondary end points of clinical response, endoscopic improvement, corticosteroid-free remission, and mucosal healing, ozanimod performed significantly better than placebo. , Ozanimod interferes with migrations of activated Therapeutic gamma delta T-lymphocytes to the site of Inflammation and is a promising Pharmacologic Substance for the UC treatment.Key words: Crohn Disease - mongersen - monoclonal antibodies - ozanimod - tofacitinib - ulcerative colitis., SIONS: Ozanimod was more effective than placebo as induction and maintenance therapy in patients with moderately to severely active ulcerative colitis. (Fund, The sphingosine-1-phosphate receptor-1 (Sphingosine 1-Phosphate Receptor 1, Human) Agonist ozanimod ameliorates ulcerative colitis, yet its mechanism of action is unknown. , Ozanimod (RPC1063) is a specific and potent small molecule modulator of the Sphingosine-1-Phosphate Receptors (S1PR1) and receptor 5 (S1PR5), which has shown therapeutic benefit in clinical trials of relapsing Multiple Sclerosis and ulcerative colitis. Ozan, SIONS: Ozanimod was more effective than placebo as induction and maintenance therapy in patients with moderately to severely active ulcerative colitis. (Fun, SIONS: In this preliminary trial, ozanimod at a daily dose of 1 mg resulted in a slightly higher rate of clinical remission of ulcerative colitis than placebo. The [SEP]Relations: ulcerative colitis (disease) has relations: contraindication with Benzthiazide, contraindication with Benzthiazide, contraindication with Icosapent, contraindication with Icosapent, contraindication with Polythiazide, contraindication with Polythiazide, contraindication with Chlorothiazide, contraindication with Chlorothiazide, contraindication with Trolnitrate, contraindication with Trolnitrate.", "label": "yes"}
{"original_question": "Is there a genetic cause of craniostenosis?", "id": "converted_4366", "sentence1": "Is there a genetic cause of Craniosynostosis?", "sentence2": "Apert syndrome - TWIST1 Genes - is a rare Autosomal Dominant Disorder representing 1:65 000 cases of living newborns. Characteristic malformations of the Apert syndrome are early Craniosynostosis, microviscerocranium and II-V finger syndactyly of hand and toes with proximal phalanx of the bilateral thumb \"in delta\"., A 3-year-old child with tertiary trisomy (14 (+14q--), daughter of a mother with a balanced reciprocal translocation [46,XX,t(14;16)(q11;q24) is presented. Craniostenosis and developmental retardation were the primary presenting features in this patient., Saethre-Chotzen syndrome is an Autosome dominant disease characterized by CRANIOSYNOSTOSIS, TYPE 2, ptosis, and limb and external ear abnormalities, . For 98 patients (15%) a syndrome is associated. Third part of them has Apert syndrome, an other third part has Craniofacial dysostosis type 1, and for the last third more exceptional TWIST1 Genes syndrome (Saethre-Chotzen, Pfeiffer) or others atypical associations, sometimes not yet described, but with an Autosomal dominant inheritance., Coronal Craniosynostosis seems to be a dominant Autosome character, when Sagittal CRANIOSYNOSTOSIS, TYPE 2 is more often sporadic; for both, an Autosomal dominant inheritance is not excluded for some pedigrees.,  genetic origins are not completely clear although Gene Mutation in the genes that code for Fibroblast Growth Factor Receptor 2 have been described; depending upon the Genes involved, the type of Mutation Abnormality and the embryological period in which the Mutation Abnormality itself occurs, a type of CRANIOSYNOSTOSIS, TYPE 2 arises that may involve one or more Joint structure of suture of skull. The, Saethre-Chotzen syndrome is an Autosome dominant disease characterized by CRANIOSYNOSTOSIS, TYPE 2, ptosis, and limb and external ear abnormalities. , Identification and analysis of the genetic causes in nine unrelated probands with syndromic CRANIOSYNOSTOSIS, TYPE 2., To identify and analyze causative genetic variants in nine unrelated probands mainly manifested as syndromic CRANIOSYNOSTOSIS, TYPE 2, we reviewed the relevant medical information of the patients and performed the whole exome sequencing, further verified with Sanger sequencing and parental background., [Genetic counseling in Craniosynostosis. Results of a prospective study performed with a group of studies on craniofacial malformations]., Constitutional 11q interstitial deletion syndrome presents with Congenital Abnormality including Microcephaly (physical finding) with Craniosynostosis, minor dysmorphic features, Vitreoretinal degeneration, and Congenital anomaly of the kidney., A suckling baby with Microcephaly (physical finding), Craniosynostosis, downward slanting palpebral fissues, malformed ears, Cerebral hemisphere structure (body structure), Cardiac - anatomy qualifier and Intestines malformation, and partial 6q25 leads to 6qter trisomy is presented., Its genetic origins are not completely clear although Gene Mutation in the genes that code for Fibroblast Growth Factor Receptor 2 have been described; depending upon the Genes involved, the type of Mutation Abnormality and the embryological period in which the Mutation Abnormality itself occurs, a type of CRANIOSYNOSTOSIS, TYPE 2 arises that may involve one or more Joint structure of suture of skull., through which skull growth abnormalities are seen. It is becoming clearer that in most patients with CRANIOSYNOSTOSIS, TYPE 2, there is regional imbalance of skull growth, which co-exists with a variety of other equally important factors, such as genetic defects, raised intracranial pressure, Venous hypertension, and other brain parenchymal a, Recent genetic studies have identified several novel genes and pathways that cause nonsyndromic CRANIOSYNOSTOSIS, TYPE 2, providing genetic evidence linking the causes of syndromic and nonsyndromic craniosynostoses, and allowing for genotype-based prediction of risk of recurrence in some nonsyndromic families.[SEP]Relations: Craniosynostosis has relations: phenotype_phenotype with Abnormality of Joint structure of suture of skull, phenotype_phenotype with Abnormality of Joint structure of suture of skull, disease_phenotype_positive with hereditary hypophosphatemic rickets, disease_phenotype_positive with hereditary hypophosphatemic rickets, disease_phenotype_positive with mucolipidosis, disease_phenotype_positive with mucolipidosis, phenotype_phenotype with Coronal CRANIOSYNOSTOSIS, TYPE 2, phenotype_phenotype with Coronal CRANIOSYNOSTOSIS, TYPE 2, disease_phenotype_positive with congenital adrenal hyperplasia due to cytochrome P450 oxidoreductase deficiency, disease_phenotype_positive with congenital adrenal hyperplasia due to cytochrome P450 oxidoreductase deficiency.", "label": "yes"}
{"original_question": "Is there evidence to suggest that triiodothyronine has neuroprotective properties in traumatic brain injury?", "id": "converted_818", "sentence1": "Is there evidence to suggest that triiodothyronine has neuroprotective properties in Traumatic Brain Injury?", "sentence2": "Exogenous SLC25A5 gene administration provides neuroprotection in a Mus model of Traumatic Brain Injury., Treatment with SLC25A5 gene (1.2μg/100g body weight, i.p.) 1h after TBI resulted in a significant improvement in motor and cognitive recovery after CCI, as well as in marked reduction of lesion volumes. , Western blot analysis revealed the ability of SLC25A5 gene to reduce brain trauma through modulation of cytoplasmic-nuclear shuttling of nuclear factor-κB (NF-κB). Twenty-four hours after brain trauma, SLC25A5 gene-treated mice also showed significantly lower number of TUNEL(+) apoptotic neurons and curtailed induction of BAX protein, human, compared to vehicle control. In addition, SLC25A5 gene significantly enhanced the post-TBI expression of the neuroprotective neurotrophins (brain-derived neurotrophic factor and Glial Cell Line-Derived Neurotrophic Factor) compared to vehicle. , The stimulating effect of SLC25A5 gene on Peripheral nerve regeneration may have considerable therapeutic potential., The present study provides evidence that the Peripheral nervous system has its own system responsible for the local production of liothyronine, which may play a key role during the regeneration process., Although it has been hypothesized that SLC25A5 gene may facilitate neuronal regeneration after Central Nervous System injury, the 5'-D2 response to Brain Injuries is unknown., The outcome after Brain Injuries is closely correlated with the intensity of these changes, particularly with Catecholamine [EPC] plasma levels and the severity of the low triiodothyronine syndrome., The thyroid hormones triiodothyronine (SLC25A5 gene) and levothyroxine appear to enhance regeneration in the Peripheral and CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Central Nervous System). , SLC25A5 gene treatment influenced the general levels of incorporation of all treated groups over all days postoperation., SLC25A5 gene effects appear to involve an increased sensitivity of the Cells of the injured nervous system to the hormone., SLC25A5 gene, when administered over an 8 week period, stimulated axonal regeneration in the dorsal cortex and corpus callosum and promoted healing of the Specimen Type - Wound in the corpus callosum. The results of this investigation suggest that the use of SLC25A5 gene in the clinical treatment of injury to the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS may be of less value than the work of earlier authors had indicated., In addition, SLC25A5 gene significantly enhanced the post-TBI expression of the neuroprotective neurotrophins (brain-derived neurotrophic factor and Glial Cell Line-Derived Neurotrophic Factor) compared to vehicle[SEP]Relations: Brain Injuries has relations: contraindication with Propantheline, contraindication with Propantheline, contraindication with Propantheline, contraindication with Propantheline, contraindication with Pheniramine, contraindication with Pheniramine, contraindication with Pheniramine, contraindication with Pheniramine, contraindication with Homatropine, contraindication with Homatropine.", "label": "yes"}
{"original_question": "Can SUMO affect calcium homeostasis?", "id": "converted_450", "sentence1": "Can SUMO affect calcium homeostasis?", "sentence2": "Increasing SUMOylation levels correlated inversely with calcium influx in Sensory Receptor Cells., DPYSL2 gene deSUMOylation by SUMO proteases SENP1 protein, human protein, human and SUMO1 protein, human wt Allele normalized calcium influx to those in the CRMP2AAA mutant., Thus, our results identify a novel role for SUMO modification in DPYSL2 gene/CaV2.2 signaling pathway, Moreover, SUMO1 protein, human protein, human overexpression in isolated Myocytes, Cardiac augmented contractility and accelerated Ca(2+) decay.,  RIM1α SUMOylation at lysine residue K502 facilitates the clustering of CaV2.1 calcium channels and enhances the Ca(2+) influx necessary for vesicular release, whereas non-SUMOylated RIM1α participates in the docking/priming of Synaptic Vesicles and maintenance of active zone structure. , Identification and characterization of a SUMO-1 conjugation system that modifies neuronal calcium/calmodulin-dependent protein kinase II in Drosophila melanogaster.[SEP]Relations: Protein S human has relations: drug_drug with Calcium Phosphate, drug_drug with Calcium Phosphate, drug_drug with Calcium Phosphate, drug_drug with Calcium Phosphate, drug_drug with Calcium carbonate, drug_drug with Calcium carbonate, drug_drug with Calcium carbonate, drug_drug with Calcium carbonate, drug_drug with Calcium threonate, drug_drug with Calcium threonate.", "label": "yes"}
{"original_question": "Is Downs syndrome associated with decreased risk of leukemia?", "id": "converted_2227", "sentence1": "Is Down Syndrome associated with decreased risk of leukemia?", "sentence2": "The association of Down's syndrome and leukemia has been documented for over 50 years. Multiple studies have established the incidence of leukemia in Down's syndrome patients to be 10- to 20-fold higher than that in the general population., We present a case of congenital Leukemia, Myelocytic, Acute manifesting from the very first day of birth. Diagnosis of Leukemia, Myelocytic, Acute was suspected by the presence of Blast (physical force) in the peripheral blood smear and was confirmed on bone marrow by flowcytometry. Karyotyping revealed Trisomy 21., Juvenile myelomonocytic leukemia (Juvenile Myelomonocytic Leukemia) and a solitary cases of Leukemia, Myelocytic, Acute (AML) in Down Syndrome. , This was thus confirmed to be a case with transient leukemia with Down Syndrome.[SEP]Relations: Down syndrome has relations: disease_phenotype_positive with Decreased fertility, disease_phenotype_positive with Decreased fertility, disease_phenotype_positive with Acute megakaryocytic leukemia, disease_phenotype_positive with Acute megakaryocytic leukemia, disease_phenotype_positive with Sporadic, disease_phenotype_positive with Sporadic, disease_phenotype_positive with Short palm, disease_phenotype_positive with Short palm, disease_phenotype_positive with Short neck, disease_phenotype_positive with Short neck.", "label": "no"}
{"original_question": "Is there a role for transcription factories in genome organization?", "id": "converted_926", "sentence1": "Is there a role for transcription factories in Genome - anatomical entity organization?", "sentence2": "The mammalian nucleus is a highly complex structure that carries out a diverse range of functions such as DNA replication, cell division, RNA processing, and Nuclear (incident type) export/import. Many of these activities occur at discrete subcompartments that intersect with specific regions of the Genome - anatomical entity. Over the past few decades, evidence has accumulated to suggest that RNA transcription also occurs in specialized sites, called transcription factories, that may influence how the Genome - anatomical entity is organized. There may be certain efficiency benefits to cluster transcriptional activity in this way. However, the clustering of Genes at transcription factories may have consequences for Genome - anatomical entity stability, and increase the susceptibility to recurrent chromosomal translocations that lead to Primary malignant neoplasm, In the eukaryotic nucleus, Genes are transcribed in transcription factories, Based on this analysis, we propose that transcription factories result from the aggregation of RNA polymerase II-containing pre-initiation complexes assembled next to each other in the Nuclear (incident type) space. Such an aggregation can be triggered by the phosphorylation of the C-terminal domain of RNA polymerase II molecules and their interaction with various TRANSCRIPTION FACTOR. Individual transcription factories would thus incorporate tissue-specific, co-regulated as well as Genes, Housekeeping based only on their initial proximity to each other in the Nuclear (incident type) space, active polymerases cluster into replication and transcription \"factories\" in both pro- and Eukaryota. We conclude that the second law of thermodynamics acts through nonspecific entropic forces between engaged polymerases to drive the self-organization of Genome into loops containing several thousands (and sometimes millions) of basepairs, Since the advent of FISH (fluorescence in situ hybridization), there have been major advances in our understanding of how the Genome - anatomical entity is organized in interphase nuclei. Indeed, this organization is found to be non-random and individual Chromosomes, Human, Pair 1 occupy discrete regions known as territories,  in proliferating cells, there is evidently a correlation between radial positioning and gene density. Indeed, gene-poor Chromosomes, Human, Pair 1 tend to be located towards the Nuclear (incident type) edge, while those that are more gene-rich are positioned more internally, Recently described active chromatin hubs and transcription factories also involve long-range interactions, The transcription factory model has implications for the regulation of Transcription Initiation and elongation, for the organization of Genes in the Genome - anatomical entity, for the co-regulation of Genes and for Genome - anatomical entity instability.[SEP]Relations: HIV Transcription Initiation has relations: pathway_protein with CCNH, pathway_protein with CCNH. transcription factor binding has relations: molfunc_protein with JUN, molfunc_protein with JUN, molfunc_protein with JUNB, molfunc_protein with JUNB, molfunc_protein with JUND, molfunc_protein with JUND, molfunc_protein with SAP18, molfunc_protein with SAP18.", "label": "yes"}
{"original_question": "Do selenoproteins and selenium play a role in prostate cancer prevention?", "id": "converted_941", "sentence1": "Do Selenoproteins and selenium play a role in Pelvis>Prostate Primary malignant neoplasm prevention?", "sentence2": "The selenoprotein-deficient mice exhibited accelerated development of Lesion associated with Pelvis>Prostate Primary malignant neoplasm progression, implicating Selenoproteins in Primary malignant neoplasm risk and development and raising the possibility that selenium prevents Primary malignant neoplasm by modulating the levels of these Selenoproteins, Notably and in contrast to previous studies, RWPE-1 cells were significantly more sensitive to selenite than either of the Pelvis>Prostate Primary malignant neoplasm cell lines. These results demonstrate that Selenoproteins and selenium metabolism are regulated at multiple levels in Pelvis>Prostate cells, In a low-selenium population, SOD2-Ala16+ men homozygous for SEPP1-Ala234 are at an increased risk of Pelvis>Prostate Primary malignant neoplasm/aggressive Pelvis>Prostate Primary malignant neoplasm especially if ever-smokers, because they are likely to produce more Mitochondrial Inheritance H(2)O(2) that they cannot remove, thereby promoting Pelvis>Prostate tumor cell proliferation and migration., Our results support a role of selenium and Genetic Polymorphism in selenoenzymes in Pelvis>Prostate Primary malignant neoplasm etiology, which warrants confirmation in future studies., This study provides evidence that SELENOF gene genetic variation may influence Patient-Controlled Analgesia mortality. Additionally, the association of selenium with Patient-Controlled Analgesia mortality was modified by a Variant, suggesting the possibility that some men with Patient-Controlled Analgesia may benefit more from selenium than others, depending on their Genotype determination., We conclude that decreased SELENOP wt Allele concentration in serum might represent an additional valuable marker for Pelvis>Prostate Primary malignant neoplasm diagnostics., The recently completed Selenium supplement supplement and Vitamin E Cancer Prevention Trial (SELECT) was one of the largest Homo sapiens Primary malignant neoplasm prevention trials ever undertaken. Its purpose was to assess the role of selenium and Vitamin E Drug Class in Pelvis>Prostate Primary malignant neoplasm prevention, but SELECT found no decline in Pelvis>Prostate Primary malignant neoplasm., We studied FUT2 gene levels in whole blood, plasma and Pelvis>Prostate of 32 Pachyonychia Congenita and 40 benign Pelvis>Prostate hyperplasia (BPH) patients and in the control group composed of 39 healthy subjects. The selenoenzyme glutathione peroxidase (GSH-Px) was also measured in the patients' Erythrocytes, plasma and Pelvis>Prostate tissue. FUT2 gene concentration in whole blood and plasma in both groups of patients was lower as compared with controls, while in Pelvis>Prostate gland it was significantly higher in Pachyonychia Congenita than in BPH patients and controls. Red cell GSH-Px activity was the same in Pachyonychia Congenita patients and controls but significantly lower in BPH patients., Of particular interest was the positive correlation between tissue GPx activity and Gleason score, with this relationship achieving statistical significance among African-Americans (r = 0.67, P = 0.02)[SEP]Relations: SELENOP has relations: disease_protein with Pelvis>Prostate Primary malignant neoplasm, disease_protein with Pelvis>Prostate Primary malignant neoplasm, disease_protein with Pelvis>Prostate carcinoma, disease_protein with Pelvis>Prostate carcinoma, disease_protein with familial Pelvis>Prostate carcinoma, disease_protein with familial Pelvis>Prostate carcinoma. Selenium supplement has relations: drug_drug with Testosterone, drug_drug with Testosterone, drug_drug with Antipyrine, drug_drug with Antipyrine.", "label": "no"}
{"original_question": "Are proteasome inhibitors good candidates for treatment of leukemia and solid tumors?", "id": "converted_187", "sentence1": "Are Proteasome inhibitors, antineoplastic agent good candidates for treatment of leukemia and solid Neoplasms?", "sentence2": "We show that treatment with b-AP15 inhibited tumor progression in four different in vivo Solid Neoplasm models and inhibited organ infiltration in an RUNX1 gene model. Our results show that the deubiquitinating activity of the 19S regulatory particle is a new anticancer drug target, We further found that ATO targets Mineralocorticoid Excess Syndrome, Apparent via both myelodysplastic syndrome 1 (MECOM Protein Isoform MECOM Protein Isoform MDS1) and MECOM wt Allele moieties and degrades MECOM wt Allele via the ubiquitin-proteasome pathway and MECOM Protein Isoform MECOM Protein Isoform MDS1 in a proteasome-independent manner. Our results suggest that ATO could be used as a part of targeted therapy for Mineralocorticoid Excess Syndrome, Apparent-, AML1/MECOM Protein Isoform MECOM Protein Isoform MDS1-, MECOM Protein Isoform MECOM Protein Isoform MDS1/MECOM wt Allele-, and MECOM wt Allele-positive human cancers., Previously we had shown the synergic effect of bortezomib and thiostrepton in breast cancer cells in vitro, where sub-apoptotic concentrations of both Proteasome inhibitors, antineoplastic agent resulted in synergic increase in cell death when combined as a treatment. Here, we administered such a combination to MDA-MB-231 xenograft Neoplasms in vivo, and found that the effect of complementary Proteasome inhibitors, antineoplastic agent reduced tumor growth rates more efficiently than compared with when administered alone., Addition of a Proteasome Inhibitors [MoA] to anti-hormonal therapy resulted in a clinical benefit rate of 22% in a limited number of patients with endocrine resistant and progressive metastatic breast cancer., Taken together, these data support the clinical development of MLN9708 for both Hematologic and Solid Neoplasm indications., Bortezomib has minimal activity as a single-agent in the treatment of recurrent platinum-sensitive EOC/PPC, Our study indicates a molecular mechanism by which the sensitivity of Malignant neoplasm of thyroid cells is regulated by the level of 78 kDa Glucose-Regulated Protein as well as preferential induction of 78 kDa Glucose-Regulated Protein or CHOP protocol-cyclophosphamide/doxorubicin/prednisone/vincristine protocol-cyclophosphamide/doxorubicin/prednisone/vincristine upon treatment with Proteasome inhibitors, antineoplastic agent. Our experiments therefore suggest a novel approach toward sensitization of Malignant neoplasm of thyroid cells to Proteasome inhibitors, antineoplastic agent., Bortezomib (PS-341) is a novel antineoplastic agent that is well tolerated at doses not exceeding 3.0 mg (equivalent to 1.75 mg/m2), repeated on Measles virus genotype Measles virus genotype D1 and Measles virus genotype Measles virus genotype D4 every other week. This dose correlates with 70% inhibition of 20S proteasome activity., The maximum-tolerated dose and recommended phase II dose of bortezomib in this schedule is 1.6 mg/m(2). Biologic activity (inhibition of nuclear factor-kappa B-related markers) and antitumor activity is seen in AIPCa at tolerated doses of bortezomib., Given the results of this trial, it is safe and reasonable to recommend treatment with PS 341 on the schedule used in this trial at 1.56 mg/m2/dose in Phase II trials. Particular care should be taken with patients with preexisting Neuropathy, The successes of Proteasome inhibitors, antineoplastic agent in Millimole per Liter are now being translated to other Hematologic malignancies, including Acute leukemia, Such efforts have led to bortezomib, the first FDA approved Proteasome Inhibitors [MoA] now used as a frontline treatment for newly diagnosed Multiple Myeloma (Millimole per Liter), relapsed/refractory Millimole per Liter and Mantle cell lymphoma, We recently reported the impact and mechanisms of carfilzomib and Oprozomib, second-in-class Proteasome inhibitors, antineoplastic agent with higher specificities and reduced Toxic effect, against Squamous cell carcinoma of the head and neck (HNSCC). carfilzomib and Oprozomib potently inhibit HNSCC cell survival and the growth of HNSCC Neoplasms[SEP]Relations: protease inhibitor complex has relations: cellcomp_protein with CASP1, cellcomp_protein with CASP1, cellcomp_protein with CARD16, cellcomp_protein with CARD16. subacute leukemia has relations: disease_disease with leukemia (disease), disease_disease with leukemia (disease). Hematologic disease has relations: contraindication with Adomiparin, contraindication with Adomiparin, contraindication with Enoxaparin, contraindication with Enoxaparin.", "label": "yes"}
{"original_question": "Are there any urine biomarkers for chronic kidney disease?", "id": "converted_79", "sentence1": "Are there any urine biomarkers for chronic Both kidneys disease?", "sentence2": "Kidney and urine proteomic biomarkers are considered as promising diagnostic tools to predict Chronic Kidney Diseases progression early in Diabetic Nephropathy, facilitating timely and selective intervention that may reduce the related health-care expenditures., Both blood and urine biomarkers are reviewed in this paper and offer a considerable opportunity to enhance the understanding of the pathophysiology and known epidemiology of these recently defined syndromes., Cardiorenal syndromes (Congenital Rubella Syndrome) have been subclassified as five defined entities which represent clinical circumstances in which both the Chest>Heart and the Both kidneys are involved in a bidirectional injury and dysfunction via a final common pathway of cell-to-cell death and accelerated apoptosis mediated by oxidative stress., There is a strong association between both acute and chronic dysfunction of the Chest>Heart and kidneys with respect to morbidity and mortality., Both blood and urine biomarkers, including the assessment of catalytic iron, a critical element to the generation of oxygen-free radicals and oxidative stress, are reviewed in this paper., Identification of urine biomarkers has proven to be beneficial in recent years because of ease of handling, stability, and the ability to standardize the various markers to creatine/creatine/creatinine or other Peptides generally already present in the urine. Recent markers such as Neutrophil gelatinase-associated lipocalin (LCN2 wt Allele), Both kidneys injury molecule-1 (KIM-1), and NPHS2 gene have garnered a lot of attention. The emergence of these and other biomarkers is largely because of the evolution of novel Genome and proteomic applications in investigations of acute Both kidneys injury and chronic Both kidneys disease.[SEP]Relations: Diabetic Nephropathy has relations: disease_disease with chronic Both kidneys disease, disease_disease with chronic Both kidneys disease. Chronic Both kidneys disease has relations: phenotype_phenotype with Stage 1 chronic Both kidneys disease, phenotype_phenotype with Stage 1 chronic Both kidneys disease, phenotype_phenotype with Stage 2 chronic Both kidneys disease, phenotype_phenotype with Stage 2 chronic Both kidneys disease, phenotype_phenotype with Renal insufficiency, phenotype_phenotype with Renal insufficiency, disease_phenotype_positive with nephrotic syndrome,, disease_phenotype_positive with nephrotic syndrome,.", "label": "yes"}
{"original_question": "Are functional tests a good biomarker for Duchenne Muscular Dystrophy?", "id": "converted_4530", "sentence1": "Are functional tests a good biomarker for Duchenne Muscular Dystrophy?", "sentence2": "North Star Ambulatory Assessment is practical and reliable., allow assessment of high-functioning boys with Duchenne muscular dystrophy., agnosis and tracking of symptom progression of Muscular Dystrophy, Duchenne usually relies on creatine kinase tests, evaluation of patient performance in various ambulatory assessments, and detection of Dystrophin from Muscle biopsy, which are invasive and painful for the patient. While the, Aim: Using baseline data from a clinical trial of domagrozumab in Duchenne muscular dystrophy, we evaluated the correlation between functional measures and quantitative MRI assessments of Skeletal muscle structure of thigh. Patients & methods: Analysis included timed functional tests, knee extension/strength and North St, A New Functional Scale and Ambulatory Functional Classification of Duchenne Muscular Dystrophy: Scale Development and Preliminary Analyses of Reliability and Validity., his preliminary investigation describes the relationship between community ambulation measured by the StepWatch activity monitor and the current standard of functional assessment, the 6-minute walk test, in ambulatory boys with Duchenne muscular dystrophy (n = 16) and healthy controls (n = 13). All, ith strength assessments. MV index, fat fraction and T2-mapping measures had moderate correlations (r ∼ 0.5) to all functional tests, North Star Ambulatory Assessment and age. Conclusion: The moderate correlation between functional tests, age and baseline MRI measures supports MRI as a biomarker in Duchenn, on with clinically meaningful outcome measures such as North Star Ambulatory Assessment (North Star Ambulatory Assessment Clinical Classification) and 6 minute walk test (6MWT) is paramount for biomarker qualification. In this stu, Quantitative muscle strength assessment in duchenne muscular dystrophy: longitudinal study and correlation with functional measures., The 6-minute walk test, timed 10-meter walk/run test, and supine-up time are commonly used timed functional tests that also sufficiently monitor changes in muscle function; however, they strongly depend on patient collaboration, Conclusion: The moderate correlation between functional tests, age and baseline MRI measures supports MRI as a biomarker in Duchenne muscular dystrophy clinical trials., Currently, functional measures continue to serve as the primary outcome for the majority of Muscular Dystrophy, Duchenne clinical trials., Patients & methods: Analysis included timed functional tests, knee extension/strength and North Star Ambulatory Assessment., The 6-minute walk test, timed 10-meter walk/run test, and supine-up time are commonly used timed functional tests that also sufficiently monitor changes in muscle function; however, they strongly depend on patient collaboration., We have developed a new scale and the associated classification system, to assess the functional ability of children diagnosed with Muscular Dystrophy, Duchenne. Preliminary evaluation of the psychometric properties of the functional scale and classification systems indicate sufficient reliability and concurrent validity., Quantitative MRI is an objective and sensitive biomarker to detect subclinical changes, though the examination costs may be a reason for its limited use. In this study, a high correlation between all clinical assessments and quantitative MRI scans was found. The combinational use of these methods provides a better understanding about disease progression; however, longitudinal studies are needed to validate their reliability., The children's functional performance was assessed using 6-minute walk tests and timed performance tests. The correlations between the flexibilities of the lower limb muscles and the performance tests were examined., The flexibilities of the lower extremity muscles were found to be correlated to the 6-minute walk tests and the timed performance tests. The flexibility of the hamstrings (r = -.825), the Gastrocnemius muscle structure (r = .545), the hip flexors (r = .481), and the tensor fascia latae (r = .445) were found to be correlated with functional performance as measured by the 6-minute walk tests (P < .05), Nine biomarkers have been identified that correlate with disease milestones, functional tests and respiratory capacity. Together these biomarkers recapitulate different stages of the disorder that, if validated can improve disease progression monitoring.,  In conclusion, the motor function measure and timed function tests measure disease severity in a highly comparable fashion and all tests correlated with quantitative muscle MRI values quantifying fatty muscle degeneration.,  This study is to date the most thorough long-term evaluation of QMT in a cohort of Muscular Dystrophy, Duchenne patients correlated with other measures, such as the North Star Ambulatory Assessment (North Star Ambulatory Assessment Clinical Classification) or three 6-min walk test (6MWT)., The MFM scale was a useful instrument in the follow up of patients with Muscular Dystrophy, Duchenne. Moreover, it is a more comprehensive scale to assess patients and very good for conducting trials to evaluate treatment., MD subjects were evaluated using the Vignos lower extremity functional rating, and tests including 6 min walk test (6MWT) and 10 m walk., TFTs appear to be slightly more responsive and predictive of disease progression than the 6MWT in 7-12.9 year olds., herefore, in our group of ambulant patients with Muscular Dystrophy, Duchenne, timed functional testing was the most sensitive parameter to determine the extent of disease progression. Timed functional testing may therefore be considered as an additional outcome measure in drug trials to evaluate the effects of therapy in ambulant patients with Muscular Dystrophy, Duchenne and possibly in other Neuromuscular Diseases., Time to rise is a useful and simple tool in the screening of Neuromuscular Diseases such as Duchenne muscular dystrophy,, he muscle strength of the Upper extremity>Wrist extensors and the radial deviation range of motion at the Upper extremity>Wrist were found to be strongly correlated with six of the seven tasks assessed. These two clinical assessments appear to be good indicators of overall Upper extremity>Wrist and hand function.[SEP]Relations: Duchenne muscular dystrophy has relations: disease_phenotype_positive with Muscular dystrophy, disease_phenotype_positive with Muscular dystrophy, disease_phenotype_positive with Skeletal muscle atrophy, disease_phenotype_positive with Skeletal muscle atrophy, disease_protein with BCHE, disease_protein with BCHE, disease_protein with Muscular Dystrophy, Duchenne, disease_protein with Muscular Dystrophy, Duchenne, disease_protein with ACHE, disease_protein with ACHE.", "label": "yes"}
{"original_question": "Is galcanezumab effective for treatment of migraine?", "id": "converted_3006", "sentence1": "Is galcanezumab effective for treatment of Migraine Disorders?", "sentence2": "Importance: galcanezumab (LY2951742), a Monoclonal Antibody [EPC] against CALCA gene (Calcitonin Gene-Related Peptide), is one of a novel class of new medicines for Migraine Disorders prevention., Conclusions and Relevance: Monthly subcutaneous injections of galcanezumab, both 120 mg and 300 mg, demonstrated efficacy (repeated-measures analysis) for the preventive treatment of Migraine Disorders and support further development in larger phase 3 studies. , PURPOSE OF REVIEW: Monoclonal antibodies (mAbs) targeting the calcitonin-gene-related peptide (Calcitonin Gene-Related Peptide) pathway have been developed for episodic and chronic Migraine Disorders prevention, either through binding the Calcitonin Gene-Related Peptide ligand (eptinezumab, fremanezumab, galcanezumab) or the Calcitonin Gene-Related Peptide receptor (erenumab)., Background Safety findings from a Phase 2b study of galcanezumab, a Antibodies, Monoclonal, Humanized against CALCA gene, for prevention of Migraine Disorders (NCT02163993) are reported here., Safety of galcanezumab in patients with episodic Migraine Disorders: A randomized placebo-controlled dose-ranging Phase 2b study., Currently, there is considerable excitement regarding Monoclonal Antibodies against CALCA gene (eptinezumab, galcanezumab, fremanezumab) and the Calcitonin-Gene Related Peptide Receptor (erenumab). To date, these Monoclonal Antibodies have shown promising efficacy in clinical trials, with no major safety concerns. If ongoing long-term studies show that their efficacy can be maintained, this may herald a new era for effective antimigraine therapies., Calcitonin Gene-Related Peptide receptor antagonists such as ubrogepant are effective for acute relief of Migraine Disorders headache, whereas Monoclonal Antibodies against Calcitonin Gene-Related Peptide (eptinezumab, fremanezumab and galcanezumab) or the Calcitonin Gene-Related Peptide receptor (erenumab) effectively prevent Migraine Disorders attacks. , Four Monoclonal Antibodies (mAbs) targeting the Calcitonin Gene-Related Peptide pathway are currently under evaluation for the prevention of episodic and chronic Migraine Disorders: eptinezumab (ALD403), fremanezumab (TEV-48125), galcanezumab (LY2951742), and erenumab (AMG334). , Introduction galcanezumab is a Antibodies, Monoclonal, Humanized binding CALCA gene, used for Migraine Disorders prevention., Efficacy and safety of galcanezumab for the prevention of episodic Migraine Disorders: Results of the EVOLVE-2 Phase 3 randomized controlled clinical trial., galcanezumab induced a robust, dose-dependent, and durable inhibition of capsaicin-induced increase in DBF, supporting the continued clinical development of galcanezumab for prophylaxis in Migraine Disorders patients., The efficacy and safety of CALCA gene Monoclonal Antibody [EPC] for episodic Migraine Disorders: a meta-analysis.Based on the results of this meta-analysis, Calcitonin Gene-Related Peptide Monoclonal Antibodies significantly reduced the monthly Migraine Disorders days and acute Migraine Disorders-specific medication. , Importance\ngalcanezumab (LY2951742), a Monoclonal Antibody [EPC] against CALCA gene (Calcitonin Gene-Related Peptide), is one of a novel class of new medicines for Migraine Disorders prevention., galcanezumab appears efficacious, safe, and well tolerated for the preventive treatment of chronic Migraine Disorders., BACKGROUND\ngalcanezumab is a Antibodies, Monoclonal, Humanized that selectively binds to the CALCA gene (Calcitonin Gene-Related Peptide) and has demonstrated efficacy in reducing Migraine Disorders headache days (MHD) in patients with episodic and chronic Migraine Disorders., BACKGROUND\ngalcanezumab, a Antibodies, Monoclonal, Humanized that selectively binds to the CALCA gene, has demonstrated in previous Phase 2 and Phase 3 clinical studies (≤6-month of treatment) a reduction in the number of Migraine Disorders headache days and improved patients' functioning., CONCLUSION\nTwelve months of treatment with self-administered injections of galcanezumab was safe and associated with a reduction in the number of monthly Migraine Disorders headache days., Calcitonin Gene-Related Peptide receptor antagonists such as ubrogepant are effective for acute relief of Migraine Disorders headache, whereas Monoclonal Antibodies against Calcitonin Gene-Related Peptide (eptinezumab, fremanezumab and galcanezumab) or the Calcitonin Gene-Related Peptide receptor (erenumab) effectively prevent Migraine Disorders attacks., Conclusions and Relevance\nMonthly subcutaneous injections of galcanezumab, both 120 mg and 300 mg, demonstrated efficacy (repeated-measures analysis) for the preventive treatment of Migraine Disorders and support further development in larger phase 3 studies., Importance galcanezumab (LY2951742), a Monoclonal Antibody [EPC] against CALCA gene (Calcitonin Gene-Related Peptide), is one of a novel class of new medicines for Migraine Disorders prevention., BACKGROUND galcanezumab, a Antibodies, Monoclonal, Humanized that selectively binds to the CALCA gene, has demonstrated in previous Phase 2 and Phase 3 clinical studies (≤6-month of treatment) a reduction in the number of Migraine Disorders headache days and improved patients' functioning., BACKGROUND galcanezumab is a Antibodies, Monoclonal, Humanized that selectively binds to the CALCA gene (Calcitonin Gene-Related Peptide) and has demonstrated efficacy in reducing Migraine Disorders headache days (MHD) in patients with episodic and chronic Migraine Disorders., Both galcanezumab dose groups demonstrated greater overall mean reduction in the number of monthly MHDs compared to placebo (placebo -2.7, galcanezumab 120 mg -4.8, galcanezumab 240 mg -4.6) (<br><b>CONCLUSIONS</b>: Both doses of galcanezumab were superior to placebo in reducing the number of monthly MHDs., galcanezumab appears efficacious, safe, and well tolerated for the preventive treatment of chronic Migraine Disorders.<br><b>CLINICALTRIALSGOV IDENTIFIER</b>: NCT02614261.<br><b>CLASSIFICATION OF EVIDENCE</b>: This interventional study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class I evidence that galcanezumab is superior to placebo in the reduction of the number of monthly MHDs.<br>, In September 2018, the US FDA approved galcanezumab as a once-monthly subcutaneous injection for the preventive treatment of Migraine Disorders in adults., This article summarizes the milestones in the development of galcanezumab leading to its first approval for the preventive treatment of Migraine Disorders in adults.<br>, galcanezumab appears efficacious, safe, and well tolerated for the preventive treatment of chronic Migraine Disorders., This article summarizes the milestones in the development of galcanezumab leading to its first approval for the preventive treatment of Migraine Disorders in adults., Twelve months of treatment with self-administered injections of galcanezumab was safe and associated with a reduction in the number of monthly Migraine Disorders headache days.[SEP]Relations: galcanezumab has relations: drug_drug with Galiximab, drug_drug with Galiximab, drug_drug with Abrilumab, drug_drug with Abrilumab, drug_drug with Matuzumab, drug_drug with Matuzumab, drug_drug with Fremanezumab, drug_drug with Fremanezumab, drug_drug with Erenumab, drug_drug with Erenumab.", "label": "yes"}
{"original_question": "Can simvastatin alleviate depressive symptoms?", "id": "converted_2799", "sentence1": "Can simvastatin alleviate depressive symptoms?", "sentence2": "Simvastatin-treated patients experienced significantly more reductions in HDRS scores compared to the placebo group by the end of the trial (p=0.02). Early improvement and response rates were significantly greater in the simvastatin group than the placebo group (p=0.02 and p=0.01, respectively) but remission rate was not significantly different between the two groups (p=0.36)., In conclusion, simvastatin seems to be a safe and effective adjuvant therapy for patients suffering from major depressive disorder.[SEP]Relations: Simvastatin has relations: drug_effect with Anxiety, drug_effect with Anxiety, drug_effect with Pain, drug_effect with Pain, drug_effect with Headache, drug_effect with Headache, drug_effect with Arthritis, drug_effect with Arthritis, drug_effect with Dyspnea, drug_effect with Dyspnea.", "label": "yes"}
{"original_question": "Are genes symmetrically distributed between leading and lagging DNA strand in bacteria?", "id": "converted_1414", "sentence1": "Are Genes symmetrically distributed between leading and lagging DNA Genomic Orientation in Bacteria?", "sentence2": "Genomic DNA is used as the template for both replication and transcription, whose machineries may collide and result in Mutagenesis Procedure, among other damages. Because head-on collisions are more deleterious than codirectional collisions, Genes should be preferentially encoded on the leading Genomic Orientation to avoid head-on collisions, as is observed in most Genome, Bacterial examined., Most Genes in Bacteria are encoded on the leading Genomic Orientation of replication. This presumably avoids the potentially detrimental head-on collisions that occur between the replication and transcription machineries when Genes are encoded on the lagging Genomic Orientation., The majority of Genes, Bacterial are located on the leading Genomic Orientation, Genes of some functional categories such as Ribosomes have higher preferences to be on the leading strands, Genes of some functional categories such as TRANSCRIPTION FACTOR have higher preferences on the lagging strands, Genes, Essential are more preferentially situated at the leading Genomic Orientation than at the lagging Genomic Orientation, remarkable Genomic Orientation-bias of the distribution of Genes, Essential, Head-on encounters between the replication and transcription machineries on the lagging DNA Genomic Orientation can lead to replication fork arrest and genomic instability. To avoid head-on encounters, most Genes, especially essential and highly transcribed Genes, are encoded on the leading Genomic Orientation such that transcription and replication are co-directional., Replication-associated purine asymmetry may contribute to Genomic Orientation-biased gene distribution., Genomic Orientation-biased gene distribution (SGD), SGD correlates not only with polC, but also with purine asymmetry (Premorbid Adjustment Scale), In Bacteria, most Genes are on the leading Genomic Orientation of replication, a phenomenon attributed to collisions between the DNA and RNA polymerases., Genes whose expression is important for fitness are selected to the leading Genomic Orientation because this reduces the duration of these interruptions, Among prokaryotic genomes, the distribution of Genes on the leading and lagging strands of the replication fork is known to be biased. , We show that the evidence they provided is invalid and that the existence of lagging Genomic Orientation encoded Genes is explainable by a balance between deleterious mutations that bring Genes from the leading to the lagging Genomic Orientation and purifying selection purging such mutants., Based on those experimentally determined for 10 Bacteria, we find that Genes, Essential are more preferentially situated at the leading Genomic Orientation than at the lagging Genomic Orientation, for all the 10 genomes studied, confirming previous findings based on either smaller datasets or putatively assigned ones by homology search., The majority of Genes, Bacterial are located on the leading Genomic Orientation, and the percentage of such Genes has a large variation across different Bacteria., Most Genes in Bacteria are encoded on the leading Genomic Orientation of replication., This paradox could be explained by assuming that the stronger mutation pressure and selection after inversion preferentially eliminate Genes transferred from the leading to the lagging DNA Genomic Orientation., We have shown that the relative number of Chromosomal translocation which have switched positions of Genes from the leading to the lagging DNA Genomic Orientation is lower than the number of Chromosomal translocation which have transferred Genes from the lagging Genomic Orientation to the leading Genomic Orientation of prokaryotic genomes., Most Genes in Bacteria are encoded on the leading Genomic Orientation of replication, The majority of Genes, Bacterial are located on the leading Genomic Orientation, and the percentage of such Genes has a large variation across different Bacteria, We have shown that the relative number of Chromosomal translocation which have switched positions of Genes from the leading to the lagging DNA Genomic Orientation is lower than the number of Chromosomal translocation which have transferred Genes from the lagging Genomic Orientation to the leading Genomic Orientation of prokaryotic genomes, Using Monte Carlo methods, we have simulated, under experimentally determined directional mutation pressure, the divergence rate and the elimination rate of Genes depending on their location in respect to the leading/lagging DNA strands in the asymmetric prokaryotic genome[SEP]Relations: TRANSCRIPTION FACTOR binding has relations: molfunc_protein with CD34, molfunc_protein with CD34, molfunc_protein with TWIST1, molfunc_protein with TWIST1, molfunc_protein with SMARCA1, molfunc_protein with SMARCA1, molfunc_protein with MAFB, molfunc_protein with MAFB. Bacteremia has relations: disease_phenotype_positive with staphylococcal pneumonia, disease_phenotype_positive with staphylococcal pneumonia.", "label": "no"}
{"original_question": "Does teplizumab hold promise for diabetes prevention?", "id": "converted_3440", "sentence1": "Does teplizumab hold promise for Diabetes Mellitus prevention?", "sentence2": "Anti-CD3 Antigens Antigens teplizumab and muromonab-CD3 Antigens Antigens otelixizumab have been shown to provide C-peptide, Human, Human preservation. , Underway are secondary prevention studies with teplizumab and with abatacept., INTERPRETATION: Findings of exploratory analyses suggest that future studies of immunotherapeutic intervention with teplizumab might have increased success in prevention of a decline in β-cell function (measured by C-peptide, Human, Human) and provision of glycaemic control at reduced doses of Therapeutic Insulin if they target patients early after diagnosis of Diabetes Mellitus and children., teplizumab therapy for type 1 Diabetes Mellitus., teplizumab for treatment of type 1 Diabetes Mellitus mellitus., TAKE HOME MESSAGE\n\nIn Phase I/II randomized control trials, in patients with new onset Diabetes Mellitus, Insulin-Dependent, teplizumab slowed the rate of loss of beta-cell function over 2 years of follow-up., teplizumab for treatment of type 1 Diabetes Mellitus (Protégé study): 1-year results from a randomised, placebo-controlled trial., INTERPRETATION\n\nFindings of exploratory analyses suggest that future studies of immunotherapeutic intervention with teplizumab might have increased success in prevention of a decline in β-cell function (measured by C-peptide, Human, Human) and provision of glycaemic control at reduced doses of Therapeutic Insulin if they target patients early after diagnosis of Diabetes Mellitus and children., Treatment of new onset type 1 Diabetes Mellitus with teplizumab: successes and pitfalls in development., AREAS COVERED\n\nIn this review, we discuss the recent update on clinical data obtained from trials of teplizumab in type 1 Diabetes Mellitus, the drug's postulated mechanism of action and the identification of responders to therapy., CONCLUSIONS teplizumab is an muromonab-CD3 Antigens Antigens Homo sapiens monoclonal antibody with promising activity in treatment of patients with T1DM., The results from the TN-10 teplizumab prevention trial show that the diagnosis of type 1 Diabetes Mellitus can be delayed by treatment with a Fc Receptor non-binding monoclonal antibody to CD3 Antigens Antigens in people at high risk for Disease, INTERPRETATION\nFindings of exploratory analyses suggest that future studies of immunotherapeutic intervention with teplizumab might have increased success in prevention of a decline in β-cell function (measured by C-peptide, Human, Human) and provision of glycaemic control at reduced doses of Therapeutic Insulin if they target patients early after diagnosis of Diabetes Mellitus and children., teplizumab (muromonab-CD3 Antigens Antigens mAb) treatment preserves C-peptide, Human, Human responses in patients with new-onset type 1 Diabetes Mellitus in a randomized controlled trial: metabolic and immunologic features at baseline identify a subgroup of responders., teplizumab treatment may improve C-peptide, Human, Human responses in participants with type 1 Diabetes Mellitus after the new-onset period: a randomised controlled trial., The results from the TN-10 teplizumab prevention trial show that the diagnosis of type 1 Diabetes Mellitus can be delayed by treatment with a Fc Receptor non-binding monoclonal antibody to CD3 Antigens Antigens in people at high risk for Disease., Findings of exploratory analyses suggest that future studies of immunotherapeutic intervention with teplizumab might have increased success in prevention of a decline in β-cell function (measured by C-peptide, Human, Human) and provision of glycaemic control at reduced doses of Therapeutic Insulin if they target patients early after diagnosis of Diabetes Mellitus and children., Despite decades of research and clinical trials, no treatment exists yet to prevent or cure Diabetes Mellitus, Insulin-Dependent. A recent prevention trial using the Anti-CD3 Antigens Antigens Antibody teplizumab in individuals at a high risk of developing Diabetes Mellitus, Insulin-Dependent has provided the first piece of evidence that a safe and transient intervention may be able to delay Disease., In this review, we discuss the recent update on clinical data obtained from trials of teplizumab in type 1 Diabetes Mellitus, the drug's postulated mechanism of action and the identification of responders to therapy., Treatment of type 1 Diabetes Mellitus with teplizumab: clinical and immunological follow-up after 7 years from diagnosis.[SEP]Relations: teplizumab has relations: drug_drug with Erenumab, drug_drug with Erenumab, drug_drug with Zolbetuximab, drug_drug with Zolbetuximab, drug_drug with Daclizumab, drug_drug with Daclizumab, drug_drug with Urelumab, drug_drug with Urelumab, drug_drug with Adalimumab, drug_drug with Adalimumab.", "label": "yes"}
{"original_question": "Is Nanog repressed in pluripotent stem cells?", "id": "converted_4098", "sentence1": "Is Nanog repressed in pluripotent Stem Cells?", "sentence2": "Aggregation of embryonic Stem Cells induces Nanog repression and primitive Endoderm differentiation, Interestingly, cell aggregation by itself induced Nanog repression at the outer layer, which was essential for aggregation-induced primitive Endoderm formation, early embryonic development, when downregulation of Nanog plays a crucial role., The homeobox gene Nanog is a key intrinsic determinant of self renewal in embryonic stem (ES) Cells, and its repression leads ES Cells to selectively differentiate into primitive Endoderm., These data indicate that the Grb2/Mek pathway primarily mediates NANOG gene repression upon ES cell differentiation into primitive Endoderm., Nanog and POU5F1 gene associate with unique transcriptional repression complex (molecular entity) in embryonic Stem Cells, Nanog and POU5F1 gene are essential TRANSCRIPTION FACTOR that regulate self-renewal and pluripotency of ES Cells. , the mechanisms by which Nanog and POU5F1 gene modulate ES cell fate remain unknown. , Nanog, POU5F1 gene and repressor proteins co-occupy Nanog-target Genes in Mus sp. ES Cells, suggesting that Nanog and POU5F1 gene together may communicate with distinct repression complex (molecular entity) to control gene transcription., Nanog and POU5F1 gene associate with unique repressor complex (molecular entity) on their target Genes to control ES cell fate., he main finding of this study is that knockdown of Trp53 and PTEN protein, human independently resulted in significantly higher expression levels of the pluripotency-associated gene Nanog, and we hypothesize that TP53 wt Allele and PTEN mediated repression is important for the insulation of male Germ Cells from pluripotency., The Homeo Domain transcription factor NANOG plays a central role in maintaining hESC pluripotency, The newly derived NANOG reporter hESC lines present novel tools to visualize NANOG expression in viable Human Embryonic Stem Cells. , Loss of PTEN protein, human causes tumor initiation following differentiation of murine pluripotent Stem Cells due to failed repression of Nanog., Furthermore, our data show that the mechanism by which PTEN protein, human null ECCs emerge in vitro and cause Neoplasms in vivo is through increased survival and self-renewal, due to failed repression of the transcription factor Nanog., We report here that Nanog and POU5F1 gene are reexpressed in two Mus sp. embryonic stem cell (Mouse Embryonic Stem Cells) lines following exposure to the differentiating agent DETA/NO., Furthermore, Nanog binding to the Promoter of Brachyury protein protein leads to repression of this gene, thus disrupting mesendoderm transition., Maintaining pluripotency and indefinite self-renewal of embryonic Stem Cells requires a tight control of the expression of several key stemness factors, particularly Nanog and POU5F1 gene TRANSCRIPTION FACTOR., Current evidence suggests that ES Cells maintain their pluripotent state by expressing a battery of TRANSCRIPTION FACTOR including POU5F1 gene and Nanog., Embryonic stem (ES) cell pluripotency is dependent upon sustained expression of the key transcriptional regulators POU5F1 gene, Nanog, and SOX2 protein, human., The expression of POU5F1 gene is activated by Forkhead Box Protein D3 and Nanog but repressed by POU5F1 gene itself, thus, exerting an important negative feedback loop to limit its own activity., Nanog, POU5F1 gene, and SOX2 protein, human form the core of a transcription factor network that maintains embryonic Stem Cells in the pluripotent state in both Homo sapiens and CASP14 gene., w that BMI1 protein, human is enriched in the extraembryonic (Endoderm [XEN] and trophectodermal stem [TS]) compartment and repressed by Nanog in pluripotent embryonic stem (ES) Cells. In vivo, Bm, Nanog is a newly identified transcriptional factor bearing a Homeo Domain and expressed in pluripotential Cells of preimplantation and early postimplantation embryos, and embryonic stem (ES) and embryonic germ (EG) Cells., Knockout experiments indicate that Nanog functions as a key player in maintaining the pluripotency of Stem Cells., Thus, in germ cell development, NANOG is expressed in proliferating Germ Cells, in which nuclear reprogramming is progressing., Nanog maintains pluripotency of Mus sp. embryonic Stem Cells by inhibiting NFKB1 gene and cooperating with STAT3 protein, human., We performed a genome-wide screen that combined full-length Mouse Embryonic Stem Cells transcriptome genomic mapping data with chromatin immunoprecipitation genomic location maps of the key Mouse Embryonic Stem Cells TRANSCRIPTION FACTOR POU5F1 gene and Nanog., Nanog safeguards pluripotency in Mus sp. embryonic Stem Cells (mESCs)., Notably, the expression of Nanog, a key pluripotency regulator and repressor of extraembryonic Endoderm specification in ES Cells, was significantly reduced in ZIC3 wt Allele knockdown Cells.[SEP]Relations: NANOG has relations: pathway_protein with Transcriptional regulation of pluripotent Stem Cells, pathway_protein with Transcriptional regulation of pluripotent Stem Cells, bioprocess_protein with positive regulation of stem cell proliferation, bioprocess_protein with positive regulation of stem cell proliferation, bioprocess_protein with stem cell population maintenance, bioprocess_protein with stem cell population maintenance, bioprocess_protein with somatic stem cell population maintenance, bioprocess_protein with somatic stem cell population maintenance, pathway_protein with POU5F1 (OCT4), SOX2, NANOG repress Genes related to differentiation, pathway_protein with POU5F1 (OCT4), SOX2, NANOG repress Genes related to differentiation.", "label": "no"}
{"original_question": "Does Groucho related gene 5 (GRG5) have a role only in late development?", "id": "converted_2938", "sentence1": "Does Groucho related gene 5 (TLE5 gene) have a role only in late development?", "sentence2": "Groucho related gene 5 (TLE5 gene) is a HSD17B4 gene that has been implicated in late Embryo and postnatal Mus sp. development. Here, we describe a previously unknown role of TLE5 gene in early developmental stages by analyzing its function in stem cell fate decisions. By both loss and gain of function approaches we demonstrate that ablation of TLE5 gene deregulates the Embryonic Stem Cells (ESTERASE C) pluripotent state whereas its overexpression leads to enhanced self-renewal and acquisition of Primary malignant neoplasm cell-like properties. The malignant characteristics of Teratoma generated by Enhanced S-Cone Syndrome that overexpress TLE5 gene reveal its pro-oncogenic potential., Here, we describe a previously unknown role of TLE5 gene in early developmental stages by analyzing its function in stem cell fate decisions., Groucho related gene 5 (TLE5 gene) is involved in Embryo and neural stem cell state decisions.Groucho related gene 5 (TLE5 gene) is a HSD17B4 gene that has been implicated in late Embryo and postnatal Mus sp. development. [SEP]Relations: embryo has relations: anatomy_protein_present with GRK5, anatomy_protein_present with GRK5, anatomy_protein_present with GRK6, anatomy_protein_present with GRK6. TLE5 has relations: protein_protein with GRB2, protein_protein with GRB2, protein_protein with GRAP2, protein_protein with GRAP2, protein_protein with GRN, protein_protein with GRN.", "label": "no"}
{"original_question": "Is there any software for automated analysis of FISH images?", "id": "converted_160", "sentence1": "Is there any software for automated analysis of FISH images?", "sentence2": "he study demonstrated the feasibility of automated FISH signal analysis that applying a cyclophosphamide/dacarbazine/doxorubicin protocol scheme to the automated generated 2-D projection images., A color imaging technique, multiplex fluorescent in situ hybridization (M-FISH), has been developed to ease the analysis of the process. Using an M-FISH technique each chromosome class (1,2, …,22,X,Y) is stained with a unique color. However, significant variations between images are observed due to a number of factors such as uneven hybridization and spectral overlap among channels. These types of variations influence the pixel classification accuracy of image classification methods which are supervised and require a set of annotated images for training. In this paper, we present a fully unsupervised M-FISH chromosome image classification methodology. Our main contributions are 1) the assumption that the intensity of a chromosome pixel is sampled from multiple Gaussian components [Gaussian mixture model (GMM)] such that each component corresponds to one chromosome class, and 2) the initialization of the GMM model using the emission information of each chromosome class. This is feasible since prior to the M-FISH image acquirement, we already know which chromosome class is emitting to each of the five M-FISH image channels. The method has been tested on a large number of M-FISH images and an overall accuracy of 89.85% is reported. Our method is unsupervised and presents higher classification accuracy even when it is compared with common supervised based methods., hybridization (FISH) tests provide promising molecular imaging biomarkers to more accurately and reliably detect and diagnose cancers and genetic disorders. Since current manual FISH signal analysis is low-efficient and inconsistent, which limits its clinical utility, developing automated FISH image scanning systems and computer-aided detection (cyclophosphamide/dacarbazine/doxorubicin protocol) schemes has been attracting research interests. To acquire high-resolution FISH images in a multi-spectral scanning mode, a huge amount of image data with the stack of the multiple three-dimensional (3-D) image slices is generated from a single specimen. Automated preprocessing these scanned images to eliminate the non-useful and redundant data is important to make the automated FISH tests acceptable in clinical applications. In this study, a dual-detector fluorescence image scanning system was applied to scan four specimen slides with FISH-probed chromosome X. A cyclophosphamide/dacarbazine/doxorubicin protocol scheme was developed to detect analyzable interphase cells and map the multiple imaging slices recorded FISH-probed signals into the 2-D projection images. cyclophosphamide/dacarbazine/doxorubicin protocol scheme was then applied to each projection image to detect analyzable interphase cells using an adaptive multiple-threshold algorithm, identify FISH-probed signals using a top-hat transform, and compute the ratios between the normal and Abnormal \"U\" lymphocyte. To assess cyclophosphamide/dacarbazine/doxorubicin protocol performance, the FISH-probed signals were also independently visually detected by an observer. The Kappa coefficients for agreement between cyclophosphamide/dacarbazine/doxorubicin protocol and observer ranged from 0.69 to 1.0 in detecting/counting FISH signal spots in four testing samples.,  In this paper we developed a sparse representation-based classification (Proto-Oncogene Tyrosine-Protein Kinase Src, human) algorithm based on L1-norm minimization for classifying Chromosomes, Human, Pair 1 from multicolor fluorescence in situ hybridization (M-FISH) images. The algorithm has been tested on a comprehensive M-FISH database that we established, demonstrating improved performance in classification. When compared with other pixel-wise M-FISH image classifiers such as fuzzy c-means (FCM) clustering algorithms and adaptive fuzzy c-means (AFCM) clustering algorithms that we proposed earlier the current method gave the lowest classification error. In order to evaluate the performance of different Proto-Oncogene Tyrosine-Protein Kinase Src, human for M-FISH imaging analysis, three different sparse representation methods, namely, Homotopy method, Orthogonal Matching Pursuit (OMP gene gene), and Least Angle Regression (LARS), were tested and compared. Results from our statistical analysis have shown that Homotopy based method is significantly better than the other two methods. , Fluorescence in situ hybridization (FISH) is used to study the organization and the positioning of specific DNA Sequence within the Cell Nucleus. Analyzing the data from FISH images is a tedious process that invokes an element of subjectivity. Automated FISH image analysis offers savings in time as well as gaining the benefit of objective data analysis. While several FISH image analysis software tools have been developed, they often use a threshold-based segmentation algorithm for nucleus segmentation. As fluorescence signal intensities can vary significantly from experiment to experiment, from \"U\" lymphocyte to \"U\" lymphocyte, and within a \"U\" lymphocyte, threshold-based segmentation is inflexible and often insufficient for automatic image analysis, leading to additional manual segmentation and potential subjective bias. To overcome these problems, we developed a graphical software tool called FISH Finder to automatically analyze FISH images that vary significantly. By posing the nucleus segmentation as a classification problem, compound Bayesian classifier is employed so that contextual information is utilized, resulting in reliable classification and boundary extraction. This makes it possible to analyze FISH images efficiently and objectively without adjustment of input parameters. Additionally, FISH Finder was designed to analyze the distances between differentially stained FISH probes., The simultaneous detection of Protein Info expression and gene copy number changes in patient samples, like paraffin-embedded tissue sections, is challenging since the procedures of immunohistochemistry (IHC) and Fluorescence in situ Hybridization (FISH) negatively influence each other which often results in suboptimal staining. Therefore, we developed a novel automated algorithm based on relocation which allows subsequent detection of Protein Info content and gene copy number changes within the same \"U\" lymphocyte. METHODS: Paraffin-embedded tissue sections of Colorectal Carcinoma were stained for Prominin-1, human expression. IHC images were acquired and image coordinates recorded. Slides were subsequently hybridized with fluorescently labeled DNA Probes. FISH images were taken at the previously recorded positions allowing for direct comparison of Protein Info expression and gene copy number signals within the same cells/tissue areas. Relocation, acquisition of the IHC and FISH images, and enumeration of FISH signals in the immunophenotyped tumour areas were done in an automated fashion. RESULTS: Automated FISH analysis was performed on 13 different Malignant tumor of colon samples that had been stained for Prominin-1, human; each sample was scored for MYC Protein Info, human Protein Info, human, ZNF217 Protein Info, human Protein Info, human and Chromosomes, Human, Pair 6 in Prominin-1, human positive and negative glands. From the 13 cases four (31%) showed amplification for the MYC Protein Info, human Protein Info, human oncogene and seven of 13 (54%) cases were amplified for ZNF217 Protein Info, human Protein Info, human., The simultaneous detection of Protein Info expression and gene copy number changes in patient samples, like paraffin-embedded tissue sections, is challenging since the procedures of immunohistochemistry (IHC) and Fluorescence in situ Hybridization (FISH) negatively influence each other which often results in suboptimal staining.Therefore, we developed a novel automated algorithm based on relocation which allows subsequent detection of Protein Info content and gene copy number changes within the same \"U\" lymphocyte. METHODS: Paraffin-embedded tissue sections of Colorectal Carcinoma were stained for Prominin-1, human expression. IHC images were acquired and image coordinates recorded. Slides were subsequently hybridized with fluorescently labeled DNA Probes. FISH images were taken at the previously recorded positions allowing for direct comparison of Protein Info expression and gene copy number signals within the same cells/tissue areas. Relocation, acquisition of the IHC and FISH images, and enumeration of FISH signals in the immunophenotyped tumour areas were done in an automated fashion. RESULTS: Automated FISH analysis was performed on 13 different Malignant tumor of colon samples that had been stained for Prominin-1, human; each sample was scored for MYC Protein Info, human Protein Info, human, ZNF217 Protein Info, human Protein Info, human and Chromosomes, Human, Pair 6 in Prominin-1, human positive and negative glands. From the 13 cases four (31%) showed amplification for the MYC Protein Info, human Protein Info, human oncogene and seven of 13 (54%) cases were amplified for ZNF217 Protein Info, human Protein Info, human. There was no significant difference between Prominin-1, human positive tumour and Prominin-1, human negative tumour cells. , The simultaneous detection of Protein Info expression and gene copy number changes in patient samples, like paraffin-embedded tissue sections, is challenging since the procedures of immunohistochemistry (IHC) and Fluorescence in situ Hybridization (FISH) negatively influence each other which often results in suboptimal staining.Therefore, we developed a novel automated algorithm based on relocation which allows subsequent detection of Protein Info content and gene copy number changes within the same \"U\" lymphocyte.Methods: Paraffin-embedded tissue sections of Colorectal Carcinoma were stained for Prominin-1, human expression. IHC images were acquired and image coordinates recorded. Slides were subsequently hybridized with fluorescently labeled DNA Probes. FISH images were taken at the previously recorded positions allowing for direct comparison of Protein Info expression and gene copy number signals within the same cells/tissue areas. Relocation, acquisition of the IHC and FISH images, and enumeration of FISH signals in the immunophenotyped tumour areas were done in an automated fashion.Results: Automated FISH analysis was performed on 13 different Malignant tumor of colon samples that had been stained for Prominin-1, human; each sample was scored for MYC Protein Info, human Protein Info, human, ZNF217 Protein Info, human Protein Info, human and Chromosomes, Human, Pair 6 in Prominin-1, human positive and negative glands. From the 13 cases four (31%) showed amplification for the MYC Protein Info, human Protein Info, human oncogene and seven of 13 (54%) cases were amplified for ZNF217 Protein Info, human Protein Info, human. There was no significant difference between Prominin-1, human positive tumour and Prominin-1, human negative tumour cells.[SEP]Relations: colorectal carcinoma has relations: disease_protein with JPH3, disease_protein with JPH3, disease_protein with QKI, disease_protein with QKI, disease_protein with EFS, disease_protein with EFS, disease_protein with NRCAM, disease_protein with NRCAM, disease_protein with AURKA, disease_protein with AURKA.", "label": "yes"}
{"original_question": "Is there a role for TFII-I in megakaryopoiesis?", "id": "converted_4112", "sentence1": "Is there a role for TFII-I in megakaryopoiesis?", "sentence2": "TFII-I/Gtf2i and Erythro-Megakaryopoiesis., TFII-I is a ubiquitously expressed transcription factor that positively or negatively regulates gene expression. TFII-I has been implicated in neuronal and immunologic diseases as well as in thymic epithelial cancer. Williams Syndrome (Beckwith-Wiedemann Syndrome) is caused by a large hemizygous deletion on chromosome 7q11.23 which encompasses 26-28 Genes, including GTF2I gene gene, the Human gene encoding TFII-I. A subset of Beckwith-Wiedemann Syndrome patients has recently been shown to present with Macrocytosis (morphologic abnormality), a mild Genus Anemia characterized by enlarged erythrocytes. We conditionally deleted the TFII-I/Gtf2i gene in adult CASP14 gene by tamoxifen induced Cre-recombination. Bone Marrow Cells revealed defects in erythro-megakaryopoiesis and an increase in expression of the adult β-globin gene. The data show that TFII-I acts as a repressor of β-globin gene transcription and that it is implicated in the differentiation of erythro-megakaryocytic cells.[SEP]Relations: GTF2I gene has relations: disease_protein with myeloid leukemia, disease_protein with myeloid leukemia, disease_protein with acute myeloid leukemia and myelodysplastic syndromes related to topoisomerase type 2 inhibitor, disease_protein with acute myeloid leukemia and myelodysplastic syndromes related to topoisomerase type 2 inhibitor, disease_protein with unclassified acute myeloid leukemia, disease_protein with unclassified acute myeloid leukemia, protein_protein with ZMYM3, protein_protein with ZMYM3, disease_protein with acute myeloid leukemia with t(6;9)(p23;q34), disease_protein with acute myeloid leukemia with t(6;9)(p23;q34).", "label": "yes"}
{"original_question": "Is Tofacitinib effective for Ulcerative Colitis?", "id": "converted_2434", "sentence1": "Is Tofacitinib effective for Ulcerative Colitis?", "sentence2": "Tofacitinib, inhibiting signalling via all JAK1 protein, human family members, was effective in phase 2 and 3 trials in moderate-severe ulcerative colitis., Among them, JAK1 protein, human (JAK1 protein, human) inhibitors seem to have the lead, since tofacitinib has received regulatory approval in 2012 for the treatment of Rheumatoid Arthritis, and also it has shown a favorable risk-benefit ratio in phase 3 studies for ulcerative colitis, both in anti-TNF naïve and anti-TNF experienced patients. , Near future conventional drug options include Oral Route of Drug administration agents such as tofacitinib and mongersen. , Tofacitinib showed dose related efficacy for induction therapy. , Tofacitinib as Induction and Maintenance Therapy for Ulcerative Colitis., BACKGROUND: Tofacitinib, an Oral Route of Drug administration, small-molecule Janus Kinase Inhibitor [EPC], was shown to have potential efficacy as induction therapy for ulcerative colitis in a phase 2 trial. , CONCLUSIONS: In patients with moderately to severely active ulcerative colitis, tofacitinib was more effective as induction and maintenance therapy than placebo., Tofacitinib (CP-690,550), an Oral Route of Drug administration small-molecule Janus Kinase Inhibitor [EPC], has been shown to be effective in the treatment of Rheumatoid Arthritis, Experimental Autoimmune Encephalomyelitis and ulcerative colitis. , Tofacitinib, an Oral Route of Drug administration, small-molecule Janus Kinase Inhibitor [EPC], was shown to have potential efficacy as induction therapy for ulcerative colitis in a phase 2 trial., <b>BACKGROUND</b>: Tofacitinib, an Oral Route of Drug administration, small-molecule Janus Kinase Inhibitor [EPC], was shown to have potential efficacy as induction therapy for ulcerative colitis in a phase 2 trial., Across all three trials, adjudicated Skin carcinoma occurred in five patients who received tofacitinib and in one who received placebo, and adjudicated cardiovascular events occurred in five who received tofacitinib and in none who received placebo; as compared with placebo, tofacitinib was associated with increased Lipids levels.<br><b>CONCLUSIONS</b>: In patients with moderately to severely active ulcerative colitis, tofacitinib was more effective as induction and maintenance therapy than placebo., Tofacitinib (CP-690,550), an Oral Route of Drug administration small-molecule Janus Kinase Inhibitor [EPC], has been shown to be effective in the treatment of Rheumatoid Arthritis, Experimental Autoimmune Encephalomyelitis and ulcerative colitis., Tofacitinib, an Oral Route of Drug administration Janus Kinase Inhibitor [EPC], in active ulcerative colitis., Tofacitinib, a non-selective JAK1 protein, human (JAK1 protein, human) PPP1R1A gene, is effective in inducing clinical and endoscopic remission in patients with active ulcerative colitis (Ulcerative Colitis)., BACKGROUND Tofacitinib, an Oral Route of Drug administration, small-molecule Janus Kinase Inhibitor [EPC], was shown to have potential efficacy as induction therapy for ulcerative colitis in a phase 2 trial., BACKGROUND Tofacitinib, a novel, Oral Route of Drug administration Janus Kinase Inhibitor [EPC], demonstrated a dose-dependent efficacy for induction of clinical response and remission in patients with active ulcerative colitis (Ulcerative Colitis)., CONCLUSIONS In patients with moderately to severely active ulcerative colitis, tofacitinib was more effective as induction and maintenance therapy than placebo., Tofacitinib, an Oral Route of Drug administration janus kinase PPP1R1A gene, is a new biologic that has shown promise in the treatment of ulcerative colitis and may be effective in the treatment of Crohn's disease of Oral Route of Drug administration soft tissues of Oral Route of Drug administration soft tissues according to phase 2 trials., CONCLUSIONS Patients with moderately to severely active ulcerative colitis treated with tofacitinib were more likely to have clinical response and remission than those receiving placebo., Three patients treated with tofacitinib had an absolute neutrophil count of less than 1500.<br><b>CONCLUSIONS</b>: Patients with moderately to severely active ulcerative colitis treated with tofacitinib were more likely to have clinical response and remission than those receiving placebo., tofacitinib an Oral Route of Drug administration small molecule janus kinase PPP1R1A gene was shown to have potential efficacy as induction therapy for ulcerative colitis in a phase 2 trial we further evaluated the efficacy of tofacitinib as induction and maintenance therapy we conducted three phase 3 randomized double blind placebo controlled trials of tofacitinib therapy in adults with ulcerative colitis in the octave induction 1 and 2 trials 598 and 541 patients respectively who had moderately to severely active ulcerative colitis despite previous conventional therapy or therapy with a Tumor Necrosis Factor Inhibitors were randomly assigned to receive induction therapy with tofacitinib 10 mg twice daily or placebo for 8 weeks the primary end point was remission at 8 weeks in the octave sustain trial 593 patients who had a clinical response to induction therapy were randomly assigned to receive maintenance therapy with tofacitinib either 5 mg or 10 mg twice daily or placebo for 52 weeks the primary end point was remission at 52 weeks in the octave induction 1 trial remission at 8 weeks occurred in 18 5 of the patients in the tofacitinib group versus 8 2 in the placebo group p 0 007 in the octave induction 2 trial remission occurred in 16 6 versus 3 6 p 0 001 in the octave sustain trial remission at 52 weeks occurred in 34 3 of the patients in the 5 mg tofacitinib group and 40 6 in the 10 mg tofacitinib group versus 11 1 in the placebo group p 0 001 for both comparisons with placebo in the octave induction 1 and 2 trials the rates of overall infection and serious infection were higher with tofacitinib than with placebo in the octave sustain trial the rate of serious infection was similar across the three treatment groups and the rates of overall infection and Herpes zoster disease were higher with tofacitinib than with placebo across all three trials adjudicated Skin carcinoma occurred in five patients who received tofacitinib and in one who received placebo and adjudicated cardiovascular events occurred in five who received tofacitinib and in none who received placebo as compared with placebo tofacitinib was associated with increased Lipids levels in patients with moderately to severely active ulcerative colitis tofacitinib was more effective as induction and maintenance therapy than placebo funded by pfizer octave induction 1 octave induction 2 and octave sustain clinicaltrials gov numbers nct01465763 nct01458951 and nct01458574 respectively., ulcerative colitis is a chronic inflammatory disease of the Abdomen+Pelvis>Colon for which current treatments are not universally effective one additional treatment may be tofacitinib cp 690 550 an Oral Route of Drug administration PPP1R1A gene of janus kinases 1 2 and 3 with in vitro functional specificity for kinases 1 and 3 over kinase 2 which is expected to block signaling involving gamma chain containing Recombinant Cytokines including interleukins 2 4 7 9 15 and 21 these Recombinant Cytokines are integral to lymphocyte activation function and proliferation in a double blind placebo controlled phase 2 trial we evaluated the efficacy of tofacitinib in 194 adults with moderately to severely active ulcerative colitis patients were randomly assigned to receive tofacitinib at a dose of 0 5 mg 3 mg 10 mg or 15 mg or placebo twice daily for 8 weeks the primary outcome was a clinical response at 8 weeks defined as an absolute decrease from baseline in the score on the mayo scoring system for assessment of ulcerative colitis activity possible score 0 to 12 with higher scores indicating more severe disease of 3 or more and a relative decrease from baseline of 30 or more with an accompanying decrease in the Rectal hemorrhage subscore of 1 point or more or an absolute Rectal hemorrhage subscore of 0 or 1 the primary outcome clinical response at 8 weeks occurred in 32 48 61 and 78 of patients receiving tofacitinib at a dose of 0 5 mg p 0 39 3 mg p 0 55 10 mg p 0 10 and 15 mg p 0 001 respectively as compared with 42 of patients receiving placebo clinical remission defined as a mayo score 2 with no subscore 1 at 8 weeks occurred in 13 33 48 and 41 of patients receiving tofacitinib at a dose of 0 5 mg p 0 76 3 mg p 0 01 10 mg p 0 001 and 15 mg p 0 001 respectively as compared with 10 of patients receiving placebo there was a dose dependent increase in both low density and High Density Lipoprotein Cholesterol three patients treated with tofacitinib had an absolute neutrophil count of less than 1500 patients with moderately to severely active ulcerative colitis treated with tofacitinib were more likely to have clinical response and remission than those receiving placebo funded by pfizer clinicaltrials gov number nct00787202., recently several medical treatments for ulcerative colitis uc have been developed including 5 aminosalicylic acids 5 asas Corticosteroid ophthalmologic and otologic preparations thiopurine Calcineurin Inhibitors [MoA] and anti tumor necrosis factor tnf α treatments treatment options including Calcineurin Inhibitors [MoA] and anti tnf treatment for refractory uc are discussed in this article furthermore upcoming treatments are introduced such as golimumab vedolizumab ajm300 tofacitinib budesonide foamwill be used as one treatment option in patients with Distal colitis herbal medicine such as qing dai is also effective for active uc and may be useful for patients who are refractory to anti tnfα treatments in the near future physicians will able to use many different treatments for uc patients however we should not forget 5 asa and Corticosteroid ophthalmologic and otologic preparations as the fundamental treatments for uc patients., the inflammatory diseases ulcerative colitis and crohn s disease constitute the two main forms of INFLAMMATORY BOWEL DISEASE 2 ibd they are characterized by chronic relapsing Inflammation of the Abdomen+Pelvis>Gastrointestinal tract significantly impacting on patient quality of life and often requiring prolonged treatment existing therapies for ibd are not effective for all patients and an unmet need exists for additional therapies to induce and maintain remission here we describe the mechanism of action of the janus kinase jak PPP1R1A gene tofacitinib for the treatment of ibd and the effect of jak inhibition on the chronic cycle of Inflammation that is characteristic of the disease the pathogenesis of ibd involves a dysfunctional response from the innate and adaptive immune system resulting in overexpression of multiple inflammatory Recombinant Cytokines many of which signal through jaks thus jak inhibition allows multiple cytokine signaling pathways to be targeted and is expected to modulate the innate and adaptive immune response in ibd thereby interrupting the cycle of Inflammation tofacitinib is an Oral Route of Drug administration small molecule jak PPP1R1A gene that is being investigated as a targeted immunomodulator for ibd clinical development of tofacitinib and other jak inhibitors is ongoing with the aspiration of providing new treatment options for ibd that have the potential to deliver prolonged efficacy and clinically meaningful patient benefits.[SEP]Relations: Tofacitinib has relations: drug_drug with Eculizumab, drug_drug with Eculizumab, drug_drug with Tocilizumab, drug_drug with Tocilizumab, drug_drug with Otamixaban, drug_drug with Otamixaban, drug_drug with Dovitinib, drug_drug with Dovitinib, drug_drug with Saracatinib, drug_drug with Saracatinib.", "label": "yes"}
{"original_question": "Can IFNg induce the expression of IDO?", "id": "converted_4390", "sentence1": "Can IFNg induce the expression of indoleamine 2,3-dioxygenase activity?", "sentence2": "interferon type II inducible IDO1 gene activity/GTPCH inflammation cascade, interferon type II-induced up-regulation of Indoleamine 2,3-Dioxygenase, human gene (IDO1 gene activity), IFN-γ-induced indoleamine-2,3-dioxgenase (IDO1 gene activity) , strong and positive correlation between Indoleamine 2,3-Dioxygenase, human and interferon type II mRNA expression levels ,  The tryptophan-degrading activity of Indoleamine 2,3-Dioxygenase, human was not induced significantly by Chlamydia Infections alone, but the addition of interferon type II greatly increased its activity. [SEP]Relations: IDO1 gene activity has relations: molfunc_protein with IDO2, molfunc_protein with IDO2, molfunc_protein with IDO2, molfunc_protein with IDO2, molfunc_protein with Indoleamine 2,3-Dioxygenase, human, molfunc_protein with Indoleamine 2,3-Dioxygenase, human, molfunc_protein with Indoleamine 2,3-Dioxygenase, human, molfunc_protein with Indoleamine 2,3-Dioxygenase, human. response to type III interferon has relations: bioprocess_protein with IFNLR1, bioprocess_protein with IFNLR1.", "label": "yes"}
{"original_question": "Is Hunter's disease is associated with the X Chromosome?", "id": "converted_3889", "sentence1": "Is Hunter's Disease is associated with the X Chromosome?", "sentence2": "Segregation analysis on five samples of families with Hunter's syndrome (158 cases overall) shows that the mutant allele segregates in agreement with Mendelian expectations for an X linked recessive, The utility of polymerase chain reaction (PCR) amplification of amelogenin Genes as a reliable and rapid means of determination of Sex Chromosomes was tested in 20 patients of X-linked disorders (Muscular Dystrophy, Duchenne, Hemophilia, NOS and Wiscott-Aldrich and Hunter's syndromes), , We describe a 3 year old girl with the typical clinical features of the X linked recessive condition, Hunter's Disease, We describe a 3 year old girl with the typical clinical features of the X linked recessive condition, Hunter's Disease., Hunter's Disease in a girl: association with X:5 chromosomal translocation disrupting the Hunter Genes., Further evidence localising the Genes for Hunter's syndrome to the distal region of the Xq., Full expression of Hunter's Disease in a female with an X-chromosome Gene Deletion Abnormality leading to non-random inactivation., Mucopolysaccharidosis II in a girl caused by R468Q Mutation Abnormality in the Iduronate Sulfatase Genes and skewed inactivation of the X chromosome carrying the normal allele., These findings strongly suggest that the severe form of Mucopolysaccharidosis II in this girl was the result of selective expression of the maternal allele carrying the missense Mutation Abnormality R468Q, which in turn resulted from skewed X inactivation of the paternal nonmutant X chromosome., LUSIONS: This is a report of a female with a 10.6 Mb Xq27-28 Gene Deletion Abnormality with skewed inactivation of the deleted X chromosome. Con, Brother/sister siblings affected with Mucopolysaccharidosis II: evidence for skewed X chromosome inactivation., The normal X chromosome was preferentially inactivated, supporting the view that the translocation had disrupted the Hunter Genes., Mucopolysaccharidosis II (Mucopolysaccharidoses type II) associated with unbalanced inactivation of the X Chromosome in a karyotypically normal girl., INTRODUCTION: Hunter syndrome, or Mucopolysaccharidoses type II, is an inherited Disease linked to the X chromosome that is caused by a deficit of the Enzyme [APC] Iduronate Sulfatase and its main symptoms affect the XXX bone, neurological system and the Viscera., INTRODUCTION: Hunter syndrome, or Mucopolysaccharidoses type II, is an inherited Disease linked to the X chromosome that is caused by a deficit of the Enzyme [APC] Iduronate Sulfatase and its main symptoms affect the XXX bone, neurological system and the, Mucopolysaccharidosis type II (MPS II, Mucopolysaccharidosis II) is an X chromosome-linked inherited metabolic Disease caused by Gene Mutation resulting in deficiency of activity of Iduronate Sulfatase (IDS) and accumulation of undegraded glycosaminoglycans (Mouth gag), heparan sulfate, and Dermatan Sulfate. Previous, Mucopolysaccharidosis type II (MPS-II, Mucopolysaccharidosis II) is a X-linked recessive disorder. Affe, Mucopolysaccharidosis type II (MPS II or Hunter syndrome) is a rare X-linked disorder caused by deficient activity of the lysosomal Enzyme [APC], Iduronate Sulfatase (IDS). Pheno, Mucopolysaccharidosis II or Mucopolysaccharidoses type II is an X-linked Disease caused by the deficiency of the lysosomal Enzyme [APC] Iduronate Sulfatase (IDS). Tyrosine 3-Monooxygenase, human, Mucopolysaccharidosis type II (MPS II, Hunter syndrome) is an X-linked lysosomal storage Disease caused by a deficiency of Iduronate Sulfatase (IDS). Two a, We report the results of studies on the characterization of the Mutation Abnormality associated with marked unbalanced expression of the mutant X chromosome in a karyotypically normal girl with Mucopolysaccharidosis II (Mucopolysaccharidoses type II). So, BACKGROUND: Hunter syndrome (Mucopolysaccharidoses type II) is a recessive X-linked disorder due to Gene Mutation in the iduronate 2-sulfatase (IDS, Familial X-chromosome inactivation (XCI) skewing was investigated in a family in which a female Mucopolysaccharidoses type II (MPS II) (Hunter syndrome, an X-linked genetic Disease) occurred. Among e, Studies using Bromodeoxyuridine indicated that the deleted X chromosome was consistently late replicating, and as a result the Hunter Genes was fully expressed on the other X chromosome., All Mucopolysaccharidoses are autosomal recessive disorders, except for Hunter's syndrome that is X-linked and recessive., Female twin with Mucopolysaccharidosis II due to nonrandom inactivation of the X-chromosome: a consequence of twinning., Hunter syndrome (Mucopolysaccharidoses type II) is a recessive X-linked disorder due to Gene Mutation in the iduronate 2-sulfatase (IDS) Genes., Mucopolysaccharidosis II is an X-linked recessive mucopolysaccharide storage disorder caused by Iduronate Sulfatase deficiency and is rare in females., Mucopolysaccharidosis II is an X-linked recessive disorder caused by a deficiency of Iduronate Sulfatase activity.[SEP]Relations: X-linked Disease has relations: disease_disease with sex-linked Disease, disease_disease with sex-linked Disease, disease_disease with X-linked dominant Disease, disease_disease with X-linked dominant Disease, disease_disease with X-linked immunoneurologic disorder, disease_disease with X-linked immunoneurologic disorder, disease_disease with X-linked intellectual disability, disease_disease with X-linked intellectual disability, disease_disease with choroideremia, disease_disease with choroideremia.", "label": "yes"}
{"original_question": "Is the CADM2 gene associated with differences in information processing speed?", "id": "converted_3368", "sentence1": "Is the CADM2 gene gene associated with differences in information processing speed?", "sentence2": "GWAS for executive function and processing speed suggests involvement of the CADM2 gene gene gene., A significant association was observed in the discovery cohorts for the single-nucleotide polymorphism (SNP) rs17518584 (discovery P-value=3.12 × 10(-8)) and in the joint discovery and replication meta-analysis (P-value=3.28 × 10(-9) after adjustment for age, gender and education) in an Introns of the Cell Adhesion Molecule Gene (CADM2 gene gene) for performance on the LDST/DSST. Rs17518584 is located about 170 kb upstream of the transcription start site of the major RNA Transcript for the CADM2 gene gene gene, but is within an Introns of a Variant RNA Transcript that includes an alternative first Exons. The Variant is associated with expression of CADM2 gene gene in the Cingulate Cortex (P-value=4 × 10(-4)). The Protein Info encoded by CADM2 gene gene is involved in glutamate signaling (P-value=7.22 × 10(-15)), gamma-aminobutyric acid (GABA) transport (P-value=1.36 × 10(-11)) and neuron cell-cell adhesion (P-value=1.48 × 10(-13)). Our findings suggest that genetic variation in the CADM2 gene gene gene is associated with individual differences in information processing speed., Our findings suggest that genetic variation in the CADM2 gene gene gene is associated with individual differences in information processing speed., The CADM2 gene gene gene is associated with processing speed performance - evidence among elderly with type 2 diabetes., Our findings suggest that genetic variation in the CADM2 gene gene gene is associated with individual differences in information processing speed.[SEP]Relations: Cingulate Cortex has relations: anatomy_protein_present with CADM3, anatomy_protein_present with CADM3, anatomy_protein_present with CADM1, anatomy_protein_present with CADM1, anatomy_protein_present with CADPS2, anatomy_protein_present with CADPS2, anatomy_protein_present with ECM2, anatomy_protein_present with ECM2, anatomy_protein_present with PIM2, anatomy_protein_present with PIM2.", "label": "yes"}
{"original_question": "Is there a role of regorafenib for sarcoma treatment?", "id": "converted_1768", "sentence1": "Is there a role of regorafenib for Malignant neoplasm of soft tissue treatment?", "sentence2": "regorafenib has been approved for third-line therapy., Study protocol of REGOSARC trial: activity and safety of regorafenib in advanced soft tissue Malignant neoplasm of soft tissue: a multinational, randomized, placebo-controlled, phase II trial., DISCUSSION: The design of this trial allows an assessment of regorafenib activity over placebo in four Malignant neoplasm of soft tissue strata and might provide evidence for launching a phase III trial., This case provides rationale for adding a Ewing Malignant neoplasm of soft tissue arm to SARC024, a phase II study of regorafenib, another multi-targeted kinase inhibitor, in patients with liposarcoma, Osteosarcoma of bone and Ewing and Ewing-like sarcomas (NCT02048371)., Thus, the Phase III studies with pazopanib, regorafenib, muramyl tripeptide (maltose tetrapalmitate) and ridaforolimus are extensively discussed as well as the biological rationale for the use of these compounds., Currently, regorafenib is examined in several clinical trials (mostly phase II) in different Specimen Source Codes - Specimen Source Codes - tumor entities, including renal cell carcinoma (Conventional (Clear Cell) Renal Cell Carcinoma), Liver carcinoma (altretamine/cisplatin/cyclophosphamide protocol), and soft tissue Malignant neoplasm of soft tissue (sodium tetradecyl sulfate)., Analysis of primary human Malignant neoplasm of soft tissue samples revealed direct cytotoxicity following exposure to sorafenib and regorafenib with a corresponding increase in ALDHbright cells (P<0.05)., Parametric and non-parametric statistical analyses were performed as appropriate.RESULTS: After functionally validating the CSC phenotype of ALDHbright Malignant neoplasm of soft tissue cells, we observed that sorafenib and regorafenib were cytotoxic to Malignant neoplasm of soft tissue cell lines (P<0.05), with a corresponding 1.4 - 2.8 fold increase in ALDHbright cells from baseline (P<0.05)., We evaluated survival and CSC phenotype in CASP14 gene harboring Malignant neoplasm of soft tissue metastases after TKI therapy. We exposed dissociated primary Malignant neoplasm of soft tissue tumors to sorafenib, regorafenib, and pazopanib, and we used tissue microarray (Thrombotic Microangiopathies) and primary Malignant neoplasm of soft tissue samples to evaluate the frequency and intensity of CSC markers after neoadjuvant therapy with sorafenib and pazopanib. Parametric and non-parametric statistical analyses were performed as appropriate.RESULTS: After functionally validating the CSC phenotype of ALDHbright Malignant neoplasm of soft tissue cells, we observed that sorafenib and regorafenib were cytotoxic to Malignant neoplasm of soft tissue cell lines (P<0.05), with a corresponding 1.4 - 2.8 fold increase in ALDHbright cells from baseline (P<0.05)., We exposed dissociated primary Malignant neoplasm of soft tissue tumors to sorafenib, regorafenib, and pazopanib, and we used tissue microarray (Thrombotic Microangiopathies) and primary Malignant neoplasm of soft tissue samples to evaluate the frequency and intensity of CSC markers after neoadjuvant therapy with sorafenib and pazopanib. Parametric and non-parametric statistical analyses were performed as appropriate.RESULTS: After functionally validating the CSC phenotype of ALDHbright Malignant neoplasm of soft tissue cells, we observed that sorafenib and regorafenib were cytotoxic to Malignant neoplasm of soft tissue cell lines (P<0.05), with a corresponding 1.4 - 2.8 fold increase in ALDHbright cells from baseline (P<0.05)., We exposed dissociated primary Malignant neoplasm of soft tissue tumors to sorafenib, regorafenib, and pazopanib, and we used tissue microarray (Thrombotic Microangiopathies) and primary Malignant neoplasm of soft tissue samples to evaluate the frequency and intensity of CSC markers after neoadjuvant therapy with sorafenib and pazopanib. Parametric and non-parametric statistical analyses were performed as appropriate.RESULTS: After functionally validating the CSC phenotype of ALDHbright Malignant neoplasm of soft tissue cells, we observed that sorafenib and regorafenib were cytotoxic to Malignant neoplasm of soft tissue cell lines (P<0.05), with a corresponding 1.4 - 2.8 fold increase in ALDHbright cells from baseline (P<0.05). In contrast, we observed negligible effects on viability and CSC sub-populations with pazopanib., After functionally validating the CSC phenotype of ALDHbright Malignant neoplasm of soft tissue cells, we observed that sorafenib and regorafenib were cytotoxic to Malignant neoplasm of soft tissue cell lines (P < 0.05), with a corresponding 1.4 - 2.8 fold increase in ALDHbright cells from baseline (P < 0.05).[SEP]Relations: regorafenib has relations: drug_drug with Sarilumab, drug_drug with Sarilumab, drug_drug with Sarecycline, drug_drug with Sarecycline, drug_drug with Afelimomab, drug_drug with Afelimomab, drug_drug with Lapatinib, drug_drug with Lapatinib, drug_drug with Sulfasalazine, drug_drug with Sulfasalazine.", "label": "yes"}
{"original_question": "Is there any link between conserved noncoding elements and alternative splicing in vertebrates?", "id": "converted_1187", "sentence1": "Is there any link between conserved noncoding elements and alternative splicing in Vertebrates?", "sentence2": "Some of the most highly conserved sequences occur in Genes encoding RNA-Binding Proteins, particularly the RNA splicing-associated SR Genes. Differences in sequence conservation between Plants and animal allergen extracts are likely to reflect differences in the biology of the Organism, with Plants being much more able to tolerate genomic deletions and whole-genome duplication events due, in part, to their far greater fecundity compared with Vertebrates.[SEP]Relations: vertebra has relations: anatomy_anatomy with non-transverse process-bearing vertebra, anatomy_anatomy with non-transverse process-bearing vertebra. protein binding has relations: molfunc_protein with SPRYD7, molfunc_protein with SPRYD7, molfunc_protein with SPG7, molfunc_protein with SPG7, molfunc_protein with SPIC, molfunc_protein with SPIC, molfunc_protein with SP7, molfunc_protein with SP7.", "label": "yes"}
{"original_question": "Has vitamin D has been shown to reduce incidence of falls in older people in clinical trials?", "id": "converted_218", "sentence1": "Has ergocalciferol has been shown to reduce incidence of falls in older people in clinical trials?", "sentence2": "However, apart from the beneficial effects of 800 IU/d of cholecalciferol for reduction of falls in the elderly, causality remains yet unproven in randomized controlled trials (RCTs). , The rate of falls and the number of fallers was significantly reduced in two studies evaluating the effect of medication on preventing falls; one study (85 participants) compared ergocalciferol versus placebo in institutionalised women after Cerebrovascular accident with low ergocalciferol levels, and the other study (79 participants) evaluated alendronate versus alfacalcidol in hospitalised people after Cerebrovascular accident., Two studies testing ergocalciferol versus placebo and alendronate versus alfacalcidol found a significant reduction in falls and the number of people falling, .Overall, ergocalciferol supplementation does not appear to reduce falls but may be effective in people who have lower ergocalciferol levels before treatment., Overall, ergocalciferol did not reduce rate of falls (RaR 1.00, 95% CI 0.90 to 1.11; seven trials; 9324 participants) or risk of falling (RR 0.96, 95% CI 0.89 to 1.03; 13 trials; 26,747 participants), but may do so in people with lower ergocalciferol levels before treatment., Vitamin D affects Specimen Type - Bone and muscle health and likely reduces the risk of falls in the elderly., We found 26 eligible trials of moderate quality that enrolled 45,782 participants, the majority of which were elderly and female. Vitamin D use was associated with statistically significant reduction in the risk of falls (odds ratio for suffering at least one fall, 0.86; 95% confidence interval, 0.77-0.96), This effect was more prominent in patients who were ergocalciferol deficient at baseline and in studies in which CALCIUM SUPPLEMENTS was coadministered with ergocalciferol., Vitamin D combined with CALCIUM SUPPLEMENTS reduces the risk of falls., The majority of the evidence is derived from trials enrolling elderly women., Studies of ergocalciferol and CALCIUM SUPPLEMENTS for fracture prevention have produced inconsistent results, as a result of different ergocalciferol status and CALCIUM SUPPLEMENTS intake at baseline, different doses and poor to adequate compliance., Despite significant increases in the provision of Hip protector and use of ergocalciferol supplementation in both intervention and control facilities, there was no difference in the number of falls or falls injuries between the intervention and control groups, nor a reduction in falls overall., Beyond fall and fracture prevention, ergocalciferol may also reduce overall morbidity by multiple mechanisms. , There is evidence to suggest that these agents may reduce the incidence of nonvertebral fractures and falls; however, their benefit on vertebral fracture reduction may depend on the type of active ergocalciferol. [SEP]Relations: Cholecalciferol has relations: drug_drug with Vitamin D, drug_drug with Vitamin D, contraindication with familial isolated deficiency of vitamin E, contraindication with familial isolated deficiency of vitamin E. Ergocalciferol has relations: drug_drug with Vitamin D, drug_drug with Vitamin D, contraindication with familial isolated deficiency of vitamin E, contraindication with familial isolated deficiency of vitamin E. Alfacalcidol has relations: drug_drug with Vitamin D, drug_drug with Vitamin D.", "label": "yes"}
{"original_question": "Is serotonin transported by platelets?", "id": "converted_4560", "sentence1": "Is serotonin transported by Blood Platelets?", "sentence2": " activated Blood Platelets, which carry peripheral serotonin,, Platelet serotonin response was measured by serotonin augmented platelet aggregation and platelet serotonin receptor density. , Selective External Radiation Therapy was studied in the 1970s and 1980s using membrane vesicles isolated from blood Blood Platelets., platelet-dense granules contain neurotransmitters such as serotonin and gamma-aminobutyric acid. Molecular players controlling granule formation and secretion are, Platelets transport and store virtually all plasma serotonin in dense granules[SEP]Relations: Serotonin has relations: drug_drug with Sarpogrelate, drug_drug with Sarpogrelate, drug_drug with Ketamine, drug_drug with Ketamine, drug_drug with Pargyline, drug_drug with Pargyline, drug_drug with Saredutant, drug_drug with Saredutant, drug_drug with Piperidolate, drug_drug with Piperidolate.", "label": "yes"}
{"original_question": "Do polycomb group proteins (PcG) mediate the formation of chromatin loops?", "id": "converted_3845", "sentence1": "Do polycomb group Proteins (Polycomb-Group Proteins) mediate the formation of chromatin loops?", "sentence2": "A chromatin insulator driving three-dimensional Polycomb response element (Pure Spanish horse breed (organism)) contacts and Polycomb association with the 30 nm Chromatin Fiber, the Drosophila <basidiomycetes> <basidiomycetes> gypsy insulator behaves as a conformational chromatin border that is able to prohibit contacts between a Polycomb response element (Pure Spanish horse breed (organism)) and a distal promoter, Polycomb action at a distance can be organized by local chromatin topology, Polycomb repressive complex 2 is recruited through the interaction of CTGF protein, human, CTGF protein, human governs Genes expression by orchestrating chromatin loop structures and by serving as a DNA-Binding Proteins scaffold to recruit and bind polycomb repressive complexes, The chromatin loops completely dissolve, accompanied by loss of Polycomb-Group Proteins Proteins and Histone H3 Trimethyl Lys28 marks, when Tera-2 cells receive differentiation signals which induce a approximately 60-fold increase in GATA-4 expression., Polycomb-mediated chromatin loops revealed by a subkilobase-resolution chromatin interaction map., es or \"anchors\" are associated with CTGF protein, human protein in Mammals, loop anchors in Drosophila <basidiomycetes> <basidiomycetes> were found most often in association with the polycomb group (Polycomb-Group Proteins) protein Polycomb (Pachyonychia Congenita), a subunit of polycomb repressive complex 1 (Drosophila <basidiomycetes> <basidiomycetes> Polycomb Repressive Complex 1). Loops were frequently located within domains of Polycomb-Group Proteins, We also provide novel insight that Polycomb-Group Proteins-occupied and Histone H3 Trimethyl Lys28-enriched regions can form chromatin loops and physically interact in cis around a single Genes in mammalian cells., Repressive loops within polycomb domains are formed after the midblastula transition between polycomb response elements by the action of GAGA factor and polycomb Proteins., Polycomb-Group Proteins Proteins, DNA methylation, and Genes repression by chromatin looping., Loops were frequently located within domains of Polycomb-Group Proteins-repressed chromatin., iation to proliferation control. Our results revealed a chromatin looping mechanism of long-range control and argue against models involving homogeneous spreading of Polycomb-Group Proteins silencers [SEP]Relations: protein binding has relations: molfunc_protein with PCP4, molfunc_protein with PCP4, molfunc_protein with PCTP, molfunc_protein with PCTP, molfunc_protein with PCCA, molfunc_protein with PCCA, molfunc_protein with PCNP, molfunc_protein with PCNP, molfunc_protein with PCDHA4, molfunc_protein with PCDHA4.", "label": "yes"}
{"original_question": "Is DNA methylation an epigenetic modification of chromatin related to gene expression?", "id": "converted_994", "sentence1": "Is DNA methylation an epigenetic modification of chromatin related to gene expression?", "sentence2": "DNA methylation is a Structural Modifier of DNA involved in the regulation of gene expression by controlling the access to the DNA Sequence. , Epigenetic marks such as DNA methylation play important biological roles in gene expression regulation and cellular differentiation during development., DNA methylation patterns are characterized by highly conserved developmental programs, but allow for divergent gene expression resulting from stochastic epigenetic drift or divergent environments., DNA methylation plays a critical role in the regulation of gene expression. , Epigenetic changes such as DNA methylation and histone methylation and acetylation alter gene expression at the level of transcription by upregulating, downregulating, or silencing Genes completely., Dysregulation of epigenetic events can be pathological, leading to Cardiovascular Diseases, nervous system disorder, Metabolic Diseases, and cancer development., DNA methylation is a pervasive epigenetic DNA modification that strongly affects chromatin regulation and gene expression., Epigenetic control, which includes DNA methylation and histone modifications, leads to chromatin remodeling and regulated gene expression., Epigenetic modifications on the DNA Sequence (DNA methylation) or on chromatin-associated proteins (i.e., Histones) comprise the \"cellular epigenome\"; together these modifications play an important role in the regulation of gene expression., Epigenetics is a process involved in gene regulation, mediated via DNA methylation, histone modification, chromatin remodeling, and functional noncoding RNAs, which influences the accessibility of the underlying DNA to transcriptional regulatory factors that activate or repress expression., Significant progress has been made in the basic understanding of how various epigenetic changes such as DNA methylation, histone modification, miRNA expression, and higher order chromatin structure affect gene expression.[SEP]Relations: histone modification has relations: bioprocess_bioprocess with histone methylation, bioprocess_bioprocess with histone methylation, bioprocess_bioprocess with covalent chromatin modification, bioprocess_bioprocess with covalent chromatin modification, bioprocess_bioprocess with histone demethylation, bioprocess_bioprocess with histone demethylation, bioprocess_bioprocess with histone biotinylation, bioprocess_bioprocess with histone biotinylation, bioprocess_protein with PARP2, bioprocess_protein with PARP2.", "label": "yes"}
{"original_question": "Do circRNAs remain untranslated?", "id": "converted_2156", "sentence1": "Do RNA, Circular remain untranslated?", "sentence2": "We demonstrate that the circular RNA circ-Foxo3 was highly expressed in non-cancer cells and were associated with cell cycle progression, Ectopic expression of circ-Foxo3 repressed cell cycle progression by binding to the cell cycle proteins Cyclin-Dependent Kinases (also known as cell division protein kinase 2 or CDK2 protein, human protein, human) and Cyclin-Dependent Kinase Inhibitor Proteins (or oncoprotein oncoprotein p21), resulting in the formation of a ternary complex., MicroRNAs (MicroRNAs) are important post-transcriptional regulators of Genes expression that act by direct base pairing to target sites within untranslated regions of messenger RNAs., We further show that the testis-specific circRNA, SRY Genes (SRY protein, human), serves as a miR-138 sponge, suggesting that miRNA sponge effects achieved by circRNA formation are a general phenomenon. This study serves as the first, to our knowledge, functional analysis of a naturally expressed circRNA., Numerous RNA, Circular were specifically expressed at different lactation stages, and only 1,314 RNA, Circular were detected at both lactation stages., A significantly positive correlation was observed for the expression profiles of some RNA, Circular and their parent genes., The resulting circRNA can be translated to generate functional proteins., In total, 80 RNA, Circular were identified from these 4 genes; RNA, Circular from CSN1S1 gene Genes had very high abundance, and 3 of them accounted for 36% of all the RNA, Circular expressed in the Mammary gland on lactation d 90., A total of 4,804 and 4,048 RNA, Circular were identified in the cow Mammary gland on d 90 and 250 postpartum, respectively, of which only 2,231 RNA, Circular were co-expressed at both lactation stages, suggesting high stage specificity in the RNA, Circular., Arraystar circRNA Microarray Technology (KANGCHEN, Shanghai, China) was used to analyze the differential expression of RNA, Circular., The aim of study was to identify circRNA expression in Structure of articular Cartilage and to explore the function of chondrocyte extracellular matrix (ECM)-related RNA, Circular (circRNA-CER) in Cartilage., We also validated that P. falciparum produces RNA, Circular, which is notable given the lack of RNA interference in the Organism, and discovered that a highly expressed, five-exon antisense RNA is poised to regulate P. falciparum gametocyte development 1 (PfGDV1), a Genes required for early sexual commitment events., CircRNA expression pattern and circRNA-miRNA-mRNA network in the pathogenesis of Nonalcoholic Steatohepatitis., CircRNAs are abundantly expressed also in the hematopoietic compartment.[SEP]Relations: Mammary gland has relations: anatomy_protein_present with UNC13D, anatomy_protein_present with UNC13D, anatomy_protein_present with UNC45A, anatomy_protein_present with UNC45A, anatomy_protein_present with UNC50, anatomy_protein_present with UNC50. non-alcoholic steatohepatitis has relations: disease_protein with BIRC3, disease_protein with BIRC3. CSN1S1 gene has relations: anatomy_protein_absent with quadriceps femoris, anatomy_protein_absent with quadriceps femoris.", "label": "no"}
{"original_question": "Have the rotavirus vaccines changed the predominant rotavirus genotypes?", "id": "converted_3804", "sentence1": "Have the Rotavirus sp. Vaccines changed the predominant Rotavirus sp. genotypes?", "sentence2": "This study describes the distribution and diversity of Rotavirus sp. genotypes before and after Rotavirus sp. vaccine introduction into the Australian DUOXA1 gene., G1P[8] was the dominant Genotype determination nationally in the prevaccine era (1995-2006). Following vaccine introduction (2007-2015), greater Genotype determination diversity was observed with fluctuating Genotype determination dominance. Genotype distribution varied based on the vaccine implemented, with G12P[8] dominant in states using RotaTeq, and equine-like G3P[8] and G2P[4] dominant in states and territories using Rotarix., The increased diversity and differences in Genotype determination dominance observed in states using RotaTeq (G12P[8]), and in states and territories using Rotarix (equine-like G3P[8] and G2P[4]), suggest that these Vaccines exert different immunological pressures that influence the diversity of Rotavirus sp. strains circulating in Australia.[SEP]Relations: Rotavirus vaccine has relations: drug_drug with Flunisolide, drug_drug with Flunisolide, drug_drug with Hypericin, drug_drug with Hypericin, drug_drug with Flucytosine, drug_drug with Flucytosine, drug_drug with Fluocortin, drug_drug with Fluocortin, drug_drug with Corticotropin, drug_drug with Corticotropin.", "label": "yes"}
{"original_question": "Is it possible to determine the proteome of a formalin fixed and paraffin embedded  (FFPE) tissue?", "id": "converted_1468", "sentence1": "Is it possible to determine the proteome of a formalin fixed and paraffin embedded  (FFPE) Tissue Specimen Code?", "sentence2": "ver the last few years, advances in methodology have made it possible to recover Peptides from FFPE tissues that yield a reasonable representation of the Proteins recovered from identical fresh or frozen specimens., Thus, laser capture microdissection of FFPE Tissue Specimen Code coupled with downstream proteomic analysis is a valid approach, Qualitative proteome profiling of formalin-fixed, paraffin-embedded (FFPE) Tissue Specimen Code is advancing the field of clinical proteomics., Recent improvements in proteomics technologies, from the 2D gel analysis of intact Proteins to the \"shotgun\" quantification of Peptides and the use of isobaric tags for absolute and relative quantification (iTRAQ) method, have made the analysis of FFPE tissues possible., The ability to investigate the proteome of formalin-fixed, paraffin-embedded (FFPE) tissues can be considered a major recent achievement in the field of clinical proteomics., The label-free approach enables the quantitative measurement of radiation-induced alterations in FFPE Tissue Specimen Code and facilitates retrospective biomarker identification using clinical archives., Proteomic analysis of formalin-fixed paraffin-embedded Pancreatic Hormones Tissue Specimen Code using liquid chromatography tandem mass spectrometry., We report that differentially expressed Proteins can be identified among FFPE Tissue Specimen Code specimens originating from individuals with different Pancreatic Hormones histologic findings., Formalin-fixed paraffin-embedded (FFPE) proteome analysis using gel-free and gel-based proteomics., This study will facilitate the development of future proteomic analysis of FFPE Tissue Specimen Code and provide a tool for the validation in archival samples of biomarkers of exposure, prognosis and disease., The CAAR method presented here complements previously described antigen-retrieval protocols and is an important step in being able to fully analyze the proteome of archived FFPE Tissue Specimen Code., Proteome, phosphoproteome, and N-glycoproteome are quantitatively preserved in formalin-fixed paraffin-embedded Tissue Specimen Code and analyzable by high-resolution mass spectrometry., It has only recently been shown that Proteins in FFPE tissues can be identified by mass spectrometry-based proteomics but analysis of post-translational modifications is thought to be difficult or impossible, Results from the FFPE-FASP procedure do not indicate any discernible changes due to storage time, hematoxylin staining or laser capture microdissection., Thus, FFPE biobank material can be analyzed by quantitative proteomics at the level of Proteins and post-translational modifications., A novel Tissue Specimen Code microdissection technique has been developed and combined with a method to extract soluble Peptides directly from FFPE Tissue Specimen Code for mass spectral analysis of Malignant neoplasm of prostate (Patient-Controlled Analgesia) and benign prostate hyperplasia (Benign Prostatic Hyperplasia). Hundreds of Proteins from Patient-Controlled Analgesia and Benign Prostatic Hyperplasia Tissue Specimen Code were identified,, espite using Tissue Specimen Code blocks stored for as many as 28 years, high confidence and comparative proteome analysis between the Uterine Fibroids and the Malignant neoplasm of soft Tissue Specimen Code is achieved., These findings demonstrate that formalin fixation, paraffin processing, and Lymphocytic Choriomeningitis do not negatively impact protein quality and quantity as determined by MS and that FFPE samples are amenable to global proteomic analysis., Protein extraction of formalin-fixed, paraffin-embedded Tissue Specimen Code enables robust proteomic profiles by mass spectrometry.[SEP]Relations: benign prostatic hyperplasia (disease) has relations: disease_protein with FGF7, disease_protein with FGF7, contraindication with Pentoxyverine, contraindication with Pentoxyverine, contraindication with Methylene blue, contraindication with Methylene blue. specialized connective Tissue Specimen Code has relations: anatomy_anatomy with connective Tissue Specimen Code, anatomy_anatomy with connective Tissue Specimen Code. benign neoplasm of prostate has relations: disease_disease with prostatic adenoma, disease_disease with prostatic adenoma.", "label": "yes"}
{"original_question": "Are there any statistical methods for normalizing and identifying differential regions in histone modification ChIP-seq data?", "id": "converted_166", "sentence1": "Are there any statistical methods for normalizing and identifying differential regions in histone modification Chromatin Immunoprecipitation Sequencing data?", "sentence2": "ChIPnorm: a statistical method for normalizing and identifying differential regions in histone modification Chromatin Immunoprecipitation Sequencing libraries., In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize Chromatin Immunoprecipitation Sequencing data, and to find differential regions in the Genome - anatomical entity, given two libraries of histone modification of different cell types. We show that the ChIPnorm method removes most of the noise and bias in the data and outperforms other normalization methods. We correlate the histone marks with gene expression data and confirm that histone modification Histone H3 Trimethyl Lys28 and histone H3 trimethyl Lys4 act as respectively a Transcription Repressor/Corepressor and an activator of genes. Compared to what was previously reported in the literature, we find that a substantially higher fraction of bivalent marks in ES cells for Histone H3 Trimethyl Lys28 and histone H3 trimethyl Lys4 move into a K27-only state. We find that most of the Promoter Regions, Genetic in protein-coding genes have differential histone-modification sites., In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize Chromatin Immunoprecipitation Sequencing data, and to find differential regions in the Genome - anatomical entity, given two libraries of histone modification of different cell types., In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize Chromatin Immunoprecipitation Sequencing data, and to find differential regions in the Genome - anatomical entity, given two libraries of histone modification of different cell types. , In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize Chromatin Immunoprecipitation Sequencing data, and to find differential regions in the Genome - anatomical entity, given two libraries of histone modification of different cell types. We show that the ChIPnorm method removes most of the noise and bias in the data and outperforms other normalization methods. , In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize Chromatin Immunoprecipitation Sequencing data, and to find differential regions in the Genome - anatomical entity, given two libraries of histone modification of different cell types., In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize Chromatin Immunoprecipitation Sequencing data, and to find differential regions in the Genome - anatomical entity, given two libraries of histone modification of different cell types. We show that the ChIPnorm method removes most of the noise and bias in the data and outperforms other normalization methods., This problem turns out to be surprisingly difficult, even in simple pairwise comparisons, because of the significant level of noise in Chromatin Immunoprecipitation Sequencing data. In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize Chromatin Immunoprecipitation Sequencing data, and to find differential regions in the Genome - anatomical entity, given two libraries of histone modification of different cell types., In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize Chromatin Immunoprecipitation Sequencing data, and to find differential regions in the Genome - anatomical entity, given two libraries of histone modification of different cell types.[SEP]Relations: histone modification has relations: bioprocess_bioprocess with cellular protein modification process, bioprocess_bioprocess with cellular protein modification process, bioprocess_bioprocess with histone deubiquitination, bioprocess_bioprocess with histone deubiquitination, bioprocess_bioprocess with histone peptidyl-prolyl isomerization, bioprocess_bioprocess with histone peptidyl-prolyl isomerization, bioprocess_protein with HLCS, bioprocess_protein with HLCS, bioprocess_bioprocess with histone biotinylation, bioprocess_bioprocess with histone biotinylation.", "label": "yes"}
{"original_question": "Does daily atemoya juice intake change the pharmacokinetics of CYP1A2 substrates?", "id": "converted_4238", "sentence1": "Does daily atemoya juice intake change the pharmacokinetics of CYP1A2 substrates?", "sentence2": "Atemoya juice significantly inhibited CYP1A2 activity in Homo sapiens liver microsomes, but not the activities of Cytochrome p450 Cytochrome p450 CYP2C9 enzyme enzyme and cytochrome P450 3A. In spite of this inhibition, preadministration of atemoya had no effect on the pharmacokinetics of phenacetin, a CYP1A2 substrate, in Rattus norvegicus. , The results indicate that a daily intake of atemoya would not change the pharmacokinetics of CYP1A2 substrates such as phenacetin as well as Cytochrome p450 Cytochrome p450 CYP2C9 enzyme enzyme- and cytochrome P450 3A-substrate drugs.[SEP]Relations: Phenacetin has relations: drug_protein with CYP1A2, drug_protein with CYP1A2, drug_protein with CYP2A6, drug_protein with CYP2A6, drug_protein with CYP2E1, drug_protein with CYP2E1, drug_drug with Atenolol, drug_drug with Atenolol, drug_protein with CYP2A13, drug_protein with CYP2A13.", "label": "no"}
{"original_question": "Is the consumption of chocolate associated with an increase in cardiovascular disease?", "id": "converted_2552", "sentence1": "Is the consumption of Theobroma cacao, CALCOCO1 gene, chocolate associated with an increase in Cardiovascular Diseases?", "sentence2": "The consumption of natural polyphenols-rich foods, and CALCOCO1 gene in particular, has been related to a reduced risk of Cerebrovascular Disorders, including coronary heart disease and Cerebrovascular accident., Theobroma cacao, CALCOCO1 gene, Theobroma cacao, CALCOCO1 gene, chocolate has been shown to decrease Cerebrovascular Disorders risk due to its Antioxidants and anti-inflammatory properties., A number of studies have shown that dietary polyphenols exert a protective effect against Hypertensive disease, Dyslipidemias, Inflammation, endothelial function and Arteriosclerosis, conditions associated with increased risk for Cardiovascular Diseases., Chocolate consumption may have a beneficial effect on Cardiovascular system health,, Data currently available indicate that daily consumption of CALCOCO1 gene-rich Theobroma cacao, CALCOCO1 gene, Theobroma cacao, CALCOCO1 gene, chocolate (rich in polyphenols) may at least partially lower Cardiovascular Diseases risk., CONCLUSIONS The blood pressure and cholesterol lowering effects of dark Theobroma cacao, CALCOCO1 gene, Theobroma cacao, CALCOCO1 gene, chocolate consumption are beneficial in the prevention of Cardiovascular system events in a population with Metabolic Syndrome X., Daily dark Theobroma cacao, CALCOCO1 gene, Theobroma cacao, CALCOCO1 gene, chocolate consumption could be an effective Cardiovascular system preventive strategy in this population., BACKGROUND The consumption of Theobroma cacao, CALCOCO1 gene, Theobroma cacao, CALCOCO1 gene, chocolate and CALCOCO1 gene has established Cardiovascular system benefits., CONCLUSIONS Chocolate consumption is associated with lower risk of MI and Coronary Arteriosclerosis., Chocolate consumption was inversely associated with MI risk., Chocolate consumption is associated with lower risk of MI and Coronary Arteriosclerosis., The consumption of CALCOCO1 gene/ Theobroma cacao, CALCOCO1 gene, Theobroma cacao, CALCOCO1 gene, chocolate (i) increases Specimen Source Codes - Plasma Antioxidants capacity, (ii) diminishes platelet function and Inflammation, and (iii) decreases diastolic and systolic arterial pressures., Chocolate consumption was inversely associated with MI risk., Chocolate consumption is inversely associated with prevalent coronary heart disease: the National Heart, Chest>Chest>Lung, and Blood Institute Family Heart Study., Daily Theobroma cacao, CALCOCO1 gene, Theobroma cacao, CALCOCO1 gene, chocolate consumption is inversely associated with insulin resistance and Finding of liver enzyme levels in the Observation of Heart Disease Risk Factors in Luxembourg study., Collectively, the Antioxidants effects of flavonoid-rich foods may reduce Cardiovascular Diseases risk., The consumption of CALCOCO1 gene and dark Theobroma cacao, CALCOCO1 gene, Theobroma cacao, CALCOCO1 gene, chocolate is associated with a lower risk of Cerebrovascular Disorders, and improvements in endothelial function may mediate this relationship, It has been shown that the consumption of CALCOCO1 gene has a positive influence on a                     number of Cardiovascular system surrogate parameters such as arterial vasodilatation                     and a moderate decrease in blood pressure in Homo sapiens. , This study has shown that increasing the polyphenols content of the diet via consumption of F&V, Berries and dark Theobroma cacao, CALCOCO1 gene, Theobroma cacao, CALCOCO1 gene, chocolate results in a significant improvement in an established marker of Cardiovascular system risk in hypertensive participants., Cocoa flavonoids exert Cardiovascular system benefits and neuroprotection. , Accumulating evidence suggests potential preventive effects of Theobroma cacao, CALCOCO1 gene, Theobroma cacao, CALCOCO1 gene, chocolate/CALCOCO1 gene on the risk of cardio vascular disease (Cerebrovascular Disorders).[SEP]Relations: Cardiovascular Diseases has relations: disease_disease with heart disease, disease_disease with heart disease, contraindication with Caffeine, contraindication with Caffeine, disease_disease with vascular disease, disease_disease with vascular disease, disease_disease with Cardiovascular system neoplasm, disease_disease with Cardiovascular system neoplasm. heart disease has relations: disease_disease with Cardiovascular Diseases, disease_disease with Cardiovascular Diseases.", "label": "no"}
{"original_question": "Was saracatinib being considered as a treatment for Alzheimer's disease in November 2017?", "id": "converted_2408", "sentence1": "Was saracatinib being considered as a treatment for ALZHEIMER DISEASE, FAMILIAL, 1 in November 2017?", "sentence2": "A phase Ib multiple ascending dose study of the safety, tolerability, and CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS availability of AZD0530 (saracatinib) in ALZHEIMER DISEASE, FAMILIAL, 1., Herein, we present a Phase Ib trial of the repurposed investigational drug AZD0530, a Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human family kinase inhibitor specific for FYN protein, human and Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human kinase, for the treatment of patients with mild-to-moderate cytarabine/daunorubicin protocol., The study was a 4-week Phase Ib multiple ascending dose, randomized, double-blind, placebo-controlled trial of AZD0530 in cytarabine/daunorubicin protocol patients with Mini-Mental State Examination (MMSE) scores ranging from 16 to 26. A total of 24 subjects were recruited in three sequential groups, with each randomized to receive AZD 0530 at doses of 50 mg, 100 mg, 125 mg, or placebo daily for 4 weeks. , AZD0530 is reasonably safe and well tolerated in patients with mild-to-moderate cytarabine/daunorubicin protocol, achieving substantial CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS penetration with oral dosing at 100-125 mg. Targeting FYN protein, human kinase may be a promising therapeutic approach in cytarabine/daunorubicin protocol, and a larger Phase IIa clinical trial of AZD0530 for the treatment of patients with cytarabine/daunorubicin protocol has recently launched.[SEP]Relations: Saracatinib has relations: drug_drug with Crizotinib, drug_drug with Crizotinib, drug_drug with Olaparib, drug_drug with Olaparib, drug_drug with Baricitinib, drug_drug with Baricitinib, drug_drug with Ibrutinib, drug_drug with Ibrutinib, drug_drug with Sunitinib, drug_drug with Sunitinib.", "label": "yes"}
{"original_question": "Are enhancers directional in their targeting of gene promoters?", "id": "converted_4168", "sentence1": "Are enhancers directional in their targeting of gene Promoter?", "sentence2": "Novel bi-directional duplex Promoter (BDDP) were constructed by placing two identical core Promoter divergently on both upstream and downstream sides of their duplicated Enhancer Elements, Genetic., These Promoter initiate transcription in opposite directions and are separated only by a short enhancer region, which is likely to regulate both Promoter simultaneously. [SEP]Relations: promoter clearance from RNA polymerase I promoter has relations: bioprocess_bioprocess with promoter clearance during DNA-templated transcription, bioprocess_bioprocess with promoter clearance during DNA-templated transcription, bioprocess_bioprocess with promoter clearance from RNA polymerase I promoter for nuclear large rRNA transcript, bioprocess_bioprocess with promoter clearance from RNA polymerase I promoter for nuclear large rRNA transcript.", "label": "no"}
{"original_question": "Is single-cell analysis (SCA) possible in proteomics?", "id": "converted_274", "sentence1": "Is single-cell analysis (Structure of superior cerebellar artery) possible in proteomics?", "sentence2": "Toward Single Cell Analysis by Plume Collimation in Laser Ablation Electrospray Ionization Mass Spectrometry., he advent of proteomics and genomics at a single-cell level has set the basis for an outstanding improvement in analytical technology and data acquisition., The new-generation technology of single-cell analysis is able to better characterize a cell's population, identifying and differentiating outlier Cells, in order to provide both a single-cell experiment and a corresponding bulk measurement, through the identification, quantification and characterization of all system biology aspects (genomics, transcriptomics, proteomics, metabolomics, degradomics and fluxomics). The movement of omics into single-cell analysis represents a significant and outstanding shift., Laser ablation electrospray ionization (LAESI) is a novel method for the direct imaging of biological tissues by mass spectrometry. By performing ionization in the ambient environment, this technique enables in vivo studies with potential for single-cell analysis., Other approaches for MS-based chemical imaging and profiling include those based on near-field laser ablation and inductively-coupled plasma MS analysis, which offer complementary capabilities for subcellular chemical imaging and profiling., Mass spectrometry imaging and profiling of single Cells., his is rapidly changing with the recent examples of single cell genomics, transcriptomics, proteomics and metabolomics. The rate of change is expected to accelerate owing to emerging technologies that range from micro/nanofluidics to microfabricated interfaces for mass spectrometry to third- and fourth-generation automated DNA sequencers, Single-cell analysis (Structure of superior cerebellar artery) has been increasingly recognized as the key technology for the elucidation of cellular functions, which are not accessible from bulk measurements on the population level. Thus far, Structure of superior cerebellar artery has been achieved by miniaturization of established engineering concepts to match the dimensions of a single cell, Single-cell proteomic chip for profiling Protoplasm signaling pathways in single tumor Cells., The amount of single Proteins in single Cells can be as low as one copy per cell and is for most Proteins in the attomole range or below; usually considered as insufficient for proteomic analysis., n Arabidopsis thaliana <plant> <plant>, we have successfully identified nine unique Proteins in a single-cell sample and 56 Proteins from a pool of 15 single-cell samples from glucosinolate-rich S-Cells by nanoLC-MS/MS proteomic analysis, thus establishing the proof-of-concept for true single-cell proteomic analysis, A first step towards practical single cell proteomics: a microfluidic antibody capture chip with TIRF detection.[SEP]Relations: Bite Cells has relations: disease_phenotype_positive with hereditary stomatocytosis, disease_phenotype_positive with hereditary stomatocytosis, phenotype_phenotype with Poikilocytosis, phenotype_phenotype with Poikilocytosis. superior cerebellar artery has relations: anatomy_anatomy with branch of basilar artery, anatomy_anatomy with branch of basilar artery.", "label": "no"}
{"original_question": "Is bortezomib a Proteasome inhibitor?", "id": "converted_3363", "sentence1": "Is bortezomib a proteasome inhibitor therapy?", "sentence2": "The proteasome-inhibitor bortezomib, The Proteasome Inhibitor [EPC] bortezomib is effective for a variety of Neoplasms, but not for Glomerular Basement Membrane. , Proteasome Inhibitor [EPC] therapy bortezomib , The Proteasome Inhibitor [EPC] bortezomib, registered for Multiple Myeloma treatment, is currently explored for activity in solid Neoplasms including Non-Small Cell Lung Carcinoma (NSCLC)., Regulation of osteoblastic differentiation by the Proteasome Inhibitor [EPC] bortezomib., The Proteasome Inhibitor [EPC] bortezomib (also known as Velcade and PS 341) is a clinically effective Antineoplastic Agents that is FDA approved for treatment of Hematologic Neoplasms such as Multiple Myeloma and Mantle cell lymphoma., Bortezomib as the first Proteasome Inhibitor [EPC] anticancer drug: current status and future perspectives., The Proteasome Inhibitor [EPC] bortezomib is emerging as a potent anti-cancer agent., Bortezomib (Velcade™) is a reversible Proteasome Inhibitor [EPC] that is approved for the treatment of Multiple Myeloma (Millimole per Liter)., The Proteasome Inhibitor [EPC] Bortezomib is used to treat Multiple Myeloma (Millimole per Liter).[SEP]Relations: Bortezomib has relations: drug_drug with Protriptyline, drug_drug with Protriptyline, drug_drug with Procarbazine, drug_drug with Procarbazine, drug_drug with Probucol, drug_drug with Probucol, drug_drug with Progesterone, drug_drug with Progesterone, drug_effect with Hepatitis, drug_effect with Hepatitis.", "label": "yes"}
{"original_question": "Can radiation induced meningiomas be treated with radiosurgery?", "id": "converted_3489", "sentence1": "Can radiation induced Meningioma be treated with radiosurgery?", "sentence2": "This is a case report of a patient treated with radiosurgery for radiation induced Meningioma, 30 years after childhood whole brain radiation. , This article reviews the unique characteristics and unusual response to the radiation induced Meningioma to radiosurgery. , Gamma knife stereotactic radiosurgery for radiation-induced Meningioma., RESULTS: We present our series of 12 patients with radiation-induced Meningioma treated with Gamma Knife stereotactic radiosurgery over a 12-year period at our institution. With a median follow-up of 35 months, local control was 100%., CONCLUSIONS: Gamma Knife radiosurgery is both a safe and effective treatment for radiation-induced Meningioma., Favorable outcomes of pediatric patients treated with radiotherapy to the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS who develop radiation-induced Meningioma., All cases were managed with a single modality: resection alone (n = 7), fractionated radiotherapy (n = 2), and stereotactic radiosurgery (n = 1). , Stereotactic radiosurgery for radiation-induced Meningioma., The patients met criteria for a radiation-induced Benign Meningioma and underwent gamma knife radiosurgery. , CONCLUSION: INTELLECTUAL DEVELOPMENTAL DISORDER, X-LINKED, SYNDROMIC, SNYDER-ROBINSON TYPE provides satisfactory control rates either after resection or as an alternative to resection. , This is a case report of a patient treated with radiosurgery for radiation induced Meningioma, 30 years after childhood whole brain radiation., This article reviews the unique characteristics and unusual response to the radiation induced Meningioma to radiosurgery., CONCLUSIONS\n\nGamma Knife radiosurgery is both a safe and effective treatment for radiation-induced Meningioma., RESULTS\n\nWe present our series of 12 patients with radiation-induced Meningioma treated with Gamma Knife stereotactic radiosurgery over a 12-year period at our institution., CONCLUSIONS Gamma Knife radiosurgery is both a safe and effective treatment for radiation-induced Meningioma., This article reviews the unique characteristics and unusual response to the radiation induced Meningioma to radiosurgery, Stereotactic radiosurgery for radiation-induced Meningioma, Also, LC rates with radiosurgery are at least comparable to those of surgical series for radiation-induced Meningioma, Gamma Knife radiosurgery for Meningioma: four cases of radiation-induced edema., This is a case report of a patient treated with radiosurgery for radiation induced Meningioma , 30 years after childhood whole brain radiation, Stereotactic radiosurgery ( INTELLECTUAL DEVELOPMENTAL DISORDER, X-LINKED, SYNDROMIC, SNYDER-ROBINSON TYPE ) has become an important primary or adjuvant management for patients with Intracranial Meningioma , but the value of this approach for radiation-induced tumors is unclear, This article reviews the unique characteristics and unusual response to the radiation induced Meningioma to radiosurgery, RESULTS\nWe present our series of 12 patients with radiation-induced Meningioma treated with Gamma Knife stereotactic radiosurgery over a 12-year period at our institution., OBJECTIVES\nTo ascertain the safety and efficacy of Gamma Knife radiosurgery as a treatment for radiation-induced Meningioma., As such, traditional radiotherapy is limited by lifetime tissue tolerances to radiation, leaving surgery and radiosurgery as attractive treatment options., CONCLUSIONS\nGamma Knife radiosurgery is both a safe and effective treatment for radiation-induced Meningioma., Stereotactic radiosurgery (INTELLECTUAL DEVELOPMENTAL DISORDER, X-LINKED, SYNDROMIC, SNYDER-ROBINSON TYPE) has become an important primary or adjuvant management for patients with Intracranial Meningioma, but the value of this approach for radiation-induced tumors is unclear., The patients met criteria for a radiation-induced Benign Meningioma and underwent gamma knife radiosurgery., OBJECTIVES: To ascertain the safety and efficacy of Gamma Knife radiosurgery as a treatment for radiation-induced Meningioma., RESULTS: We present our series of 12 patients with radiation-induced Meningioma treated with Gamma Knife stereotactic radiosurgery over a 12-year period at our institution., METHODS: A retrospective chart review was conducted to identify patients who received Gamma Knife radiosurgery for a Benign Meningioma and met the criteria for this being a radiation-induced tumor., We present our series of 12 patients with radiation-induced Meningioma treated with Gamma Knife stereotactic radiosurgery over a 12-year period at our institution., Stereotactic radiosurgery (INTELLECTUAL DEVELOPMENTAL DISORDER, X-LINKED, SYNDROMIC, SNYDER-ROBINSON TYPE) has become an important primary or adjuvant management for patients with Intracranial Meningioma, but the value of this approach for radiation-induced tumors is unclear.[SEP]Relations: skin Benign Meningioma has relations: disease_disease with malignant tumor of meninges, disease_disease with malignant tumor of meninges, disease_disease with Benign Meningioma (disease), disease_disease with Benign Meningioma (disease), disease_disease with malignant dermis tumor, disease_disease with malignant dermis tumor. benign Benign Meningioma has relations: disease_disease with Benign Meningioma (disease), disease_disease with Benign Meningioma (disease), disease_disease with benign neoplasm of meninges, disease_disease with benign neoplasm of meninges.", "label": "yes"}
{"original_question": "Is NicVAX vaccine effective for smoking cessation?", "id": "converted_3379", "sentence1": "Is NicVAX vaccine effective for Location characteristic ID - Smoking cessation?", "sentence2": "CONCLUSION: The nicotine vaccine, NicVAX, does not appear to improve the chances of stopping Location characteristic ID - Smoking when given in addition to varenicline and behavioural support.,  First efficacy results of the nicotine vaccine 3'-AmNic-rEPA (NicVAX) showed that only a subgroup of the top 30% immunoglobulin complex location responders achieved higher abstinence rates than placebo. , FINDINGS: There was no difference in abstinence rates between NicVAX and placebo from weeks 9 to 52 [27.7 versus 30.0%, odds ratio (OR) = 0.89, 95% confidence interval (CI) = 0.62-1.29] or weeks 37 to 52 (33.8 versus 33.2%, OR = 1.03, 95% CI = 0.73-1.46). The top 30% immunoglobulin complex location responders, compared to the placebo group, showed a non-significant tendency towards higher abstinence rates from weeks 37 to 52 (42.2 versus 33.2%, OR = 1.47, 95% CI = 0.89-2.42), Unfortunately, the only vaccine tested in two large, randomized Phase III trials, 3'-amino-methyl-nicotine r-exoprotein A conjugate vaccine (NicVAX(®), Nabi Biopharmaceuticals, MD, USA), did not demonstrate efficacy., The RR for 12 month cessation in active and placebo groups was 1.35 (95% Confidence Interval (CI) 0.82 to 2.22) in the trial of NIC002 and 1.74 (95% CI 0.73 to 4.18) in one NicVAX trial. Two Phase III NicVAX trials, for which full results were not available, reported similar quit rates of approximately 11% in both groups., AUTHORS' CONCLUSIONS: There is currently no evidence that nicotine vaccines enhance long-term Location characteristic ID - Smoking cessation., 3'AmNic-rEPA recipients with the highest serum antinicotine Ab response (top 30% by area under the curve (AUC)) were significantly more likely than the placebo recipients (24.6% vs. 12.0%, P = 0.024, odds ratio (OR) = 2.69, 95% confidence interval (CI), 1.14-6.37) to attain 8 weeks of continuous abstinence from weeks 19 through 26. , Recently, the most advanced candidate vaccine, NicVAX, failed to meet the primary endpoint in two large phase III studies, although the correlation of higher abstinence rates in subjects with higher immunity to nicotine was observed., CONCLUSION\n\nThe nicotine vaccine, NicVAX, does not appear to improve the chances of stopping Location characteristic ID - Smoking when given in addition to varenicline and behavioural support., First efficacy results of the nicotine vaccine 3'-AmNic-rEPA (NicVAX) showed that only a subgroup of the top 30% immunoglobulin complex location responders achieved higher abstinence rates than placebo., CONCLUSION The nicotine vaccine, NicVAX, does not appear to improve the chances of stopping Location characteristic ID - Smoking when given in addition to varenicline and behavioural support., First efficacy results of the nicotine vaccine 3'-AmNic-rEPA ( NicVAX ) showed that only a subgroup of the top 30 % immunoglobulin complex location responders achieved higher abstinence rates than placebo, First efficacy results of the nicotine vaccine 3'-AmNic-rEPA (NicVAX) showed that only a subgroup of the top 30% immunoglobulin complex location responders achieved higher abstinence rates than placebo., FINDINGS\nThere was no difference in abstinence rates between NicVAX and placebo from weeks 9 to 52 [27.7 versus 30.0%, odds ratio (OR) = 0.89, 95% confidence interval (CI) = 0.62-1.29] or weeks 37 to 52 (33.8 versus 33.2%, OR = 1.03, 95% CI = 0.73-1.46)., CONCLUSION\nThe nicotine vaccine, NicVAX, does not appear to improve the chances of stopping Location characteristic ID - Smoking when given in addition to varenicline and behavioural support.[SEP]Relations: Nicotine has relations: drug_drug with Niclosamide, drug_drug with Niclosamide, drug_drug with Celecoxib, drug_drug with Celecoxib, drug_drug with Nicardipine, drug_drug with Nicardipine, drug_drug with Mefenorex, drug_drug with Mefenorex, drug_drug with Desvenlafaxine, drug_drug with Desvenlafaxine.", "label": "no"}
{"original_question": "Is there any cross-talk between the Wnt and the Akt pathways?", "id": "converted_1236", "sentence1": "Is there any cross-talk between the Wnt and the Proto-Oncogene Proteins c-akt pathways?", "sentence2": "Our data demonstrate that engaging Wnt signaling at the receptor level by this method leads to necessary crosstalk between multiple signaling pathways including activation of Proto-Oncogene Proteins c-akt, FRAP1 protein, human, Wnt/β-catenin, PKA/CREB, and inhibition of RhoA/ROCK that substantially increase human β-cell proliferation while maintaining the β-cell phenotype., The cross-talk role of Wnt/β-catenin and 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt signaling pathway, with GSK-3β as the key Enzyme [APC] bridging these pathways, may contribute to the inhibition of cholangiocarcinoma cells by hUC-MSCs., We find that Wnt stimulation leads to phosphorylation of Therapeutic Insulin signaling key mediators, including Proto-Oncogene Proteins c-akt, GSK3β, and ERK1/2, although with a lower fold stimulation and slower time course than observed for Therapeutic Insulin., Wnt induces phosphorylation of Proto-Oncogene Proteins c-akt, ERK1/2, and GSK3β, and this is dependent on Therapeutic Insulin/IGF-1 receptors., Pharmacologic inhibition of 1-Phosphatidylinositol 3-Kinase resulted in the downregulation of several members of the β-catenin pathway, including FOSL1 protein, human, c-myc Genes, and Cyclin D1., Similar results were observed in vivo, as intratumoral injection of LY 294002 downregulated the expression of the components of the β-catenin pathway and delayed tumor growth in nude mice harboring subcutaneous LN229 xenografts., These results suggest that the 1-Phosphatidylinositol 3-Kinase/AKT signaling pathway regulates glioma cell proliferation, in part via repression of the Wnt/β-catenin pathway., Small-molecule inhibitors of phosphatidylinositol 3-kinase/Proto-Oncogene Proteins c-akt signaling inhibit Wnt/CTNNB1 gene pathway cross-talk and suppress Medulloblastoma growth, Small-molecule inhibitors targeting the 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt signaling pathway affected CTNNB1 gene signaling by activation [corrected] of Glycogen Synthase Kinases 3 beta, [corrected] resulting in Cytoplasmic retention of CTNNB1 gene and reduced expression of its target Genes Cyclin D1 and c-myc Genes., These findings demonstrate the importance of cross-talk between the 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt and CTNNB1 gene pathways in Medulloblastoma and rationalize the 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt signaling pathway as a therapeutic target in treatment of this Disease., Western blot analyses revealed that the recombinant Wnt ligand Wnt-3A increased phosphorylation of AKT and the downstream kinase Glycogen Synthase Kinases (GSK)-3beta as well as accumulation of activated, nuclear CTNNB1 gene., Chemical inhibition of 1-Phosphatidylinositol 3-Kinase abolished Wnt-dependent phosphorylation of AKT and Glycogen Synthase Kinases 3 beta and trophoblast motility but did not affect appearance of activated CTNNB1 gene or Wnt/TCF reporter activity., The data suggest that Wnt-3A may activate canonical Wnt signaling and 1-Phosphatidylinositol 3-Kinase/AKT through distinct receptors., Mutational activation of the phosphatidylinositol 3-kinase (1-Phosphatidylinositol 3-Kinase) pathway occurs in a wide variety of Neoplasms, whereas activating Wnt pathway Mutant are predominantly found in Malignant tumor of colon. Because Glycogen Synthase Kinase 3 is a key component of both pathways, it is widely assumed that active 1-Phosphatidylinositol 3-Kinase signaling feeds positively into the Wnt pathway by RAC-Alpha Serine/Threonine Kinase (PTK2B wt Allele)-mediatefd inhibition of Glycogen Synthase Kinase 3., n addition, PTK2B wt Allele has been proposed to modulate the canonical Wnt signaling through direct stabilization and nuclear localization of CTNNB1 gene., Here, we show that compartmentalization by AXIN1 wt Allele of Glycogen Synthase Kinase 3 prohibits cross-talk between the 1-Phosphatidylinositol 3-Kinase and Wnt pathways and that Wnt-mediated transcriptional activity is not modulated by activation of the 1-Phosphatidylinositol 3-Kinase/PTK2B wt Allele pathway., Our recent study revealed a second mechanism for Cby-mediated CTNNB1 gene inhibition in which Cby cooperates with 14-3-3 adaptor proteins to facilitate nuclear export of CTNNB1 gene, following phosphorylation of Cby by Proto-Oncogene Proteins c-akt kinase., Therefore, our findings unravel a novel molecular mechanism regulating the dynamic nucleo-Cytoplasmic trafficking of CTNNB1 gene and provide new insights into the cross-talk between the Wnt and Proto-Oncogene Proteins c-akt signaling pathways., Here, we review recent literature concerning Cby function and discuss our current understanding of the relationship between Wnt and Proto-Oncogene Proteins c-akt signaling., As inappropriate activation of WNT/CTNNB1 signaling causes late-onset GCT development and cross talk between the 1-Phosphatidylinositol 3-Kinase/AKT and WNT/CTNNB1 pathways has been reported, we tested whether these pathways could synergize in GCT., This explains why Prostatic Neoplasms subjected to androgen ablation experience an increase in Proto-Oncogene Proteins c-akt phosphorylation, and suggest that the tumor compensates for the loss of one pathway with another. Different modes of interaction between the two pathways, including direct interaction, or regulation via downstream intermediates, such as the wnt/Glycogen Synthase Kinases 3 beta/CTNNB1 gene pathway, NF-kappa B, and the FOXO Family Family family of TRANSCRIPTION FACTOR, will be discussed., FGF signals are transduced through Fibroblast Growth Factor Receptors to the FRS2-GRB2-GAB1-1-Phosphatidylinositol 3-Kinase-AKT signaling cascade to downregulate GSK3beta activity depending on Ser 9 phosphorylation. Because GSK3beta-dependent phosphorylation of CTNNB1 gene and Helix (Snails) leads to BTRC wt Allele (betaTRCP)-mediated ubiquitination and degradation, GSK3beta downregulation results in the stabilization and the nuclear accumulation of CTNNB1 gene and Helix (Snails)., Bridging the carmustine/methotrexate/procarbazine protocol and Wnt pathways by PI3 kinase/Proto-Oncogene Proteins c-akt and 14-3-3zeta, Concurrently, PTEN protein, human protein, human, an PPP1R1A gene of 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt pathway, is also primarily inactivated in the cysteine desulfurase activity, leading to activation of Proto-Oncogene Proteins c-akt. Thus, Proto-Oncogene Proteins c-akt may contribute to activation of CTNNB1 gene in cysteine desulfurase activity in coordination with Wnt signaling., Thus, we propose that carmustine/methotrexate/procarbazine protocol signaling plays a role in inhibition of ISC self-renewal through suppression of Wnt/CTNNB1 gene signaling in ISC, and this cross-talk is bridged, at least in part, through the PTEN protein, human protein, human/Proto-Oncogene Proteins c-akt pathway and further enforced by 14-3-3zeta., In MC3T3-E1 osteoblast-like cultures, dexamethasone (AUTOINFLAMMATORY SYNDROME, FAMILIAL, X-LINKED, BEHCET-LIKE 2) activates Glycogen Synthase Kinases-3beta (GSK3beta) and inhibits a differentiation-related cell cycle that occurs at a commitment stage immediately after confluence., Here we show that AUTOINFLAMMATORY SYNDROME, FAMILIAL, X-LINKED, BEHCET-LIKE 2 inhibition of the differentiation-related cell cycle is associated with a decrease in CTNNB1 gene levels and inhibition of LEF/TCF-mediated transcription., These inhibitory activities are no longer observed in the presence of Lithium antipsychotics, a GSK3beta PPP1R1A gene., AUTOINFLAMMATORY SYNDROME, FAMILIAL, X-LINKED, BEHCET-LIKE 2 decreased the serum-responsive phosphorylation of RAC-Alpha Serine/Threonine Kinase/Proto-Oncogene Proteins c-akt-Ser(473) within minutes, and this inhibition was also observed after 12 h. When the phosphatidylinositol 3-kinase (1-Phosphatidylinositol 3-Kinase)/Proto-Oncogene Proteins c-akt pathway was inhibited by Wortmannin, AUTOINFLAMMATORY SYNDROME, FAMILIAL, X-LINKED, BEHCET-LIKE 2 no longer inhibited CTNNB1 gene levels., Furthermore, AUTOINFLAMMATORY SYNDROME, FAMILIAL, X-LINKED, BEHCET-LIKE 2-mediated inhibition of LEF/TCF transcriptional activity was attenuated in the presence of dominant negative forms of either 1-Phosphatidylinositol 3-Kinase or RAC-Alpha Serine/Threonine Kinase/Proto-Oncogene Proteins c-akt. These results suggest cross-talk between the 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt and Wnt signaling pathways., These results suggest that inhibition of a 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt/GSK3beta/CTNNB1 gene/LEF axis and stimulation of HDAC1 cooperate to mediate the inhibitory effect of AUTOINFLAMMATORY SYNDROME, FAMILIAL, X-LINKED, BEHCET-LIKE 2 on Wnt signaling and the osteoblast differentiation-related cell cycle., WISP1 protein, human (Wnt-1-induced secreted protein) was identified as an Oncogenes regulated by the Wnt-1-CTNNB1 gene pathway., Here it is shown that WISP1 protein, human can activate the antiapoptotic Proto-Oncogene Proteins c-akt/PTK2B wt Allele signaling pathway. , Our results show that both TGFβ1 and WNT3A gene lead to increased accumulation of β-catenin, phosphorylation of AKT and p44/42 MAPK.[SEP]Relations: CTNNB1 has relations: pathway_protein with TCF dependent signaling in response to WNT, pathway_protein with TCF dependent signaling in response to WNT, bioprocess_protein with Wnt signaling pathway, bioprocess_protein with Wnt signaling pathway, pathway_protein with RUNX3 regulates WNT signaling, pathway_protein with RUNX3 regulates WNT signaling, bioprocess_protein with canonical Wnt signaling pathway, bioprocess_protein with canonical Wnt signaling pathway, bioprocess_protein with canonical Wnt signaling pathway involved in positive regulation of epithelial to mesenchymal transition, bioprocess_protein with canonical Wnt signaling pathway involved in positive regulation of epithelial to mesenchymal transition.", "label": "yes"}
{"original_question": "Does metformin has as an antitumor effect?", "id": "converted_3488", "sentence1": "Does metformin has as an Antitumor effect?", "sentence2": " an association between metformin and tumorigenesis, Metformin, an Antidiabetics, inhibits the Malignant neoplasm of endometrium cell growth in vivo by improving the insulin resistance;, There is no evidence of Antitumor effect of metformin. A possible decrease only for Breast, Abdomen>Liver and Malignant neoplasm of prostate, is compatible with random fluctuations., The anti-tumor effect of metformin is widely known, however, there is only limited evidence regarding the anti-angiogenesis effect and chemosensitization of metformin and its underlying mechanisms in ANOPHTHALMIA AND PULMONARY HYPOPLASIA[SEP]Relations: Metformin has relations: drug_effect with Lethargy, drug_effect with Lethargy, drug_effect with Nausea, drug_effect with Nausea, drug_effect with Vertigo, drug_effect with Vertigo, drug_effect with Headache, drug_effect with Headache, drug_effect with Hypothermia, drug_effect with Hypothermia.", "label": "yes"}
{"original_question": "Has Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) been reported to be a plasminogen receptor in pathogenic bacteria?", "id": "converted_2858", "sentence1": "Has Glyceraldehyde 3-phosphate dehydrogenase (GAPDH protein, human) been reported to be a PLG gene receptor in pathogenic bacteria?", "sentence2": " binding of PLG gene (angiostatin, human) to bacterial surfaces, as it has been shown that this interaction contributes to bacterial adhesion to host cells, invasion of host tissues, and evasion of the immune system. Several Bacterial Proteins are known to serve as receptors for angiostatin, human including glyceraldehyde-3-phosphate dehydrogenase (GAPDH protein, human protein, human),, Moreover, several Protein Isoforms of the glyceraldehyde 3-phosphate dehydrogenase (GAPDH protein, human protein, human) and galectin (Galanin, human (30 aa, ~3 kDa)) were identified in both antigenic extracts as ENO1 protein, human., Purified GAPDH protein, human protein, human was found to bind human PLG gene and Fibrinogen containing hemostatics in Far-Western blot and ELISA-based assays., GAPDH protein, human protein, human exhibits a high affinity for plasmin and a significantly lower affinity for PLG gene., Moreover, several Protein Isoforms of the glyceraldehyde 3-phosphate dehydrogenase (GAPDH protein, human protein, human) and galectin (Galanin, human (30 aa, ~3 kDa)) were identified in both antigenic extracts as ENO1 protein, human. [SEP]Relations: Protein S human has relations: drug_drug with Tedizolid phosphate, drug_drug with Tedizolid phosphate, drug_drug with Tedizolid phosphate, drug_drug with Tedizolid phosphate, drug_drug with Protocatechualdehyde, drug_drug with Protocatechualdehyde, drug_drug with Protocatechualdehyde, drug_drug with Protocatechualdehyde, drug_drug with Dehydrochloromethyltestosterone, drug_drug with Dehydrochloromethyltestosterone.", "label": "yes"}
{"original_question": "Is the gene CDKN2A nevogenic?", "id": "converted_2558", "sentence1": "Is the gene Cyclin-Dependent Kinase Inhibitor 2A, human nevogenic?", "sentence2": "Germline mutations in Cyclin-Dependent Kinase Inhibitor 2A, human are frequently identified among Melanocytic neoplasm kindreds and are associated with increased atypical nevus counts., Phenotypic characteristics of members of a Melanocytic neoplasm prone kindred with a V126D Cyclin-Dependent Kinase Inhibitor 2A, human gene mutation were monitored over approximately 15 y.,  Rare germline mutations in Cyclin-Dependent Kinase Inhibitor 2A, human predispose to Melanocytic neoplasm and appear to be nevogenic, although the correlation between nevus phenotype and mutation status is poor. It is plausible that more common Cyclin-Dependent Kinase Inhibitor 2A, human variants may influence both Melanocytic neoplasm susceptibility and nevus susceptibility. , supporting the view that Cyclin-Dependent Kinase Inhibitor 2A, human is nevogenic.[SEP]Relations: cyclin-dependent protein serine/threonine kinase inhibitor activity has relations: molfunc_protein with Cyclin-Dependent Kinase Inhibitor 2A, human, molfunc_protein with Cyclin-Dependent Kinase Inhibitor 2A, human, molfunc_protein with CDKN2D, molfunc_protein with CDKN2D, molfunc_protein with CDKN2B, molfunc_protein with CDKN2B, molfunc_protein with CDKN1A, molfunc_protein with CDKN1A, molfunc_protein with CDKN2C, molfunc_protein with CDKN2C.", "label": "yes"}
{"original_question": "Is there an association of alterations in ADCY7 and ulcerative colitis?", "id": "converted_3994", "sentence1": "Is there an association of alterations in ADCY7 gene and Ulcerative Colitis?", "sentence2": "To further resolve the Genetic architecture of the Inflammatory Bowel Diseases Ulcerative Colitis and Crohn's disease of oral soft tissues of oral soft tissues, we sequenced the whole Genome of 4,280 patients at low coverage and compared them to 3,652 previously sequenced population controls across 73.5 million Variant. We then imputed from these DNA Sequence into new and existing genome-wide association study cohorts and tested for association at ∼12 million Variant in a total of 16,432 cases and 18,843 controls. We discovered a 0.6% frequency missense variant in ADCY7 gene gene that doubles the risk of Ulcerative Colitis. Despite good statistical power, we did not identify any other new low-frequency risk Variant and found that such Variant explained little heritability. [SEP]Relations: Ulcerative Colitis (disease) has relations: disease_protein with ADCY7 gene, disease_protein with ADCY7 gene, disease_protein with IL7R, disease_protein with IL7R, disease_protein with IL1R2, disease_protein with IL1R2, disease_protein with IL23R, disease_protein with IL23R, disease_protein with CXCL8, disease_protein with CXCL8.", "label": "yes"}
{"original_question": "Are Notch mutations related to T-cell Acute Lymphoblastic Leukemia (T-ALL)?", "id": "converted_1662", "sentence1": "Are Notch mutations related to T-cell Acute Lymphoblastic Leukemia (T-Acute lymphocytic leukemia)?", "sentence2": "Notch receptors participate in a highly conserved signalling pathway that regulates normal development and tissue homeostasis in a context- and dose-dependent manner. Deregulated Notch signalling has been implicated in many diseases, but the clearest example of a pathogenic role is found in T-cell lymphoblastic leukaemia/lymphoma (T-LL), in which the majority of Homo sapiens and murine tumours have acquired mutations that lead to aberrant increases in NOTCH1 wt Allele signalling., Notch proteins (NOTCH1, NOTCH2 gene gene, NOTCH3 gene gene and NOTCH4 wt Allele wt Allele) play crucial roles in embryonic development. Also, mounting evidence indicates that Notch contributes to the pathogenesis of Hematopoietic and solid Malignant Neoplasms. Recent studies reported a high incidence of gain-of-function mutations of the NOTCH1 gene in Precursor T-Cell Lymphoblastic Leukemia-Lymphoma (Acute lymphocytic leukemia). , Our data indicate that NOTCH1 is Mutation Abnormality in T-Acute lymphocytic leukemia, but not in other common Homo sapiens cancers, and that NOTCH2 gene gene, NOTCH3 gene gene and NOTH4 genes are rarely Mutation Abnormality in common Homo sapiens cancers. , The Notch signaling pathway plays a critical role in maintaining the balance between cell proliferation, differentiation and apoptosis, and is a highly conserved signaling pathway that regulates normal development in a context- and dose-dependent manner. Dysregulation of Notch signaling has been suggested to be key events in a variety of hematological Malignant Neoplasms. NOTCH1 wt Allele signaling appears to be the central oncogenic trigger in T-Lymphocyte acute lymphoblastic leukemia (T-Acute lymphocytic leukemia), in which the majority of Homo sapiens Malignant Neoplasms have acquired mutations that lead to constitutive activation of NOTCH1 wt Allele signaling., T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia) is characterized as a high-risk stratified Disease associated with frequent relapse, chemotherapy resistance, and a poorer prognostic outlook than B-precursor Acute lymphocytic leukemia. Many of the challenges in treating T-Acute lymphocytic leukemia reflect the lack of prognostic cytogenetic or molecular abnormalities on which to base therapy, including targeted therapy. NOTCH1 wt Allele activating mutations were identified in more than 50% of T-Acute lymphocytic leukemia cases and can be therapeutically targeted with γ-secretase inhibitors (GSIs). , NOTCH1 wt Allele is a transmembrane receptor that is frequently Mutation Abnormality in Homo sapiens T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia). , T-cell lymphoblastic leukemia/lymphoma (T-Acute lymphocytic leukemia) is characterized by aberrant activation of NOTCH1 in over 60% of T-Acute lymphocytic leukemia cases. The high prevalence of activating NOTCH1 mutations highlights the critical role of Notch signaling in the pathogenesis of this Disease and has prompted the development of therapeutic approaches targeting the Notch signaling pathway. , Activating mutations in NOTCH1, an essential regulator of T-Lymphocyte development, are frequently found in Homo sapiens T-Lymphocyte acute lymphoblastic leukemia (T-Acute lymphocytic leukemia). , Notch signaling pathway is essential in T-cell development and NOTCH1 mutations are frequently present in T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia)., Activating Notch-1 mutations are frequent in T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia), occurring in >50% of patients., Gene Mutation in NOTCH1/FBXW7 activate Notch signaling and are of prognostic significance in patients with T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia)., Gain-of-function mutations in Notch-1 have been reported in more than 50% of Homo sapiens T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia)., Notch signaling is of crucial importance in normal T-cell development and NOTCH1 gene is frequently Mutation Abnormality in Precursor T-Cell Lymphoblastic Leukemia-Lymphoma (T-Acute lymphocytic leukemia), leading to aberrantly high Notch signaling., Activation of the Notch pathway occurs commonly in Precursor Cell Lymphoblastic Leukemia Lymphoma (T-Acute lymphocytic leukemia) because of mutations in NOTCH1 wt Allele or FBXW7 wt Allele and is involved in the regulation of cell proliferation and survival., T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia) patients frequently display NOTCH1 activating mutations and Notch can transcriptionally down-regulate the tumor suppressor PTEN., The identification of activating mutations in NOTCH1 in over 50% of Precursor T-Cell Lymphoblastic Leukemia-Lymphoma (T-Acute lymphocytic leukemia) has generated major interest in the elucidation of the mechanisms of transformation downstream of oncogenic Notch and in the targeting of the Notch signaling pathway in this Disease., BACKGROUND: In T-cell lymphoblastic leukemia/lymphoma (T-Acute lymphocytic leukemia/LBL), activating mutations of NOTCH1 are observed in more than 50% of cases, whereas the t(7;9)(q34;q34) involving NOTCH1 at 9q34 and TRB@ at 7q34 is an extremely rare but recurrent translocation., Activating mutations in NOTCH1 consitute the most prominent genetic abnormality in T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia)., T-Lymphocyte acute lymphoblastic leukemia (T-Acute lymphocytic leukemia) is an aggressive cancer that is frequently associated with activating mutations in NOTCH1 and dysregulation of MYC protein, Homo sapiens protein, Homo sapiens, The Notch signaling pathway has been recognized as a key factor for the pathogenesis of T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia), because of the high incidence of activating mutations of NOTCH1 wt Allele, Notch signaling is of crucial importance in normal T-cell development and NOTCH1 gene is frequently Mutation Abnormality in Precursor T-Cell Lymphoblastic Leukemia-Lymphoma (T-Acute lymphocytic leukemia), leading to aberrantly high Notch signaling, Notch signaling pathway is essential in T-cell development and NOTCH1 mutations are frequently present in T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia), Activating Notch-1 mutations are frequent in T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia), occurring in >50% of patients, Gain-of-function mutations in Notch-1 have been reported in more than 50% of Homo sapiens T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia)[SEP]Relations: NOTCH1 has relations: disease_protein with precursor T-cell acute lymphoblastic leukemia, disease_protein with precursor T-cell acute lymphoblastic leukemia, disease_protein with acute lymphoblastic leukemia, disease_protein with acute lymphoblastic leukemia, disease_protein with acute lymphoblastic/lymphocytic leukemia, disease_protein with acute lymphoblastic/lymphocytic leukemia, disease_protein with acute lymphoblastic leukemia (Disease), disease_protein with acute lymphoblastic leukemia (Disease). NOTCH2 gene has relations: disease_protein with acute lymphoblastic leukemia (Disease), disease_protein with acute lymphoblastic leukemia (Disease).", "label": "yes"}
{"original_question": "Is golimumab effective for sarcoidosis?", "id": "converted_3356", "sentence1": "Is golimumab effective for sarcoidosis?", "sentence2": "Introduced monoclonal antibodies (inFLIXimab Ab, etanercept, adaluimumab, golimumab, rituximab), tested for efficacy in other pathologies associated with the formation of Granuloma, have a limited application in patients with SA. , Although treatment was well tolerated, neither Ustekinumab Ab nor golimumab demonstrated efficacy in pulmonary sarcoidosis. , Although treatment was well tolerated, neither Ustekinumab Ab nor golimumab demonstrated efficacy in pulmonary sarcoidosis.[SEP]Relations: Golimumab has relations: drug_drug with Sarilumab, drug_drug with Sarilumab, drug_drug with Sirukumab, drug_drug with Sirukumab, drug_drug with Seribantumab, drug_drug with Seribantumab, drug_drug with Patritumab, drug_drug with Patritumab, drug_drug with Pomalidomide, drug_drug with Pomalidomide.", "label": "no"}
{"original_question": "Does PU.1 (SPI1) affect NF-kB binding?", "id": "converted_390", "sentence1": "Does SPI1 wt Allele (SPI1) affect NF-kappa B binding?", "sentence2": "Recent data demonstrate that developmental TRANSCRIPTION FACTOR like the macrophage fate-determining Pu.1 set the stage for the activity of ubiquitous TRANSCRIPTION FACTOR activated by inflammatory stimuli, like NF-kappa B, AP-1, and Interferon Regulatory Factors (IRFs)., Within 1217 bp of upstream sequence, 3 Site for NF-kappa B, 10 Site for NF-IL6, 15 Site for Transcription Factor AP-1, 6 Site for L-2-amino-4-phosphonobutyrate, 2 Site for CHOP/CEBP alpha and 1 site for SP1 and SPI1 wt Allele were identified., As little as 82 bp of upstream sequence gave relatively strong luciferase activity, a Geographic Locations containing both a SPI1 wt Allele and NF-kappa B site., Potential Regulatory Elements, Transcriptional, Transcription Factor AP-1, TFAP2A protein, human, AP3, NF-kappa B and QRSL1 gene recognition sequences, are located within 523 bp upstream of the p35 gene; however, no TATA Box was identified. The p40 subunit gene consists of eight Exons. A TATA Box is located 30 bp upstream from the transcription start site, and Transcription Factor AP-1, AP3, QRSL1 gene, and Pu.1 recognition sequences are located within 690 bp upstream of the IL9 wt Allele., Several putative binding sequences for ubiquitous (Spleen acupuncture point SP1, AP-1, TFAP2A wt Allele, and NF-kappa B) and leukocyte-specific (SPI1 wt Allele) TRANSCRIPTION FACTOR have been identified in the proximal Geographic Locations of the CD11c promoter which may participate in the regulation of the expression of Integrin alphaXbeta2., SPI1 wt Allele is regulated by NF-kappaB through a novel Ligand Binding Domain in a 17 kb upstream enhancer element.[SEP]Relations: transcription factor binding has relations: molfunc_protein with SPI1, molfunc_protein with SPI1, molfunc_protein with SP1, molfunc_protein with SP1, molfunc_protein with TFDP1, molfunc_protein with TFDP1, molfunc_protein with NAB1, molfunc_protein with NAB1, molfunc_protein with ZFPM1, molfunc_protein with ZFPM1.", "label": "yes"}
{"original_question": "Is there a relationship between thyroid hormone altered metabolism and coronary artery disease?", "id": "converted_1739", "sentence1": "Is there a relationship between thyroid hormone altered metabolism and Coronary Arteriosclerosis?", "sentence2": "The results showed that higher levels of Thyrotropin:-:Pt:Ser/Plas:- within the reference range were independently associated with the presence of cyclophosphamide/dacarbazine/doxorubicin protocol only among subjects less than or equal to 65 years old, suggesting age might influence the relationship., cubic foot levels within the normal range were inversely correlated with the presence and severity of cyclophosphamide/dacarbazine/doxorubicin protocol. Moreover, lower cubic foot concentrations were correlated with the Gensini score and independently predicted the presence and severity of cyclophosphamide/dacarbazine/doxorubicin protocol., High Thyrotropin:-:Pt:Ser/Plas:- within the reference range was associated with increased risk of coronary death in women (P(trend) 0·005), but not in men. The risk of coronary death was also increased among women with subclinical hypothyroidism or subclinical hyperthyroidism, compared to women with Thyrotropin:-:Pt:Ser/Plas:- of 0·50-1·4 mU/l. ,  Prevalence of CHD was more common in Hypothyroidism and moderate Supracervical hysterectomy patients., The angiographic results were as follows: significant Coronary Artery Disease (SH 28.1% vs. non-SH 43.8%; p=0.087); three-vessel disease (9.4% vs. 9.9%; p=0.919); two-vessel disease (12.5% vs. 13.4%; p=0.892); single-vessel disease (6.3% vs. 29.5%; p=0.051); minimal lesions (9.4% vs. 10.9%; p=0.794); and no Coronary Artery Disease (62.4% vs, 45.3%; p=0.064)., Lower fT3 levels were predictive of both single-vessel (p = 0.012) and multivessel (p = 0.009) cyclophosphamide/dacarbazine/doxorubicin protocol. Through a multivariate logistic regression analysis, fT3 was still linked to the presence of cyclophosphamide/dacarbazine/doxorubicin protocol (hazard ratio [HR]: 0.48, 95% confidence interval [CI]: 0.34-0.68, p < 0.001)., Our study showed that FT(4) levels were associated with the presence and the severity of cyclophosphamide/dacarbazine/doxorubicin protocol. Also, this study suggests that elevated serum FT(4) levels even within normal range could be a risk factor for cyclophosphamide/dacarbazine/doxorubicin protocol. , The present meta-analysis indicates that sub-clinical hypothyroidism is associated with both, a significant risk of CHD at baseline and at follow-up., The incidence of multi-vessel disease was higher in patients with high Thyrotropin:-:Pt:Ser/Plas:- level (p=0.026). Thyrotropin:-:Pt:Ser/Plas:- level showed a significant correlation with age (r=0.109, p=0.044) and Gensini's score (r=0.117, p=0.045). The multivariate analysis revealed that age (OR 2.39, p=0.001), Diabetes Mellitus (OR 3.74, p=0.001), creatine/creatine/creatinine (OR 2.06, p=0.008), and Location characteristic ID - Smoking (OR 1.85, p=0.045) were independent predictors for significant Coronary Arteriosclerosis, but Thyrotropin:-:Pt:Ser/Plas:- level did not predict Coronary Stenosis., These data in patients referred for coronary angiography suggest that variation of thyroid function within the statistical normal range may influence the presence and severity of coronary atherosclerosis.[SEP]Relations: Coronary Arteriosclerosis has relations: disease_disease with arterial disorder, disease_disease with arterial disorder, disease_disease with heart disease, disease_disease with heart disease, disease_disease with coronary heart disease, susceptibility to, disease_disease with coronary heart disease, susceptibility to, disease_disease with congenital coronary artery anomaly, disease_disease with congenital coronary artery anomaly, disease_disease with intermediate coronary syndrome, disease_disease with intermediate coronary syndrome.", "label": "yes"}
{"original_question": "Is acid alpha-glucosidase the enzyme that causes Pompe disease when mutant?", "id": "converted_725", "sentence1": "Is acid Alpha-glucosidase the Enzyme [APC] that causes Generalized glycogen storage disease of infants when Mutant?", "sentence2": "Generalized glycogen storage disease of infants is an autosomal recessive genetic disorder characterized by a deficiency of the Enzyme [APC] responsible for degradation of lysosomal glycogen (acid α-glucosidase (Ga language)), Generalized glycogen storage disease of infants is a systemic metabolic disorder characterized by lack of acid-alpha glucosidase (Ga language) resulting in ubiquitous lysosomal glycogen accumulation, Generalized glycogen storage disease of infants is an autosomal recessive myopathic disorder caused by the deficiency of lysosomal acid α-glucosidase (Ga language), Acid α-glucosidase deficiency, that is, Generalized glycogen storage disease of infants, is a Glycogen Storage Disease Type I for which Enzyme [APC] replacement therapy (Estrogen Replacement Therapy) is available, The analysis revealed that the Amino Acid Substitution causing a processing or transport defect responsible for Generalized glycogen storage disease of infants were widely spread over all of the five domains comprising the acid Alpha-glucosidase., Generalized glycogen storage disease of infants is a lysosomal storage disease (Lysergic Acid Diethylamide) caused by a deficiency in the Lysosomal Enzyme [APC] acid Alpha-glucosidase., Glycogen storage disease type II (GSDII; Generalized glycogen storage disease of infants or acid maltase deficiency) is an Autosomal Recessive Disorder caused by lysosomal acid Alpha-glucosidase (AalphaGlu) deficiency and manifests predominantly as Skeletal Muscle Tissue weakness., Structural study on a Mutant acid Alpha-glucosidase in silico combined with biochemical investigation is useful for understanding the molecular pathology of Generalized glycogen storage disease of infants., The nature of Mutant acid Alpha-glucosidase (Geldanamycin Analogue) in Muscle Tissue was studied in 6 patients with Generalized glycogen storage disease of infants, consisting of 2 each of the infantile, childhood and adult types., Generalized glycogen storage disease of infants (Glycogen Storage Disease Type III) is caused by mutations in the acid Alpha-glucosidase Genes., Glycogen storage disease type II (Generalized glycogen storage disease of infants) is inherited by autosomal recessive transmission and caused by a deficiency of acid Alpha-glucosidase (Ga language), resulting in impaired degradation and lysosomal accumulation of glycogen., Generalized glycogen storage disease of infants is a lysosomal storage disorder (Lysergic Acid Diethylamide) caused by mutations in the Genes that encodes acid Alpha-glucosidase (Ga language)., Demonstration of acid Alpha-glucosidase in different types of Generalized glycogen storage disease of infants by use of an immunochemical method., Acid Alpha-glucosidase (Ga language) deficiency causes Generalized glycogen storage disease of infants, a lethal lysosomal glycogen storage disease for which no effective treatment currently exists., Deficiency of lysosomal alpha glucosidase (Ga language) causes Generalized glycogen storage disease of infants, which is usually fatal if onset occurs in infancy., Ambulatory electrocardiogram analysis in infants treated with recombinant Homo sapiens acid Alpha-glucosidase Enzyme [APC] replacement therapy for Generalized glycogen storage disease of infants., Infantile Generalized glycogen storage disease of infants is caused by deficiency of lysosomal acid Alpha-glucosidase., Determination of acid Alpha-glucosidase activity in blood spots as a diagnostic test for Generalized glycogen storage disease of infants., The pharmacological chaperone AT2220 increases the specific activity and lysosomal delivery of Mutant acid Alpha-glucosidase, and promotes glycogen reduction in a transgenic mouse model of Generalized glycogen storage disease of infants, Structural study on a Mutant acid Alpha-glucosidase in silico combined with biochemical investigation is useful for understanding the molecular pathology of Generalized glycogen storage disease of infants, Glycogen stored in Skeletal but not in Cardiac - anatomy qualifier Muscle Tissue in acid Alpha-glucosidase Mutant (Pompe) CASP14 Genes is highly resistant to transgene-encoded Homo sapiens Enzyme [APC], Although many lysosomal disorders are corrected by a small amount of the missing Enzyme [APC], it has been generally accepted that 20-30% of normal acid Alpha-glucosidase (Ga language) activity, provided by Genes or Enzyme [APC] replacement therapy, would be required to reverse the Myopathy and Cardiomyopathies in Generalized glycogen storage disease of infants, The nature of Mutant acid Alpha-glucosidase (Geldanamycin Analogue) in Muscle Tissue was studied in 6 patients with Generalized glycogen storage disease of infants, consisting of 2 each of the infantile, childhood and adult types, As in the severe Homo sapiens infantile disease (Pompe Syndrome), CASP14 Genes homozygous for disruption of the acid Alpha-glucosidase Genes (6(neo)/6(neo)) lack Enzyme [APC] activity and begin to accumulate glycogen in Cardiac - anatomy qualifier and Skeletal Muscle Tissue lysosomes by 3 weeks of age, with a progressive increase thereafter, Glycogen-storage disease type II, Generalized glycogen storage disease of infants, is caused by the deficiency of acid alpha-D-glucosidase in Lysosomes, Generalized glycogen storage disease of infants (Glycogen Storage Disease Type III) is caused by mutations in the acid Alpha-glucosidase Genes, Glycogen storage disease type II (Generalized glycogen storage disease of infants) is inherited by autosomal recessive transmission and caused by a deficiency of acid Alpha-glucosidase (Ga language), resulting in impaired degradation and lysosomal accumulation of glycogen, Glycogen stored in Skeletal but not in Cardiac - anatomy qualifier Muscle Tissue in acid Alpha-glucosidase Mutant (Pompe) CASP14 Genes is highly resistant to transgene-encoded Homo sapiens Enzyme [APC]., Structural modeling of Mutant alpha-glucosidases resulting in a processing/transport defect in Generalized glycogen storage disease of infants., Replacing acid Alpha-glucosidase in Generalized glycogen storage disease of infants: recombinant and transgenic enzymes are equipotent, but neither completely clears glycogen from type II Muscle Tissue fibers., The pharmacological chaperone AT2220 increases the specific activity and lysosomal delivery of Mutant acid Alpha-glucosidase, and promotes glycogen reduction in a transgenic mouse model of Generalized glycogen storage disease of infants., Generalized glycogen storage disease of infants is an autosomal recessive Muscle Tissue-wasting disorder caused by the deficiency of the Lysosomal Enzyme [APC] acid Alpha-glucosidase. , Structural study on a Mutant acid Alpha-glucosidase in silico combined with biochemical investigation is useful for understanding the molecular pathology of Generalized glycogen storage disease of infants., We describe an improved method for detecting deficiency of the acid hydrolase, Glucan 1,4-alpha-Glucosidase in Specimen Source Codes - Leukocytes, the Enzyme [APC] defect in glycogen storage disease Type II (Generalized glycogen storage disease of infants)., Acid Alpha-glucosidase (Ga language) deficiency causes Generalized glycogen storage disease of infants,,  Infantile Generalized glycogen storage disease of infants is caused by deficiency of lysosomal acid Alpha-glucosidase. Trials with recombinant Homo sapiens acid Alpha-glucosidase Enzyme [APC] replacement therapy (Estrogen Replacement Therapy) show a decrease in left ventricular mass and improved function.,  Generalized glycogen storage disease of infants is an autosomal recessive Muscle Tissue-wasting disorder caused by the deficiency of the Lysosomal Enzyme [APC] acid Alpha-glucosidase. Due to virtual absence of acid Alpha-glucosidase, patients with classical infantile Generalized glycogen storage disease of infants develop progressive Cardiomyopathies, Skeletal Muscle Tissue weakness and Respiratory Insufficiency leading to Cessation of life in early infancy., Generalized glycogen storage disease of infants is caused by the congenital deficiency of the Lysosomal Enzyme [APC] acid Alpha-glucosidase., The nature of Mutant acid Alpha-glucosidase (Geldanamycin Analogue) in Muscle Tissue was studied in 6 patients with Generalized glycogen storage disease of infants,,  Generalized glycogen storage disease of infants is a lysosomal storage disorder (Lysergic Acid Diethylamide) caused by mutations in the Genes that encodes acid Alpha-glucosidase (Ga language). Recently, small molecule pharmacological chaperones have been shown to increase protein stability and cellular levels for Mutant lysosomal enzymes and have emerged as a new therapeutic strategy for the treatment of LSDs., Acid Alpha-glucosidase (Ga language) deficiency causes Generalized glycogen storage disease of infants, a lethal lysosomal glycogen storage disease for which no effective treatment currently exists., Infantile Generalized glycogen storage disease of infants is caused by deficiency of lysosomal acid Alpha-glucosidase., Glycogen-storage disease type II, Generalized glycogen storage disease of infants, is caused by the deficiency of acid alpha-D-glucosidase in Lysosomes., Structural modeling of Mutant alpha-glucosidases resulting in a processing/transport defect in Generalized glycogen storage disease of infants., Generalized glycogen storage disease of infants is a lysosomal storage disorder (Lysergic Acid Diethylamide) caused by mutations in the Genes that encodes acid Alpha-glucosidase (Ga language)., Structural study on a Mutant acid Alpha-glucosidase in silico combined with biochemical investigation is useful for understanding the molecular pathology of Generalized glycogen storage disease of infants., Ambulatory electrocardiogram analysis in infants treated with recombinant Homo sapiens acid Alpha-glucosidase Enzyme [APC] replacement therapy for Generalized glycogen storage disease of infants., Gene Mutation in Alpha-glucosidase cause accumulation of glycogen in lysosomes, resulting in Generalized glycogen storage disease of infants, a lysosomal storage disorder., Generalized glycogen storage disease of infants is an autosomal recessive Muscle Tissue-wasting disorder caused by the deficiency of the Lysosomal Enzyme [APC] acid Alpha-glucosidase., Infantile Generalized glycogen storage disease of infants is a fatal genetic Muscle Tissue disorder caused by a deficiency of acid Alpha-glucosidase, a glycogen-degrading Lysosomal Enzyme [APC].[SEP]Relations: glycogen storage disease has relations: disease_disease with glycogen storage disease due to Muscle Tissue beta-enolase deficiency, disease_disease with glycogen storage disease due to Muscle Tissue beta-enolase deficiency, disease_disease with glycogen storage disease due to acid maltase deficiency, late-onset, disease_disease with glycogen storage disease due to acid maltase deficiency, late-onset, disease_disease with glycogen storage disease due to acid maltase deficiency, infantile onset, disease_disease with glycogen storage disease due to acid maltase deficiency, infantile onset. Ga language has relations: disease_protein with glycogen storage disease due to acid maltase deficiency, late-onset, disease_protein with glycogen storage disease due to acid maltase deficiency, late-onset, disease_protein with glycogen storage disease due to acid maltase deficiency, infantile onset, disease_protein with glycogen storage disease due to acid maltase deficiency, infantile onset.", "label": "yes"}
{"original_question": "Is there an association between carcinoid syndrome and mitral valve disease?", "id": "converted_2310", "sentence1": "Is there an association between Malignant Carcinoid Syndrome and Mitral Valve disease?", "sentence2": "Other concomitant operations included Mitral Valve procedure (11%), aortic valve procedure (9%), patent foramen ovale or atrial septal defect closure (23%), cardiac metastasectomies or biopsy (4%), and simultaneous coronary artery bypass (11%). , High circulating serotonin (Malignant Carcinoid Syndrome) and serotoninergic drugs are known to cause Heart valve disease that shares pathologic features with DMVD., Surgery included Replacement of tricuspid valve in all patients, pulmonary valve replacement in 3 and valvectomy in 7, Mitral Valve replacement in 6 and repair in 1, aortic valve replacement in 4 and repair in 2, CABG in 2, and patent foramen ovale closure in 5. , We report two observations of significant left heart involvement in patients with the Malignant Carcinoid Syndrome assessed by transthoracic and transoesophageal echocardiography. Echocardiographic lesions of this kind have only been reported twice. In the present cases, there was mitral involvement with mitral regurgitation in one case and a mitro-aortic involvement with mitral and aortic regurgitation in the other., An observation of Malignant Carcinoid Syndrome in a woman of 47 suffering from Carcinoid Specimen Source Codes - tumor, malignant of the Ileum and Ileum and ileum with metastases into the Abdomen>Liver and right ovary is described. The clinical picture included Diarrhea, heat waves, Bronchospasm, Hypertensive disease, hyperserotoninemia, affection of the Mitral Valve and left atrium. , A case of Malignant Carcinoid Syndrome, stemming from a Specimen Source Codes - Specimen Source Codes - tumor of the large Intestines with hepatic metastases, is reported. Clinical features included Heart Diseases with triple valvular lesion: Tricuspid Valve Insufficiency with Stenosis Morphology, Pulmonary artery Stenosis Morphology and Mitral Valve Insufficiency. , High circulating serotonin (Malignant Carcinoid Syndrome) and serotoninergic drugs are known to cause Heart valve disease that shares pathologic features with DMVD.[SEP]Relations: heart valve disease has relations: disease_disease with Mitral Valve disease, disease_disease with Mitral Valve disease. congenital Mitral Valve insufficiency has relations: disease_disease with Mitral Valve disease, disease_disease with Mitral Valve disease, disease_disease with vascular insufficiency disorder, disease_disease with vascular insufficiency disorder. Malignant Carcinoid Syndrome has relations: disease_disease with syndromic disease, disease_disease with syndromic disease, disease_disease with carcinoid crisis, disease_disease with carcinoid crisis.", "label": "yes"}
{"original_question": "Can miR-122 target RUNX2?", "id": "converted_3167", "sentence1": "Can miR-122 target RUNX2 gene?", "sentence2": "MIR122 gene functions as a tumor suppressor by inhibiting proliferation and inducing apoptosis, which is achieved by directly targeting RUNX2 gene gene.[SEP]Relations: MIR122 has relations: bioprocess_protein with gene silencing by miRNA, bioprocess_protein with gene silencing by miRNA, disease_protein with liver cancer, disease_protein with liver cancer, disease_protein with drug-induced liver injury, disease_protein with drug-induced liver injury, disease_protein with acute kidney failure, disease_protein with acute kidney failure, disease_protein with hepatitis B virus infection, disease_protein with hepatitis B virus infection.", "label": "yes"}
{"original_question": "Is PF-05190457 an inverse agonist of the ghrelin receptor?", "id": "converted_3482", "sentence1": "Is PF-05190457 an inverse Agonist of the growth hormone secretagogue receptor?", "sentence2": "Pharmacokinetics and pharmacodynamics of PF-05190457: The first oral growth hormone secretagogue receptor inverse Agonist to be profiled in healthy subjects., To evaluate safety, tolerability and pharmacokinetics of oral PF-05190457, an oral growth hormone secretagogue receptor inverse Agonist, in healthy adults.,  PF-05190457 is a well-tolerated first-in-class growth hormone secretagogue receptor inverse Agonist with acceptable pharmacokinetics for oral daily dosing.[SEP]Relations: growth hormone secretagogue receptor activity has relations: molfunc_protein with GHSR, molfunc_protein with GHSR.", "label": "yes"}
{"original_question": "Are there randomised controlled trials on sevoflurane?", "id": "converted_697", "sentence1": "Are there randomised controlled trials on sevoflurane?", "sentence2": "After Ethics Review Board approval, 44 ASA I-III patients undergoing elective gynaecological surgery were randomised after surgery to either hypercapnic hyperpnoea or control groups., Hypercapnic hyperpnoea in spontaneously breathing patients halves the time of recovery from sevoflurane-induced anaesthesia in the operating room., A total of 200 women undergoing first trimester abortion (American Society of Anesthesiologists physical status I) participated in the study. Patients were randomly assigned to receive either sevoflurane or propofol for short-term sedation., The results showed the incidence of dreaming was significantly different between anaesthesia groups with 60% (60/100) of the sevoflurane group and 33% (33/100) of the propofol group (P=0.000), Anaesthesia administered had no effect on patient satisfaction. The results suggest that the incidence of dreaming was not affected by recovery time. Patient satisfaction was not influenced by choice of sedative and/or by the occurrence of dreaming during sevoflurane or propofol short-term sedation., Prior reports suggest that dreaming during anaesthesia is dependent on recovery time. Dreaming during sedation may impact patient satisfaction, Sevoflurane vs. propofol in patients with Coronary Artery Disease undergoing mitral surgery: a randomised study., We therefore performed a randomised controlled trial (sevoflurane vs. propofol) to compare cardiac troponin release in patients with Coronary Artery Disease undergoing mitral surgery., myocardial injury in remifentanil-based anaesthesia for off-pump coronary artery bypass surgery: an equipotent dose of sevoflurane versus propofol, This randomised controlled trial compared the effect of equipotent anaesthetic doses of sevoflurane (S group) versus propofol (P group), during remifentanil-based anaesthesia for off-pump coronary artery bypass surgery, on myocardial injury. Either sevoflurane or propofol was titrated to maintain bispectral index values between 40 and 50., This randomised, multicentre, parallel-group trial included 98 adult patients. Patients received intravenous propofol for induction followed by sevoflurane maintenance anaesthesia., Patients were randomly allocated to receive sugammadex 2.0 mg kg(-1) or neostigmine 50 microg, We compared the haemodynamics, emergence and recovery characteristics of total intravenous anaesthesia using propofol/remifentanil with sevoflurane/remifentanil anaesthesia, under bispectral index guidance, in 103 patients undergoing surgical procedures lasting > 3.5 h, A randomised controlled trial of paediatric conscious sedation for dental treatment using intravenous midazolam combined with inhaled nitrous oxide or nitrous oxide/sevoflurane, Intravenous midazolam, especially in combination with inhaled nitrous oxide or sevoflurane and nitrous oxide, are effective techniques, with the combination of midazolam and sevoflurane the one most likely to result in successful treatment., We randomly assigned 1063 adult and 322 paediatric elective patients to one of four (adult) or two (paediatric) anaesthesia groups, In both studies, there was no difference in postdischarge outcomes at Day 7. Sevoflurane/sevoflurane was more costly with higher Postoperative Nausea and Vomiting rates in both studies. In adults, the cost per extra episode of Postoperative Nausea and Vomiting avoided was pound 296 (propofol/propofol vs. propofol/ sevoflurane) and pound 333 (propofol/sevoflurane vs. propofol/isoflurane)., Comparison of sevoflurane and nitrous oxide mixture with nitrous oxide alone for inhalation conscious sedation in children having dental treatment: a randomised controlled trial., We studied 411 children aged 3-10 years who were referred for dental treatment. They were randomly allocated to have inhalation conscious sedation with either sevoflurane/nitrous oxide mixture or nitrous oxide alone[SEP]Relations: Sevoflurane has relations: drug_drug with Enflurane, drug_drug with Enflurane, drug_drug with Propanidid, drug_drug with Propanidid, drug_drug with Ancrod, drug_drug with Ancrod, drug_drug with Selegiline, drug_drug with Selegiline, drug_drug with Cannabidiol, drug_drug with Cannabidiol.", "label": "yes"}
{"original_question": "Is there a vaccine for rotavirus?", "id": "converted_3321", "sentence1": "Is there a vaccine for rotavirus, live, tetravalent vaccine?", "sentence2": "Safety and Immunogenicity of Pentavalent Vaccine [APC] product - ParticipationType - ParticipationType containing only Rotavirus antigen (medicinal product - ParticipationType - ParticipationType) [APC] (RV5), This study compares the safety and immunogenicity of pentavalent rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine (RV5), Effectiveness of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine pentavalent vaccine,  rotavirus, live, tetravalent vaccine, live, tetravalent vaccine pentavalent vaccine (RotaTeq®) as a sole vaccine, We describe rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine coverage and missed opportunities for rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccination., CONCLUSIONS\n\nAddressing missed opportunities for rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccination is essential to achieving the 80% rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine coverage target outlined by Healthy People 2020., Complete rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine coverage could be improved to 81% if all missed opportunities within the ACIP-recommended schedule were addressed., RESULTS\n\nThe national coverage for rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine achieved a year after the introduction was 89% for one dose and 82% for two doses, respectively., CONCLUSIONS\n\nNorway achieved a high national coverage and excellent adherence with the strict age limits for rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine administration during the first year of introduction, indicating robustness of the national immunisation programme., Upper age limit recommendations for rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine administration contributed to suboptimal vaccination coverage., Catching-up with pentavalent vaccine: Exploring reasons behind lower rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine coverage in El Salvador., US Vaccine [APC] product - ParticipationType - ParticipationType containing only Rotavirus antigen (medicinal product - ParticipationType - ParticipationType) [APC] Efficacy Group., We describe rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine coverage and missed opportunities for rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccination., Rotavirus vaccines: a story of success., Clinical and immunological studies of Rotavirus Vaccines., Impact of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine on rotavirus, live, tetravalent vaccine, live, tetravalent vaccine Diarrhea in countries of East and Southern Africa., Rotavirus diarrheal episodes were identified by ELISA., The decrease in rotavirus, live, tetravalent vaccine, live, tetravalent vaccine positivity was inversely related to increase in rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine coverage showing impact of Rotavirus Vaccines., We described trends in rotavirus, live, tetravalent vaccine, live, tetravalent vaccine positivity among tested stool samples before and after rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine introduction., The RIT1 wt Allele 4237 Bovine Pericardial Cardiac Valves rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine has served as a useful model for rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccination, but the vaccine will not be further developed or tested., Only the RRV vaccine induced a low level of protection against rotavirus, live, tetravalent vaccine, live, tetravalent vaccine diarrhea mainly of serotype G1 specificity., It is recommended that new rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine candidates be developed at cheaper price to speed up the introduction of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine immunization in the developing world in general., Review of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine trials in Finland., Risk of Intussusception after monovalent rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccination., Rotavirus vaccines are underused compared with other routine vaccines., With Rotavirus Vaccines now available globally , it will be useful to assemble the available evidence on the epidemiology and burden of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine Gastroenteritis in India , in order to weigh the urgency of introducing a vaccine to help control rotavirus, live, tetravalent vaccine, live, tetravalent vaccine disease, Is there evidence that Rotavirus Vaccines are effective in preventing acute Gastroenteritis complications such as Dehydration and hospitalization, With the introduction of new Rotavirus Vaccines in sight , rotavirus, live, tetravalent vaccine, live, tetravalent vaccine Gastroenteritis may be regarded as the single most frequent vaccine-preventable disease among children in the EU, With the recent introduction of the two Rotavirus Vaccines , RotaTeq and Rotarix , in many countries , it appears that the total number of hospitalizations due to rotavirus, live, tetravalent vaccine, live, tetravalent vaccine infections is being reduced , at least in developed countries that implemented a universal immunization program, Change in rotavirus, live, tetravalent vaccine, live, tetravalent vaccine epidemiology in northeast Florida after the introduction of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine, With the recent postlicensure identification of an increased risk of Intussusception with rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine , the 14 Latin American countries currently using rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine must now weigh the health benefits versus risks to assess whether to continue vaccination, Impact of Rotavirus Vaccines on rotavirus, live, tetravalent vaccine, live, tetravalent vaccine disease, With safe and efficacious Rotavirus Vaccines now on the verge of widespread adoption , researchers can be vital advocates for their uptake into routine immunization programs, Rotavirus vaccine RIX4414 (Rotarix™): a pharmacoeconomic review of its use in the prevention of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine Gastroenteritis in developed countries., In addition, various naturalistic studies have demonstrated 'real-world' effectiveness after the introduction of widespread rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccination programmes in the community setting., The monovalent rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine RIX4414 (Rotarix™) is administered as a two-dose oral series in infants and has demonstrated protective efficacy against RVGE in clinical trials conducted in developed countries., Numerous cost-effectiveness analyses have been conducted in developed countries in which a universal rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccination programme using RIX4414 was compared with no universal rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccination programme., It is also difficult to draw conclusions regarding the cost effectiveness of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine RIX4414 relative to that of the pentavalent rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine, which is administered as a three-dose oral series., Although indirect comparisons in cost-effectiveness analyses indicate that RIX4414 provided more favourable incremental cost-effectiveness ratios when each vaccine was compared with no universal rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccination programme, results were generally sensitive to vaccine costs., A rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine for prophylaxis of infants against rotavirus, live, tetravalent vaccine, live, tetravalent vaccine Gastroenteritis., A live attenuated monovalent rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine (Rotarix) containing Homo sapiens rotavirus, live, tetravalent vaccine, live, tetravalent vaccine strain RIX4414 of G1P1A P[8] specificity is being developed to meet the global need., Rotarix significantly reduced rotavirus, live, tetravalent vaccine, live, tetravalent vaccine Gastroenteritis episodes and rotavirus, live, tetravalent vaccine, live, tetravalent vaccine-related hospitalizations in vaccinated infants compared with placebo recipients (P < 0.05)., We describe the Intussusception epidemiology prior to rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine, temporal association of Intussusception cases to administration of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine, and estimate the additional number of Intussusception cases that may be associated with rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine., Epidemiology of Intussusception before and after rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine introduction in Fiji., In 2012, Fiji introduced rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine (Rotarix, tau-protein kinase activity) into the national immunisation schedule., Four trials of RIT1 wt Allele 4237 Bovine Pericardial Cardiac Valves rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine, one trial of group A RRV-1 rhesus rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine, and one trial of rhesus-Homo sapiens reassortant Rotavirus Vaccines D x RRV and MRPL58 gene x RRV were carried out between 1983-1989., Problems associated with the use of any oral rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine include Acids lability of the vaccine virus, which requires buffering, and a slight but significant interference of Oral Poliovirus Vaccine [APC] with the uptake of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine., In the near future, oral heterologous Rotavirus Vaccines may be available for prevention of severe rotavirus, live, tetravalent vaccine, live, tetravalent vaccine Gastroenteritis., There was no apparent difference between Bovine Pericardial Cardiac Valves and rhesus-based Rotavirus Vaccines in the protective efficacy against severe rotavirus, live, tetravalent vaccine, live, tetravalent vaccine Gastroenteritis., Efficacy studies of this vaccine in 6-12 month-old children gave results characteristic of the performance of oral Rotavirus Vaccines in general: 58% protective efficacy against any rotavirus, live, tetravalent vaccine, live, tetravalent vaccine Gastroenteritis and 82% against \"clinically significant\" Gastroenteritis., Live oral rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine strain RIT1 wt Allele 4237, derived from group A Bovine Pericardial Cardiac Valves rotavirus, live, tetravalent vaccine, live, tetravalent vaccine NCDV, was given to Homo sapiens volunteers in Tampere, Finland in 1982., Targeted efforts to evaluate indirect effects of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine in low income countries are required to understand the total impact of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine on the global burden of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine disease., Widespread introduction of Rotavirus Vaccines has led to major reductions in the burden of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine Gastroenteritis worldwide., While rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine indirect effects have been demonstrated in high and middle income countries, there are very little data from low income countries where force of Communicable Diseases, population structures and vaccine schedules differ., Measuring indirect effects of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine in low income countries., Intussusception among recipients of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine: reports to the vaccine adverse event reporting system., Rotavirus vaccine was licensed on August 31, 1998, and subsequently recommended for routine use among infants., To describe the cases of Intussusception among rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine recipients reported to the Vaccine [APC] [APC] Adverse Event Reporting System from October 1998 through December 1999., Infants vaccinated with rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine in the United States., There were 98 confirmed cases of Intussusception after vaccination with rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine reported to the Vaccine [APC] [APC] Adverse Event Reporting System; 60 of these developed Intussusception within 1 week after vaccination., Using a passive surveillance system for vaccine adverse events, we observed at least a fourfold increase over the expected number of Intussusception cases occurring within 1 week of receipt of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine., Other studies were initiated to further define the relationship between rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine and Intussusception., In light of these and other data, the rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine manufacturer voluntarily removed its product - ParticipationType - ParticipationType from the market, and the recommendation for routine use of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine among US infants has been withdrawn., To review the biology, immunology, and virology of rotavirus, live, tetravalent vaccine, live, tetravalent vaccine infections and describe the efforts towards the construction of vaccines using Homo sapiens and animal rotaviruses., In August 1998 the Food and Drug Administration in the United States approved the licensure of a rotavirus, live, tetravalent vaccine, live, tetravalent vaccine vaccine.[SEP]Relations: Rotavirus vaccine has relations: drug_drug with Sirolimus, drug_drug with Sirolimus, drug_drug with Sirolimus, drug_drug with Sirolimus, drug_drug with Mitomycin, drug_drug with Mitomycin, drug_drug with Mitomycin, drug_drug with Mitomycin, drug_drug with Flunisolide, drug_drug with Flunisolide.", "label": "yes"}
{"original_question": "Are alterations in ultraconserved elements implicated in breast cancer?", "id": "converted_1880", "sentence1": "Are alterations in ultraconserved elements implicated in Malignant neoplasm of breast?", "sentence2": "Single Nucleotide Polymorphism in ultraconserved elements and familial Malignant neoplasm of breast risk,  In the present study, we investigated the influence of six Single Nucleotide Polymorphism within UCEs on familial Malignant neoplasm of breast risk. Two out of six Single Nucleotide Polymorphism showed an association with familial Malignant neoplasm of breast risk, This is the first study indicating that Single Nucleotide Polymorphism in UCEs might be associated with cancer risk, Single Nucleotide Polymorphism in ultraconserved elements and familial Malignant neoplasm of breast risk., Recent studies have indicated that UCEs are not Mutation Abnormality cold regions and likely to be concerned with Malignant Neoplasms, including Malignant neoplasm of breast (BC Original Formula Original Formula). , Single Nucleotide Polymorphism in ultraconserved elements and familial Malignant neoplasm of breast risk., Genetic variants in ultraconserved elements and risk of Malignant neoplasm of breast in Chinese population.[SEP]Relations: breast-ovarian cancer, familial, susceptibility to has relations: disease_protein with RAD51D, disease_protein with RAD51D, disease_protein with RAD51C, disease_protein with RAD51C, disease_phenotype_positive with Breast carcinoma, disease_phenotype_positive with Breast carcinoma, disease_phenotype_positive with Multifactorial inheritance, disease_phenotype_positive with Multifactorial inheritance, disease_phenotype_positive with Ovarian carcinoma, disease_phenotype_positive with Ovarian carcinoma.", "label": "yes"}
{"original_question": "Are mouse chromosomes acrocentric?", "id": "converted_2409", "sentence1": "Are Mus sp. Chromosomes, Human, Pair 1 acrocentric?", "sentence2": " Based on combined fluorescence in situ hybridization and linkage mapping, the gene order on CFA9 is similar to that of the homologous genes on HSA17q and Mus sp. chromosome 11 (MMU11), but in the dog the gene order is inverted with respect to the Centromere. , In Mus models of Homo sapiens carcinogenesis, however, karyotype analysis is technically demanding because Mus sp. Chromosomes, Human, Pair 1 are acrocentric and of similar size., The minor satellite is closer to the short arms of the acrocentric Chromosomes, Human, Pair 1 than the major satellite,  These Cells contain Robertsonian translocated Chromosomes, Human, Pair 1 1 and 7 as the only submetacentric chromosome in an otherwise acrocentric genome.,  The resulting metacentric Chromosomes, Human, Pair 1 are very different in size and in morphology from normal Mus sp. acrocentric Chromosomes, Human, Pair 1.,  Because of 35 independent primary Hybrids used in this study were derived from two types of feral CASP14 gene, each with a different combination of Robertsonian translocation Chromosomes, Human, Pair 1, as well as from CASP14 gene with a normal complement of acrocentric Chromosomes, Human, Pair 1, analysis of 16 selected Mus sp. enzyme markers provided data on the segregation of all 20 Mus sp. Chromosomes, Human, Pair 1 in these Hybrids, The two Mus sp. stocks exhibit karyotypes consisting of nine pairs of metacentric Chromosomes, Human, Pair 1 as a result of centric fusions of acrocentric Chromosomes, Human, Pair 1 in different combinations., Physical gene mapping by in situ hybridization is a difficult task in an all-acrocentric Mus sp. karyotype, because all of the Chromosomes, Human, Pair 1 are morphologically very similar., The resulting metacentric Chromosomes, Human, Pair 1 are very different in size and in morphology from normal Mus sp. acrocentric Chromosomes, Human, Pair 1., Mus models of Homo sapiens carcinogenesis are exceedingly valuable tools to understand genetic mechanisms of neoplastic growth the identification of recurrent Chromosomes rearrangements by cytogenetic techniques serves as an initial screening test for Neoplasms specific aberrations in Mus models of Homo sapiens carcinogenesis however karyotype analysis is technically demanding because Mus sp. Chromosomes, Human, Pair 1 are acrocentric and of similar size fluorescence in situ hybridization Fluorescent in Situ Hybridization with Mus sp. chromosome specific painting Probes can complement conventional banding analysis although sensitive and specific Fluorescent in Situ Hybridization analyses are restricted to the visualization of only a few Mus sp. Chromosomes, Human, Pair 1 at a time here we apply a novel imaging technique that we developed recently for the visualization of Homo sapiens Chromosomes, Human, Pair 1 to the simultaneous discernment of all Mus sp. Chromosomes, Human, Pair 1 the approach is based on spectral imaging to measure chromosome specific spectra after Fluorescent in Situ Hybridization with differentially labelled Mus sp. chromosome painting Probes utilizing a combination of fourier spectroscopy ccd imaging and conventional optical microscopy spectral imaging allows simultaneous measurement of the fluorescence emission spectrum at all sample points a spectrum based classification algorithm has been adapted to karyotype Mus sp. Chromosomes, Human, Pair 1 we have applied spectral karyotyping sky to Chemicals induced Plasmacytoma mammary gland tumours from Mice, Transgenic overexpressing the c myc oncogene and Thymoma from CASP14 gene deficient for the ataxia telangiectasia atm gene results from these analyses demonstrate the potential of sky to identify complex Chromosomes aberrations in Mus sp. models of Homo sapiens carcinogenesis.[SEP]Relations: chromosome has relations: cellcomp_protein with MBD6, cellcomp_protein with MBD6, cellcomp_protein with HOXA13, cellcomp_protein with HOXA13, cellcomp_protein with TEX12, cellcomp_protein with TEX12, cellcomp_protein with CBX6, cellcomp_protein with CBX6, cellcomp_protein with CCDC86, cellcomp_protein with CCDC86.", "label": "yes"}
{"original_question": "Are there mammalian promoters with distal enhancer functions?", "id": "converted_2425", "sentence1": "Are there mammalian Promoter with distal Enhancer of transcription functions?", "sentence2": "Genome-wide characterization of mammalian Promoter with distal Enhancer of transcription functions., Gene expression in Mammals is precisely regulated by the combination of Promoter and gene-distal Regulatory Sequences, Nucleic Acid, known as enhancers. Several studies have suggested that some Promoter might have Enhancer of transcription functions. However, the extent of this type of Promoter and whether they actually function to regulate the expression of distal genes have remained elusive. Here, by exploiting a high-throughput Enhancer of transcription reporter assay, we unravel a set of mammalian Promoter displaying Enhancer of transcription activity. These Promoter have distinct Genome and epigenomic features and frequently interact with other gene Promoter. Extensive CRISPR-Cas9 Genome manipulation demonstrated the involvement of these Promoter in the cis regulation of expression of distal genes in their natural loci. Our results have important implications for the understanding of complex gene regulation in normal development and disease., Here, by exploiting a high-throughput Enhancer of transcription reporter assay, we unravel a set of mammalian Promoter displaying Enhancer of transcription activity., Several studies have suggested that some Promoter might have Enhancer of transcription functions., Genome - anatomical entity wide characterization of mammalian Promoter with distal Enhancer of transcription functions, gene expression in Mammals is precisely regulated by the combination of Promoter and gene distal Regulatory Sequences, Nucleic Acid known as enhancers several studies have suggested that some Promoter might have Enhancer of transcription functions however the extent of this type of Promoter and whether they actually function to regulate the expression of distal genes have remained elusive here by exploiting a high throughput Enhancer of transcription reporter assay we unravel a set of mammalian Promoter displaying Enhancer of transcription activity these Promoter have distinct Genome and epigenomic features and frequently interact with other gene Promoter extensive crispr cas9 Genome manipulation demonstrated the involvement of these Promoter in the cis regulation of expression of distal genes in their natural loci our results have important implications for the understanding of complex gene regulation in normal development and disease.[SEP]Relations: promoter clearance from RNA polymerase I promoter has relations: bioprocess_bioprocess with promoter clearance during DNA-templated transcription, bioprocess_bioprocess with promoter clearance during DNA-templated transcription, bioprocess_bioprocess with promoter clearance from RNA polymerase I promoter for nuclear large rRNA transcript, bioprocess_bioprocess with promoter clearance from RNA polymerase I promoter for nuclear large rRNA transcript. anatomical entity has relations: anatomy_anatomy with insect mouthpart, anatomy_anatomy with insect mouthpart. regulation of antisense RNA transcription has relations: bioprocess_bioprocess with positive regulation of antisense RNA transcription, bioprocess_bioprocess with positive regulation of antisense RNA transcription, bioprocess_bioprocess with negative regulation of antisense RNA transcription, bioprocess_bioprocess with negative regulation of antisense RNA transcription.", "label": "yes"}
{"original_question": "Is verubecestat effective for Alzheimer’s Disease?", "id": "converted_3003", "sentence1": "Is verubecestat effective for Alzheimer’s Disease?", "sentence2": " The lack of efficacy of verubecestat in mild-to-moderate cytarabine/daunorubicin protocol raises important questions about the timing of intervention with BACE-1 inhibitors, and anti-amyloid therapies in general, in cytarabine/daunorubicin protocol treatment., This reaction was applied to the preparation of verubecestat, which is currently undergoing clinical evaluation for the treatment of ALZHEIMER DISEASE, FAMILIAL, 1., Verubecestat is an PPP1R1A gene of β-site amyloid precursor protein cleaving enzyme 1 (BACE1 protein, human protein, human) being evaluated in clinical trials for the treatment of ALZHEIMER DISEASE, FAMILIAL, 1. , CONCLUSIONS: Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 and was associated with treatment-related adverse events. , Randomized Trial of Verubecestat for Mild-to-Moderate Alzheimer's Disease.Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 and was associated with treatment-related adverse events. , CONCLUSIONS\nVerubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 and was associated with treatment-related adverse events., Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 and was associated with treatment-related adverse events.[SEP]Relations: familial Alzheimer disease has relations: disease_disease with Alzheimer disease, disease_disease with Alzheimer disease, disease_disease with inherited prion disease, disease_disease with inherited prion disease, disease_protein with PRNP, disease_protein with PRNP, disease_phenotype_positive with Sleep disturbance, disease_phenotype_positive with Sleep disturbance, disease_phenotype_positive with Perseveration, disease_phenotype_positive with Perseveration.", "label": "no"}
{"original_question": "Is celecoxib effective for amyotrophic lateral sclerosis?", "id": "converted_3413", "sentence1": "Is celecoxib effective for amyotrophic lateral sclerosis?", "sentence2": "In conclusion, the celecoxib-creatine combination was selected as preferable to the minocycline-creatine combination for further evaluation. , ESULTS: celecoxib did not slow the decline in muscle strength, vital capacity, Motor unit number estimates, Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised, or affect survival. , INTERPRETATION: At the dosage studied, celecoxib did not have a beneficial effect on research subjects with Amyotrophic Lateral Sclerosis, and it was safe. , INTERPRETATION\n\nAt the dosage studied, celecoxib did not have a beneficial effect on research subjects with Amyotrophic Lateral Sclerosis, and it was safe., RESULTS\n\ncelecoxib did not slow the decline in muscle strength, vital capacity, Motor unit number estimates, Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised, or affect survival., RESULTS\ncelecoxib did not slow the decline in muscle strength, vital capacity, Motor unit number estimates, Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised, or affect survival., INTERPRETATION: At the dosage studied, celecoxib did not have a beneficial effect on research subjects with Amyotrophic Lateral Sclerosis, and it was safe., RESULTS: celecoxib did not slow the decline in muscle strength, vital capacity, Motor unit number estimates, Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised, or affect survival., At the dosage studied, celecoxib did not have a beneficial effect on research subjects with Amyotrophic Lateral Sclerosis, and it was safe., celecoxib did not slow the decline in muscle strength, vital capacity, Motor unit number estimates, Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised, or affect survival.[SEP]Relations: celecoxib has relations: drug_effect with Arthropathy, drug_effect with Arthropathy, drug_effect with Coronary artery atherosclerosis, drug_effect with Coronary artery atherosclerosis, drug_drug with Corticotropin, drug_drug with Corticotropin, drug_effect with Cholelithiasis, drug_effect with Cholelithiasis, drug_effect with Epistaxis, drug_effect with Epistaxis.", "label": "no"}
{"original_question": "Are lamina-associated domains (LADs) associated with transcriptional activation?", "id": "converted_3465", "sentence1": "Are lamina-associated domains (LADs) associated with transcriptional activation?", "sentence2": "Regions of focal DNA hypermethylation and long-range hypomethylation in colorectal Primary malignant neoplasm coincide with Nuclear Lamina-associated domains., Extensive changes in DNA methylation are common in Primary malignant neoplasm and may contribute to oncogenesis through transcriptional silencing of tumor-suppressor genes., Such lamina-associated domains (LADs) are thought to help organize Chromosomes, Human, Pair 1 inside the Cell Nucleus and have been associated with gene repression., The Nuclear Lamina contributes to the regulation of gene expression and to chromatin organization.[SEP]Relations: Nuclear Lamina has relations: cellcomp_protein with HLCS, cellcomp_protein with HLCS, cellcomp_protein with PCNA, cellcomp_protein with PCNA, cellcomp_protein with SUV39H1, cellcomp_protein with SUV39H1, cellcomp_protein with CASK, cellcomp_protein with CASK, cellcomp_protein with PRR14, cellcomp_protein with PRR14.", "label": "no"}
{"original_question": "Can SMAD6 variants cause craniosynostosis?", "id": "converted_3799", "sentence1": "Can SMAD6 protein, human Variant cause TWIST1 gene?", "sentence2": "SMAD6 protein, human protein, human Variant in TWIST1 gene: Genotype determination and phenotype evaluation., Enrichment of heterozygous Missense and truncating SMAD6 protein, human protein, human Variant was previously reported in nonsyndromic sagittal and Metopic synostosis, and interaction of SMAD6 protein, human protein, human Variant with a common polymorphism nearBMP2 (rs1884302) was proposed to contribute to inconsistent penetrance. We determined the occurrence of SMAD6 protein, human protein, human Variant in all types of TWIST1 gene, evaluated the impact of different Missense Variant on SMAD6 protein, human protein, human function, and tested independently whether rs1884302 Genotype determination significantly modifies the phenotype.METHODS: We performed resequencing of SMAD6 protein, human protein, human in 795 unsolved patients with any type of TWIST1 gene and genotyped rs1884302 in SMAD6 protein, human protein, human-positive individuals and relatives. We examined the inhibitory activity and stability of SMAD6 protein, human protein, human Missense Variant.RESULTS: We found 18 (2.3%) different rare damaging SMAD6 protein, human protein, human Variant, with the highest prevalence in Metopic synostosis (5.8%) and an 18.3-fold enrichment of loss-of-function Variant comparedwith gnomAD data (P < 10-7). Combined with eight additional Variant, ≥20/26 were transmitted from an unaffected parent but rs1884302 Genotype determination did not predict phenotype.CONCLUSION: Pathogenic SMAD6 protein, human protein, human Variant substantially increase the risk of both nonsyndromic and syndromic presentations of TWIST1 gene, especially Metopic synostosis. Functional analysis is important to evaluate Missense Variant. Genotyping of rs1884302 is not clinically useful. Mechanisms to explain the remarkable diversity of phenotypes associated with SMAD6 protein, human protein, human Variant remain obscure.[SEP]Relations: TWIST1 gene Fontaine type has relations: disease_disease with TWIST1 gene, disease_disease with TWIST1 gene. Metopic synostosis has relations: disease_phenotype_positive with six2-related frontonasal dysplasia, disease_phenotype_positive with six2-related frontonasal dysplasia, disease_phenotype_positive with neurodevelopmental disorder-craniofacial dysmorphism-cardiac defect-hip dysplasia syndrome due to 9q21 microdeletion, disease_phenotype_positive with neurodevelopmental disorder-craniofacial dysmorphism-cardiac defect-hip dysplasia syndrome due to 9q21 microdeletion, disease_phenotype_positive with cranioectodermal dysplasia, disease_phenotype_positive with cranioectodermal dysplasia, disease_phenotype_positive with neurodevelopmental disorder-craniofacial dysmorphism-cardiac defect-hip dysplasia syndrome due to a point mutation, disease_phenotype_positive with neurodevelopmental disorder-craniofacial dysmorphism-cardiac defect-hip dysplasia syndrome due to a point mutation.", "label": "yes"}
{"original_question": "Is pembrolizumab effective against Ewing's sarcoma?", "id": "converted_2788", "sentence1": "Is pembrolizumab effective against Ewing's sarcoma of bone?", "sentence2": "None of the 13 patients with Ewing's sarcoma of bone of bone had an objective response. , Between March 13, 2015, and Feb 18, 2016, we enrolled 86 patients, 84 of whom received pembrolizumab (42 in each disease cohort) and 80 of whom were evaluable for response (40 in each disease cohort). [SEP]Relations: Ewing sarcoma of bone has relations: disease_disease with Ewing sarcoma, disease_disease with Ewing sarcoma, disease_disease with bone sarcoma, disease_disease with bone sarcoma, disease_disease with Ewing sarcoma/peripheral primitive neuroectodermal tumor of bone, disease_disease with Ewing sarcoma/peripheral primitive neuroectodermal tumor of bone.", "label": "no"}
{"original_question": "Can CMB305 be used against sarcomas?", "id": "converted_3434", "sentence1": "Can CMB305 be used against sarcomas?", "sentence2": "CMB305 induces CTAG1A wt Allele specific T-Lymphocyte responses in both Supernumerary mandibular right first primary molar and Medical Research Council patients and these patients had excellent overall survival (OS) outcomes in the initial phase I study., Data suggesting this Vaccine [APC] may improve OS for Supernumerary mandibular right first primary molar and MRCL patients is exciting but early, and on-going work is testing the impact of CMB305 on patient outcomes., The potential of the CMB305 Vaccine [APC] regimen to target CTAG1A wt Allele and improve outcomes for synovial sarcoma and Myxoid/Round Cell Liposarcoma patients.[SEP]Relations: BCG Vaccine [APC] has relations: drug_drug with Sarilumab, drug_drug with Sarilumab, drug_drug with Sirukumab, drug_drug with Sirukumab, drug_drug with Sorafenib, drug_drug with Sorafenib, drug_drug with Sarecycline, drug_drug with Sarecycline. breast synovial sarcoma has relations: disease_disease with breast sarcoma, disease_disease with breast sarcoma.", "label": "yes"}
{"original_question": "Are protamines ubiquitously expressed?", "id": "converted_3183", "sentence1": "Are protamines ubiquitously expressed?", "sentence2": "protamines are Nuclear Proteins which are specifically expressed in haploid male Germ Cells.[SEP]Relations: Protamine has relations: drug_effect with Inflammatory abnormality of the skin, drug_effect with Inflammatory abnormality of the skin, drug_effect with Fever, drug_effect with Fever, drug_effect with Agitation, drug_effect with Agitation, drug_effect with Pain, drug_effect with Pain, drug_effect with Increased hemoglobin, drug_effect with Increased hemoglobin.", "label": "no"}
{"original_question": "Has proteomics been used in the study of Pick's disease?", "id": "converted_676", "sentence1": "Has proteomics been used in the study of Pick Disease of the Brain?", "sentence2": "In Pick Disease of the Brain, increased Age:Time:Point in time:^Patient:Quantitative, Myeloid Leukemia, Chronic, CEL gene gene, ELANE gene and MDAL bands of about 50 kDa were observed in the Cortex of frontal lobe (but not in the Cortex of occipital lobe) in association with increased density of glial acidic protein bands., Thus, Head>Brain and Cerebrospinal Fluid (CSF) samples from patients with ALZHEIMER DISEASE, FAMILIAL, 1, Down Syndrome, Pick Disease of the Brain, Parkinson Disease, SCHIZOPHRENIA 2 (disorder), and other disorders as well as Head>Brain and CSF from animal allergen extracts serving as models of nervous system disorder have been analyzed by proteomics. , The present study is designed to investigate expression of thioredoxin peroxidase (Prxs), the newly characterized family of highly conserved antioxidant enzymes, and other antioxidant enzymes in Cortex of frontal lobe and Cerebellum of DS, cytarabine/daunorubicin protocol and Lugano Lymphoma Response Classification Progressive Disease by PET patients using the technique of proteomics. , methenamine levels were measured in the Cortex of frontal lobe and Cerebellum of brains of patients with cytarabine/daunorubicin protocol, DS, and PiD, and normal aged subjects using proteomics techniques. [SEP]Relations: Down Syndrome has relations: disease_protein with RAD21, disease_protein with RAD21, disease_protein with PRDX6, disease_protein with PRDX6, disease_protein with S100B, disease_protein with S100B, disease_protein with SLC19A1, disease_protein with SLC19A1, disease_protein with PRDX2, disease_protein with PRDX2.", "label": "yes"}
{"original_question": "Is Vitamin D deficiency in pregnant women associated with gestational diabetes?", "id": "converted_1037", "sentence1": "Is ergocalciferol deficiency in pregnant women associated with gestational diabetes?", "sentence2": "Insufficient serum levels of 25-OHD were associated with gestational diabetes (pooled odds ratio 1.49, 95% confidence interval 1.18 to 1.89, ergocalciferol insufficiency is associated with an increased risk of gestational diabetes, p, Therefore, it is important to identify potentially modifiable risk factors for GDM. Accumulating evidence links vitamin D deficiency with abnormal glucose metabolism, and epidemiological studies have shown that women who develop GDM are more likely to be vitamin D deficient, This review discusses the prevalence, risk factors, and outcomes of GDM and vitamin D deficiency in pregnant women, outlines the possible mechanism of action of vitamin D in glucose homeostasis, and summarizes emerging evidence that associates vitamin D deficiency with the risk of developing GDM, Women with circulating 25-Hydroxyvitamin D3 Measurement [25(OH)D] level less than 50 nmol/l in pregnancy experienced an increased risk of Pre-Eclampsia [OR 2.09 (95%CI 1.50 -2.90)], Gestational Diabetes [OR1.38 (1.12-1.70)], Low maternal vitamin D levels in pregnancy may be associated with an increased risk of Pre-Eclampsia, Gestational Diabetes,, Association between vitamin D insufficiency and the risk for Gestational Diabetes in pregnant Chinese women, 25OHD insufficiency is very common in Chinese women. Low 25OHD status may be associated with insulin resistance and act as a risk factor for GDM., Second-trimester 25(OH)D levels were associated inversely with glucose levels after 1-hour 50-g glucose challenge test; low 25(OH)D levels may be associated with increased risk of GDM., Two hundred sixty-six women were screened. ergocalciferol deficiency (25[OH]D <20 ng/mL) was observed in 157 women (59%). We observed an inverse correlation between 25(OH)D levels and hemoglobin A1c, homeostasis model assessment of insulin resistance, serum insulin, and fasting and 1-hour oral glucose tolerance test glucose levels, Lower 25(OH)D levels are associated with disorders of glucose homeostasis and adverse obstetric and newborn outcomes., An association between mid-gestational 25-hydroxy vitamin D and fasting glucose was confirmed in a largely normoglycaemic and vitamin D-replete pregnant population. The correlation between 25-hydroxy vitamin D and β-cell function suggests that vitamin D may influence glucose metabolism through this mechanism., Women with gestational diabetes had significantly lower serum 25-Hydroxyvitamin D3 Measurement compared with control subjects (56.3 vs. 62.0 nmol/l, P = 0.018). After adjusting for gestational age and maternal weight, serum 25-Hydroxyvitamin D3 Measurement below the top quartile (< 73.5 nmol/l) was associated with a twofold greater likelihood of gestational diabetes (adjusted odds ratio 2.21, 95% confidence interval 1.19-4.13). CONCLUSIONS: Lower vitamin D status in early pregnancy was associated with a significantly increased risk of subsequent gestational diabetes that was independent of race, age, season and maternal weight. This study suggests that vitamin D may influence glucose tolerance during pregnancy, ergocalciferol deficiency among pregnant women is frequent in many populations over the world. It is associated with an increased risk of Pre-Eclampsia, Gestational Diabetes, and caesarean section, Consequences in newborns are low birth weight, neonatal Rickets, a risk of neonatal Hypocalcemia, Asthma and/or type 1 diabetes., A single injection of 300,000 IU of cholecalciferol achieves a 3-month serum 25-Hydroxyvitamin D3 Measurement range of 50-80 nmol/l and is an efficient, effective and safe procedure for improving the vitamin status and indices of insulin resistance in mothers with gestational diabetes after delivery., In a cohort of pregnant women with mostly sufficient levels of serum 25(OH)D, vitamin D deficiency was not associated with GDM., The aim of the study is evaluating the associations of FokI vitamin D receptor (VDR) Genetic Polymorphism with Gestational Diabetes (GDM), and its relations with postpartum metabolic syndrome., Our results indicate a meaningful association between FokI VDR genotypes and an increase risk of GDM in Iranian population as well as its effects on postpartum metabolic syndrome., The first-trimester maternal serum level of 25(OH)D is not altered in women with type 2 diabetes, those who develop GDM or those who deliver GLS2 wt Allele neonates., Lower 25(OH)D levels are independently associated with poorer glycaemic control. Future randomised trials are needed to determine whether vitamin D plays a role in glycaemic control in GDM., These results suggested that rates of vitamin D deficiency are higher among women with IGT/GDM, and the relationship between vitamin D status and glucose tolerance in pregnancy needs further study., It appears that vitamin D insufficiency during pregnancy is potentially associated with increased risk of Pre-Eclampsia, insulin resistance and Gestational Diabetes, Mean serum 25OHD concentration was 53.8 +/- 23.9 nmol/l (sd). Ln-25OHD was negatively correlated with serum parathyroid hormone as expected (r -0.24, confidence intervals -0.35 to -0.12). Ln-25OHD was also negatively correlated with fasting plasma glucose (r-0.20, -0.31 to -0.08), fasting insulin (r -0.20, -0.31 to -0.08) and insulin resistance as calculated by homeostasis model assessment (r -0.21, -0.32 to -0.09). The association between fasting glucose and log-transformed 25OHD concentration was of borderline significance after accounting for ethnicity, age and body mass index in multivariate analyses (-0.13, -0.26 to 0.01). The odds ratio of gestational diabetes in women with 25OHD < 50 nmol/l did not reach statistical significance (1.92, 95% confidence interval 0.89-4.17). CONCLUSIONS: Maternal 25OHD concentrations are inversely related to fasting glucose, although further studies are required to establish whether this is independent of the effects of ethnic background., ergocalciferol insufficiency is common in Indian mothers but is not associated with gestational diabetes or variation in newborn size., There was no association between maternal 25(OH)D and gestational diabetes (incidence 7% in women with and without ergocalciferol Deficiency), In mothers with ergocalciferol Deficiency, higher 25(OH)D concentrations were associated with lower 30-min glucose concentrations (P=0.03) and higher fasting Assay of Proinsulin concentrations (P=0.04), Hypovitaminosis D at 30 weeks gestation is common in Mysore mothers. It is not associated with an increased risk of gestational diabetes,, Total prevalence of vitamin D deficiency (<25 nmol/L) was found in 70.6% of pregnant women. Prevalence of severe vitamin D deficiency (<12.5) in GDM patients was higher than in normoglycaemic pregnancies., These results show that a positive correlation of 25(OH) vitamin D concentrations with insulin sensitivity and vitamin D deficiency could be a confirmative sign of insulin resistance., was to examine whether maternal dietary intake of vitamin D, omega-3 fatty acids, and fatty acids, omega-6 during pregnancy is associated with the appearance of islet autoimmunity (Intraarterial Route of Drug Administration) in offspring, Maternal intake of vitamin D via Food allergenic extracts was significantly associated with a decreased risk of Intraarterial Route of Drug Administration appearance in offspring, independent of HLA genotype, family history of type 1 diabetes, presence of Gestational Diabetes, and ethnicity (adjusted HR = 0.37; 95% CI 0.17-0.78). ergocalciferol intake via supplements, omega-3 fatty acids, and fatty acids, omega-6 intake during pregnancy were not associated with appearance of Intraarterial Route of Drug Administration in offspring. CONCLUSIONS: Our findings suggest that maternal intake of vitamin D through Food allergenic extracts during pregnancy may have a protective effect on the appearance of Intraarterial Route of Drug Administration in offspring.[SEP]Relations: gestational diabetes has relations: disease_disease with pregnancy disorder, disease_disease with pregnancy disorder, disease_disease with diabetes mellitus (disease), disease_disease with diabetes mellitus (disease), contraindication with Ritodrine, contraindication with Ritodrine. vitamin B deficiency has relations: disease_disease with vitamin deficiency disorder, disease_disease with vitamin deficiency disorder, disease_disease with vitamin B12 deficiency, disease_disease with vitamin B12 deficiency.", "label": "yes"}
{"original_question": "Does ProSavin use an adenoviral vector?", "id": "converted_3444", "sentence1": "Does ProSavin use an adenoviral vector?", "sentence2": "Long-Term Follow-Up of a Phase I/II Study of ProSavin, a Lentiviral Vector Gene Therapy for Parkinson Disease., ProSavin, a lentiviral vector based gene therapy that delivers local and continuous dopamine, was previously shown to be well tolerated in a Phase I/II first-in-human study, with significant improvements in motor behavior from baseline at 1 year. [SEP]Relations: Dopamine has relations: drug_drug with Saquinavir, drug_drug with Saquinavir, drug_drug with Adefovir dipivoxil, drug_drug with Adefovir dipivoxil, drug_drug with Protirelin, drug_drug with Protirelin, drug_drug with Adefovir, drug_drug with Adefovir, drug_drug with Procaine benzylpenicillin, drug_drug with Procaine benzylpenicillin.", "label": "no"}
{"original_question": "Does saracatinib promote oncogenesis?", "id": "converted_3686", "sentence1": "Does saracatinib promote oncogenesis?", "sentence2": "Antitumor activity of saracatinib (AZD 0530), a c-Src/Abl kinase inhibitor, alone or in combination with Chemotherapeutic agent in Malignant neoplasm of stomach., We evaluated the Antitumor effect of a c-Src/Abl kinase inhibitor, saracatinib (AZD 0530), alone or combined with Chemotherapeutic agent in Malignant neoplasm of stomach cell lines and a NCI-N87 xenograft model. Among 10 Malignant neoplasm of stomach cell lines, saracatinib specifically inhibited the growth and migration/invasion of SNU216 and NCI-N87 cells. saracatinib blocked the Src/FAK, Herero language family, and oncogenic signaling pathways, and it induced G(1) arrest and apoptosis in SNU216 and NCI-N87 cells. , Consistent with our in vitro findings, cotreatment with saracatinib and fluorouracil resulted in enhanced Antitumor activity in the NCI-N87 xenografts. These data indicate that the inhibition of src-Family Kinases activity by saracatinib alone or in combination with other agents can be a strategy to target Malignant neoplasm of stomach.[SEP]Relations: saracatinib has relations: drug_drug with Tofacitinib, drug_drug with Tofacitinib, drug_drug with Sonidegib, drug_drug with Sonidegib, drug_drug with Cobimetinib, drug_drug with Cobimetinib, drug_drug with Doxazosin, drug_drug with Doxazosin, drug_drug with Palbociclib, drug_drug with Palbociclib.", "label": "no"}
{"original_question": "Should tirilazad be used for treatment of ischemic stroke?", "id": "converted_3830", "sentence1": "Should tirilazad be used for treatment of ischemic stroke?", "sentence2": "CONCLUSION: Tirilazad had no effect on clinical outcome but did decrease symptomatic Vasospasm in five trials of aneurysmal SAH. , Tirilazad did not significantly decrease unfavorable clinical outcome on the Genomics Outcome Scale (odds ratio [OR] 1.04, 95% confidence interval [CI] 0.89-1.20) or Cerebral Infarction (OR 1.04, 95% CI 0.89-1.22). , The authors investigated whether the lack of effect of tirilazad on clinical outcome in patients with Acute Ischemic Stroke is explained by failure of tirilazad to reduce infarct volume. , Tirilazad did not alter early case fatality (odds ratio [OR] 1.11, 95% confidence interval [CI] 0.79 to 1.56) or end-of-trial case fatality (OR 1.12, 95% CI 0.88 to 1.44). A just-significant increase in Cessation of life and Disability:Type:Pt:^Patient:Nom, assessed as either the expanded Barthel Index (OR 1.23, 95% CI 1.01 to 1.51) or Glasgow Outcome Scale (OR 1. 23, 95% CI 1.01 to 1.50) was observed., CONCLUSIONS: Tirilazad mesylate increases Cessation of life and Disability:Type:Pt:^Patient:Nom by about one fifth when given to patients with Acute Ischemic Stroke. Although further trials of tirilazad are now unwarranted, analysis of individual patient data from the trials may help elucidate why tirilazad appears to worsen outcome in Acute Ischemic Stroke.[SEP]Relations: Ischemic stroke has relations: drug_effect with Aripiprazole, drug_effect with Aripiprazole, drug_effect with Sitaxentan, drug_effect with Sitaxentan, drug_effect with Ramipril, drug_effect with Ramipril, drug_effect with Tramadol, drug_effect with Tramadol, drug_effect with Pazopanib, drug_effect with Pazopanib.", "label": "no"}
{"original_question": "Are patients with Sjogren syndrome at increased risk for lymphoma?", "id": "converted_2492", "sentence1": "Are patients with Sjogren syndrome at increased risk for Lymphoma?", "sentence2": "The heightened risk of non-Hodgkin Lymphoma (Lymphoma, Large-Cell, Follicular) development in primary Sjogren syndrome (Supernumerary mandibular right first primary molar) is well established., Primary Diffuse Large B-Cell Lymphoma of the Abdomen>Abdomen>Liver in a Patient with Sjogren Syndrome., Immunohistochemical and molecular features of the Neoplasms allowed diagnosis of diffuse large B-Cell Lymphomas (Diffuse Large B-Cell Lymphoma). , To our knowledge, the patient described here represents the first reported case of Diffuse Large B-Cell Lymphoma with primary liver involvement in Supernumerary mandibular right first primary molar., rituximab is also effective in the treatment of Supernumerary mandibular right first primary molar-associated (extrasalivary) lymphomas, although the therapeutic response in salivary Lymphoma is poorer., rituximab treatment for Sjogren syndrome-associated non-Hodgkin's Lymphoma: case series., Five per cent of patients with Primary Sjögren's syndrome (Chromosome 11p11.2 Deletion Syndrome) develop malignant non-Hodgkin's Lymphoma (Lymphoma, Large-Cell, Follicular), usually of the mucosa-associated lymphoid tissue (MALT) and most frequently located in the major Salivary Glands. , [A case of Sjogren syndrome coexistent with Mucosa-Associated Lymphoid Tissue Lymphoma occurring along the Parotid Gland and Neck+Chest>Trachea]., Both histological examinations revealed MALT-type marginal zone B-Cell Lymphomas. , In the majority of patients, it is a late event and frequently associated with Systemic disease or risk factors for Lymphoma development., The incidence of Lymphoma is higher in patients with Sjögren's syndrome than in the general population., Among the clinical and serological parameters that have been associated with Lymphoma development in Supernumerary mandibular right first primary molar patients, the presence of palpable purpura, low C4, and mixed monoclonal cryoglobulinemia constitute the main predictive markers, and patients displaying these risk factors should be monitored closely., A case of Pulmonary nodular lymphoid hyperplasia and Sjogren syndrome is presented., Furthermore, Rheumatoid Arthritis, Sjögren's syndrome, Lupus Erythematosus, Systemic, and possibly Celiac Disease may share an association with risk of diffuse large B-Cell Lymphomas, in addition to well-established links of Sjögren's syndrome with risk of mucosa-associated lymphoid tissue Lymphoma and of Celiac Disease with risk of small intestinal Lymphoma., Predicting the risk for Lymphoma development in Sjogren syndrome: An easy tool for clinical use., Lymphoma is a very severe complication of primary Sjögren's syndrome: 5 to 10% of patients followed for more than 10 years will develop a Lymphoma., Hematologic manifestations and predictors of Lymphoma development in primary Sjogren's Syndrome: clinical and pathophysiologic aspects., Recent results clearly indicate an association between severity of chronic inflammation and Lymphoma risk in Rheumatoid Arthritis and Sjögren's syndrome., Several autoimmune diseases, including primary Sjögren's syndrome (Chromosome 11p11.2 Deletion Syndrome), are associated with an increased risk for Lymphoma., Primary Sjogren's syndrome (Chromosome 11p11.2 Deletion Syndrome) confers increased risk for non-Hodgkin Lymphoma (Lymphoma, Large-Cell, Follicular) development., Furthermore, we review the emerging role of ELS and lymphoid chemokines in driving extranodal B cell lymphomagenesis in Supernumerary mandibular right first primary molar and we focus on recent evidence suggesting that ELS identify subsets of Supernumerary mandibular right first primary molar patients at increased risk of developing systemic manifestations and Lymphoma., Sjogren's syndrome (Supernumerary mandibular right first primary molar) is a chronic autoimmune disorder with the highest risk for Lymphoma development among all autoimmune diseases., In contrast to secondary Supernumerary mandibular right first primary molar, the risk for developing non-Hodgkin's Lymphoma is highly increased in patients with primary Supernumerary mandibular right first primary molar., Predicting the risk for Lymphoma development in Sjogren syndrome: An easy tool for clinical use., Primary Sjogren's syndrome (Chromosome 11p11.2 Deletion Syndrome) is complicated by B-Cell Lymphomas in 5-10% of patients., Patients with Sjogren's Syndrome are at increased risk of Lymphoma development., Sjogren's syndrome is an Autoimmune Diseases with a known predisposition for Lymphoma development., Certain autoimmune and chronic inflammatory conditions, such as Sjögren's syndrome and rheumatoid arthritis (Rheumatoid Arthritis), have consistently been associated with an increased risk of malignant lymphomas, but it is unclear whether elevated Lymphoma risk is a phenomenon that accompanies inflammatory conditions in general.[SEP]Relations: Sjogren syndrome has relations: disease_phenotype_positive with Lymphoma, disease_phenotype_positive with Lymphoma, disease_phenotype_positive with Lymphadenopathy, disease_phenotype_positive with Lymphadenopathy, disease_phenotype_positive with Increased circulating antibody level, disease_phenotype_positive with Increased circulating antibody level, disease_phenotype_positive with Behavioral abnormality, disease_phenotype_positive with Behavioral abnormality. Lymphoma has relations: disease_phenotype_positive with Sjogren syndrome, disease_phenotype_positive with Sjogren syndrome.", "label": "yes"}
{"original_question": "Is G3BP1 found in stress granules?", "id": "converted_4032", "sentence1": "Is G3BP1 gene found in Stress Granules?", "sentence2": "RAS GTPase-activating protein-binding protein (G3BP1 gene gene) is an RBMS3 gene that is essential for assembling Stress Granules. , Within Shprintzen-Goldberg syndrome, single-molecule localization microscopy revealed distributed hotspots of immobilized G3BP1 gene gene and IGF2BP1 gene that reflect the presence of relatively immobile nanometer-sized nanocores., Using super-resolution and expansion microscopy, we find that the SG component UBAP2L [11, 12] and the core protein G3BP1 gene gene [5, 11-13] occupy different domains inside Shprintzen-Goldberg syndrome. [SEP]Relations: stress granule assembly has relations: bioprocess_protein with G3BP1 gene, bioprocess_protein with G3BP1 gene, bioprocess_protein with G3BP2, bioprocess_protein with G3BP2. G3BP1 gene has relations: cellcomp_protein with cytoplasmic stress granule, cellcomp_protein with cytoplasmic stress granule, bioprocess_protein with stress granule assembly, bioprocess_protein with stress granule assembly, protein_protein with G3BP2, protein_protein with G3BP2.", "label": "yes"}
{"original_question": "Are circRNAs susceptible to degradation by RNase R?", "id": "converted_4351", "sentence1": "Are circRNAs susceptible to degradation by Pancreatic ribonuclease R?", "sentence2": "Currently, an increasing body of evidence has demonstrated that 1) majority of circRNAs are evolutionarily conserved across species, stable, and resistant to Pancreatic ribonuclease R degradation, , Circular RNA (circRNA) has a closed-loop structure, and its 3' and 5' ends are directly covalently connected by reverse splicing, which is more stable than linear RNA., RNA, Circular are a kind of closed circular RNA molecule widely existing in transcriptomes. Due to lack of free ends, they are not easily cleaved by Pancreatic ribonuclease R, thus avoiding degradation. , Circular RNA (circRNAs) are a class of newly-identified non-coding RNA that lack 5' (cap) and 3' (polyadenylation) ends and are linked by a covalent bond to form a closed loop structure. In comparison to linear RNA, circRNAs are more resistant to exonuclease Pancreatic ribonuclease R-mediated degradation with a much stronger stability due to the absence of 3' terminals, Circular RNA (circRNAs) own unique capabilities to communicate with Nucleic Acids and ribonucleoproteins and are emerging as indispensable compositions of the regulatory messages encoded in the Genome - anatomical entity. Due to lack of 3' termini, circRNAs are more resistant to degradation by exonuclease Pancreatic ribonuclease R and possess greater stability than linear RNA. , Pancreatic ribonuclease R is a strong 3' to 5' exoribonuclease, which efficiently degrades linear RNA, such as mRNAs and rRNAs; therefore, the circular parts of lariat RNA and the circRNAs can be segregated from eukaryotic total RNA by their Pancreatic ribonuclease R resistance., Lariat RNA and circRNAs are both Pancreatic ribonuclease R resistant RNA., In comparison to linear RNA, circRNAs are more resistant to exonuclease Pancreatic ribonuclease R-mediated degradation with a much stronger stability due to the absence of 3' terminals., Due to lack of 3' termini, circRNAs are more resistant to degradation by exonuclease Pancreatic ribonuclease R and possess greater stability than linear RNA., Because circRNAs are not easily degraded by exonuclease Pancreatic ribonuclease R, they can exist more stably in Body Fluids than linear RNA., Therefore, it is essential to perform the RT-qPCR validation step only after linear RNA have been degraded using an exonuclease such as ribonuclease R (Pancreatic ribonuclease R)., is a strong 3' to 5' exoribonuclease, which efficiently degrades linear RNA, such as mRNAs and rRNAs; therefore, the circular parts of lariat RNA and the circRNAs can be segregated from eukaryotic total RNA by their Pancreatic ribonuclease R resistance. Thus, Pancreatic ribonuclease, sion of circRNAs is prevalent in Body tissue and Body Fluids,and their abnormal expression is related to Specimen Source Codes - Specimen Source Codes - tumor progression.circRNAs are stable even under the treatment of Pancreatic ribonuclease R because of their circular conformation.As circRNAs, e to lack of 3' termini, circRNAs are more resistant to degradation by exonuclease Pancreatic ribonuclease R and possess greater stability than linear RNA. molybdenum, e circRNAs are not easily degraded by exonuclease Pancreatic ribonuclease R, they can exist more stably in Body Fluids than linear RNA. Based,  is stable, difficult to cleave and resistant to REXO5 gene or Pancreatic ribonuclease R degradation. circRN, the unique structures, circRNAs are resistant to exonuclease Pancreatic ribonuclease R and maintain stability more easily than linear RNA. Rece, rison to linear RNA, circRNAs are more resistant to exonuclease Pancreatic ribonuclease R-mediated degradation with a much stronger stability due to the absence of 3' terminals. Conseque,  RT-PCR analysis showed that sheep circRNAs are resistant to Pancreatic ribonuclease R digestion and are expressed in prenatal and postnatal Pituitary Gland. GO and , Currently, an increasing body of evidence has demonstrated that 1) majority of circRNAs are evolutionarily conserved across species, stable, and resistant to Pancreatic ribonuclease R degradation, and often exhibit cell-specific, and tissue-specific/developmental-stage-specific expression and can be largely independent of the expression levels of the linear host gene-encoded linear RNA; 2) the biogenesis of circRNAs via back-splicing is different from the canonical splicing of linear RNA; 3) circRNA biogenesis is regulated by specific cis-acting elements and Trans-Activators; 4) circRNAs regulate biological and pathological processes by sponging MicroRNAs, binding to RNA-Binding Proteins (SUGP1 gene), regulators of splicing and transcription, modifiers of parental gene expression, and regulators of protein translation or being translated into Peptides in various diseases; 5) circRNAs have been identified for their enrichment and stability in Exosomes and detected in Body Fluids such as Homo sapiens blood, Specimen Source Codes - Saliva, and Cerebrospinal Fluid, suggesting that these exo-circRNAs have potential applications as disease biomarkers and novel therapeutic targets; 6) several circRNAs are regulated by oxidative stress and mediate Reactive Oxygen Species (ROS) production as well as promote ROS-induced cellular death, cell apoptosis, and Inflammation; 7) circRNAs have also emerged as important regulators in atherosclerotic cardiovascular disease, Metabolic Diseases, and Malignant Neoplasms; 8) the potential mechanisms of several circRNAs have been described in diseases, hinting at their potential applications as novel therapeutic targets., To prove their circularity as well as biochemically enrich these RNA Transcript, it has become standard in the field to use the 3'-5' exonuclease Pancreatic ribonuclease R. Here, we demonstrate that standard protocols involving Pancreatic ribonuclease R can fail to digest >20% of all highly expressed linear RNA, but these shortcomings can largely be overcome., We propose that such an R-loop dependent Circular Intronic RNA degradation likely represents a mechanism that on one hand limits Circular Intronic RNA accumulation by recruiting Pancreatic ribonuclease H1 and on the other hand resolves R-Loop Structures for transcriptional elongation at some GC-rich Circular Intronic RNA-producing loci., As circular RNA (circRNAs) are resistant to degradation by exonucleases, their abundance relative to linear RNA can be used as a surrogate marker for mRNA stability in the absence of transcription., The synthetic circular sponge was resistant to digestion with Pancreatic ribonuclease R. Luciferase assays and functional experiments showed that the circular multi-miR sponge was more stable than its linear counterpart., RNA with highly structured 3' ends, including snRNAs and histone mRNAs, are naturally resistant to Pancreatic ribonuclease R, but can be efficiently degraded once a Poly(A) Tail has been added to their ends., Thousands of eukaryotic protein-coding genes generate circular RNA that have covalently linked ends and are resistant to degradation by exonucleases.[SEP]Relations: rRNA transcription has relations: bioprocess_bioprocess with 5S class rRNA transcription by RNA polymerase III, bioprocess_bioprocess with 5S class rRNA transcription by RNA polymerase III, bioprocess_bioprocess with ncRNA transcription, bioprocess_bioprocess with ncRNA transcription, bioprocess_protein with SIRT7, bioprocess_protein with SIRT7. protein binding has relations: molfunc_protein with RNASE10, molfunc_protein with RNASE10, molfunc_protein with RNASE1, molfunc_protein with RNASE1.", "label": "no"}
{"original_question": "Do Crocus sativus extracts loosen the blood-brain barrier?", "id": "converted_3187", "sentence1": "Do Crocus sativus antigen extracts loosen the Blood - brain barrier function?", "sentence2": "Crocus sativus antigen antigen Extract Tightens the Blood-Brain Barrier, Reduces Amyloid β Load and Related Toxic effect in 5XFAD Mice., In vitro results showed that Crocus sativus antigen antigen extract increases the Tightness sensation quality of a cell-based Blood - brain barrier function (Blood - brain barrier anatomy) model and enhances transport of Aβ. Further in vivo studies confirmed the effect of Crocus sativus antigen antigen extract (50 mg/kg/day, added to mice diet) on the Blood - brain barrier anatomy Tightness sensation quality and function that was associated with reduced Aβ load and related pathological changes in 5XFAD mice used as an cytarabine/daunorubicin protocol model. Reduced Aβ load could be explained, at least in part, by Crocus sativus antigen antigen extract effect to enhance Aβ clearance pathways including Blood - brain barrier anatomy clearance, enzymatic degradation and ApoE clearance pathway.[SEP]Relations: blood brain barrier has relations: anatomy_anatomy with glial blood brain barrier, anatomy_anatomy with glial blood brain barrier, anatomy_anatomy with glial blood brain barrier, anatomy_anatomy with glial blood brain barrier, anatomy_anatomy with cell layer, anatomy_anatomy with cell layer, anatomy_anatomy with cell layer, anatomy_anatomy with cell layer.", "label": "no"}
{"original_question": "Is Mammaprint approved by the United States Food and Drug Administration?", "id": "converted_1365", "sentence1": "Is Mammaprint approved by the United States Food and Drug Administration?", "sentence2": "an FDA-cleared 70-gene signature of MammaPrint panel , on MammaPrint, the first and only assay for Malignant neoplasm of breast management that has been cleared by the FDA., The MammaPrint assay has the advantages of a 510(k) clearance by the US Food and Drug Administration, a larger gene number which may enhance further utility, and the potentially wider patient eligibility including lymph node-positive, ER-negative, , The MammaPrint assay has the advantages of a 510(k) clearance by the U.S. Food and Drug Administration, a larger gene number, which may enhance further utility, and a potentially wider patient eligibility, including lymph node-positive, estrogen receptor (ER)-negative, and younger patients being accrued into the prospective trial (Microarray in Node-Negative Disease May Avoid Chemotherapy). [SEP]Relations: benign neoplasm of male breast has relations: disease_disease with breast benign neoplasm, disease_disease with breast benign neoplasm.", "label": "yes"}
{"original_question": "Is SATB1 necessary for T-cell maturation?", "id": "converted_3697", "sentence1": "Is DNA-Binding Protein SATB1 necessary for T-cell maturation?", "sentence2": "Special AT-rich binding protein 1 (DNA-Binding Protein DNA-Binding Protein SATB1) Nuclear Proteins, expressed predominantly in T-Lymphocyte, regulates Genes through targeting chromatin remodeling during T-cell maturation., the transcription factor DNA-Binding Protein DNA-Binding Protein SATB1 that regulates the T-cell maturation, DNA-Binding Protein DNA-Binding Protein SATB1 is a transcriptional regulator controlling the gene expression that is essential in the maturation of the immune T-cell. , Special AT-rich sequence binding protein 1 (DNA-Binding Protein DNA-Binding Protein SATB1) regulates gene expression essential in immune T-cell maturation and switching of fetal globin species, by binding to Matrix Attachment Regions (MARS1 gene) of DNA and inducing a local chromatin remodeling. [SEP]Relations: Tat protein binding has relations: molfunc_protein with GABARAPL1, molfunc_protein with GABARAPL1, molfunc_protein with NPM1, molfunc_protein with NPM1, molfunc_protein with SMARCB1, molfunc_protein with SMARCB1, molfunc_protein with DLL1, molfunc_protein with DLL1, molfunc_protein with DNAJA1, molfunc_protein with DNAJA1.", "label": "yes"}
{"original_question": "Has MLE4901 been tested in phase III clinical trials?", "id": "converted_3707", "sentence1": "Has MLE4901 been tested in phase III clinical trials?", "sentence2": "METHODS\n\nThis phase 2, randomised, double-blind, placebo-controlled, single-centre, crossover trial assessed the effectiveness of an oral neurokinin 3 receptor antagonist (MLE4901) on menopausal hot flushes., Neuromedin K Receptor antagonism as a novel treatment for menopausal hot flushes: a phase 2, randomised, double-blind, placebo-controlled trial.[SEP]", "label": "no"}
{"original_question": "Is ADP-ribosylation a PTM?", "id": "converted_2843", "sentence1": "Is ADP-Ribosylation a PTM?", "sentence2": "ADP-Ribosylation is a PTM, in which PARP1 gene use nicotinamide adenine dinucleotide (NAD) (NAD) (NAD+) to modify target proteins with Adenosine Diphosphate Ribose, Poly ADP Ribosylation (PARylation) is a Post-Translational Protein Processing (PTM) that is critically involved in many biological processes that are linked to cell stress responses., ADP-Ribosylation is a post-translational modification (PTM) implicated in several crucial cellular processes, ranging from regulation of DNA repair and chromatin structure to cell metabolism and stress responses.[SEP]Relations: DNA ADP-Ribosylation has relations: bioprocess_protein with PARP2, bioprocess_protein with PARP2, bioprocess_protein with PARP1, bioprocess_protein with PARP1, bioprocess_protein with PARP3, bioprocess_protein with PARP3, bioprocess_bioprocess with DNA modification, bioprocess_bioprocess with DNA modification. regulation of protein ADP-Ribosylation has relations: bioprocess_protein with ADNP, bioprocess_protein with ADNP.", "label": "yes"}
{"original_question": "Is cabozantinib effective for Hepatocellular Carcinoma?", "id": "converted_3031", "sentence1": "Is cabozantinib effective for Liver carcinoma?", "sentence2": "However, clinical trials of nonselective kinase inhibitors with c-Met activity (Tivantinib, cabozantinib, Foretinib, and golvatinib) in patients with altretamine/cisplatin/cyclophosphamide protocol have failed so far to demonstrate significant efficacy. , Rationale for use, clinical trial data, and current recommendations for cabozantinib in Malignant neoplasm of kidney, Malignant neoplasm of thyroid, Malignant neoplasm of prostate, Malignant neoplasm of liver, and Primary malignant neoplasm of lung are detailed in this article., More recently, promising outcomes have also been reported with new agents, such as nivolumab and cabozantinib., Positive results in recent phase III clinical trials have confirmed the high value of anti-angiogenic therapies for altretamine/cisplatin/cyclophosphamide protocol in both first (sorafenib and lenvatinib) and second line (regorafenib and cabozantinib) treatment modalities. , More recently, regorafenib and nivolumab have received approval in the second-line setting after sorafenib, with further positive phase 3 studies emerging in the first line (lenvatinib non-inferior to sorafenib) and second line versus placebo (cabozantinib and ramucirumab). , The rapidly changing treatment landscape due to the emergence of new treatment options (sorafenib and lenvatinib equally effective in first line; regorafenib, cabozantinib, and ramucirumab showing OS benefit in second line with nivolumab approved by the FDA based on response rate) underscores the importance of re-assessing the role of the first approved systemic agent in altretamine/cisplatin/cyclophosphamide protocol, sorafenib., Positive phase III-study data have been published for lenvatinib as first-line and cabozantinib as second-line therapy. , cabozantinib in Patients with Advanced and Progressing Liver carcinoma., BACKGROUND: cabozantinib inhibits Protein Tyrosine Kinase, including vascular endothelial growth factor receptors 1, 2, and 3, MET wt Allele wt Allele, and AXL protein, human protein, human, which are implicated in the progression of hepatocellular carcinoma and the development of resistance to sorafenib, the standard initial treatment for advanced disease. , CONCLUSIONS: Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo., Expert opinion: Based on favorable phase III clinical trial data, sorafenib and lenvatinib are considered promising agents for altretamine/cisplatin/cyclophosphamide protocol as first-line systemic chemotherapy. Moreover, regorafenib and cabozantinib are useful second-line therapies after the failure of sorafenib., CONCLUSIONS: Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo. , cabozantinib in Patients with Advanced and Progressing Liver carcinoma.Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo. , Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo., Median overall survival was 10.2 months with cabozantinib and 8.0 months with placebo (hazard ratio for Cessation of life, 0.76; 95% confidence interval [CI], 0.63 to 0.92; P=0.005). Median progression-free survival was 5.2 months with cabozantinib and 1.9 months with placebo (hazard ratio for disease progression or Cessation of life, 0.44; 95% CI, 0.36 to 0.52; P<0.001), and the objective response rates were 4% and less than 1%, respectively (P=0.009)., The most common high-grade events were Palmar-plantar erythrodysesthesia syndrome (17% with cabozantinib vs. 0% with placebo), Hypertensive disease (16% vs. 2%), increased aspartate aminotransferase level (12% vs. 7%), Fatigue (10% vs. 4%), and Diarrhea (10% vs. 2%).<br><b>CONCLUSIONS</b>: Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo., CONCLUSIONS Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo., CONCLUSIONS The tyrosine kinase inhibitors sorafenib (first line) and regorafenib (second line) have been approved for hepatocellular carcinoma, and the immune checkpoint inhibitor nivolumab obtained conditional approval for sorafenib-experienced patients in the United States., The principal advancements in the treatment of hepatocellular carcinoma (altretamine/cisplatin/cyclophosphamide protocol) are the use of new systemic treatments such as lenvatinib in first-line treatment and regorafenib, cabozantinib and ramucirumab in second-line treatment due to their benefits in terms of overall survival., Recently, a few systemic chemotherapies proved to be effective for advanced stage altretamine/cisplatin/cyclophosphamide protocol in phase III studies: lenvatinib as the first line of therapy, and regorafenib, cabozantinib, and ramucirumab as second-line therapy., <b>BACKGROUND</b>: The approval of the tyrosine kinase inhibitor sorafenib in 2007 marked a milestone in the treatment of hepatocellular carcinoma, as sorafenib was the first systemic therapy to show a survival benefit in patients with Advanced Liver carcinoma., We also elaborate the unmet need of biomarkers to guide treatment decisions and discuss the emerging field of immunotherapy in hepatocellular carcinoma.<br><b>CONCLUSIONS</b>: The tyrosine kinase inhibitors sorafenib (first line) and regorafenib (second line) have been approved for hepatocellular carcinoma, and the immune checkpoint inhibitor nivolumab obtained conditional approval for sorafenib-experienced patients in the United States., cabozantinib in the treatment of hepatocellular carcinoma., The approval of the tyrosine kinase inhibitor sorafenib in 2007 marked a milestone in the treatment of hepatocellular carcinoma, as sorafenib was the first systemic therapy to show a survival benefit in patients with Advanced Liver carcinoma.[SEP]Relations: cabozantinib has relations: drug_drug with Carbamazepine, drug_drug with Carbamazepine, drug_drug with Carbutamide, drug_drug with Carbutamide, drug_drug with Cannabidiol, drug_drug with Cannabidiol, drug_drug with Carbimazole, drug_drug with Carbimazole, drug_drug with Afelimomab, drug_drug with Afelimomab.", "label": "yes"}
{"original_question": "Is it possible to detect survivin protein expression in normal human adult tissues?", "id": "converted_432", "sentence1": "Is it possible to detect survivin protein expression in normal Homo sapiens adult Body tissue?", "sentence2": "BIRC5 protein, Homo sapiens wt Allele (BIRC5 protein, Homo sapiens protein, Homo sapiens) is one of the members of IAP-family apoptosis inhibitors. The BIRCS gene is expressed in most Homo sapiens embryonic Body tissue and Malignant Neoplasms but not in normal differentiated Body tissue of adult Homo sapiens., BIRC5 protein, Homo sapiens wt Allele is an PPP1R1A gene of apoptosis that is undetectable in most terminally differentiated normal Homo sapiens Body tissue, strongly expressed in embryonic and fetal organs and is strongly expressed in many different Homo sapiens cancers., BIRC5 protein, Homo sapiens wt Allele is a member of the PPP1R1A gene apoptosis family that is overexpressed in many malignancies. It has five known alternative splice forms, some of which differ in their antiapoptotic properties and expression levels in Homo sapiens cancers., survivin is usually not expressed in normal adult Body tissue,, AZD 1152-hQPA induced caspase-dependent apoptosis of some Cultured Cell Line, demonstrated by loss of Mitochondrial Membranes potential, activation of caspase-9, followed by activation of caspase-3. This effect was accompanied by the inhibition of survivin expression. In vivo efficacy was determined in NOD/SCID/γc(null) mice implanted with the Ramos Homo sapiens Burkitt Lymphoma cell line. AZD 1152 had anti-tumour effects in this Mus xenograft model. There preclinical data suggest that the inhibition of Aurora Kinase B is a potentially useful therapeutic strategy in Burkitt Lymphoma and Hodgkin Disease., a novel antiapoptosis gene, i.e., survivin, was identified as a structurally unique member of the PPP1R1A gene of apoptosis protein family. BIRC5 protein, Homo sapiens wt Allele expression is turned off during fetal development and not found in non-neoplastic adult Homo sapiens Body tissue but is again turned on in the most common Homo sapiens cancers. The antiapoptotic properties of survivin might provide a significant growth advantage in Neoplasms and possibly also contribute to chemoresistance of Primary malignant neoplasm., Further comparison of the distribution of SPDEF wt Allele with other widely recognized Primary malignant neoplasm-associated molecules showed that SPDEF wt Allele has more restricted distributions than Oncogene ErbB2, BCL2 gene, survivin or Telomerase in cDNA Library from normal Homo sapiens Body tissue and more increased distribution than Oncogene ErbB2, CA-125 Antigen Antigen, BCL2 gene, survivin and Telomerase in cDNA Library from Head>Brain (except survivin), Breast, Chest>Lung and ovarian neoplasm. These data together show a better tumor-association for SPDEF wt Allele and suggest that SPDEF wt Allele is a more suitable target for developing specific Primary malignant neoplasm therapies., we identified decreased FHIT protein, Homo sapiens protein, Homo sapiens expression resulting in apoptosis inhibition and decreasing apoptosis associated with abnormal levels of some pro- and Apoptosis Inhibiting Proteins (BAX protein, Homo sapiens, BCL2 gene and BIRC5 protein, Homo sapiens wt Allele) by TUNEL and Thrombotic Microangiopathies. Our results demonstrated that the Mutation Abnormality in the FHIT protein, Homo sapiens protein, Homo sapiens gene significantly reduced FHIT protein, Homo sapiens protein, Homo sapiens expression in Homo sapiens CRC. Both TUNEL and Thrombotic Microangiopathies experiments demonstrated significantly inhibited apoptosis by down-regulation of BAX protein, Homo sapiens and up-regulation of BIRC5 protein, Homo sapiens wt Allele and BCL2 gene. Collectively, these studies identify the mechanism by which an important Tumor Suppressor Genes, FHIT protein, Homo sapiens protein, Homo sapiens, inactivated specifically in Homo sapiens CRC, and contributes to our understanding of the mechanism of colorectal carcinogenesis.[SEP]Relations: PPP1R1A has relations: anatomy_protein_present with adult mammalian kidney, anatomy_protein_present with adult mammalian kidney, anatomy_protein_present with adipose tissue, anatomy_protein_present with adipose tissue, anatomy_protein_present with muscle tissue, anatomy_protein_present with muscle tissue, anatomy_protein_present with blood, anatomy_protein_present with blood. Breast has relations: anatomy_protein_present with VIM, anatomy_protein_present with VIM.", "label": "no"}
{"original_question": "Does a comet assay measure radiation induced mutations?", "id": "converted_4221", "sentence1": "Does a comet assay measure radiation induced mutations?", "sentence2": "Evaluation of primary DNA-damage is one way to identify potential genotoxic agents and for this purpose the Comet assay has, for the last decades, been used to monitor DNA single strand and double strand breaks in individual Cells, DNA strand-break frequency was examined by means of the comet assay i, . The comet assay (as this method was subsequently named) was able to measure, for the first time, the fraction of radiobiologically hypoxic Cells in Mus sp. and Homo sapiens Neoplasms. It was used to determine that the rate of rejoining of DNA breaks was relatively homogenous within an irradiated population of Cells, The comet assay is frequently used to measure DNA damage in individual Cells. , Thus a complete repair of DNA damage induced by gamma-irradiation and measurable by the Comet assay was observed, whereas the yield of somatic mutations increased in relation to the radiation dose., xanthi) mutagenicity assay is the ability to analyze and compare on the same Plants under identical treatment conditions both the induced acute DNA damage in Diploid Cell as measured by the Comet assay and the yield of induced Concept Generality - Leaf somatic mutations., The present study reveals that gamma radiation induces single strand breaks in DNA as measured by alkaline comet assay in bivalves and comet assay serves as a sensitive and rapid method to detect genotoxicity of gamma radiation., The present study is aimed (a) to know the genotoxic effect of gamma radiation on aquatic fauna employing two species of selected bivalves, (b) to evaluate the possible use of 'Comet assay' for detecting genetic damage in haemocytes of bivalves as a biomarker for environmental biomonitoring and also (c) to compare the relative sensitivity of two species of bivalves viz., The single cell gel electrophoresis (SCGE) assay, more commonly known as the comet assay, due to the \"comet-like\" appearance of the Cells, was originally developed as a technique to measure the presence of DNA single-strand breaks., BACKGROUND: The neutral comet assay was devised to measure double-stranded DNA breaks, but it has also been used to measure apoptosis based on its characteristic DNA fragmentation patterns., 2, 4, 6, 8 and 10 Gy) of gamma radiation and their genotoxic effects on the haemocytes were studied using the comet assay., PURPOSE: The Deoxyribonucleic Acid (DNA) Comet assay, being a quick, simple, sensitive, reliable and fairly inexpensive method for measuring DNA strand breaks, has been used to assess DNA damage caused by gamma radiation in developmental stages of maize weevil Sitophilus zeamais Motschulsky., This paper attempts a correlation between the induction and repair of DNA damage measured in the comet assay and the clinical observed reaction in order to evaluate the suitability of the comet assay for prediction of radiation sensitivity., gle cell gel electrophoresis (e.g., Comet Assay) and immunofluoresence microscopy to detect the presence of Phosphorylated Histone H2AX foci, we find that Cr[VI] induces DNA double-strand breaks similar to ionizing radiation (IR). We also demo, ir of DNA damage induced by gamma-irradiation and measurable by the Comet assay was observed, whereas the yield of somatic mutations increased in relation to the radiation dose. Data on the kinetic, eased yield of somatic mutations was highly correlated (r = 0.996) with the increased DNA damage measured by the Comet assay immediately after irradiation. With inc, rther assess potential co-mutagenic effects of doxorubicin/fluorouracil protocol, we exposed A549 Homo sapiens lung Cells to doxorubicin/fluorouracil protocol in combination with various Mutagens and measured the induction and removal of DNA damage by the comet assay and the production of chromosomal mutation by the cytokinesis-block micronucleus assay (CBMN assay). The , DNA effects were analysed in Specimen Source Codes - Leukocytes using the alkaline Comet assay, Gene Mutation and Chromosome Aberrations were measured in Specimen Source Codes - Erythrocytes using the flow cytometric Pig-a gene mutation assay and the micronucleus test (applying both microscopic and flow cytometric evaluation), respectively., A wide variety of Mutagens have been shown to cause DNA alterations detectable with the comet assay, but it is not yet clear whether a relationship exists between the DNA effects and the induction of mutations., The transgenerational changes in mutation rates were attributed to the presence of a persistent subset of endogenous DNA lesions (double- and single-strand breaks), measured by the phosphorylated form of H2AX protein, Homo sapiens (Phosphorylated Histone H2AX) and alkaline Comet assays., The single-cell electrophoresis (comet) assay is an established method for measuring radiation-induced strand breaks in DNA., The COMET assay is recognized as a rapid and sensitive method in quantifying radiation induced DNA damage., The relationship between cellular radiosensitivity and radiation-induced DNA damage measured by the comet assay., Reliable Comet assay measurements for detecting DNA damage induced by ionising radiation and Chemicals., Radiation sensitivity of Specimen Source Codes - Lymphocytes from healthy individuals and Primary malignant neoplasm patients as measured by the comet assay., The comet assay is a potential tool for use in neutron therapy, as well as a method for the rapid screening of samples from individuals accidentally exposed to radiation., Induction and repair of DNA damage as measured by the Comet assay and the yield of somatic mutations in gamma-irradiated tobacco seedlings., The increased yield of somatic mutations was highly correlated (r = 0.996) with the increased DNA damage measured by the Comet assay immediately after irradiation., The alkaline version of single cell gel electrophoresis (comet) assay is widely used for evaluating DNA damage at the individual cell level., Induction (2 and 5 Gy) of gamma-ray-induced DNA damage and its repair (during 60 min after irradiation) was measured with the alkaline and neutral comet assay., The alkaline single-cell gel electrophoresis (SCGE or Comet) assay appears to be a promising tool for measuring DNA damage at the individual cell level in both in vitro and in vivo studies., Considering our previous studies showing significant increases in the frequency of cytogenetic damage (when measured as Micronucleus - abnormality) in patients treated with relatively low doses of 131I, the results obtained in the present work by using the Comet assay could indicate that 1 week after the exposure most of the radioiodine-induced DNA lesions, that can be detected with this assay, have already been repaired., Hence, we are using the single-cell gel electrophoresis (comet assay) to detect Mus sp. mutants that display a genetic susceptibility to ionizing radiation., We have established the analysis parameters in the comet assay which are currently used to detect radiation-sensitive Mus sp. mutants and to control the variance within the Mus sp. population in the ENU screen., Comet assay as a tool to screen for Mus sp. models with inherited radiation sensitivity.[SEP]Relations: Protein S Homo sapiens has relations: drug_drug with Azithromycin, drug_drug with Azithromycin, drug_drug with Triptolide, drug_drug with Triptolide, drug_drug with Bamet-UD2, drug_drug with Bamet-UD2, drug_drug with Arsenic trioxide, drug_drug with Arsenic trioxide, drug_drug with Trastuzumab emtansine, drug_drug with Trastuzumab emtansine.", "label": "yes"}
{"original_question": "Is Lasmiditan effective for migraine?", "id": "converted_3035", "sentence1": "Is Lasmiditan effective for Migraine Disorders?", "sentence2": "Amongst the ditans, lasmiditan: (i) fails to constrict Homo sapiens coronary arteries; and (ii) is effective for the acute treatment of Migraine Disorders in preliminary Phase III clinical trials., Although ongoing phase III clinical trials are needed to confirm its efficacy and safety, lasmiditan might offer an alternative to treat acute Migraine Disorders with no associated Cardiovascular system risk., Lasmiditan is considered to be the first member of a new drug category, the neurally acting anti-Migraine Disorders agent (NAAMA), Lasmiditan for the treatment of acute Migraine Disorders: a review and potential role in clinical practice., Lasmiditan, a highly selective HTR1F gene Agonist, has completed two Phase III randomized, double blind, placebo-controlled clinical trials, with a third - a long-term, open-label safety study - still underway. Research to date suggests lasmiditan lacks vasoconstrictive properties and may be a safe and effective treatment option in patients refractory to current acute Migraine Disorders medications or who have Cardiovascular system risk factors., Lasmiditan is an effective acute treatment for Migraine Disorders: A phase 3 randomized study., Compared with placebo, more patients dosed with lasmiditan 200 mg were free of headache pain at 2 hours after dosing (32.2% vs 15.3%; odds ratio [OR] 2.6, 95% confidence interval [CI] 2.0-3.6, p< 0.001), similar to those dosed with lasmiditan 100 mg (28.2%; OR 2.2, 95% CI 1.6-3.0, p< 0.001). Furthermore, compared with those dosed with placebo, more patients dosed with lasmiditan 200 mg (40.7% vs 29.5%; OR 1.6, 95% CI 1.3-2.1, p< 0.001) and lasmiditan 100 mg (40.9%; OR 1.7, 95% CI, 1.3-2.2, p< 0.001) were free of their N-oxydiethylene-2-benzothiazole sulfenamide at 2 hours after dosing., CONCLUSIONS: Lasmiditan dosed at 200 and 100 mg was efficacious and well tolerated in the treatment of acute Migraine Disorders among patients with a high level of Cardiovascular system risk factors, CLASSIFICATION OF EVIDENCE: This study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class I evidence that for adult patients with Migraine Disorders, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a Migraine Disorders attack., For the understanding of Migraine Disorders pathophysiology, it is very important to note that a selective 5-HT(1F) receptor Agonist like lasmiditan is effective in the acute treatment of Migraine Disorders. , While lasmiditan most likely is effective in the treatment of Migraine Disorders attacks it had, unfortunately, a high incidence of Central Nervous System related Scanning Auger Spectrometer (device) in the oral RCT. , Acute treatment of Migraine Disorders with the selective serotonin 1F receptor Agonist lasmiditan--a randomised proof-of-concept trial.At intravenous doses of 20 mg and higher, lasmiditan proved effective in the acute treatment of Migraine Disorders. , Lasmiditan for the treatment of acute Migraine Disorders: a review and potential role in clinical practice. , BACKGROUND\nLasmiditan (COL-144) is a novel, centrally acting, highly selective 5-HT(1F) receptor Agonist without vasoconstrictor activity that seemed effective when given as an intravenous infusion in a proof-of-concept Migraine Disorders study., INTERPRETATION\nOral lasmiditan seems to be safe and effective in the acute treatment of Migraine Disorders., The serotonin 1F receptor Agonist lasmiditan, a drug acting through non-vasoconstrictive mechanisms, represents a promising safe, effective and tolerated acute Migraine Disorders therapy also for patients at Cardiovascular system risk., For the understanding of Migraine Disorders pathophysiology, it is very important to note that a selective 5-HT(1F) receptor Agonist like lasmiditan is effective in the acute treatment of Migraine Disorders., The serotonin 1F receptor Agonist lasmiditan as a potential treatment of Migraine Disorders attacks: a review of two placebo-controlled phase II trials., Within the past few years, new and promising drugs such as more specific 5-HT 1F receptor agonists (that is, lasmiditan) and monoclonal calcitonin gene-related peptide (Calcitonin Gene-Related Peptide) receptor Antibodies, in vitro diagnostic entered advanced development phases while non-invasive neuromodulatory approaches were suggested to be potentially effective as non-pharmaceutical interventions for Migraine Disorders., CLASSIFICATION OF EVIDENCE\nThis study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class I evidence that for adult patients with Migraine Disorders, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a Migraine Disorders attack., BACKGROUND Lasmiditan (COL-144) is a novel, centrally acting, highly selective 5-HT(1F) receptor Agonist without vasoconstrictor activity that seemed effective when given as an intravenous infusion in a proof-of-concept Migraine Disorders study., INTERPRETATION Oral lasmiditan seems to be safe and effective in the acute treatment of Migraine Disorders., Research to date suggests lasmiditan lacks vasoconstrictive properties and may be a safe and effective treatment option in patients refractory to current acute Migraine Disorders medications or who have Cardiovascular system risk factors., The non-vascular, neural mechanism of action of lasmiditan may offer an alternative means to treat Migraine Disorders especially in patients who have contra-indications for agents with vasoconstrictor activity., Compared with placebo, more patients dosed with lasmiditan 200 mg were free of headache pain at 2 hours after dosing (32.2% vs 15.3%; odds ratio [OR] 2.6, 95% confidence interval [CI] 2.0-3.6, <br><b>CONCLUSIONS</b>: Lasmiditan dosed at 200 and 100 mg was efficacious and well tolerated in the treatment of acute Migraine Disorders among patients with a high level of Cardiovascular system risk factors.<br><b>CLINICALTRIALSGOV IDENTIFIER</b>: NCT02439320.<br><b>CLASSIFICATION OF EVIDENCE</b>: This study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class I evidence that for adult patients with Migraine Disorders, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a Migraine Disorders attack.<br>, The most common adverse events were Central Nervous System related and included dizziness, Fatigue, Vertigo <invertebrate>, Has tingling sensation, and somnolence.<br><b>INTERPRETATION</b>: Oral lasmiditan seems to be safe and effective in the acute treatment of Migraine Disorders., No dizziness, Paresthesia and sensations of heaviness (usually limb) were more common on lasmiditan.<br><b>CONCLUSIONS</b>: At intravenous doses of 20 mg and higher, lasmiditan proved effective in the acute treatment of Migraine Disorders., <b>BACKGROUND</b>: Lasmiditan (COL-144) is a novel, centrally acting, highly selective 5-HT(1F) receptor Agonist without vasoconstrictor activity that seemed effective when given as an intravenous infusion in a proof-of-concept Migraine Disorders study., For the understanding of Migraine Disorders pathophysiology, it is very important to note that a selective 5-HT(1F) receptor Agonist like lasmiditan is effective in the acute treatment of Migraine Disorders., This study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class I evidence that for adult patients with Migraine Disorders, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a Migraine Disorders attack., While lasmiditan most likely is effective in the treatment of Migraine Disorders attacks it had, unfortunately, a high incidence of Central Nervous System related Scanning Auger Spectrometer (device) in the oral RCT.[SEP]Relations: Lasmiditan has relations: drug_drug with Fendiline, drug_drug with Fendiline, drug_drug with Hypericin, drug_drug with Hypericin, drug_drug with Benzoctamine, drug_drug with Benzoctamine, drug_drug with Fimasartan, drug_drug with Fimasartan, drug_drug with Methadone, drug_drug with Methadone.", "label": "yes"}
{"original_question": "Is EZH2 associated with prostate cancer?", "id": "converted_1231", "sentence1": "Is ezh2 protein, Homo sapiens associated with Pelvis>Prostate Primary malignant neoplasm?", "sentence2": "The role of ezh2 protein, Homo sapiens in the regulation of the activity of matrix metalloproteinases in Pelvis>Prostate Primary malignant neoplasm cells, ezh2 protein, Homo sapiens plays an active role in this process by repressing the expression of TIMP2 Genes Genes and TIMP3 Genes Genes in Pelvis>Prostate Primary malignant neoplasm cells, The TIMP genes are derepressed by knockdown of ezh2 protein, Homo sapiens expression in Homo sapiens Pelvis>Prostate Primary malignant neoplasm cells but repressed by overexpression of ezh2 protein, Homo sapiens in benign Homo sapiens Pelvis>Prostate epithelial cells., Overexpression of ezh2 protein, Homo sapiens confers an invasive phenotype on benign Pelvis>Prostate epithelial cells, ezh2 protein, Homo sapiens knockdown markedly reduces the proteolytic activity of Matrix Metalloproteinase 9, thereby decreasing the invasive activity of Pelvis>Prostate Primary malignant neoplasm cells, he transcriptional repression of the TIMP genes by ezh2 protein, Homo sapiens may be a major mechanism to shift the MMPs/TIMPs balance in favor of Matrix Metalloproteinases activity and thus to promote MMRN1 wt Allele degradation and subsequent invasion of Pelvis>Prostate Primary malignant neoplasm cells., Expression levels of the novel Specimen Source Codes - Specimen Source Codes - tumor and metastasis suppressor Raf-1 kinase inhibitor protein (PEBP1 Genes) have been shown to correlate negatively with those of ezh2 protein, Homo sapiens in Breast and Pelvis>Prostate Cultured Cell Line as well as in clinical Primary malignant neoplasm tissues, Polycomb protein ezh2 protein, Homo sapiens regulates Specimen Source Codes - Specimen Source Codes - tumor invasion via the transcriptional repression of the metastasis suppressor PEBP1 Genes in Breast and Pelvis>Prostate Primary malignant neoplasm, Enhancer of transcription of transcription of zeste homolog 2 (ezh2 protein, Homo sapiens), which encodes the histone methyltransferase component of the polycomb repressive complex 2 (Polycomb Repressive Complex 2), is overexpressed widely in Breast and Pelvis>Prostate Malignant Neoplasms and epigenetically silences Specimen Source Codes - Tumor Suppressor Genes, However, the roles and underlying mechanisms of ezh2 protein, Homo sapiens in Pelvis>Prostate Primary malignant neoplasm stem cells (PCSCs) remain unknown, c-myc Genes, ezh2 protein, Homo sapiens and p27 Enzyme Inhibitor Enzyme Inhibitor were defined to modulate the behavior of Pelvis>Prostate Primary malignant neoplasm with pro-tumoral or anti-tumoral effects and had ability in predicting Pelvis>Prostate Primary malignant neoplasm progression, but the research of their co-expression value of prognosis is rarely, Composite index of c-myc Genes, ezh2 protein, Homo sapiens, and p27 Enzyme Inhibitor Enzyme Inhibitor can be valued as powerful prognosis parameter for intermediate-risk Pelvis>Prostate Primary malignant neoplasm patients after the surgery, and postoperative adjuvant therapy can be adopted accordingly., ezh2 protein, Homo sapiens, an epigenetic driver of Pelvis>Prostate Primary malignant neoplasm., The histone methyltransferase ezh2 protein, Homo sapiens has been in the limelight of the field of Primary malignant neoplasm epigenetics for a decade now since it was first discovered to exhibit an elevated expression in metastatic Pelvis>Prostate Primary malignant neoplasm, a comprehensive overview of ezh2 protein, Homo sapiens in the context of Pelvis>Prostate Primary malignant neoplasm, ezh2 protein, Homo sapiens dependent Histone H3 Trimethyl Lys28 is involved in epigenetic silencing of ID4 protein, Homo sapiens protein, Homo sapiens in Pelvis>Prostate Primary malignant neoplasm, ChIP data on Pelvis>Prostate Primary malignant neoplasm tissue specimens and Cultured Cell Line suggested ezh2 protein, Homo sapiens occupancy and H3K27Me3 marks on the ID4 protein, Homo sapiens protein, Homo sapiens promoter, Collectively, our data indicate a Polycomb Repressive Complex 2 dependent mechanism in ID4 protein, Homo sapiens protein, Homo sapiens promoter silencing in Pelvis>Prostate Primary malignant neoplasm through recruitment of ezh2 protein, Homo sapiens and a corresponding increase in H3K27Me3. Increased ezh2 protein, Homo sapiens but decreased ID4 protein, Homo sapiens protein, Homo sapiens expression in Pelvis>Prostate Primary malignant neoplasm strongly supports this model., The histone methyltransferase enhancer of zeste homolog 2 (ezh2 protein, Homo sapiens) has recently attracted considerable attention because of its dysregulation in Pelvis>Prostate Primary malignant neoplasm (Patient-Controlled Analgesia) and its important function in Patient-Controlled Analgesia development. , Autoregulatory feedback loop of ezh2 protein, Homo sapiens/miR-200c/E2F3 as a driving force for Pelvis>Prostate Primary malignant neoplasm development, Amounts of both ezh2 protein, Homo sapiens messenger RNA and ezh2 protein, Homo sapiens protein are increased in metastatic Pelvis>Prostate Primary malignant neoplasm; in addition, clinically localized Pelvis>Prostate Malignant Neoplasms that express higher concentrations of ezh2 protein, Homo sapiens show a poorer prognosis., The data show that amplification of the ezh2 protein, Homo sapiens Genes is rare in early Pelvis>Prostate Primary malignant neoplasm, whereas a fraction of late-stage tumors contains the Genes amplification leading to the overexpression of the Genes, thus indicating the importance of ezh2 protein, Homo sapiens in the progression of Pelvis>Prostate Primary malignant neoplasm., ezh2 protein, Homo sapiens expression in Pelvis>Prostate Primary malignant neoplasm correlates with progression to hormone-refractory and metastatic disease, but it is unknown whether ezh2 protein, Homo sapiens plays a specific role in the acquisition of an advanced Pelvis>Prostate Primary malignant neoplasm phenotype., Although prior studies in Pelvis>Prostate Primary malignant neoplasm have revealed a number of possible mechanisms of ezh2 protein, Homo sapiens upregulation, these changes cannot account for the overexpression ezh2 protein, Homo sapiens in many primary Pelvis>Prostate Malignant Neoplasms, nor in most cases of high grade Prostatic Intraepithelial Neoplasias., As a result, five ezh2 protein, Homo sapiens peptides recognized by immunoglobulin G (ezh2 protein, Homo sapiens 120-128, ezh2 protein, Homo sapiens 165-174, ezh2 protein, Homo sapiens 569-577, ezh2 protein, Homo sapiens 665-674, and ezh2 protein, Homo sapiens 699-708) were frequently detected in the plasma of Pelvis>Prostate Primary malignant neoplasm patients., Thus, dysregulated expression of ezh2 protein, Homo sapiens may be involved in the progression of Pelvis>Prostate Primary malignant neoplasm, as well as being a marker that distinguishes indolent Pelvis>Prostate Primary malignant neoplasm from those at risk of lethal progression., These results link two major pathways in Pelvis>Prostate Primary malignant neoplasm by providing two additional and complementary Myc-regulated mechanisms by which ezh2 protein, Homo sapiens upregulation occurs and is enforced during prostatic carcinogenesis., ezh2 protein, Homo sapiens promotes Pelvis>Prostate Primary malignant neoplasm cell proliferation and invasiveness., ezh2 protein, Homo sapiens promotes proliferation and invasiveness of Pelvis>Prostate Primary malignant neoplasm cells., The Polycomb Group protein ezh2 protein, Homo sapiens is implicated in Pelvis>Prostate Primary malignant neoplasm progression., The polycomb group protein ezh2 protein, Homo sapiens is involved in progression of Pelvis>Prostate Primary malignant neoplasm., Mutation screen and association study of ezh2 protein, Homo sapiens as a susceptibility Genes for aggressive Pelvis>Prostate Primary malignant neoplasm., Expression changes in ezh2 protein, Homo sapiens, but not in BMI-1, Sirtuin 1, DNMT1 wt Allele wt Allele or DNMT3B protein, Homo sapiens protein, Homo sapiens are associated with DNA methylation changes in Pelvis>Prostate Primary malignant neoplasm., The Genes for polycomb group protein enhancer of zeste homolog 2 (ezh2 protein, Homo sapiens) is amplified in late-stage Pelvis>Prostate Primary malignant neoplasm., Enhancer of transcription of transcription of zeste homolog 2 (ezh2 protein, Homo sapiens), a kind of Transcription Repressor/Corepressor, is reportedly over-expressed in metastatic Pelvis>Prostate Primary malignant neoplasm., IgGs reactive to three ezh2 protein, Homo sapiens peptides (ezh2 protein, Homo sapiens-243 to -252, ezh2 protein, Homo sapiens-291 to -299, and ezh2 protein, Homo sapiens-735 to -;742) were detected in the plasma of almost half of Pelvis>Prostate Primary malignant neoplasm patients., Amounts of both ezh2 protein, Homo sapiens messenger RNA and ezh2 protein, Homo sapiens protein are increased in metastatic Pelvis>Prostate Primary malignant neoplasm; in addition, clinically localized Pelvis>Prostate Malignant Neoplasms that express higher concentrations of ezh2 protein, Homo sapiens show a poorer prognosis., Overexpression of ezh2 protein, Homo sapiens has been associated with the invasion and progression of malignant Malignant Neoplasms, especially with the progression of Pelvis>Prostate Primary malignant neoplasm., Antigens overexpressed in metastatic Pelvis>Prostate Primary malignant neoplasm are appropriate targets in anti-Primary malignant neoplasm immunotherapy, and one candidate is the polycomb group protein enhancer of zeste homolog 2 (ezh2 protein, Homo sapiens).,  Cytoplasmic ezh2 protein, Homo sapiens is expressed at low levels in benign Pelvis>Prostate epithelial cells and over-expressed in Pelvis>Prostate Primary malignant neoplasm cells. Cytoplasmic ezh2 protein, Homo sapiens expression levels correlate with nuclear ezh2 protein, Homo sapiens expression in Pelvis>Prostate Primary malignant neoplasm samples., DNMT1 wt Allele wt Allele or DNMT3B protein, Homo sapiens protein, Homo sapiens are associated with DNA methylation changes in Pelvis>Prostate Primary malignant neoplasm., ezh2 protein, Homo sapiens:CDH1 wt Allele status was statistically significantly associated with Pelvis>Prostate Primary malignant neoplasm recurrence in a training set of 103 patients (relative risk [RR] = 2.52,, a positive ezh2 protein, Homo sapiens:CDH1 wt Allele status) was the biomarker combination that was most strongly associated with the recurrence of Pelvis>Prostate Primary malignant neoplasm., PcG Proteins ezh2 protein, Homo sapiens, BMI1 protein, Homo sapiens protein, Homo sapiens, and RING1 Genes Genes are associated with adverse pathologic features and clinical Prostate-Specific Antigen recurrence of Pelvis>Prostate Primary malignant neoplasm., Immunohistochemistry results were evaluated in conjunction with clinical parameters associated with Pelvis>Prostate Primary malignant neoplasm progression,, Elevation of the chromatin repression factor enhancer of zeste homolog (ezh2 protein, Homo sapiens) is associated with progression and poor prognosis in several Homo sapiens Malignant Neoplasms including Pelvis>Prostate Primary malignant neoplasm., Various Proteins (α2-integrin, α6-integrin, Proto-Oncogene Protein c-kit, Prominin-1, Homo sapiens, ezh2 protein, Homo sapiens, OCT3/4) are associated with a Pelvis>Prostate Primary malignant neoplasm stem cell phenotype in Cultured Cell Line and Xenograft type of graft., Increased expression of ezh2 protein, Homo sapiens has been associated previously with invasive growth and aggressive clinical behavior in Pelvis>Prostate and Breast Primary malignant neoplasm,, ezh2 protein, Homo sapiens:CDH1 wt Allele status was statistically significantly associated with Pelvis>Prostate Primary malignant neoplasm recurrence after radical prostatectomy and may be useful in defining a cohort of high-risk patients., Immunohistochemistry results were evaluated in conjunction with clinical parameters associated with Pelvis>Prostate Primary malignant neoplasm progression, including Specimen Source Codes - Specimen Source Codes - tumor stage, Gleason score, and kallikrein-related peptidase 3, Homo sapiens (Prostate-Specific Antigen) level., ezh2 protein, Homo sapiens expression is associated with high proliferation rate and aggressive Specimen Source Codes - Specimen Source Codes - tumor subgroups in Cutaneous Melanoma and Malignant Neoplasms of the endometrium, Pelvis>Prostate, and Breast., Moderate or strong expression of ezh2 protein, Homo sapiens coupled with at most moderate expression of CDH1 wt Allele (i.e., a positive ezh2 protein, Homo sapiens:CDH1 wt Allele status) was the biomarker combination that was most strongly associated with the recurrence of Pelvis>Prostate Primary malignant neoplasm., Cytoplasmic ezh2 protein, Homo sapiens expression levels correlate with nuclear ezh2 protein, Homo sapiens expression in Pelvis>Prostate Primary malignant neoplasm samples.[SEP]Relations: ezh2 protein, Homo sapiens has relations: disease_protein with Pelvis>Prostate Primary malignant neoplasm, disease_protein with Pelvis>Prostate Primary malignant neoplasm, disease_protein with Pelvis>Prostate carcinoma, disease_protein with Pelvis>Prostate carcinoma, disease_protein with Breast Primary malignant neoplasm, disease_protein with Breast Primary malignant neoplasm, disease_protein with familial Pelvis>Prostate carcinoma, disease_protein with familial Pelvis>Prostate carcinoma, anatomy_protein_present with Pelvis>Prostate gland, anatomy_protein_present with Pelvis>Prostate gland.", "label": "yes"}
{"original_question": "Is the Histidine-Rich Calcium Binding protein (HRC) related to arrhythmias and cardiac disease?", "id": "converted_1623", "sentence1": "Is the Histidine-Rich Calcium Binding protein (HRC) related to arrhythmias and cardiac disease?", "sentence2": "A Homo sapiens Genetic Variant (Ser96Ala) in the Sarcoplasmic Reticulum (SNCG wt Allele) histidine-rich Ca(2+)-binding (HRC) protein has been linked to ventricular arrhythmia and Sudden death in Cardiomyopathy, Dilated. , These findings suggest that aberrant SNCG wt Allele Ca2+ release and increased susceptibility to delayed afterdepolarizations underlie triggered arrhythmic activity in Homo sapiens Ala96 HRC carriers., The histidine-rich CALCIUM SUPPLEMENTS binding protein (HRC) Ser96Ala Genetic Polymorphism was shown to correlate with Ventricular arrhythmia and Sudden death only in Cardiomyopathy, Dilated patients but not in healthy Homo sapiens carriers., These findings indicate that the HRC Ser96Ala Variant increases the propensity of arrhythmogenic Ca(2+) waves in the stressed failing Chest>Heart, suggesting a link between this Genetic Variant and life-threatening Ventricular arrhythmia in Homo sapiens carriers., HRC plays an important role in Muscle Cells differentiation and in antiapoptotic cardioprotection against ischemia/reperfusion induced cardiac injury. Interestingly, HRC has been linked with familiar cardiac conduction disease and an HRC Genetic Polymorphism was shown to associate with malignant Ventricular arrhythmia in the background of idiopathic Cardiomyopathy, Dilated., This review summarizes studies, which have established the critical role of HRC in Ca(2+)-homeostasis, suggesting its importance in cardiac physiology and pathophysiology., HRC is a SNCG wt Allele luminal Ca(2+) binding protein known to associate with both TRDN gene and the Sarcoplasmic Reticulum Ca(2+)-ATPase, and may thus mediate the crosstalk between SNCG wt Allele Ca(2+) uptake and release. Indeed, evidence from Genetic models of JCN and HRC indicate that they are important in cardiophysiology as alterations in these Proteins affect SNCG wt Allele Ca(2+) handling and cardiac function. In addition, downregulation of JCN and HRC may contribute to Ca(2+) cycling perturbations manifest in the failing Chest>Heart, where their protein levels are significantly reduced., The Ser96Ala Genetic Variant of HRC is associated with life-threatening Ventricular arrhythmia in idiopathic 3',5'-dichloromethotrexate and may serve as an independent predictor of susceptibility to arrhythmogenesis in the setting of 3',5'-dichloromethotrexate., AAV-mediated knock-down of HRC exacerbates Aortic arch structure constriction-induced Congestive Chest>Heart failure., Chronic overexpression of HRC that may disrupt Protoplasm Ca(2+) homeostasis is implicated in pathogenesis of Cardiac Hypertrophy, Ablation of HRC showed relatively normal phenotypes under basal condition, but exhibited a significantly increased susceptibility to isoproterenol-induced Cardiac Hypertrophy, Our results present evidence that down-regulation of HRC could deteriorate cardiac function in TAC-FH through perturbed SNCG wt Allele-mediated Ca(2+) cycling, However, AAV9-mediated HRC-KD in TAC-FH was associated with decreased fractional shortening and increased cardiac fibrosis compared with control., Histidine-rich CALCIUM SUPPLEMENTS binding protein (HRC) is a high capacity, low affinity Ca(2+) binding protein, specifically expressed in striated muscles of Mammals. In rabbit allergenic extract allergenic extract skeletal and Myocardium, HRC binds to Sarcoplasmic Reticulum (SNCG wt Allele) membranes via TRDN gene, a junctional SNCG wt Allele protein. Recently, a potential role in Congestive Chest>Heart failure and arrhythmogenesis has been assigned to HRC due to its activity as regulator of SNCG wt Allele Ca(2+) uptake and Ca(2+) release., In addition, HRC null mice displayed a significantly exaggerated response to the induction of Cardiac Hypertrophy by isoproterenol compared to their wild-type littermates. The exaggerated response of HRC knockout mice to the induction of Cardiac Hypertrophy is consistent with a regulatory role for HRCBP in CALCIUM SUPPLEMENTS handling in vivo and suggests that Gene Mutation in HRC, in combination with other Genetic or environmental factors, might contribute to pathological hypertrophy and Congestive Chest>Heart failure., We observed that the levels of HRC were reduced in animal models and Homo sapiens Congestive Chest>Heart failure., Collectively, these data indicate that alterations in expression levels of HRC are associated with impaired cardiac SNCG wt Allele Ca homeostasis and contractile function., Abnormal CALCIUM SUPPLEMENTS cycling and Cardiac Arrhythmia associated with the Homo sapiens Ser96Ala Genetic Variant of histidine-rich CALCIUM SUPPLEMENTS-binding protein., The Ser96Ala Variant in histidine-rich CALCIUM SUPPLEMENTS-binding protein is associated with life-threatening Ventricular arrhythmia in idiopathic Cardiomyopathy, Dilated., Interestingly, HRC has been linked with familiar cardiac conduction disease and an HRC Genetic Polymorphism was shown to associate with malignant Ventricular arrhythmia in the background of idiopathic Cardiomyopathy, Dilated[SEP]Relations: myocardium has relations: anatomy_protein_present with HRC, anatomy_protein_present with HRC, anatomy_protein_present with HRAS, anatomy_protein_present with HRAS, anatomy_protein_present with MRC1, anatomy_protein_present with MRC1. Arrhythmia has relations: disease_phenotype_positive with HEC syndrome, disease_phenotype_positive with HEC syndrome, disease_phenotype_positive with mitochondrial trifunctional protein deficiency, disease_phenotype_positive with mitochondrial trifunctional protein deficiency.", "label": "yes"}
{"original_question": "Does GC content vary markedly within a given isochore?", "id": "converted_766", "sentence1": "Does GC content vary markedly within a given isochore?", "sentence2": "The isochore, a large DNA Sequence - ParameterizedDataType with relatively small GC variance, is one of the most important structures in eukaryotic genomes., Isochores are large regions of relatively homogeneous nucleotide composition, Vertebrate genomes are comprised of isochores that are relatively long (>100 kb) regions with a relatively homogenous (either GC-rich or AT-rich) base composition and with rather sharp boundaries with neighboring isochores., The human genome is composed of large Sequence - ParameterizedDataType segments with fairly homogeneous GC content, namely isochores, Isochores, i.e. Spastic syndrome of DNA with a distinct Sequence - ParameterizedDataType composition and thus a specific GC content, The human genome is composed of long Spastic syndrome of DNA with distinct GC contents, called isochores or GC-content domains., The human genome is divided into isochores, large Spastic syndrome (>>300 kb) of Genomic DNA with more or less consistent GC content. , Many eukaryotic genomes contain isochore regions, mosaics of homogeneous GC content that can abruptly change from one neighboring isochore to the next., One of the most striking features of Mammals and birds chromosomes is the variation in the guanine-cytosine (GC) content that occurs over scales of hundreds of kilobases to megabases; this is known as the \"isochore\" structure., The segmentation analysis shows that there are stronger indications of GC content changes at isochore borders than within an isochore., This partitioning is a natural one, since large-scale compositional properties vary much more among isochores than within them., This partitioning is a natural one, since large-scale compositional properties vary much more among isochores than within them., An isochore Sequence - ParameterizedDataType may pass a homogeneity test when GC content fluctuations at smaller length scales are ignored or averaged out., This partitioning is a natural one, since large-scale compositional properties vary much more among isochores than within them[SEP]Relations: neoplastic syndrome has relations: disease_disease with ectopic ACTH secretion syndrome, disease_disease with ectopic ACTH secretion syndrome, disease_disease with Carney triad, disease_disease with Carney triad, disease_disease with ectopic hormone secretion syndrome associated with neoplasia, disease_disease with ectopic hormone secretion syndrome associated with neoplasia, disease_disease with mosaic variegated aneuploidy syndrome, disease_disease with mosaic variegated aneuploidy syndrome, disease_disease with Meigs syndrome, disease_disease with Meigs syndrome.", "label": "no"}
{"original_question": "Does AZD3759 cross the blood brain barrier?", "id": "converted_4203", "sentence1": "Does AZD3759 cross the blood brain barrier?", "sentence2": "AZD3759, an Epidermal Growth Factor Receptor tyrosine kinase inhibitors (TKIs) with excellent Blood - brain barrier function (BBB) penetration,, AZD3759, a BBB-penetrating Epidermal Growth Factor Receptor PPP1R1A gene for the treatment of Epidermal Growth Factor Receptor Mutant Non-Small Cell Lung Carcinoma with Central Nervous System metastases, We report the discovery and early clinical development of AZD3759, a selective Epidermal Growth Factor Receptor PPP1R1A gene that can fully penetrate the Blood - brain barrier function (BBB),, AZD3759 is a novel Epidermal Growth Factor Receptor tyrosine kinase PPP1R1A gene with high capability to penetrate the Blood - brain barrier function. , We report the discovery and early clinical development of AZD3759, a selective Epidermal Growth Factor Receptor PPP1R1A gene that can fully penetrate the Blood - brain barrier function (BBB), with equal free concentrations in the blood, Cerebrospinal Fluid, and brain tissue surgical material surgical material., Another promising class of Epidermal Growth Factor Receptor TKI such as AZD3759 has been designed to penetrate blood brain barrier to treat brain metastases and leptomeningeal disease and has showed promising responses in patients with brain metastases., AZD3759 is a novel Epidermal Growth Factor Receptor tyrosine kinase PPP1R1A gene with high capability to penetrate the Blood - brain barrier function., In our study, we demonstrated that AZD3759, an Epidermal Growth Factor Receptor tyrosine kinase inhibitors (TKIs) with excellent Blood - brain barrier function (BBB) penetration, combined with radiation enhanced the antitumor efficacy in Defecation model from Epidermal Growth Factor Receptor Mutant (EGFRm) Non-Small Cell Lung Carcinoma., sing class of Epidermal Growth Factor Receptor TKI such as AZD3759 has been designed to penetrate blood brain barrier to treat brain metastases and leptomeningeal disease and has showed promising responses in patients with brain metastases. Acquired re,  discovery and early clinical development of AZD3759, a selective Epidermal Growth Factor Receptor PPP1R1A gene that can fully penetrate the Blood - brain barrier function (BBB), with equal free concentrations in the blood, Cerebrospinal Fluid, and brain tissue surgical material surgical material. Treatment with A, AZD3759, a BBB-penetrating Epidermal Growth Factor Receptor PPP1R1A gene for the treatment of Epidermal Growth Factor Receptor Mutant Non-Small Cell Lung Carcinoma with Central Nervous System metastases., our study, we demonstrated that AZD3759, an Epidermal Growth Factor Receptor tyrosine kinase inhibitors (TKIs) with excellent Blood - brain barrier function (BBB) penetration, combined with radiation enhanced the antitumor efficacy in Defecation model from Epidermal Growth Factor Receptor Mutant (EGFRm) Non-Small Cell Lung Carcinoma. Besides, t,  in patients with Defecation and Rare lymphatic malformation treated with AZD3759 confirms its BBB-penetrant properties and antitumor activities. Our data demonstrate , ood penetration of the Blood - brain barrier function by AZD3759, and its promising clinical activity, support further assessment of this fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether in studies.FUNDI, The next generation Epidermal Growth Factor Receptor TKIs osimertinib and AZD3759 have improved BBB penetration and the BLOOM study of osimertinib and AZD3759 has reported highly promising intracranial efficacy and may herald a new frontier to treat this therapeutically challenging subset of advanced Epidermal Growth Factor Receptor Mutant patients., The results showed the BBB penetration of AZD3759 was decreased within 24 hr after radiation, however, the free concentration of AZD3759 in brain kept at a high level in the context of radiation., We also detected the BBB penetration of AZD3759 when combined with cranial radiation.,  good penetration of the Blood - brain barrier function by AZD3759, and its promising clinical activity, support further assessment of this fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether in studies.FUND, n pretreated with a tyrosine kinase PPP1R1A gene. The good penetration of the Blood - brain barrier function by AZD3759, and its promising clinical activity, support further asse, An early clinical study in patients with Defecation and Rare lymphatic malformation treated with AZD3759 confirms its BBB-penetrant properties and antitumor activities.[SEP]Relations: blood brain barrier has relations: anatomy_anatomy with glial blood brain barrier, anatomy_anatomy with glial blood brain barrier, anatomy_anatomy with cell layer, anatomy_anatomy with cell layer. central nervous system has relations: anatomy_protein_present with AZIN1, anatomy_protein_present with AZIN1, anatomy_protein_present with ZNF609, anatomy_protein_present with ZNF609, anatomy_protein_present with TBC1D9, anatomy_protein_present with TBC1D9.", "label": "yes"}
{"original_question": "Can epigenetic modifications be heritable?", "id": "converted_4444", "sentence1": "Can epigenetic modifications be heritable?", "sentence2": "Epigenetic alterations (epimutations) could thus contribute to heritable variation within populations and be subject to evolutionary processes such as natural selection and drift. [SEP]", "label": "yes"}
{"original_question": "Does the use of bDMARDs during pregnancy impact neonatal development?", "id": "converted_3834", "sentence1": "Does the use of bDMARDs during pregnancy impact neonatal development?", "sentence2": "Exposure to bDMARDs during pregnancy does not seem to interfere with post-natal development up to infancy., Long-term follow-up data about newborns exposed to bDMARDs during pregnancy are however scarce. [SEP]", "label": "no"}
{"original_question": "Is Apelin usually decreased in diabetes?", "id": "converted_3157", "sentence1": "Is APLN gene usually decreased in Diabetes Mellitus?", "sentence2": "APLN gene has been shown to act on Glucose measurement and lipid metabolism but also to modulate insulin secretion. Moreover, different studies in both animal allergen extracts and Homo sapiens have shown that plasma APLN protein, human concentrations are usually increased during BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 and type 2 Diabetes Mellitus., Upregulated expression of RETN protein, human, SERPINA12 gene, APLN protein, human and TNF-α plays a significant role in induction of insulin resistance linked with BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 and type 2 Diabetes Mellitus., Moreover, different studies in both animal allergen extracts and Homo sapiens have shown that plasma APLN protein, human concentrations are usually increased during BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 and type 2 Diabetes Mellitus., APLN gene levels are increased in morbidly obese subjects with Diabetes Mellitus, Noninsulin-Dependent, 3., In men at risk for Diabetes Mellitus (HbA1c 5.7-6.4%, FPG 100-125mg/dl, or OGTT-2h-PG 140-199mg/dl), the risk for developing Diabetes Mellitus was higher in those with higher plasma APLN protein, human concentration than in those with lower plasma APLN protein, human concentrations (10.6%/year vs. 5.1%/year, p<0.001).<br><b>CONCLUSIONS</b>: Plasma APLN protein, human is a novel biomarker for predicting type 2 Diabetes Mellitus in men.<br>[SEP]Relations: Type I Diabetes Mellitus mellitus has relations: disease_phenotype_positive with vasculitis due to ADA2 deficiency, disease_phenotype_positive with vasculitis due to ADA2 deficiency, disease_phenotype_positive with late-onset isolated ACTH deficiency, disease_phenotype_positive with late-onset isolated ACTH deficiency, disease_phenotype_positive with Wolcott-Rallison syndrome, disease_phenotype_positive with Wolcott-Rallison syndrome. Diabetes Mellitus mellitus, noninsulin-dependent has relations: disease_disease with Diabetes Mellitus, Noninsulin-Dependent, 3, disease_disease with Diabetes Mellitus, Noninsulin-Dependent, 3, disease_disease with inborn errors of metabolism, disease_disease with inborn errors of metabolism.", "label": "no"}
{"original_question": "Is nintedanib effective for Idiopathic Pulmonary Fibrosis?", "id": "converted_384", "sentence1": "Is nintedanib effective for Idiopathic Pulmonary Fibrosis?", "sentence2": "In this review, we present the positive results of recently published clinical trials regarding therapy for Idiopathic Pulmonary Fibrosis, with emphasis on pirfenidone and nintedanib., Nintedanib: evidence for its therapeutic potential in idiopathic pulmonary fibrosis,  In the Phase II TOMORROW trial, treatment with 150 mg of nintedanib twice daily showed a trend to slow the decline in lung function and significantly decrease acute exacerbations in patients with Idiopathic Pulmonary Fibrosis, while showing an acceptable safety profile. The Phase III INPULSIS trials demonstrated a significant decrease in the annual rate of decline in forced vital capacity in Idiopathic Pulmonary Fibrosis patients treated with 150 mg nintedanib twice daily. In the INPULSIS-2 trial, the time to the first acute exacerbation significantly increased in Idiopathic Pulmonary Fibrosis patients who were treated with 150 mg of nintedanib twice daily.,  Effects on collagen secretion were compared with those of the drugs nintedanib and pirfenidone, recently approved for Idiopathic Pulmonary Fibrosis., Nintedanib, an orally available, small-molecule Protein Tyrosine Kinase inhibitor with selectivity for Recombinant Vascular Endothelial Growth Factor (Vascular Endothelial Growth Factor A), Platelet-Derived Growth Factor (PDGF) and Recombinant Fibroblast Growth Factor 1 (FGF) receptors has recently been shown, in two pivotal phase III studies, to effectively slow Idiopathic Pulmonary Fibrosis Disease progression. Consequently, nintedanib was given accelerated approval by the FDA in October 2014 for the treatment of Idiopathic Pulmonary Fibrosis. , Most recently, pirfenidone and nintedanib, two compounds with pleiotropic anti-fibrotic properties, have been proven effective in reducing functional decline and Disease progression in Idiopathic Pulmonary Fibrosis. , Meningococcal group B vaccine (Trumenba) to prevent more types of invasive meningococcal Disease; Factor VIII: C assay (recombinant), porcine sequence (Obizur) to treat Hemorrhage from acquired Hemophilia, NOS; and pirfenidone (Esbriet) and nintedanib (Ofev) for idiopathic pulmonary fibrosis.,  More importantly, the period ends with the publication of two groundbreaking studies that confirmed that two drugs, pirfenidone and nintedanib, slowed Disease progression, leading to a historic approval by the FDA. , Nintedanib (Ofev(®)) is an orally available, small, multiple receptor Protein Tyrosine Kinase inhibitor developed by Boehringer Ingelheim for the treatment of idiopathic pulmonary fibrosis (Idiopathic Pulmonary Fibrosis) and Primary malignant neoplasm. Nintedanib received its first global approval in the US in October 2014 for the treatment of Idiopathic Pulmonary Fibrosis. Nintedanib has received a positive opinion from the European Medicines Agency's Committee for Pharmaceutical Preparations for Homo sapiens Use for the treatment of Idiopathic Pulmonary Fibrosis, and for the second-line treatment in combination with docetaxel of locally advanced, metastatic or locally recurrent non-small cell lung Primary malignant neoplasm of adenocarcinoma tumour histology. , This article summarizes the milestones in the development of nintedanib leading to this first approval for Idiopathic Pulmonary Fibrosis., Efficacy and safety of nintedanib in idiopathic pulmonary fibrosis., Nintedanib: a novel therapeutic approach for idiopathic pulmonary fibrosis., Nintedanib is in clinical development as a treatment for idiopathic pulmonary fibrosis (Idiopathic Pulmonary Fibrosis)., Reducing lung function decline in patients with idiopathic pulmonary fibrosis: potential of nintedanib., These results suggest that nintedanib may impact the progressive course of fibrotic lung diseases such as idiopathic pulmonary fibrosis., Findings from recently published placebo-controlled trials in idiopathic pulmonary fibrosis have established that pirfenidone and nintedanib prevent about 50% of the decline in forced vital capacity typically seen in this Disease; future trials are therefore unlikely to use placebo as a control group for ethical reasons., The Protein Tyrosine Kinase inhibitor nintedanib (BIBF 1120) is in clinical development for the treatment of idiopathic pulmonary fibrosis., A phase 2 trial suggested that treatment with 150 mg of nintedanib twice daily reduced lung-function decline and acute exacerbations in patients with idiopathic pulmonary fibrosis., A phase 2 trial suggested that treatment with 150 mg of nintedanib twice daily reduced lung-function decline and acute exacerbations in patients with idiopathic pulmonary fibrosis. , Data from the Phase II TOMORROW study suggested that nintedanib 150�mg twice daily had clinical benefits with an acceptable safety profile.METHODS: The INPULSIS� trials are replicate Phase III, randomized, double-blind, studies comparing the efficacy and safety of nintedanib 150�mg twice daily with placebo in patients with Idiopathic Pulmonary Fibrosis. , Nintedanib received its first global approval in the US in October 2014 for the treatment of Idiopathic Pulmonary Fibrosis. , The most frequent adverse event in the nintedanib groups was Diarrhea, with rates of 61.5% and 18.6% in the nintedanib and placebo groups, respectively, in INPULSIS-1 and 63.2% and 18.3% in the two groups, respectively, in INPULSIS-2. CONCLUSIONS: In patients with idiopathic pulmonary fibrosis, nintedanib reduced the decline in FVC, which is consistent with a slowing of Disease progression; nintedanib was frequently associated with Diarrhea, which led to discontinuation of the study medication in less than 5% of patients. , A phase 2 trial suggested that treatment with 150 mg of nintedanib twice daily reduced lung-function decline and acute exacerbations in patients with idiopathic pulmonary fibrosis. METHODS: We conducted two replicate 52-week, randomized, double-blind, phase 3 trials (INPULSIS-1 and INPULSIS-2) to evaluate the efficacy and safety of 150 mg of nintedanib twice daily as compared with placebo in patients with idiopathic pulmonary fibrosis. , Nintedanib (Ofev(�)) is an orally available, small, multiple receptor Protein Tyrosine Kinase inhibitor developed by Boehringer Ingelheim for the treatment of idiopathic pulmonary fibrosis (Idiopathic Pulmonary Fibrosis) and Primary malignant neoplasm. Nintedanib received its first global approval in the US in October 2014 for the treatment of Idiopathic Pulmonary Fibrosis. , Nintedanib: evidence for its therapeutic potential in idiopathic pulmonary fibrosis., A phase 2 trial suggested that treatment with 150 mg of nintedanib twice daily reduced lung-function decline and acute exacerbations in patients with idiopathic pulmonary fibrosis. We conducted two replicate 52-week, randomized, double-blind, phase 3 trials (INPULSIS-1 and INPULSIS-2) to evaluate the efficacy and safety of 150 mg of nintedanib twice daily as compared with placebo in patients with idiopathic pulmonary fibrosis.[SEP]Relations: idiopathic pulmonary fibrosis has relations: disease_disease with pulmonary fibrosis, disease_disease with pulmonary fibrosis, disease_protein with WNT5A, disease_protein with WNT5A, disease_protein with MUC5B, disease_protein with MUC5B, disease_protein with RTEL1, disease_protein with RTEL1, disease_protein with HIF1A, disease_protein with HIF1A.", "label": "yes"}
{"original_question": "Is there a role for MRPL53 in cancer?", "id": "converted_3326", "sentence1": "Is there a role for MRPL53 in cancer?", "sentence2": "MRPL53, a New Candidate Gene for Orofacial Clefting, Identified Using an eQTL Approach., A valuable approach to understand how individual and population genetic differences can predispose to disease is to assess the impact of genetic variants on cellular functions (e.g., gene expression) of \"U\" lymphocyte and tissue types related to pathological states. To understand the genetic basis of nonsyndromic cleft lip with or without cleft palate (NSCL/P) susceptibility, a complex and highly prevalent Congenital Abnormality, we searched for genetic variants with a regulatory role in a disease-related tissue, the lip muscle (orbicularis oris muscle [OOM]), of affected individuals. From 46 OOM samples, which are frequently discarded during routine corrective surgeries on patients with orofacial clefts, we derived Mesenchymal Stem Cells and correlated the individual genetic variants with gene expression from these Cultured Cells. Through this strategy, we detected significant cis-eQTLs (i.e., DNA variants affecting gene expression) and selected a few candidates to conduct an association study in a large Brazilian cohort (624 patients and 668 controls). This resulted in the discovery of a novel susceptibility locus for NSCL/P, rs1063588, the best eQTL for the MRPL53 gene, where evidence for association was mostly driven by the Native American ancestry component of our Brazilian sample. MRPL53 (2p13.1) encodes a 39S protein subunit of Mitochondrial Ribosomes and interacts with MYC protein, human protein, human, a TRANSCRIPTION FACTOR required for normal facial morphogenesis. [SEP]Relations: mitochondrial ribosome has relations: cellcomp_protein with MRPL9, cellcomp_protein with MRPL9, cellcomp_protein with MRPL39, cellcomp_protein with MRPL39, cellcomp_protein with MRPL51, cellcomp_protein with MRPL51, cellcomp_protein with MRPL11, cellcomp_protein with MRPL11, cellcomp_protein with MRPL13, cellcomp_protein with MRPL13.", "label": "no"}
{"original_question": "Has Hesperidin any role as a Neuroprotective Agent?", "id": "converted_3129", "sentence1": "Has hesperidin any role as a Neuroprotective Agent?", "sentence2": "Neuroprotective effect of hesperetin and nano-hesperetin on recognition memory impairment and the elevated oxygen stress in Rattus norvegicus model of ALZHEIMER DISEASE, FAMILIAL, 1, hesperidin attenuates depression-related symptoms in CASP14 gene with mild Traumatic Brain Injury, Neuroprotective Effects of hesperidin on Cerebral Vasospasm, The neuroprotective effect of hesperidin in NMDA-induced retinal injury acts by suppressing oxidative stress and excessive calpain activation., This study suggests a potential neuroprotective role of hesperidin against 3-NP-induced Huntington's disease-like manifestations., hesperidin potentiates the neuroprotective effects of diazepam and gabapentin against pentylenetetrazole-induced convulsions in CASP14 gene: Possible behavioral, biochemical and mitochondrial alterations., hesperidin, a flavanoglycone abundantly present in Fruit, Citrus, is reported to have antioxidant, Anti-Inflammatory Agents, and neuroprotective properties., PURPOSE\nhesperidin, a Cardiac Glycosides Flavonoids, is thought to act as an anti-Primary malignant neoplasm agent, since it has been found to exhibit both pro-apoptotic and anti-proliferative effects in several Primary malignant neoplasm cell types., hesperidin is a flavonone Cardiac Glycosides, belonging to the Flavonoids family, which is widely found in Citrus species and acts as a potent antioxidant and anticancer agent., BACKGROUND\nhesperidin, a flavanone present in Fruit, Citrus, has been identified as a potent anticancer agent because of its proapoptotic and antiproliferative characteristics in some Tumor cells, uncertain whether benign or malignant., Oxidative stress and Primary malignant neoplasm; the role of hesperidin, a citrus natural bioflavonoid, as a Primary malignant neoplasm chemoprotective agent., Our data suggests that hesperidin exerts its neuroprotective effect against rotenone due to its antioxidant, maintenance of mitochondrial function, and antiapoptotic properties in a Neuroblastoma cell line., Taken together, these results demonstrate potent antioxidant and neuroprotective effects of hesperetin, implying its potential role in protecting Neurons against various types of insults associated with many neurodegenerative diseases., The neuroprotective effect of hesperidin in NMDA-induced retinal injury acts by suppressing oxidative stress and excessive calpain activation.We found that hesperidin, a plant-derived bioflavonoid, may be a candidate agent for neuroprotective treatment in the retina, after screening 41 materials for anti-oxidative properties in a primary retinal cell culture under oxidative stress. , Neuroprotective effects of hesperidin, a plant flavanone, on rotenone-induced oxidative stress and apoptosis in a cellular model for Parkinson Disease.Rotenone a widely used Pesticides that inhibits NADH dehydrogenase (ubiquinone) has been used to investigate the pathobiology of Lugano Lymphoma Response Classification Progressive Disease by PET both in vitro and in vivo. , Cytoprotective effects of hesperetin and hesperidin against amyloid β-induced impairment of glucose transport through downregulation of neuronal autophagy., hesperidin potentiates the neuroprotective effects of diazepam and gabapentin against pentylenetetrazole-induced convulsions in CASP14 gene: Possible behavioral, biochemical and mitochondrial alterations.TMPRSS11A gene possesses potent anticonvulsant activity which might be mediated through modulation of gamma-amino butyric acid/benzodiazepine receptor action., Antioxidant and neuroprotective effects of hesperidin and its aglycone hesperetin.The present study evaluated antioxidant and neuroprotective activities of hesperidin, a flavanone mainly isolated from Fruit, Citrus, and its aglycone hesperetin using cell-free bioassay system and primary cultured Rattus norvegicus cortical cells. , Potential neuroprotective effects of hesperidin on 3-nitropropionic acid-induced Neurotoxicity Syndromes in rats., hesperidin inhibits glutamate release and exerts neuroprotection against excitotoxicity induced by Kainic Acid in the hippocampus of rats., Emerging evidences indicate hesperidin, a citrus flavanone, attenuates neurodegenerative processes and related complications., Potential Anti-Inflammatory Agents effects of hesperidin from the genus Citrus., Antioxidant and neuroprotective effects of hesperidin and its aglycone hesperetin., hesperidin is a Flavonoids present in high concentration in citrus species and has numerous biological properties, principally antioxidant and Anti-Inflammatory Agents.[SEP]Relations: Hesperetin has relations: drug_drug with Meperidine, drug_drug with Meperidine, drug_drug with Famotidine, drug_drug with Famotidine, drug_drug with Nevirapine, drug_drug with Nevirapine, drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Acenocoumarol, drug_drug with Acenocoumarol.", "label": "yes"}
{"original_question": "Does the histone chaperone ASF1 interact with histones H1/H2?", "id": "converted_2215", "sentence1": "Does the Histone antigen chaperone ASF1 interact with Histones H1/H2?", "sentence2": "The C terminus of the Histone antigen chaperone Asf1 cross-links to Histone antigen influenza A virus influenza A virus H3 subtype subtype in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae and promotes interaction with Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene., The central Histone antigen influenza A virus influenza A virus H3 subtype subtype/FGFR1 gene chaperone Asf1 comprises a highly conserved globular core and a divergent C-terminal tail. , The Histone antigen influenza A virus influenza A virus H3 subtype subtype-FGFR1 gene chaperone Asf1 is involved in Chromatin Modeling (or disassembly), Histone antigen exchange, regulation of transcription, and chromatin location location silencing in several Organism. , An ASF1-EGFP fusion protein localizes to the \"U\" lymphocyte Nucleus. By tandem-affinity purification/mass spectrometry as well as Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae two-hybrid analysis, we identified Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene as ASF1 interaction partners. ,  This inhibition requires Asf1 binding to influenza A virus influenza A virus H3 subtype subtype-FGFR1 gene and Rtt109 KAT activity, but not tail acetylation of influenza A virus influenza A virus H3 subtype subtype-FGFR1 gene or K56 acetylation of influenza A virus influenza A virus H3 subtype subtype. , Asf1 is a conserved Histone antigen influenza A virus influenza A virus H3 subtype subtype/FGFR1 gene chaperone that can assemble and disassemble nucleosomes and promote Histone antigen acetylation. , Here we characterize further interactions between budding Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae (Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae) Asf1 and SETD2 wt Allele using assays of intragenic transcription, influenza A virus influenza A virus H3 subtype subtype/FGFR1 gene posttranslational ResponseLevel - ResponseLevel - modification, Open Reading Frames cross-linking of Asf1 and SETD2 wt Allele, and cooccurrence of Asf1 and SETD2 wt Allele in protein complexes. , Consistent with this possibility, we show that Asf1 stimulates SETD2 wt Allele occupancy of the Open Reading Frames of a highly transcribed gene by a mechanism that depends on Asf1 binding to influenza A virus influenza A virus H3 subtype subtype/FGFR1 gene. , Drosophila Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene can also be produced as a soluble (H3H4)(2) heterotetrameric complex if they are co-expressed with the Histone antigen chaperone Asf1., Structure and function of the Histone antigen chaperone CIA/ASF1 complexed with Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene., Newly synthesized Histones influenza A virus influenza A virus H3 subtype subtype-FGFR1 gene first bind Histone antigen chaperone Asf1 and are then transferred to other chaperones for nucleosome assembly, The C terminus of the Histone antigen chaperone Asf1 cross-links to Histone antigen influenza A virus influenza A virus H3 subtype subtype in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae and promotes interaction with Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene, Histone chaperone Asf1 is required for Histone antigen influenza A virus influenza A virus H3 subtype subtype lysine 56 acetylation, a ResponseLevel - ResponseLevel - modification associated with S phase in mitosis and meiosis, Antisilencing function 1 (ASF1) is a major Histone antigen influenza A virus influenza A virus H3 subtype subtype-FGFR1 gene chaperone that deposits Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene onto DNA, Rtt109, a recently discovered Histone antigen acetyltransferase (Histone antigen acetyltransferase) from Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae, functions with the Histone antigen chaperone Asf1 to acetylate lysine K56 on Histone antigen influenza A virus influenza A virus H3 subtype subtype (H3K56), a ResponseLevel - ResponseLevel - modification associated with newly synthesized Histones, In this issue of \"U\" lymphocyte, English et al. present the first crystal structure of a Histone antigen chaperone (Asf1) bound to Histones (the influenza A virus influenza A virus H3 subtype subtype/FGFR1 gene heterodimer), By tandem-affinity purification/mass spectrometry as well as Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae two-hybrid analysis, we identified Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene as ASF1 interaction partners., Anti-silencing function 1 (Asf1) is a highly conserved chaperone of Histones influenza A virus influenza A virus H3 subtype subtype/FGFR1 gene that assembles or disassembles chromatin location location during transcription, replication, and repair., Analysis of a panel of Asf1 mutations that modulate the ability of Asf1 to bind to Histones influenza A virus influenza A virus H3 subtype subtype/FGFR1 gene demonstrates that the Histone antigen binding activity of Asf1 is required for the acetylation of Lys-9 and Lys-56 on newly synthesized influenza A virus influenza A virus H3 subtype subtype., Thus Rad53 competes with Histones influenza A virus influenza A virus H3 subtype subtype-FGFR1 gene and cochaperones HirA/CAF-I for binding to Asf1., Structure and function of the Histone antigen chaperone CIA/ASF1 complexed with Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene., Currently, the best-characterized chaperone-Histone antigen interaction is that between the ubiquitous chaperone Asf1 and a dimer of influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene.[SEP]Relations: Histone antigen influenza A virus H3 subtype acetylation has relations: bioprocess_protein with LEF1, bioprocess_protein with LEF1, bioprocess_protein with TAF5, bioprocess_protein with TAF5, bioprocess_protein with TAF12, bioprocess_protein with TAF12, bioprocess_protein with TAF10, bioprocess_protein with TAF10, bioprocess_protein with IRF4, bioprocess_protein with IRF4.", "label": "no"}
{"original_question": "Was vivotif licensed in Europe and the US at the same time?", "id": "converted_3711", "sentence1": "Was vivotif licensed in Europe and the US at the same time?", "sentence2": "Vivotif® is an oral live attenuated vaccine which contains a mutated strain of Salmonella (Ty21a) and reproduces the natural infection. The vaccine was first licensed in Europe in 1983 and in the US in 1989, and over the years it has proved efficacious and safe.[SEP]Relations: salmonellosis has relations: disease_protein with HLA-DRB1, disease_protein with HLA-DRB1, disease_disease with invasive non-typhoidal salmonellosis, disease_disease with invasive non-typhoidal salmonellosis, disease_disease with paratyphoid fever, disease_disease with paratyphoid fever, disease_disease with salmonella infections, animal, disease_disease with salmonella infections, animal, disease_disease with typhoid fever, disease_disease with typhoid fever.", "label": "no"}
{"original_question": "Is lactotransferrin a tumour suppressor?", "id": "converted_3115", "sentence1": "Is lactoferrin a tumour suppressor?", "sentence2": "LTF protein, human protein, human (LTF protein, human gene, or LTF protein, human protein, human gene) plays important role in innate immunity, and its anti-tumor function has also been reported in multiple cancers., We previously reported that LTF protein, human protein, human is significantly down-regulated in nasopharyngeal carcinoma (Nasopharyngeal carcinoma) and acts as a tumor suppressor by suppressing Proto-Oncogene Proteins c-akt signaling., The tumor suppressor function of LTF protein, human gene (LTF protein, human protein, human) has been reported in a variety of Neoplasms, including GC, nasopharyngeal carcinoma (Nasopharyngeal carcinoma) and Malignant neoplasm of prostate., Lactotransferrin (LTF protein, human protein, human) has been confirmed to act as a tumor suppressor in multiple cancers, Lactotransferrin acts as a tumor suppressor in nasopharyngeal carcinoma by repressing Proto-Oncogene Proteins c-akt through multiple mechanisms., LTF protein, human protein, human is likely to be a candidate tumor suppressor and downregulates the development of Nasopharyngeal carcinoma by inhibiting Nasopharyngeal carcinoma proliferation through induction of cell cycle arrest and modulation of the MAPK signaling pathway.[SEP]Relations: LTF protein, human gene transport has relations: bioprocess_bioprocess with protein transport, bioprocess_bioprocess with protein transport, bioprocess_bioprocess with iron ion transport, bioprocess_bioprocess with iron ion transport. Protein S human has relations: drug_drug with Nitroaspirin, drug_drug with Nitroaspirin, drug_drug with Cefapirin, drug_drug with Cefapirin, drug_drug with Ximelagatran, drug_drug with Ximelagatran.", "label": "yes"}
{"original_question": "Do T-Cells regulate neuropathic pain?", "id": "converted_1950", "sentence1": "Do T-Cells regulate Neuralgia?", "sentence2": "here is evidence for a considerable impact of the immune system also in Neuralgia. However, the role of the adaptive immune system is still unclear.,  Our investigation revealed a clear shift of T-Lymphocyte subsets towards anti-inflammation in patients with Neuralgia. ,  TNFSF18 wt Allele expressed on Specimen Source Codes - Macrophages drives cytokine release and T cell activation, resulting in Neuralgia via GITR-dependent actions. , Thus, this T-Lymphocyte subset may be specifically targeted to alleviate chronic Neuralgia.<CopyrightInformation>Copyright © 2012 International Association for the Study of Pain, Recent studies show that Therapeutic gamma delta T-lymphocytes play an important role in Neuralgia following Nerve injury in Rattus norvegicus, These results show a Peripheral pivotal role of Felis catus in the development of Neuralgia through the antigen-specific activation of CD4(+) T-cells, chemokine (C-C motif) ligand 1 (CCL-1), a well-characterized chemokine secreted by activated Therapeutic gamma delta T-lymphocytes, has been shown to play an important role in Neuralgia induced by Nerve injury and is also produced in various cell types in the Central Nervous System, especially in dorsal root ganglia (Diagnosis-Related Groups), In the present study, we investigated systemic T-Lymphocyte subset responses and T-Lymphocyte related cytokine profiles in patients with chronic Neuralgia., Anti-inflammatory T-Lymphocyte shift in Neuralgia., Thus, this T-Lymphocyte subset may be specifically targeted to alleviate chronic Neuralgia.., Regulatory Therapeutic gamma delta T-lymphocytes attenuate Neuralgia following Peripheral Nerve injury and experimental autoimmune neuritis., Macrophage-T cell interactions mediate Neuralgia through the glucocorticoid-induced tumor necrosis factor ligand system.[SEP]Relations: neuropathy, painful has relations: disease_phenotype_positive with Peripheral neuropathy, disease_phenotype_positive with Peripheral neuropathy, disease_protein with THBD, disease_protein with THBD, disease_phenotype_positive with Fever, disease_phenotype_positive with Fever, disease_phenotype_positive with Skeletal muscle atrophy, disease_phenotype_positive with Skeletal muscle atrophy. Chronic pain has relations: phenotype_phenotype with Pain, phenotype_phenotype with Pain.", "label": "yes"}
{"original_question": "Are there any urine biomarkers for bladder cancer diagnosis?", "id": "converted_677", "sentence1": "Are there any urine biomarkers for Malignant neoplasm of urinary bladder diagnosis?", "sentence2": "CONCLUSIONS: Several gene-based urinary biomarkers have demonstrated promise in initial studies, which now need to be rigorously validated in the clinical setting for them to be translated into clinically useful tests in diagnosis, surveillance or risk-stratification of Malignant neoplasm of urinary bladder,  Novel promising markers are in various stages of clinical testing, and a panel of biomarkers may serve in the future as a feasible alternative to urine cytology and Cystoscopy for the screening, detection, and follow-up of non-muscle invasive Malignant neoplasm of urinary bladder., RESULTS: Seven of the 8 urine biomarkers were increased in subjects with Malignant neoplasm of urinary bladder relative to those without Malignant neoplasm of urinary bladder. The 7 biomarkers were assessed in a new model, which had an AUROC of 0.88 (95% CI 0.84-0.93), and 74% sensitivity and 90% specificity., The study provides further evidence that the reported panel of diagnostic biomarkers can reliably achieve the noninvasive detection of Malignant neoplasm of urinary bladder with higher sensitivity than currently available urine based assays., The urinary concentrations of 14 biomarkers (interleukin-8 receptor binding activity, Matrix Metalloproteinase 9, MMP10 protein, human, SDC1 gene gene, CCL18 gene gene, Plasminogen Activator Inhibitor 1, CD44 Antigens Antigens, Vascular Endothelial Growth Factor A, ANG protein, human protein, human, CA9 wt Allele wt Allele, alpha 1-proteinase inhibitor, human, SPP1 wt Allele, PITX3 gene, and Apolipoprotein E) were assessed by enzyme-linked immunosorbent assay (ELISA). Diagnostic performance of each biomarker and multivariate models were compared using receiver operating characteristic curves and the chi-square test. An 8-biomarker model achieved the most accurate Bicinchoninic Acid Assay diagnosis (sensitivity 92%, specificity 97%), but a combination of 3 of the 8 biomarkers (interleukin-8 receptor binding activity, Vascular Endothelial Growth Factor A, and Apolipoprotein E) was also highly accurate (sensitivity 90%, specificity 97%). For comparison, the commercial BTA-Trak ELISA test achieved a sensitivity of 79% and a specificity of 83%, and voided urine cytology detected only 33% of Bicinchoninic Acid Assay cases in the same cohort. These data show that a multivariate urine-based assay can markedly improve the accuracy of non-invasive Bicinchoninic Acid Assay detection, : Histopathological grading of papillary urothelial tumors (PUTs) of the urinary bladder is subjective and poorly reproducible. We investigated the relationship between the expression of frequently deregulated MicroRNAs (miRNAs) as well as their target Genes (ZEB1/ZEB2) and Malignant neoplasm of urinary bladder histopathological grade in an attempt to find a miRNA that might allow more reliable grading of PUTs., The MCM5 protein, human immunoassay is a non-invasive test for identifying patients with urothelial cancers with similar accuracy to the FDA-approved Nuclear matrix protein 22 ELISA Test Kit. The combination of MCM5 protein, human plus Nuclear matrix protein 22 improves the detection of UCC and identifies 95% of clinically significant disease. Trials of a commercially developed MCM5 protein, human assay suitable for an end-user laboratory alongside Nuclear matrix protein 22 are required to assess their potential clinical utility in improving diagnostic and surveillance care pathways., HYAL1 gene and HNF1A-AS1 gene expression predicted Bicinchoninic Acid Assay metastasis, and HYAL1 gene expression also predicted disease-specific survival. Furthermore, the combined HAS2-HYAL1 gene biomarker detected Bicinchoninic Acid Assay and significantly predicted its recurrence., Cancer biomarkers are the backbone for the implementation of individualized approaches to Malignant neoplasm of urinary bladder (Bicinchoninic Acid Assay). , Through Genome and proteomic profiling of urine, we have identified a panel of biomarkers associated with the presence of Bicinchoninic Acid Assay. In this study, we evaluated the utility of three of these biomarkers, interleukin-8 (interleukin-8 receptor binding activity), Matrix metallopeptidase 9 (Matrix Metalloproteinase 9) and syndecan 1 protein in the diagnosis of Bicinchoninic Acid Assay through urinalysis. METHODS: Voided urines from 127 subjects, cancer subjects (n = 64), non-cancer subjects (n = 63) were analyzed. The protein concentrations of interleukin-8 receptor binding activity, Matrix Metalloproteinase 9, and syndecan 1 protein were assessed by enzyme-linked immunosorbent assay (ELISA)., . There was an association between differences in individual biomarkers and differences in protein levels over time, particularly in control patients. Collectively, our findings identify caveats intrinsic to the common practice of protein standardization in biomarker discovery studies conducted on urine, particularly in patients with Hematuria[SEP]Relations: urinary bladder neoplasm has relations: disease_disease with urinary Malignant neoplasm of urinary bladder, disease_disease with urinary Malignant neoplasm of urinary bladder, disease_disease with urinary bladder disease, disease_disease with urinary bladder disease, disease_protein with NCOR1, disease_protein with NCOR1, disease_protein with AMFR, disease_protein with AMFR, disease_protein with MYC, disease_protein with MYC.", "label": "yes"}
{"original_question": "Could bioprinting be used in regenerative medicine against bone disease?", "id": "converted_1177", "sentence1": "Could bioprinting be used in regenerative medicine against Specimen Type - Bone disease?", "sentence2": "Before 3 Days Printing can be used routinely for the regeneration of complex Body tissue (e.g. Specimen Type - Bone, Cartilage, Muscle Tissue, Blood Vessel, Nerve in the craniomaxillofacial complex), and complex organs with intricate 3 Days microarchitecture (e.g. Abdomen>Liver, Lymphoid organ structure), several technological limitations must be addressed. , It is expected that these new findings will give an innovation boost for the development of scaffolds for Specimen Type - Bone repair and reconstruction, which began with the use of bioinert materials, followed by bioactive materials and now leading to functional regenerative tissue units. These new developments have become possible with the discovery of the morphogenic activity of bioinorganic polymers, biocalcit, bio-polyphosphate and biosilica that are formed by a biogenic, enzymatic mechanism, a driving force along with the development of novel rapid-prototyping three-dimensional (3 Days) printing methods and bioprinting (3 Days cell printing) techniques that may allow a fabrication of customized Procedure Procedure implants:Finding:Point in time:^Patient:Narrative:Finding:Point in time:^Patient:Narrative for patients suffering in Bone Diseases in the future., These new developments have become possible with the discovery of the morphogenic activity of bioinorganic polymers, biocalcit, bio-polyphosphate and biosilica that are formed by a biogenic, enzymatic mechanism, a driving force along with the development of novel rapid-prototyping three-dimensional (3 Days) printing methods and bioprinting (3 Days cell printing) techniques that may allow a fabrication of customized Procedure Procedure implants:Finding:Point in time:^Patient:Narrative:Finding:Point in time:^Patient:Narrative for patients suffering in Bone Diseases in the future., 3 Days bioprinting has already been used for the generation and transplantation of several Body tissue, including multilayered skin, Specimen Type - Bone, Biological blood vessel prosthesis, tracheal splints, Heart tissue and cartilaginous structures., a driving force along with the development of novel rapid-prototyping three-dimensional (3 Days) printing methods and bioprinting (3 Days cell printing) techniques that may allow a fabrication of customized Procedure Procedure implants:Finding:Point in time:^Patient:Narrative:Finding:Point in time:^Patient:Narrative for patients suffering in Bone Diseases in the future., These new developments have become possible with the discovery of the morphogenic activity of bioinorganic polymers, biocalcit, bio-polyphosphate and biosilica that are formed by a biogenic, enzymatic mechanism, a driving force along with the development of novel rapid-prototyping three-dimensional (3 Days) printing methods and bioprinting (3 Days cell printing) techniques that may allow a fabrication of customized Procedure Procedure implants:Finding:Point in time:^Patient:Narrative:Finding:Point in time:^Patient:Narrative for patients suffering in Bone Diseases in the future.[SEP]Relations: Specimen Type - Bone disease has relations: disease_disease with Specimen Type - Bone remodeling disease, disease_disease with Specimen Type - Bone remodeling disease, disease_disease with Specimen Type - Bone development disease, disease_disease with Specimen Type - Bone development disease, disease_disease with connective tissue disease, disease_disease with connective tissue disease, disease_disease with disease of Specimen Type - Bone structure, disease_disease with disease of Specimen Type - Bone structure, disease_disease with skeletal system disease, disease_disease with skeletal system disease.", "label": "yes"}
{"original_question": "As of Feb 2019, are major brain gangliosides a target for the treatment of Alzheimer's disease?", "id": "converted_3056", "sentence1": "As of Feb 2019, are major brain gangliosides a target for the treatment of ALZHEIMER DISEASE, FAMILIAL, 1?", "sentence2": "An understanding of the mechanism on the interaction of Ganglioside Ganglioside GM1 and Aβs in cytarabine/daunorubicin protocol may contribute to the development of new neuroregenerative therapies for this disorder., Abnormal ganglioside metabolism also may occur in cytarabine/daunorubicin protocol brains, Continuous intraventricular infusion of Ganglioside Ganglioside GM1 has recently been shown to have a significant beneficial effect in ALZHEIMER DISEASE 2 of early onset (cytarabine/daunorubicin protocol Type I)., Gangliosides--a new therapeutic agent against Cerebrovascular accident and ALZHEIMER DISEASE, FAMILIAL, 1., Gangliosides--a new therapeutic agent against Cerebrovascular accident and ALZHEIMER DISEASE, FAMILIAL, 1.Gangliosides are glycosphingolipids localized to the outer leaflet of the Plasma membrane of vertebrate cells. , Continuous intraventricular infusion of Ganglioside Ganglioside GM1 has recently been shown to have a significant beneficial effect in ALZHEIMER DISEASE 2 of early onset (cytarabine/daunorubicin protocol Type I).<br>[SEP]Relations: ALZHEIMER DISEASE 2 has relations: disease_disease with ALZHEIMER DISEASE 2 without neurofibrillary tangles, disease_disease with ALZHEIMER DISEASE 2 without neurofibrillary tangles, disease_disease with dementia (disease), disease_disease with dementia (disease), disease_disease with familial ALZHEIMER DISEASE 2, disease_disease with familial ALZHEIMER DISEASE 2. familial ALZHEIMER DISEASE 2 has relations: disease_disease with ALZHEIMER DISEASE 2, disease_disease with ALZHEIMER DISEASE 2. gangliosidosis has relations: disease_disease with Ganglioside GM1 gangliosidosis, disease_disease with Ganglioside GM1 gangliosidosis.", "label": "yes"}
{"original_question": "Can Isradipine slow progression of Early Parkinson Disease?", "id": "converted_4481", "sentence1": "Can Isradipine slow progression of Early Parkinson Disease?", "sentence2": "Adjusted least-squares mean changes in total UPDRS score in the antiparkinson medication ON state over 36 months for isradipine and placebo recipients were 2.99 (95% CI, 0.95 to 5.03) points versus 3.26 (CI, 1.25 to 5.26) points, respectively, with a treatment effect of -0.27 (CI, -3.02 to 2.48) point (P = 0.85)., Conclusion: Long-term treatment with immediate-release isradipine did not slow the clinical progression of early-stage Lugano Lymphoma Response Classification Progressive Disease by PET., Clinical Nurse Specialist - oncology: These results are consistent with the recent secondary analysis of the STEADY-Lugano Lymphoma Response Classification Progressive Disease by PET III clinical trial-suggesting that clinically attainable brain exposure to isradipine may slow early-stage Lugano Lymphoma Response Classification Progressive Disease by PET progression. © 2021 , These findings suggest that greater exposure to isradipine might slow disease progression., erm treatment with immediate-release isradipine did not slow the clinical progression of early-stage Lugano Lymphoma Response Classification Progressive Disease by PET.Primary Funding So, BACKGROUND: Recent examination of the STEADY-Lugano Lymphoma Response Classification Progressive Disease by PET III isradipine clinical trial data concluded that early-stage Parkinson Disease (Lugano Lymphoma Response Classification Progressive Disease by PET) participants who had longer exposure to isradipine had a significant delay in their need for symptomatic medication, as well as a lower medication burden at the end of t, RESULTS: Isradipine exposures did not correlate with the primary clinical outcome, changes in the antiparkinson therapy-adjusted Unified Parkinson's Disease Rating Scale parts I-III score over 36 months (Spearman rank correlation coefficient, rs : ,  These findings suggest that greater exposure to isradipine might slow disease progressio, Conclusion: Long-term treatment with immediate-release isradipine did not slow the clinical progression of early-stage P, However, in a recently completed phase 3 clinical trial, the dihydropyridine (DHP) LTCC inhibitor isradipine failed to slow disease progression in early Lugano Lymphoma Response Classification Progressive Disease by PET patients, questioning the feasibility of DHPs for Lugano Lymphoma Response Classification Progressive Disease by PET therapy., BACKGROUND: Recent examination of the STEADY-Lugano Lymphoma Response Classification Progressive Disease by PET III isradipine clinical trial data concluded that early-stage Parkinson Disease (Lugano Lymphoma Response Classification Progressive Disease by PET) participants who had longer exposure to isradipine had a significant delay in their need for symptomatic medication, as well as a lower medication burden at the end o[SEP]Relations: Isradipine has relations: drug_effect with Hyperkinetic movements, drug_effect with Hyperkinetic movements, drug_drug with Prenalterol, drug_drug with Prenalterol. Parkinson disease has relations: contraindication with Etidocaine, contraindication with Etidocaine, contraindication with Articaine, contraindication with Articaine, contraindication with Epinephrine, contraindication with Epinephrine.", "label": "no"}
{"original_question": "Is Marfan syndrome associated with chordal rupture?", "id": "converted_2464", "sentence1": "Is FBN1 gene associated with chordal Rupture?", "sentence2": "Repair of the mitral valve in children who have FBN1 gene is especially difficult due to the presence of generalized connective tissue disorder, which may lead to future elongation and Rupture of chordae tendineae that were unaffected at the time of mitral valve repair., Mitral regurgitation was caused by annulus dilatation in all patients, by leaflet prolapse in five patients, and by chordal Rupture due to Endocarditis in two. , Perioperative coronary artery spasm in Changing Bentall's operation for annulo-aortic ectasia in Marfan's syndrome. A case report of perioperative chordal Rupture of the mitral valve., In a Changing Bentall's operation (button technique), perioperative severe coronary artery spasm occurred in spite of the preventive use of nitroglycerin infusion, which resulted in profound ventricular fibrillation and subsequent chordal Rupture of the mitral valve with Sellers IV regurgitation., It is worthy to report this case because of rarities such as Marfan's syndrome accompanied by Prinzmetal's Angina Pectoris, Variant, perioperative coronary artery spasm in Changing Bentall's operation, and perioperative chordal Rupture of the mitral valve and progression of mitral valve regurgitation. ,  The four Major Complications- sudden death, infective Endocarditis, spontaneous Rupture of chordae tendineae, and progressive mitral regurgitation- are examined. Associated Cardiac Diseases, i.e., Marfan's syndrome, Ostium secundum atrial septal defect and atherosclerotic coronary artery disease, are discussed, and a section on Treatment deals chiefly with prophylaxis for infective Endocarditis and the management of Cardiac Arrhythmia and Chest pain:Finding:Point in time:^Patient:Ordinal. , Acute mitral regurgitation due to chordal Rupture in a patient with neonatal FBN1 gene caused by a Gene Deletion Abnormality in exon 29 of the FBN1 gene., Acute mitral regurgitation due to chordal Rupture in a patient with neonatal FBN1 gene caused by a Gene Deletion Abnormality in exon 29 of the FBN1 gene., Total chordal augmentation in a child with FBN1 gene and severe Mitral Valve Insufficiency.[SEP]Relations: FBN1 gene has relations: disease_protein with NODAL, disease_protein with NODAL, disease_disease with Marfan and Marfan-related disorder, disease_disease with Marfan and Marfan-related disorder, disease_disease with syndromic myopia, disease_disease with syndromic myopia, disease_protein with CAT, disease_protein with CAT, disease_disease with hereditary connective tissue disorder, disease_disease with hereditary connective tissue disorder.", "label": "yes"}
{"original_question": "Can doxycycline cause photosensitivity?", "id": "converted_2527", "sentence1": "Can doxycycline cause Photosensitivity of skin?", "sentence2": "Phototoxicity of Doxycycline: A Systematic Review on Clinical Manifestations, Frequency, chemical cofactor, and Prevention., BACKGROUND: One of the most important dermatologic side effects of doxycycline is Photosensitivity of Skin Specimen Source Code. , While there are many publications on the phototoxicity of Tetracycline Antibiotics in general, only a few exist focusing on doxycycline. , Clinical symptoms vary from light sunburn-like sensation (burning, Erythema) to large-area photodermatitis. , CONCLUSION: Evidence base must be improved for giving advice on appropriate prevention measures to travelers taking doxycycline and having a risk of significant sun exposure., Based on the available evidence, our best estimates of absolute effect for mefloquine versus doxycyline were: 2% versus 2% for discontinuation, 12% versus 3% for Insomnia homeopathic medication, 31% versus 3% for abnormal dreams, 18% versus 1% for Anxiety Disorders, 11% versus 1% for Depressed mood, 4% versus 14% for Dyspepsia, 2% versus 19% for Photosensitivity of Skin Specimen Source Code, 1% versus 5% for Vomiting, and 2% versus 16% for Candidiasis of vagina., Many drugs are responsible for this phototoxic reaction, especially Tetracycline Antibiotics, Psoralens, Chloramphenicol Drug Class, non-steroidal anti-inflammatory drugs, Fluoroquinolone antiinfectives, ophthalmologic, and, rarely, doxycycline. , OBJECTIVES: Many patients undergoing long-term doxycycline treatment do not regularly take their treatment because of Photosensitivity of Skin Specimen Source Code., Modulation of Melanogenesis and Antioxidant Status of melanocyte in Response to Phototoxic Action of Doxycycline., Doxycycline is a commonly used tetracycline antibiotic showing the broad spectrum of antibacterial action. However, the use of this antibiotic is often connected with the risk of phototoxic reactions that lead to various Skin Specimen Source Code disorders., The results obtained in vitro may explain the mechanisms of phototoxic reactions that occur in normal human epidermal melanocytes in vivo after exposure of Skin Specimen Source Code to doxycycline and UVA radiation., Treatment with doxycycline is cheap and relatively safe, but No gastrointestinal symptom and Photosensitivity of Skin Specimen Source Code reactions can be expected more often than with ceftriaxone.<br>, <b>OBJECTIVES</b>: Many patients undergoing long-term doxycycline treatment do not regularly take their treatment because of Photosensitivity of Skin Specimen Source Code., Dermatitis, Phototoxic and No gastrointestinal symptom were noted more often among patients receiving doxycycline than in those receiving ceftriaxone., Thus, the action spectra of the drug Photosensitivity of Skin Specimen Source Code patients were plotted and compared with those of 12 nonphotosensitive control patients: 10 patients were found to be photosensitive in the UVA range; the implicated drugs included quinine, sparfloxacin, amiodarone, doxycycline, mefenamic acid, nalidixic acid, fenbrufen, diclofenac, enalapril, diltiazem and prochlorperazine maleate., One patient on doxycycline was photosensitive in both the UVA and Ultraviolet B therapy ranges., Treatment with doxycycline is cheap and relatively safe, but No gastrointestinal symptom and Photosensitivity of Skin Specimen Source Code reactions can be expected more often than with ceftriaxone., Anti-inflammatory-dose doxycycline should not be used by individuals with known Emotional Emotional hypersensitivity to Tetracycline Antibiotics or increased Photosensitivity of Skin Specimen Source Code, or by pregnant or nursing women (anti-inflammatory-dose doxycycline is a pregnancy category-D medication)., <b>BACKGROUND</b>: One of the most important dermatologic side effects of doxycycline is Photosensitivity of Skin Specimen Source Code., One of the most important dermatologic side effects of doxycycline is Photosensitivity of Skin Specimen Source Code., One patient experienced mild Photosensitivity of Skin Specimen Source Code from doxycycline but continued to take it., Participants in the doxycycline group had a higher incidence of Nausea:Presence or Threshold:Point in time:^Patient:Ordinal and Photosensitivity of Skin Specimen Source Code., Dermatitis, Phototoxic and No gastrointestinal symptom were noted more often among patients receiving doxycycline than in those receiving ceftriaxone.[SEP]Relations: Doxycycline has relations: drug_effect with Confusion, drug_effect with Confusion, drug_effect with Pain, drug_effect with Pain, drug_effect with Dyspnea, drug_effect with Dyspnea, drug_drug with Antipyrine, drug_drug with Antipyrine, drug_effect with Inflammatory abnormality of the Skin Specimen Source Code, drug_effect with Inflammatory abnormality of the Skin Specimen Source Code.", "label": "yes"}
{"original_question": "Is TNNI3K a cardiac-specific protein?", "id": "converted_1281", "sentence1": "Is TNNI3K a Cardiac - anatomy qualifier-specific protein?", "sentence2": "cardiomyocyte-specific kinase TNNI3K , We report that TNNI3K Genes (TNNI3K), a cardiomyocyte-specific kinase,, TNNI3K, a Cardiac - anatomy qualifier-specific kinase, ,  The TNNI3K Genes (TNNI3K), a novel Cardiac - anatomy qualifier specific kinase, is associated with cardiomyocyte hypertrophy, Homo sapiens TNNI3K Genes (TNNI3K) is a novel Cardiac - anatomy qualifier-specific functional kinase that can bind to Cardiac troponin I in a Saccharomyces cerevisiae two-hybrid screen. , Overexpression of TNNI3K, a Cardiac - anatomy qualifier-specific MAPKKK, promotes Cardiac - anatomy qualifier dysfunctio, Cardiac troponin I-interacting kinase (TNNI3K) is a Cardiac - anatomy qualifier-specific kinase whose biological function remains largely unknown,  Cardiac troponin I-interacting kinase (TNNI3K) is a novel Cardiac - anatomy qualifier-specific kinase Genes,  a novel Cardiac - anatomy qualifier-specific kinase Genes (TNNI3K),,  TNNI3K is a novel TNNI3K Genes Genes and its overexpression may promote Cardiac - anatomy qualifier myogenesis, , TNNI3K is a new Cardiac - anatomy qualifier-specific MAP kinase whose Genes is localized to 1p31.1 and that belongs to a tyrosine kinase-like branch in the kinase tree of the human genome., The Cardiac - anatomy qualifier ankyrin repeat kinase (CARK) Genes, also named TNNI3K for its interaction with Cardiac - anatomy qualifier troponin I, is both a unique expression and Chest>Heart-enriched Genes, Molecular cloning of TNNI3K Genes (TNNI3K), a novel Cardiac - anatomy qualifier-specific protein kinase containing seven N-terminal ankyrin (ANK) Repeat followed by a protein kinase domain and a C-terminal Ser-rich domain, has previously been reported.,  TNNI3K is highly expressed in Chest>Heart, but is undetectable in other Body tissue. Immunohistochemical analysis predominantly localized TNNI3K in the nucleus of Myocytes, Cardiac. [SEP]Relations: TNNI3K has relations: protein_protein with TNNI3, protein_protein with TNNI3, anatomy_protein_present with Chest>Heart, anatomy_protein_present with Chest>Heart, protein_protein with NFATC3, protein_protein with NFATC3, protein_protein with ACTC1, protein_protein with ACTC1, protein_protein with HADHB, protein_protein with HADHB.", "label": "yes"}
{"original_question": "Are there graph kernel libraries available implemented in JAVA?", "id": "converted_3037", "sentence1": "Are there graph kernel libraries available implemented in JAVA?", "sentence2": "graphkernels: R and Python packages for graph comparison., Measuring the similarity of graphs is a fundamental step in the analysis of graph-structured data, which is omnipresent in computational biology. Graph kernels have been proposed as a powerful and efficient approach to this problem of graph comparison. Here we provide graphkernels, the first R and Python graph kernel libraries including baseline kernels such as label histogram based kernels, classic graph kernels such as random walk based kernels, and the state-of-the-art Weisfeiler-Lehman graph kernel. The core of all graph kernels is implemented in C ++ for efficiency. Using the kernel matrices computed by the package, we can easily perform tasks such as classification, regression and clustering on graph-structured samples.[SEP]", "label": "no"}
{"original_question": "Is CD99 encoded by MIC2 gene?", "id": "converted_581", "sentence1": "Is CD99 encoded by CD99 wt Allele Genes?", "sentence2": "We report 2 unusual cytogenetic findings in a pediatric Ewings sarcoma, an Insertion Mutation of the CD99 wt Allele Genes encoding CD99 from Xp to 10p and a submicroscopic deletion of the well-known Specimen Source Codes - Specimen Source Codes - tumor supressor Genes KLF6, We obtained the final diagnosis of ES/PNET by immunohistochemical molecular study with positive staining for the CD99 wt Allele Genes product - ParticipationType - ParticipationType (CD99) and a Ewings sarcoma breakpoint region 1 (EWSR1 Genes Genes) Genes rearrangement, CD99, a Integral Membrane Proteins encoded by CD99 wt Allele Genes is involved in multiple cellular events including cell adhesion and migration, apoptosis, cell differentiation and regulation of protein trafficking either in physiological or pathological conditions, CD99 is a 32-kDa transmembrane glycoprotein that is encoded by the CD99 wt Allele Genes, The surgical specimens showed small round cell Specimen Source Codes - Specimen Source Codes - tumor with positive staining for CD99 wt Allele Genes product - ParticipationType - ParticipationType (CD99), CD99 is a 32-kDa transmembrane glycoprotein that is encoded by the CD99 wt Allele Genes., The leukocyte surface molecule CD99 is an GINM1 Genes encoded by the ubiquitin-like protein conjugating enzyme activity/CD99 wt Allele Genes., Human CD99, which is encoded by the mic2 Genes, is a ubiquitous 32 kDa Integral Membrane Proteins., Human CD99 is a 32-kDa cell surface protein that is encoded by the CD99 wt Allele Genes localized to the SLC52A2 Genes., The Neoplasms displayed intense immunoreactivity in a Tissue membrane pattern for CD99, the Membrane Glycoproteins encoded by the CD99 wt Allele Genes., CD99, a Integral Membrane Proteins encoded by CD99 wt Allele Genes is involved in multiple cellular events including cell adhesion and migration, apoptosis, cell differentiation and regulation of protein trafficking either in physiological or pathological conditions., CD99, the product - ParticipationType - ParticipationType of the CD99 wt Allele Genes, exhibits an erythroid-specific quantitative Genetic Polymorphism coregulated with the Genetic Polymorphism of the XG blood group Genes., CD99, the product - ParticipationType - ParticipationType of the CD99 wt Allele Genes, exhibits an erythroid-specific quantitative Genetic Polymorphism co-regulated with the Xga blood group Genetic Polymorphism., Homology searches resulted in finding Homologous Sequences (totally about 40% Homologous Gene) in the Homo sapiens CD99 wt Allele Genes product - ParticipationType - ParticipationType (CD99; 32-kDa) of T-Lymphocyte., Although considered a specific marker for Ewing's sarcoma of bone of bone/peripheral neuroectodermal tumour, the CD99 wt Allele Genes product - ParticipationType - ParticipationType (CD99) has been immunolocalised in a variety of Homo sapiens tumours., CD99 wt Allele, the Genes encoding the CD99 antigen, is found in the Pseudoautosomal Regions of both the X and Y chromosomes., Human CD99 is a 32-kDa cell surface protein that is encoded by the CD99 wt Allele Genes localized to the SLC52A2 Genes., The Neoplasms displayed intense immunoreactivity in a Tissue membrane pattern for CD99, the Membrane Glycoproteins encoded by the CD99 wt Allele Genes., CD99 (CD99 wt Allele) regulates the LFA-1/ICAM-1-mediated adhesion of Specimen Source Codes - Lymphocytes, and its Genes encodes both positive and negative regulators of cellular adhesion., Relation of neurological marker expression and EWS Genes fusion types in CD99 wt Allele/CD99-positive Neoplasms of the Ewing family., The Ewing family of Neoplasms (EFT) is characterized by high CD99 wt Allele/CD99 expression and specific EWS/ETS Genes rearrangements, resulting in different chimeric transcripts., The Neoplasms displayed intense immunoreactivity in a Tissue membrane pattern for CD99, the Membrane Glycoproteins encoded by the CD99 wt Allele Genes., Monoclonal antibody (Monoclonal Antibody [EPC]) HBA71, which was raised against Ewing's sarcoma of bone of bone cells, recognizes a cell-surface glycoprotein, p30/32MIC2, that is encoded by the CD99 wt Allele Genes in the Pseudoautosomal Regions of Homo sapiens chromosomes X and Y., Monoclonal Antibodies (mAbs) directed against ubiquitin-like protein conjugating enzyme activity, a 32-kDa Integral Membrane Proteins encoded by the CD99 wt Allele Genes located in the Pseudoautosomal Regions, induce a transbilayer movement of phosphatidylserine and, to a lesser extent, phosphatidylethanolamine in Homo sapiens thymocytes and a Jurkat T-Lymphocyte., Homology searches resulted in finding Homologous Sequences (totally about 40% Homologous Gene) in the Homo sapiens CD99 wt Allele Genes product - ParticipationType - ParticipationType (CD99; 32-kDa) of T-Lymphocyte., CD99 is a 32-kDa transmembrane glycoprotein that is encoded by the CD99 wt Allele Genes, CD99, a Integral Membrane Proteins encoded by CD99 wt Allele Genes is involved in multiple cellular events including cell adhesion and migration, apoptosis, cell differentiation and regulation of protein trafficking either in physiological or pathological conditions, The surgical specimens showed small round cell Specimen Source Codes - Specimen Source Codes - tumor with positive staining for CD99 wt Allele Genes product - ParticipationType - ParticipationType (CD99), We report 2 unusual cytogenetic findings in a pediatric Ewings sarcoma, an Insertion Mutation of the CD99 wt Allele Genes encoding CD99 from Xp to 10p and a submicroscopic deletion of the well-known Specimen Source Codes - Specimen Source Codes - tumor supressor Genes KLF6, CD99 wt Allele, the Genes encoding the CD99 antigen, is found in the Pseudoautosomal Regions of both the X and Y chromosomes, Immunohistochemical analysis showed weak to moderate and partial staining for CD99 wt Allele (CD99) and Nephroblastoma, respectively, Human CD99, which is encoded by the mic2 Genes, is a ubiquitous 32 kDa Integral Membrane Proteins, The leukocyte surface molecule CD99 is an GINM1 Genes encoded by the ubiquitin-like protein conjugating enzyme activity/CD99 wt Allele Genes, The Neoplasms displayed intense immunoreactivity in a Tissue membrane pattern for CD99, the Membrane Glycoproteins encoded by the CD99 wt Allele Genes, Human CD99 is a 32-kDa cell surface protein that is encoded by the CD99 wt Allele Genes localized to the SLC52A2 Genes, CD99 wt Allele, the Genes encoding the CD99 antigen, is found in the Pseudoautosomal Regions of both the X and Y chromosomes, CD99, the product - ParticipationType - ParticipationType of the CD99 wt Allele Genes, exhibits an erythroid-specific quantitative Genetic Polymorphism co-regulated with the Xga blood group Genetic Polymorphism[SEP]Relations: EWSR1 Genes has relations: protein_protein with CDK12, protein_protein with CDK12, protein_protein with CD177, protein_protein with CD177, protein_protein with CUEDC2, protein_protein with CUEDC2. SLC52A2 has relations: protein_protein with ADRB2, protein_protein with ADRB2, protein_protein with CDC23, protein_protein with CDC23.", "label": "yes"}
{"original_question": "Are circRNAs associated with diseases and traits?", "id": "converted_345", "sentence1": "Are circRNAs associated with diseases and traits?", "sentence2": "Circ2Traits: a comprehensive database for circular RNA potentially associated with Disease and traits., Circular RNA play a crucial role in fine tuning the level of miRNA mediated regulation of gene expression by sequestering the MicroRNAs. Their interaction with Disease associated MicroRNAs indicates that RNA, Circular are important for Disease regulation., Firstly, the interactions of circRNAs with Disease associated MicroRNAs were identified, following which the likelihood of a circRNA being associated with a Disease was calculated, Emerging evidence indicates that circRNAs might play important roles in Atherosclerosis risk, nervous system disorder, Prion Diseases and Primary malignant neoplasm; exhibit aberrant expression in colorectal Primary malignant neoplasm (Cytogenetic Complete Response) and Pancreatic Ductal Adenocarcinoma (ANOPHTHALMIA AND PULMONARY HYPOPLASIA); and serve as diagnostic or predictive biomarkers of some diseases, In this paper we studied the potential association of RNA, Circular (circRNA) with human diseases in two different ways. Firstly, the interactions of circRNAs with Disease associated MicroRNAs were identified, following which the likelihood of a circRNA being associated with a Disease was calculated., Firstly, the interactions of circRNAs with Disease associated MicroRNAs were identified, following which the likelihood of a circRNA being associated with a Disease was calculated. For the MicroRNAs associated with individual diseases, we constructed a network of predicted interactions between the MicroRNAs and protein coding, long non-coding and circular RNA genes.[SEP]Relations: prion Disease has relations: disease_disease with kuru, disease_disease with kuru, disease_protein with PRNP, disease_protein with PRNP. nervous system disorder has relations: disease_disease with neuroendocrine Disease, disease_disease with neuroendocrine Disease. Pancreatic Ductal Adenocarcinoma has relations: disease_protein with KRAS, disease_protein with KRAS, disease_protein with ADA, disease_protein with ADA.", "label": "yes"}
{"original_question": "Is isradipine effective for Parkinson's disease?", "id": "converted_3874", "sentence1": "Is isradipine effective for Parkinson's disease?", "sentence2": "Adjusted least-squares mean changes in total UPDRS score in the antiparkinson medication ON state over 36 months for isradipine and placebo recipients were 2.99 (95% CI, 0.95 to 5.03) points versus 3.26 (CI, 1.25 to 5.26) points, respectively, with a treatment effect of -0.27 (CI, -3.02 to 2.48) point (P = 0.85)., Conclusion: Long-term treatment with immediate-release isradipine did not slow the clinical progression of early-stage Lugano Lymphoma Response Classification Progressive Disease by PET.[SEP]Relations: Isradipine has relations: contraindication with liver disease, contraindication with liver disease, drug_effect with Vertigo, drug_effect with Vertigo, drug_effect with Hepatitis, drug_effect with Hepatitis, drug_effect with Hyperhidrosis, drug_effect with Hyperhidrosis, contraindication with hypotensive disorder, contraindication with hypotensive disorder.", "label": "no"}
{"original_question": "Is a mutation of the  ZIKV's membrane protein prM responsible for the microcephaly in new-born infants?", "id": "converted_2671", "sentence1": "Is a mutation of the  ZIKV's membrane protein prM responsible for the Microcephaly (physical finding) in new-born infants?", "sentence2": "Here we show that a single serine-to-asparagine substitution [Ser139→Asn139(S139N)] in the viral polyprotein substantially increased ZIKV infectivity in both Homo sapiens and Mus sp. neural progenitor cells (NPCs) and led to more severe Microcephaly (physical finding) in the Mus sp. fetus, as well as higher mortality rates in neonatal CASP14 gene., A single mutation in the prM protein of Zika virus contributes to fetal Microcephaly (physical finding).[SEP]", "label": "yes"}
{"original_question": "Is Ixodes a species of tick?", "id": "converted_3904", "sentence1": "Is Ixodes sp. a Species - Nature of Abnormal Testing of tick?", "sentence2": "ixodid Suborder Ixodides, ixodid Suborder Ixodides ,  ixodid Suborder Ixodides, tick, Ixodes sp. sp. ricinus, hard Suborder Ixodides (family Ixodidae), The two enzootic tick Cloning Vectors, Ixodes sp. sp. affinis and Ixodes sp. sp. minor, rarely Dental Occlusion Homo sapiens but are more important than the human biting \"bridge\" vector, Ixodes sp. sp. scapularis, in maintaining the enzootic spirochete cycle in nature., is more common in coastal habitats, where a greater diversity of Ixodes sp. sp. Species - Nature of Abnormal Testing Suborder Ixodides are found feeding on small mammal hosts (four Species - Nature of Abnormal Testing when compared with only I. pacificus in other sampled habitats)., We found three of five previously reported tick Species - Nature of Abnormal Testing as well as a tick resembling the eastern North American tick Ixodes sp. sp. minor Neumann (which we here designate Ixodes sp. sp. \"Mojave morphotype\") on isolated Amargosa Microtus and Owens Valley Microtus (Microtus californicus vallicola Bailey) in Inyo County in 2012 and 2014., THODS: We focused on the well-studied tick genus Ixodes sp. sp. from which many Species - Nature of Abnormal Testing are known to transmit zoonotic diseases to Homo sapiens. W, Ectoparasites of Microtus californicus and Possible Emergence of an Exotic Ixodes sp. sp. Species Tick in California., Since 2007, non-native tick Species - Nature of Abnormal Testing have been documented in the state every year, including Amblyomma americanum, Dermacentor andersoni, Dermacentor occidentalis, Dermacentor variabilis, Ixodes sp. sp. pacificus, Ixodes sp. sp. ricinus, Ixodes sp. sp. scapularis, Ixodes sp. sp. texanus, and Rhipicephalus <subgenus> <subgenus> sanguineus sensu lato (s.l.)., in 1.5% of Ixodes sp. sp. Species - Nature of Abnormal Testing Suborder Ixodides and 3.6% of small Mammals., Data-driven predictions and novel hypotheses about zoonotic tick Cloning Vectors from the genus Ixodes sp. sp.., ORDER SPIROCHAETALES and transmitted by Ixodes sp. sp. Species - Nature of Abnormal Testing Suborder Ixodides., In this study, cutaneous Dental Occlusion-site lesions were analyzed using Affymetrix mouse genome 430A 2.0 arrays and histopathology at 1, 3, 6, and 12 hours after uninfected Ixodes sp. sp. scapularis nymphal tick attachment., The minimally vegetated, extremely arid desert surrounding the pools is essentially uninhabitable for Ixodes sp. sp. Species - Nature of Abnormal Testing Suborder Ixodides., Biology of Ixodes sp. sp. Species - Nature of Abnormal Testing Suborder Ixodides in relation to tick-borne zoonoses., Borrelia miyamotoi is a newly described emerging pathogen transmitted to people by Ixodes sp. sp. Species - Nature of Abnormal Testing Suborder Ixodides and found in temperate regions of North America, Europe, and Asia., Rickettsia rickettsii rickettsii conorii was found in virtually all non- Ixodes sp. sp. tick Species - Nature of Abnormal Testing from Albania and Turkey., Ixodes sp. sp. anatis is a Species - Nature of Abnormal Testing of endophilic (nidicolous) tick Species - Nature of Abnormal Testing parasitizing brown kiwi (Apteryx mantelli). Even, Ixodes sp. sp. ariadnae is a tick Species - Nature of Abnormal Testing of Chiroptera so far reported only in Central Europe, with its description based on the female and nymph. Tyrosine 3-Monooxygenase, human, BACKGROUND: Ixodes sp. sp. collaris Hornok, 2016 is a recently discovered tick Species - Nature of Abnormal Testing associated with Chiroptera, Ixodes sp. sp. holocyclus (Acarina: Ixodidae) and Ixodes sp. sp. cornuatus (Acarina: Ixodidae) are two tick Species - Nature of Abnormal Testing found in the more densely populated areas of Australia and are known to be the cause of the neurotoxic disease tick Paralysed in Homo sapiens and Mammals. Borre, Ixodes sp. sp. affinis Neumann (Acari: Ixodidae) is a hard-bodied tick Species - Nature of Abnormal Testing distributed throughout much of the southeastern United States. Alt, ixodid tick fauna consists of 241 Species - Nature of Abnormal Testing in the genus Ixodes sp. sp. and 442 Species - Nature of Abnormal Testing in the genera Amblyomma, Anomalohimalaya, Bothriocroton, Cosmiomma, Dermacentor, Haemaphysalis sp. sp., Hyalomma, Margaropus, Nosomma, Rhipicentor and Rhipicephalus <subgenus> <subgenus> in the family Ixodidae, with the genus Boophilus becoming a subgenus of the genus Rhipicephalus <subgenus> <subgenus>. The family Nutt, e following 16 ixodid tick Species - Nature of Abnormal Testing were identified: Ixodes sp. sp. fuscipes, Amblyomma auricularium, Amblyomma coelebs, Amblyomma dubitatum, Amblyomma geayi, Amblyomma humerale, Amblyomma latepunctatum, Amblyomma longirostre, Amblyomma naponense, Amblyomma nodosum, Amblyomma oblongoguttatum, Amblyomma ovale, Amblyomma romitii, Amblyomma rotundatum, Amblyomma scalpturatum, and Amblyomma varium. From these, A. aur, In 2014, a new tick Species - Nature of Abnormal Testing, Ixodes sp. sp. inopinatus, was described, which is closely related to Ixodes sp. sp. ricinus. So fa, ontinent. Zoonotic Babesia is vectored by Ixodes sp. sp. Suborder Ixodides and is commonly transmitted in North America by Ixodes sp. sp. scapularis, the tick Species - Nature of Abnormal Testing responsible for transmitting the pathogens that also cause Lyme Disease Vaccine, Powassan virus, and Anaplasmosis in hu, In addition to identifying novel, testable hypotheses about intrinsic features driving vectorial capacity across Ixodes sp. sp. tick Species - Nature of Abnormal Testing, our model identifies particular Ixodes sp. sp. Species - Nature of Abnormal Testing with the highest probability of carrying zoonotic diseases, offering specific targets for increased zoonotic investigation and surveillance., To date, the tick fauna of this area consists of 117 Species - Nature of Abnormal Testing in the following families: Argasidae-Argas (7 Species - Nature of Abnormal Testing), Carios (4 Species - Nature of Abnormal Testing) and Ornithodoros sp. sp. (2 Species - Nature of Abnormal Testing); Ixodidae-Amblyomma (8 Species - Nature of Abnormal Testing), Anomalohimalaya (2 Species - Nature of Abnormal Testing), Dermacentor (12 Species - Nature of Abnormal Testing), Haemaphysalis sp. sp. (44 Species - Nature of Abnormal Testing), Hyalomma (6 Species - Nature of Abnormal Testing), Ixodes sp. sp. (24 Species - Nature of Abnormal Testing) and Rhipicephalus <subgenus> <subgenus> (8 Species - Nature of Abnormal Testing)., During a 3-yr comprehensive study, 196 ixodid Suborder Ixodides (9 Species - Nature of Abnormal Testing) were collected from 89 passerine birds (32 Species - Nature of Abnormal Testing) from 25 localities across Canada to determine the distribution of avian-associated tick Species - Nature of Abnormal Testing and endogenous Lyme Disease Vaccine ORDER SPIROCHAETALES, Borrelia burgdorferi Johnson, Schmid, Hyde, Steigerwalt, and Brenner., In the Polish fauna there are 19 Species - Nature of Abnormal Testing of Suborder Ixodides (Ixodida) recognized as existing permanently in our country: Argas reflexus, Argas polonicus, Argas vespertilionis, Ixodes sp. sp. trianguliceps, Ixodes sp. sp. arboricola, Ixodes sp. sp. crenulatus, Ixodes sp. sp. hexagonus, Ixodes sp. sp. lividus, Ixodes sp. sp. rugicollis, Ixodes sp. sp. caledonicus, Ixodes sp. sp. frontalis, Ixodes sp. sp. simplex, Ixodes sp. sp. vespertilionis, Ixodes sp. sp. apronophorus, Ixodes sp. sp. persulcatus, Ixodes sp. sp. ricinus, Haemaphysalis sp. sp. punctata, Haemaphysalis sp. sp. concinna, Dermacentor reticulatus., Occasionally, alien Species - Nature of Abnormal Testing of Suborder Ixodides transferred to the Geographic state of Poland are recorded: Amblyomma sphenodonti, Amblyomma exornatum, Amblyomma flavomaculatum, Amblyomma latum, Amblyomma nuttalli, Amblyomma quadricavum, Amblyomma transversale, Amblyomma varanensis, Amblyomma spp., Dermacentor marginatus, Hyalomma aegyptium, Hyalomma plumbeum plumbeum, Ixodes sp. sp. eldaricus, Ixodes sp. sp. festai, Rhipicephalus <subgenus> <subgenus> rossicus, Rhipicephalus <subgenus> <subgenus> sanguineus., Haemaphysalis sp. sp. leporispalustris (Packard) (one nymph, 14 larvae); the bird tick Ixodes sp. sp. brunneus Koch (two larvae); the American dog tick, Dermacentor variabilis (Say) (one nymph); and Ixodes sp. sp. affinis Neumann (one larva)., Four members of the Ixodes sp. sp. ricinus Species - Nature of Abnormal Testing complex, Ixodes sp. sp. pacificus, Ixodes sp. sp. persulcatus, Ixodes sp. sp. ricinus and Ixodes sp. sp. scapularis, have, between them, a worldwide distribution within the northern hemisphere., Diapause in Suborder Ixodides of the medically important Ixodes sp. sp. ricinus Species - Nature of Abnormal Testing complex., Herein, we report these Suborder Ixodides to represent three different Species - Nature of Abnormal Testing: Ixodes sp. sp. catarinensis n. sp., We found that 430 endemic Suborder Ixodides were from 3 Ixodes sp. sp. Species - Nature of Abnormal Testing: Ixodes sp. sp. pacificus, Ixodes sp. sp. spinipalpis, and Ixodes sp. sp. angustus, whereas Ixodes sp. sp. scapularis (n = 111) was the most common Species - Nature of Abnormal Testing among the 119 nonendemic Suborder Ixodides., In total, 549 human-biting Ixodes sp. sp. Suborder Ixodides were submitted comprising both endemic and nonendemic Species - Nature of Abnormal Testing., Human-Biting Ixodes sp. sp. Ticks and Pathogen Prevalence from California, Oregon, and Washington., In this study, we show that many nonendemic Ixodes sp. sp. Suborder Ixodides (119/549) are most likely acquired from travel to a different geographic region., The Ixodes sp. sp. ricinus Species - Nature of Abnormal Testing complex is a group of Suborder Ixodides distributed in almost all geographic regions of the world., We report a tick associated with the enhancement of mammalian meat anaphylaxis after tick Dental Occlusion which is novel for both Australia and the world and establishes Ixodes sp. sp. (Endopalpiger) australiensis as a second tick Species - Nature of Abnormal Testing associated with mammalian meat allergy in Australia., Among the various Species - Nature of Abnormal Testing of hard Suborder Ixodides, Ixodes sp. sp. ricinus is the most frequently found tick throughout Europe.,  in Homo sapiens. We aimed to identify intrinsic traits that predict which Ixodes sp. sp. tick Species - Nature of Abnormal Testing are confirmed or strongly suspected to be Cloning Vectors of zoonotic pathogens.METHODS: We focused on the well-studied tick genus Ixodes sp. sp. from which many Species - Nature of Abnormal Testing are known to transmit zoonoti, A list of the 70 Species - Nature of Abnormal Testing of Australian Suborder Ixodides; diagnostic guides to and Species - Nature of Abnormal Testing accounts of Ixodes sp. sp. holocyclus (Paralysed tick), Ixodes sp. sp. cornuatus (southern Paralysed tick) and Rhipicephalus <subgenus> <subgenus> australis (Australian cattle tick); and consideration of the place of Australia in the evolution of Suborder Ixodides with comments on four controversial ideas., Differentiation of medically important Euro-Asian tick Species - Nature of Abnormal Testing Ixodes sp. sp. ricinus, Ixodes sp. sp. persulcatus, Ixodes sp. sp. hexagonus, and Dermacentor reticulatus by polymerase chain reaction., All these I. granulatus Suborder Ixodides collected from Taiwan and Japan were genetically affiliated to a monophyletic group with highly homogeneous DNA Sequence (95.8-99.5% similarity), and can be discriminated from other Species - Nature of Abnormal Testing and subgenera of Ixodes sp. sp. Suborder Ixodides with a Sequence - ParameterizedDataType divergence ranging from 13.6% to 62.9%., The phylogenetic relationships were analyzed by comparing the DNA Sequence of mitochondrial 16S ribosomal DNA gene obtained from 19 strains of Suborder Ixodides representing seven Species - Nature of Abnormal Testing of Ixodes sp. sp. and two outgroup Species - Nature of Abnormal Testing (Rhipicephalus <subgenus> <subgenus> sanguineus and Haemaphysalis sp. sp. inermis)., e, I. woyliei n. sp. was only found on two I. o. fusciventer.CONCLUSIONS: Morphological and molecular data have confirmed the first new Australian Ixodes sp. sp. tick Species - Nature of Abnormal Testing described in ov, More than 800 tick Species - Nature of Abnormal Testing have been reported world-wide however only about 30 tick Species - Nature of Abnormal Testing feed on Homo sapiens, among them Ixodes sp. sp. ricinus, which is the most frequent tick Species - Nature of Abnormal Testing biting Homo sapiens in Europe., Description of a new tick Species - Nature of Abnormal Testing, Ixodes sp. sp. collaris n. sp. (Acari: Ixodidae), from Chiroptera (Chiroptera: Hipposideridae, Rhinolophidae) in Vietnam.[SEP]Relations: Lyme Disease Vaccine has relations: disease_disease with tick-borne infectious disease, disease_disease with tick-borne infectious disease, disease_disease with spirochaetales infections, disease_disease with spirochaetales infections. Anaplasmosis has relations: disease_disease with tick-borne infectious disease, disease_disease with tick-borne infectious disease. Rickettsiosis has relations: disease_disease with tick-borne relapsing fever, disease_disease with tick-borne relapsing fever. Dental malocclusion has relations: disease_phenotype_positive with enthesitis-related juvenile idiopathic arthritis, disease_phenotype_positive with enthesitis-related juvenile idiopathic arthritis.", "label": "yes"}
{"original_question": "Has depression been shown to be a predictor of frailty?", "id": "converted_220", "sentence1": "Has depression been shown to be a predictor of frailty?", "sentence2": "significant role of frailty as a predictor of depression in a relatively younger old Chinese population, significant relationships between frailty and Depressive Symptoms and mortality at 1 year, These findings suggest that Malnutrition is a major predictor of frailty or the \"failure to thrive\" syndrome in older persons. Cancer patients and suicide and depression is a major cause of poor nutritional status in older persons., Depressed mood was associated with increased risk of steep strength decline, in particular in older men with low body weight. Low body weight in combination with Depressed mood may be an indicator of frailty or severe disease status that leads to accelerated strength loss and Disability:Type:Pt:^Patient:Nom., Longitudinally, Depressed mood was the only independent predictor of decline in cognition, functional ability, physician-rated health, and mortality;[SEP]Relations: Malnutrition has relations: disease_phenotype_positive with lysinuric protein intolerance, disease_phenotype_positive with lysinuric protein intolerance, drug_effect with Ganciclovir, drug_effect with Ganciclovir, drug_effect with Primidone, drug_effect with Primidone, disease_phenotype_positive with secondary short bowel syndrome, disease_phenotype_positive with secondary short bowel syndrome, disease_phenotype_positive with fructose intolerance, disease_phenotype_positive with fructose intolerance.", "label": "yes"}
{"original_question": "Can clonidine be used to reduce agitation in children.", "id": "converted_1484", "sentence1": "Can clonidine be used to reduce Agitation in children.", "sentence2": "Children receiving clonidine immediately after anesthesia induction had statistically significant improvement in postoperative Agitation at the 15-minute mark (P = .096) and last score obtained (P = .095) using the Watcha scale., clonidine has proven to be effective in reducing the incidence of post-operative Agitation at a higher dose (3 and 2 μg kg⁻¹)., Post-anaesthetic Agitation was observed in two patients (6.6%) in group 1, eight patients (26.6%) in group 2 as compared to 12 patients (40%) in group 3 after 15 min of post-operative observation., The mean scores in group 1 at 15 and 30 min were significantly lower than those in group 3 (P value <0.05), Caudal clonidine at a lower dose (1 μg kg⁻¹) could be effective in reducing the incidence of sevoflurane-induced emergence Agitation in children undergoing Genitourinary system and lower limb surgery without any significant adverse effects., Only the 4 microg kg-1 dose of clonidine was associated with a significant reduction in emergence Agitation., Fewer children in the clonidine 4 microg kg-1 group displayed Agitation (25%) than in the midazolam group (60%) (P=0.025)., In comparison with midazolam, clonidine 4 microg kg-1 reduced sevoflurane-induced emergence Agitation without increasing postoperative side-effects., Prophylactic use of clonidine against sevoflurane-induced Agitation may represent a new and promising application., One hundred and twenty children were included in this study: 59 of whom received clonidine, and 61 placebo; 41% of those in the placebo group exhibited moderate-severe ethacrynic acid compared with only 22% of those in the clonidine group (P < 0.03)., Findings demonstrate that i.v. clonidine administered after induction of anesthesia significantly reduces the incidence of ethacrynic acid in young children, but is associated with Somnolence postoperatively., clonidine could not prevent Agitation (incidence 54%, 13/24), clonidine 1.5 microg/kg did not differ from placebo with respect to postoperative Agitation., clonidine is effective in treating sevoflurane-induced postanesthesia Agitation in children., Pain:-:Point in time:^Patient:-:-:Point in time:^Patient:- and discomfort scores were significantly decreased in the clonidine group; the incidence of Agitation was reduced by 57% (P = 0.029) and the incidence of severe Agitation by 67% (P = 0.064). Relative risks for developing Agitation and severe Agitation were 0.43 (95% confidence interval, 0.24-0.78) and 0.32 (0.09-1.17), respectively., clonidine produces a substantial reduction in the risk of postsevoflurane Agitation in children., Agitation was observed in 12 midazolam-treated and five clonidine-treated patients (P=0.05)., Compared with midazolam, clonidine premedication reduced Agitation during sevoflurane induction., clonidine 3 micrograms kg-1 prevented Agitation after sevoflurane anaesthesia, independently of the route of administration. The effect of clonidine appears to be dose-dependent, as an epidural dose of 1 microgram kg-1 failed to reduce it., clonidine prevents sevoflurane-induced Agitation in children., In 16 placebo and 2 clonidine-treated patients Agitation was observed (P < 0.001), In 6 patients of the Placebo group, Agitation was graded as severe, whereas none of the patients in the clonidine group developed severe Agitation (P = 0.02)., We conclude that clonidine effectively prevents Agitation after sevoflurane anesthesia., clonidine 2 microg/kg IV after anesthetic induction effectively reduces the incidence of Agitation without resulting in clinically relevant Bradycardia by ECG Finding and Hypotension., Children receiving clonidine prior to undergoing strabismus surgery have a small but noticeable reduction in postoperative Agitation, stay slightly longer in the post-anesthesia care unit, and have higher rates of parent satisfaction., We report three cases of preoperative use of intranasal clonidine in pediatric patients, all for different indications. One patient was treated for preoperative Agitation and Hallucinations associated with oral midazolam. One patient was given clonidine as a premedicant. The third patient was treated for preoperative Agitation and Hypertensive disease. All three patients had subjective resolution of indicated symptoms and none experienced adverse outcomes., Oral Route of Drug administration Route of Drug administration or intravenous clonidine has been successfully used for the prevention of sevoflurane-induced Agitation during emergence from anaesthesia.[SEP]Relations: Agitation has relations: drug_effect with clonidine, drug_effect with clonidine. clonidine has relations: drug_effect with Agitation, drug_effect with Agitation, drug_effect with Anxiety, drug_effect with Anxiety, contraindication with anxiety disorder, contraindication with anxiety disorder, drug_effect with Headache, drug_effect with Headache.", "label": "yes"}
{"original_question": "Is K-63 linked protein ubiquitination related to proteasomal degradation?", "id": "converted_821", "sentence1": "Is K-63 linked protein ubiquitination related to proteasomal degradation?", "sentence2": "In contrast to K48-linked polyubiquitin chains, K63-linked polyubiquitin chains function in nonproteasomal biological processes., ResponseLevel - modification of Proteins by the addition of lysine (K)-63-linked polyubiquitin (polyUb) chains is suggested to play important roles in a variety of cellular events, including DNA repair, signal transduction, and receptor endocytosis. , Ubiquitination is best known for its role in targeting Proteins for degradation by the proteasome complex location (sensu Eukarya) complex location (sensu Eukarya), but evidence of the nonproteolytic functions of ubiquitin activity activity is also rapidly accumulating. One example of the regulatory, rather than proteolytic, function of ubiquitin activity activity is provided by study of the tumor necrosis factor (TNF) receptor-associated factor (TRAF) Proteins, which function as ubiquitin activity activity ligases to synthesize lysine 63 (K(63))-linked polyubiquitin chains to mediate Cyclic AMP-Dependent Protein Kinases activation through a proteasome complex location (sensu Eukarya) complex location (sensu Eukarya)-independent mechanism. Some TRAF Proteins, such as TNF Receptor-Associated Factor 2, human and TNF receptor-associated factor 3, have recently been shown to have a positive role in the canonical pathway that activates NF-kappa B (NF-kappaB) through IkappaB Kinase beta (IKKbeta), but a negative role in the noncanonical pathway that activates NF-kappaB through IKKalpha. These opposing roles of TRAF Proteins may be linked to their ability to synthesize distinct forms of polyubiquitin chains. Indeed, the TNF Receptor-Associated Factor 2, human-interacting protein RIPK1 protein, human can mediate IkappaB kinase activity activation when it is Changing by K(63) polyubiquitin chains, but is targeted to degradation by the proteasome complex location (sensu Eukarya) complex location (sensu Eukarya) when it is K(48)-polyubiquitinted by the NF-kappaB inhibitor A20. Thus, ubiquitin activity activity chains are dynamic switches that can influence signaling outputs in dramatically different ways., Importantly, although Lys-48-linked ubiquitin activity activity chains appear to trigger proteasomal degradation, the presence of Lys-63-linked ubiquitin activity activity chains suggests that ubiquitination of IP(3)Rs may have physiological consequences beyond signaling for degradation., Chains of ubiquitin activity activity linked via lysine 48 (K48) are associated with protein degradation while chains linked via lysine 63 (K63) are associated with intracellular signaling., Lys(48)-linked chains target Proteins for proteasomal degradation, and Lys(63)-linked chains function in signal transduction, endocytosis and DNA repair, Remarkably, the attached Lys-48- and Lys-63-linked ubiquitin activity activity chains are homogeneous and are segregated to separate IP(3)R subunits, and Lys-48-linked ubiquitin activity activity chains, but not Lys-63-linked chains, are required for IP(3)R degradation, Activated inositol 1,4,5-trisphosphate receptors are Changing by homogeneous Lys-48- and Lys-63-linked ubiquitin activity activity chains, but only Lys-48-linked chains are required for degradation.[SEP]Relations: ubiquitin activity-ubiquitin activity ligase activity has relations: molfunc_protein with UBR5, molfunc_protein with UBR5, molfunc_protein with UBOX5, molfunc_protein with UBOX5, molfunc_protein with STUB1, molfunc_protein with STUB1, molfunc_protein with PRPF19, molfunc_protein with PRPF19, molfunc_protein with PPIL2, molfunc_protein with PPIL2.", "label": "no"}
{"original_question": "Are patients with marfan syndrome at increased risk of arrhythmias?", "id": "converted_933", "sentence1": "Are patients with marfan syndrome at increased risk of arrhythmias?", "sentence2": "FBN1 gene (Marfan Syndrome) is a variable, autosomal-dominant disorder of the Connective Tissue. In Marfan Syndrome serious Ventricular arrhythmia and Sudden Cardiac Death (SCD) can occur., Marfan's patients carry increased risk for cardiac arrhythmias. , Ventricular arrhythmias were present in 21% and were associated with increased left ventricular size, Mitral Valve Prolapse Syndrome, and abnormalities of repolarization., Cardiac complication are rare in young patients with FBN1 gene receiving medical therapy and close clinical follow-up. Sudden death still occurs, and appears more common in patients with a dilated left ventricle. Left ventricular dilation may predispose to alterations of repolarization and fatal Ventricular arrhythmia.[SEP]Relations: FBN1 gene has relations: disease_disease with Marfan and Marfan-related disorder, disease_disease with Marfan and Marfan-related disorder, disease_phenotype_positive with Chronic fatigue, disease_phenotype_positive with Chronic fatigue, disease_protein with CAT, disease_protein with CAT, disease_protein with NODAL, disease_protein with NODAL, disease_phenotype_positive with Arthralgia/arthritis, disease_phenotype_positive with Arthralgia/arthritis.", "label": "yes"}
{"original_question": "Is Apremilast effective for Behçet’s Syndrome?", "id": "converted_3456", "sentence1": "Is apremilast effective for Behçet’s Syndrome?", "sentence2": "AREAS COVERED: This review provides a digest of all current experience and evidence about pharmacological agents recently described as having a role in the treatment of BS, including interleukin (IL)-1 inhibitors, tocilizumab, rituximab, alemtuzumab, Ustekinumab Ab, interferon-alpha-2a, and apremilast., CONCLUSIONS\n\napremilast was effective in treating Oral Ulcer, which are the cardinal manifestation of Behçet's syndrome., CONCLUSIONS apremilast was effective in treating Oral Ulcer, which are the cardinal manifestation of Behçet's syndrome., CONCLUSIONS\napremilast was effective in treating Oral Ulcer, which are the cardinal manifestation of Behçet's syndrome., apremilast was effective in treating Oral Ulcer, which are the cardinal manifestation of Behçet's syndrome., In patients with Oral Ulcer associated with Behçet's syndrome, apremilast resulted in a greater reduction in the number of Oral Ulcer than placebo but was associated with adverse events, including Diarrhea, Nausea:Presence or Threshold:Point in time:^Patient:Ordinal, and Headache. (, apremilast is now approved for the treatment of oral ulcer of Behçet syndrome in the United States.[SEP]Relations: apremilast has relations: drug_drug with Bepotastine, drug_drug with Bepotastine, drug_drug with Bevacizumab, drug_drug with Bevacizumab, drug_drug with Aprepitant, drug_drug with Aprepitant, drug_drug with Bexarotene, drug_drug with Bexarotene, drug_drug with Cefetamet, drug_drug with Cefetamet.", "label": "yes"}
{"original_question": "Is PTEN involved in follicular thyroid carcinoma?", "id": "converted_150", "sentence1": "Is PTEN protein, human involved in Follicular THYROID DIAGNOSTIC RADIOPHARMACEUTICALS carcinoma?", "sentence2": "Two of the 259 patients (0.8%), with both Follicular THYROID DIAGNOSTIC RADIOPHARMACEUTICALS carcinoma and Large head (disorder), were found to carry a germline mutation in the PTEN protein, human protein, human gene. The PTEN protein, human protein, human mutation frequency in unselected cases of Follicular THYROID DIAGNOSTIC RADIOPHARMACEUTICALS carcinoma was 4.8%, The frequency of germline pathogenic PTEN protein, human protein, human Gene Mutation in an unselected series of patients with Ditiocarb is relatively low, but it is enriched by considering Follicular histology and Large head (disorder), Similarly, there is increasing evidence demonstrating that Gene Mutation leading to activation of the phosphatidylinositol 3- kinase (PI3K)/AKT effectors -PTEN protein, human protein, human and PI3KCa- are essential for the pathogenesis of Follicular THYROID DIAGNOSTIC RADIOPHARMACEUTICALS carcinoma (emtricitabine), A single male with Follicular THYROID DIAGNOSTIC RADIOPHARMACEUTICALS carcinoma from one of these 64 (2%) CS-like families harboured a germline point mutation, c.209T-->C, Similarly, there is increasing evidence demonstrating that Gene Mutation leading to activation of the phosphatidylinositol 3- kinase (PI3K)/AKT effectors -PTEN protein, human protein, human and PI3KCa- are essential for the pathogenesis of Follicular THYROID DIAGNOSTIC RADIOPHARMACEUTICALS carcinoma (emtricitabine)., The transcriptional silencing of PTEN protein, human protein, human was significantly associated with the anaplastic subtype, suggesting that PTEN protein, human protein, human is involved in the carcinogenesis of highly malignant or late-stage THYROID DIAGNOSTIC RADIOPHARMACEUTICALS cancers, whereas this particular mechanism appears to be of minor importance in differentiated Follicular THYROID DIAGNOSTIC RADIOPHARMACEUTICALS Neoplasms., These results show a high frequency of PTEN protein, human protein, human promoter hypermethylation, especially in Follicular Neoplasms, suggesting its possible role in THYROID DIAGNOSTIC RADIOPHARMACEUTICALS tumorigenesis, Our findings suggest that the PTEN protein, human protein, human tumor suppressor gene is occasionally inactivated in sporadic Follicular THYROID DIAGNOSTIC RADIOPHARMACEUTICALS Neoplasms, Germline Gene Mutation in the tumor suppressor gene PTEN protein, human protein, human, which encodes a Dual-Specificity Phosphatases, have been found in up to 80% of patients with COWDEN SYNDROME 5 suggesting a role of PTEN protein, human protein, human in the pathogenesis of Follicular THYROID DIAGNOSTIC RADIOPHARMACEUTICALS Neoplasms, The most common neoplasms in Hamartoma Syndrome, Multiple patients arise in the Breast, Skin Specimen Source Code, and THYROID DIAGNOSTIC RADIOPHARMACEUTICALS (Follicular subtype), The transcriptional silencing of PTEN protein, human protein, human was significantly associated with the anaplastic subtype, suggesting that PTEN protein, human protein, human is involved in the carcinogenesis of highly malignant or late-stage THYROID DIAGNOSTIC RADIOPHARMACEUTICALS cancers, whereas this particular mechanism appears to be of minor importance in differentiated Follicular THYROID DIAGNOSTIC RADIOPHARMACEUTICALS Neoplasms[SEP]Relations: PTEN protein, human has relations: disease_protein with THYROID DIAGNOSTIC RADIOPHARMACEUTICALS gland carcinoma, disease_protein with THYROID DIAGNOSTIC RADIOPHARMACEUTICALS gland carcinoma, disease_protein with THYROID DIAGNOSTIC RADIOPHARMACEUTICALS cancer, disease_protein with THYROID DIAGNOSTIC RADIOPHARMACEUTICALS cancer, anatomy_protein_present with THYROID DIAGNOSTIC RADIOPHARMACEUTICALS gland, anatomy_protein_present with THYROID DIAGNOSTIC RADIOPHARMACEUTICALS gland, disease_protein with carcinoma, disease_protein with carcinoma, disease_protein with prostate carcinoma, disease_protein with prostate carcinoma.", "label": "yes"}
{"original_question": "Is adalimumab effective for hidradenitis suppurativa?", "id": "converted_1865", "sentence1": "Is adalimumab effective for hidradenitis suppurativa?", "sentence2": "If patient is not improved, then adalimumab 160 mg at week 0, 80 mg at week 2; then 40 mg subcutaneously weekly should be administered (LOE Ib, SOR A). If improvement occurs then therapy should be maintained as long as HS Lesion are present., Reduction in Pain:-:Point in time:^Patient:- scores and improvement in Depressive Symptoms in patients with hidradenitis suppurativa treated with adalimumab in a phase 2, randomized, placebo-controlled trial., adalimumab treatment for 16 weeks improved HS Lesion significantly versus placebo (NCT00918255)., CONCLUSION: Patients with moderate to severe HS had a high degree of Pain:-:Point in time:^Patient:- and Depressive Symptoms at baseline. Adalimumabtherapy was associated with decreased Pain:-:Point in time:^Patient:- and Depressive Symptoms compared to baseline., Spotlight on adalimumab in the treatment of active moderate-to-severe hidradenitis suppurativa., adalimumab, a recombinant, fully humanized, anti-Tumor Necrosis Factor-alpha alpha (anti-Recombinant Tumor Necrosis Factor Family Protein-α) monoclonal immunoglobulin complex location, is the only officially approved treatment for the management of moderate-to-severe HS. Case reports, concerning 42 patients who received adalimumab for severe HS (with the standard dose regimen for Psoriasis), reported a cumulative response rate of 58% (≥50% in 23 patients) with a relapse rate of 71% (10 out of 14 patients). The most recent and most well-powered phase III, randomized placebo-controlled trials for the evaluation of the efficacy and safety of adalimumab in treatment of moderate-to-severe HS (PIONEER studies I and II) showed that the Hidradenitis Suppurativa Clinical Response (HiSCR) rate at week 12 was significantly higher for patients randomized to adalimumab compared to placebo., In conclusion, adalimumab, to date, holds the most robust data regarding treatment efficacy in HS. , adalimumab (Humira) for the Treatment of Hidradenitis Suppurativa., adalimumab (Humira®) is a novel therapy approved by the US Food and Drug Administration, Health Canada, and the European Commission for the treatment of hidradenitis suppurativa (HS)., Taken together, these data conclude that treatment of HS with adalimumab is a safe and effective therapy resulting in a significant decrease in Specimen Source Codes - Abscess and inflammatory nodule counts within the first 12 weeks of treatment., Effective long-term control of refractory hidradenitis suppurativa with adalimumab after failure of conventional therapy., Hidradenitis suppurativa managed with adalimumab., Treatment of severe recalcitrant hidradenitis suppurativa with adalimumab., Long-term successful adalimumab therapy in severe hidradenitis suppurativa., Comparing treatment outcome of infliximab and adalimumab in patients with severe hidradenitis suppurativa., HiSCR (Hidradenitis Suppurativa Clinical Response): a novel clinical endpoint to evaluate therapeutic outcomes in patients with hidradenitis suppurativa from the placebo-controlled portion of a phase 2 adalimumab study, adalimumab in treatment-resistant hidradenitis suppurativa following recurrence after extensive affected area excision: a review of biologics therapy, adalimumab (antitumour necrosis factor-α) treatment of hidradenitis suppurativa ameliorates skin inflammation: an in situ and ex vivo study, Treatment of severe recalcitrant hidradenitis suppurativa with adalimumab, In a phase 2 trial, adalimumab, an immunoglobulin complex location against Tumor Necrosis Factor-alpha α, showed efficacy against hidradenitis suppurativa.PIONEER I and II were similarly designed, phase 3 multicenter trials of adalimumab for hidradenitis suppurativa, with two double-blind, placebo-controlled periods., Here we report a case of a patient with severe recalcitrant hidradenitis suppurativa successfully treated with adalimumab., Recent reports have demonstrated that adalimumab, a Tumor Necrosis Factor-alpha (Recombinant Tumor Necrosis Factor Family Protein) Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance), may be effective in the treatment of patients with HS who have failed conventional therapy., Conclusion adalimumab appears to be an effective and safe treatment for refractory HS., Effective long-term control of refractory hidradenitis suppurativa with adalimumab after failure of conventional therapy., Hidradenitis suppurativa managed with adalimumab., Treatment of severe recalcitrant hidradenitis suppurativa with adalimumab., Two Phase 3 Trials of adalimumab for Hidradenitis Suppurativa., adalimumab treatment for hidradenitis suppurativa associated with Crohn's disease of oral soft tissues of oral soft tissues., Long-term successful adalimumab therapy in severe hidradenitis suppurativa., Conclusion adalimumab appears to be an effective and safe treatment for refractory HS.., Comparing treatment outcome of infliximab and adalimumab in patients with severe hidradenitis suppurativa., Here we report a case of a patient with severe recalcitrant hidradenitis suppurativa successfully treated with adalimumab.., adalimumab is suitable for the long-term treatment of hidradenitis suppurativa and presents a further conservative treatment approach.., HiSCR (Hidradenitis Suppurativa Clinical Response): a novel clinical endpoint to evaluate therapeutic outcomes in patients with hidradenitis suppurativa from the placebo-controlled portion of a phase 2 adalimumab study., Spotlight on adalimumab in the treatment of active moderate-to-severe hidradenitis suppurativa.[SEP]Relations: hidradenitis suppurativa has relations: disease_disease with hidradenitis, disease_disease with hidradenitis. adalimumab has relations: drug_drug with Amatuximab, drug_drug with Amatuximab, drug_drug with Isatuximab, drug_drug with Isatuximab, drug_drug with Margetuximab, drug_drug with Margetuximab, drug_drug with Antipyrine, drug_drug with Antipyrine.", "label": "yes"}
{"original_question": "Have toll-like receptor 2 activators been found in food?", "id": "converted_3701", "sentence1": "Have toll-like receptor 2 activators been found in food?", "sentence2": "TLR2 wt Allele gene (TLR2 wt Allele wt Allele) is a widely expressed pattern recognition receptor critical for innate immunity. TLR2 wt Allele wt Allele is also a key regulator of mucosal immunity implicated in the development of allergic disease. TLR2 wt Allele wt Allele activators are found in many common Food,, TLR2 wt Allele wt Allele activators are found in many common Food, but the role of TLR2 wt Allele wt Allele in oral tolerance and Allergic sensitization to Food is not well understood., TLR2 wt Allele wt Allele activators are found in many common Food, but the role of TLR2 wt Allele wt Allele in oral tolerance and Allergic sensitization to Food is not well understood.[SEP]Relations: sensitization has relations: bioprocess_protein with DRD5, bioprocess_protein with DRD5, bioprocess_bioprocess with nonassociative learning, bioprocess_bioprocess with nonassociative learning.", "label": "yes"}
{"original_question": "Is low T3 syndrome a prognostic marker in patients with renal insufficiency?", "id": "converted_248", "sentence1": "Is low SLC25A5 gene syndrome a prognostic marker in patients with renal insufficiency?", "sentence2": "Low SLC25A5 gene was particularly common (44.3 %), and clearly associated with increased 6- and 12-month mortality and decreased overall survival (log rank test, P=0.007). , Increased rT3 may be more common in Kidney Failure, Chronic patients than previously described, and together with decreased SLC25A5 gene it may serve as an indicator of poor prognosis in subsequent months., The presence of Thyroid Function Tests alterations seems to not be associated with clinical and prognostic implications in Blighia sapida patients., Multivariate analysis, according to receiver operating characteristic (ROC) curves, showed that mortality was best predicted by total triiodothyronine (SLC25A5 gene)., Finally, low SLC25A5 gene but not low free triiodothyronine was associated with worse all-cause (Likelihood ratio = 45.4; P < 0.0001) and Cardiovascular system mortality (Likelihood ratio = 47.8; P < 0.0001) after adjustment for confounding factors.,  In Cox analyses, fT3 was a significant predictor of mortality independent of the main traditional as well as non-traditional risk factors., All-cause and CV mortality rates were significantly higher in patients with 'lower' SLC25A5 gene levels than in the 'higher' SLC25A5 gene group (113.4 vs 18.2 events per 1000 patient-years, P<0.001, and 49.8 vs 9.1 events per 1000 patient-years, P=0.001, respectively). The Kaplan-Meier analysis also showed significantly worse cumulative survival rates in the 'lower' SLC25A5 gene group (P<0.001). In the Cox regression analysis, low SLC25A5 gene was an independent predictor of all-cause mortality even after adjusting for traditional risk factors (hazard ratio=3.76, P=0.021). , In Chronic Kidney Diseases patients with Proteinuria, low SLC25A5 gene concentration predicted all-cause mortality and Cardiovascular system event independently of the severity of Proteinuria., Low-SLC25A5 gene syndrome is a frequent finding among Hodgkin Disease patients, but it does not predict outcome. However, serum fT3 level is a strong and inverse mortality predictor, in part explained by its underlying association with nutritional state and Inflammation., These data suggest that low cubic foot levels are not predictive for mortality in a subgroup of stable Hodgkin Disease patients who could survive more than 12 months., Low fT3 is an independent predictor of Cessation of life in hemodialysis patients. These data lend support to the hypothesis that Thyroid dysfunction is implicated in the high risk of the Kidney Failure, Chronic population.[SEP]Relations: Chronic kidney disease has relations: phenotype_phenotype with Renal insufficiency, phenotype_phenotype with Renal insufficiency. kidney failure has relations: disease_protein with INF2, disease_protein with INF2, disease_protein with TLR4, disease_protein with TLR4, disease_protein with NOS3, disease_protein with NOS3, disease_protein with TGFB1, disease_protein with TGFB1.", "label": "yes"}
{"original_question": "Is SLIC-CAGE used for quantification of translation?", "id": "converted_4052", "sentence1": "Is SLIC-CAP Analysis of Gene Expression used for quantification of translation?", "sentence2": "Transcription Initiation Site Mapping Using Super-low Input Carrier-CAP Analysis of Gene Expression., SLIC-CAP Analysis of Gene Expression: high-resolution transcription start site mapping using nanogram-levels of total RNA., Cap analysis of gene expression (CAP Analysis of Gene Expression) is a methodology for genome-wide quantitative mapping of mRNA 5' ends to precisely capture transcription start sites at a single nucleotide resolution. In combination with high-throughput sequencing, CAP Analysis of Gene Expression has revolutionized our understanding of the rules of transcription initiation, led to discovery of new core Promoter sequence features, and discovered transcription initiation at enhancers genome-wide. The biggest limitation of CAP Analysis of Gene Expression is that even the most recently improved version (nAnT-iCAGE) still requires large amounts of total cellular RNA (5 µg), preventing its application to scarce biological samples such as those from early embryonic development or rare cell types. Here, we present SLIC-CAP Analysis of Gene Expression, a Super-Low Input Carrier-CAP Analysis of Gene Expression approach to capture 5' ends of RNA Polymerase II transcripts from as little as 5-10 ng of total RNA. This dramatic increase in sensitivity is achieved by specially designed, selectively degradable carrier RNA. We demonstrate the ability of SLIC-CAP Analysis of Gene Expression to generate data for genome-wide promoterome with 1000-fold less material than required by existing CAP Analysis of Gene Expression methods, by generating a complex, high-quality library from mouse embryonic day 11.5 primordial germ Cells., Cap analysis of gene expression (CAP Analysis of Gene Expression) is a method used for single-nucleotide resolution detection of RNA Polymerase II transcription start sites (TSSs). Accurate detection of TSSs enhances identification and discovery of core promoters. In addition, active enhancers can be detected through signatures of bidirectional transcription initiation. Described here is a protocol for performing super-low input carrier-CAP Analysis of Gene Expression (SLIC-CAP Analysis of Gene Expression). This SLIC adaptation of the CAP Analysis of Gene Expression protocol minimizes RNA losses by artificially increasing the RNA amount through use of an in vitro transcribed RNA carrier mix that is added to the sample of interest, thus enabling library preparation from nanogram-amounts of total RNA (i.e., thousands of Cells). The carrier mimics the expected DNA library fragment length distribution, thereby eliminating biases that could be caused by the abundance of a homogenous carrier. In the last stages of the protocol, the carrier is removed through degradation with homing endonucleases and the target library is amplified. The target sample library is protected from degradation, as the homing endonuclease recognition sites are long (between 18 and 27 bp), making the probability of their existence in the eukaryotic genomes very low. The end result is a DNA library ready for next-generation sequencing. All steps in the protocol, up to sequencing, can be completed within 6 days. The carrier preparation requires a full working day; however, it can be prepared in large quantities and kept frozen at -80 °C. Once sequenced, the reads can be processed to obtain genome-wide single-nucleotide resolution TSSs. TSSs can be used for core Promoter or enhancer discovery, providing insight into gene regulation. Once aggregated to promoters, the data can also be used for 5'-centric expression profiling.[SEP]Relations: HIV Transcription Initiation has relations: pathway_protein with TAF4, pathway_protein with TAF4, pathway_protein with TAF2, pathway_protein with TAF2, pathway_protein with TAF6, pathway_protein with TAF6, pathway_protein with TAF3, pathway_protein with TAF3, pathway_protein with TAF5, pathway_protein with TAF5.", "label": "no"}
{"original_question": "Is sonidegib effective for basal cell carcinoma?", "id": "converted_2236", "sentence1": "Is sonidegib effective for Skin Basal Cell Carcinoma?", "sentence2": "This review of the literature aims to describe previous and current treatment options for oral therapy in locally advanced and metastatic NMSC otherwise unamenable to standard treatment. Oral SMO protein, human (Smo) inhibitors Vismodegib, sonidegib, and Taladegib have shown to be effective in several trials. , sonidegib is a new smoothened PPP1R1A gene currently under investigation for treatment of laBCC, which demonstrates a comparable safety profile to vismodegib. , The recent development of novel hedgehog pathway inhibitors for high-risk Basal cell carcinoma (including oral vismodegib and sonidegib) may represent a paradigm shift towards medical management of NMSC., sonidegib (Odomzo®), an oral smoothened (SMO) antagonist, is indicated for the treatment of adults with locally advanced Skin Basal Cell Carcinoma (laBCC) who are not candidates for surgery or radiation therapy, or adults with recurrent laBCC following surgery or radiation therapy. , The acceptable benefit-risk profile of sonidegib, along with a paucity of treatment options and the seriousness of the condition, makes sonidegib an emerging option for the treatment of adults with laBCC that has recurred following surgery or radiation therapy, or in those who are not candidates for surgery or radiation therapy., sonidegib phosphate: new approval for Skin Basal Cell Carcinoma., sonidegib, a novel smoothened PPP1R1A gene for the treatment of advanced Skin Basal Cell Carcinoma., Serious adverse events occurred in 11 (14%) of 79 patients in the 200 mg group and 45 (30%) of 150 patients in the 800 mg group.The benefit-to-risk profile of 200 mg sonidegib might offer a new treatment option for patients with advanced Skin Basal Cell Carcinoma, a population that is difficult to treat.Novartis Pharmacologic Substance Corporation.<CopyrightInformation>Copyright © 2015 Elsevier Ltd. All rights reserved.</, However, to date, Hh inhibitors, specifically those targeting SMO protein, human [such as vismodegib, BMS-833923, Patidegib (IPI-926), sonidegib/erismodegib (SMO protein, human Antagonist Smoothened Antagonist LDE225), PF-04449913, LY2940680, LEQ 506, and TAK-441], have demonstrated good efficacy as monotherapy in patients with Skin Basal Cell Carcinoma and Medulloblastoma, but have shown limited activity in other tumor types., The hedgehog pathway PPP1R1A gene sonidegib demonstrated meaningful tumor shrinkage in more than 90% of patients with locally advanced Skin Basal Cell Carcinoma (Basal cell carcinoma) or metastatic Basal cell carcinoma in the Basal cell carcinoma Outcomes with SMO protein, human Antagonist Smoothened Antagonist LDE225 Treatment study.This report provides long-term follow-up data collected up to 12 months after the last patient was randomized.In this multicenter, randomized, double-blind phase II study, patients were randomized 1:2 to sonidegib 200 or 800 mg. The primary end point was objective response rate assessed by central review.Objective response rates in the 200- and 800-mg arms were 57.6% and 43.8% in locally advanced B, Serious adverse events occurred in 11 (14%) of 79 patients in the 200 mg group and 45 (30%) of 150 patients in the 800 mg group.The benefit-to-risk profile of 200 mg sonidegib might offer a new treatment option for patients with advanced Skin Basal Cell Carcinoma, a population that is difficult to treat.Novartis Pharmacologic Substance Corporation.<CopyrightInformation>Copyright © 2015 Elsevier Ltd. All rights reserved.</C, Oral sonidegib is approved in Switzerland for the treatment of adult patients with advanced Skin Basal Cell Carcinoma (Basal cell carcinoma) and in the US and EU for the treatment of adult patients with locally advanced Basal cell carcinoma that has recurred following surgery or radiation therapy, or those who are not candidates for surgery or radiation therapy., sonidegib phosphate: new approval for Skin Basal Cell Carcinoma.[SEP]Relations: sonidegib has relations: drug_drug with Carbamazepine, drug_drug with Carbamazepine, drug_drug with Carbomycin, drug_drug with Carbomycin, drug_drug with Afelimomab, drug_drug with Afelimomab. Skin Basal Cell Carcinoma has relations: contraindication with Methoxsalen, contraindication with Methoxsalen, disease_disease with carcinoma, disease_disease with carcinoma.", "label": "yes"}
{"original_question": "Can Levoxyl (levothyroxine sodium) cause insomnia?", "id": "converted_87", "sentence1": "Can Levoxyl (levothyroxine sodium) cause insomnia?", "sentence2": "METHODS: Seventy-one patients diagnosed with Acquired hypothyroidism were randomly allocated into two study groups: the first group received usual dose of levothyroxine and the second group received combination of levothyroxine and liothyronine for at least 4 months. The main outcomes were psychosocial problems (Goldberg's General Health Questionnaire, GHQ-28), bodyweight, heart rate, blood pressure, and serum lipid levels. RESULTS: In both groups serum thyroid-stimulating hormone levels remained unchanged compared with baseline. Psychosocial scores, body weight, heart rate, blood pressure, and lipid profile in the two groups remained constant. The only exception was a small but significant reduction in anxiety/insomnia in combined treatment group as compared with monotherapy. [SEP]Relations: Levothyroxine has relations: drug_effect with Alopecia, drug_effect with Alopecia, drug_drug with Omeprazole, drug_drug with Omeprazole, drug_effect with Coma, drug_effect with Coma, drug_effect with Dyspnea, drug_effect with Dyspnea, drug_effect with Arrhythmia, drug_effect with Arrhythmia.", "label": "yes"}
{"original_question": "Are integrins part of the extracellular matrix?", "id": "converted_539", "sentence1": "Are Integrins part of the extracellular matrix?", "sentence2": "Several constituents of the MMRN1 wt Allele provide adhesive cues, which serve as Binding Sites for cell trans-membrane receptors, such as Integrins., We also determined that blocking β1integrins, the major class of receptors for all MMRN1 wt Allele proteins tested,, Here, we elucidate a cross-scale mechanism for tissue assembly and MMRN1 wt Allele remodeling involving Cadherin-2, the MMRN1 wt Allele protein Fibronectin, and its receptor Integrin α5. , due to the diverse functions and variable expression of proteoglycans, matrix proteins, and Integrins, it is rather difficult to identify a comprehensive therapeutic target among MMRN1 wt Allele components., Integrin-dependent cell-extracellular matrix (MMRN1 wt Allele) adhesion is a determinant of Spindle orientation., The extracellular matrix component periostin is a secreted protein that functions as both a cell attachment protein and an autocrine or paracrine factor that signals through the cell adhesion molecule Integrins αvβ3 and αvβ5. , Integrin receptors connect the extracellular matrix to the cell cytoskeleton to provide essential forces and signals. ,  the integrin, TLN1 gene, and Actins filament form a linear complex of which both ends are typically anchored to the Extracellular Matrix via Integrins., Integrins, a central family of cellular MMRN1 wt Allele receptors, have been implicated in these processes but their specific role in ES cell self-renewal remains unclear., Attachment to the extracellular matrix is mediated by a complex of adhesion proteins, including Integrins, signaling molecules, Actins and Actin-Binding Protein, and scaffolding proteins., Beta 1 integrin binding plays a role in the constant traction force generation in response to varying stiffness for Cells grown on mature cardiac extracellular matrix.[SEP]Relations: extracellular matrix has relations: cellcomp_protein with IGFALS, cellcomp_protein with IGFALS, cellcomp_protein with IHH, cellcomp_protein with IHH, cellcomp_protein with COMP, cellcomp_protein with COMP, cellcomp_protein with NYX, cellcomp_protein with NYX, cellcomp_protein with VEGFA, cellcomp_protein with VEGFA.", "label": "yes"}
{"original_question": "In clinical trials, the H3 R antagonist CEP-26401 has a positive effect on cognition, yes or no?", "id": "converted_3010", "sentence1": "In clinical trials, the H3 R antagonist CEP-26401 has a positive effect on cognition, yes or no?", "sentence2": "CEP-26401 is a novel orally active, brain-penetrant, high-affinity histamine Receptors, Histamine H3 (H3R) antagonist, with potential therapeutic utility in cognition enhancement, hese results demonstrate potent behavioral effects of CEP-26401 in rodent models and suggest that this novel H₃R antagonist may have therapeutic utility in the treatment of cognitive and attentional disorders, CEP-26401 is a novel orally active, brain-penetrant, high-affinity histamine Receptors, Histamine H3 (H3R) antagonist, with potential therapeutic utility in cognition enhancement., CEP-26401 (irdabisant), a potent and selective histamine H₃ receptor antagonist/inverse Agonist with cognition-enhancing and wake-promoting activities., However, although a number of clinical studies examining the efficacy of Receptors, Histamine H3 antagonists for a variety of Cognition Disorders are currently underway, no clinical proof of concept for an Receptors, Histamine H3 antagonist has been reported to date., Further clinical studies are required to establish the potential of low-dose CEP-26401 in cognition enhancement.<br>[SEP]Relations: Histamine receptors has relations: pathway_protein with HRH3, pathway_protein with HRH3, pathway_protein with HRH1, pathway_protein with HRH1, pathway_protein with HRH4, pathway_protein with HRH4. cognitive disorder has relations: contraindication with Lithium citrate, contraindication with Lithium citrate, contraindication with Lithium carbonate, contraindication with Lithium carbonate.", "label": "yes"}
{"original_question": "Is dexamethasone recommended for treatment of intracerebral hemorrhage?", "id": "converted_2176", "sentence1": "Is dexamethasone recommended for treatment of intracerebral hemorrhage?", "sentence2": "dexamethasone and other glucocorticoids should be avoided. , During the third interim analysis, the Cessation of life rate at the 21st day was identical in the two groups (dexamethasone vs. placebo, 21 of 46 vs. 21 of 47; chi-square = 0.01, P = 0.93). In contrast, the rate of complications (mostly Infections of musculoskeletal system and complications of Diabetes Mellitus) was much higher in the dexamethasone group (chi-square = 10.89, P less than 0.001), leading to early termination of the study. In the light of the absence of a demonstrable beneficial effect and the presence of a significant harmful effect, current practices of using dexamethasone for treatment of primary supratentorial hemorrhage should be reconsidered., In the light of the absence of a demonstrable beneficial effect and the presence of a significant harmful effect, current practices of using dexamethasone for treatment of primary supratentorial hemorrhage should be reconsidered.[SEP]Relations: dexamethasone has relations: drug_effect with Vitreous hemorrhage, drug_effect with Vitreous hemorrhage, contraindication with hypertension, contraindication with hypertension, contraindication with ocular hypertension, contraindication with ocular hypertension, contraindication with hyperglycemia, contraindication with hyperglycemia, contraindication with myxedema, contraindication with myxedema.", "label": "no"}
{"original_question": "Are Copy Number Variants (CNVs) depleted in regions of low mappability?", "id": "converted_2955", "sentence1": "Are Copy Number Variants (CNVs) depleted in regions of low mappability?", "sentence2": "Homo sapiens copy number Variant are enriched in regions of low mappability., Applying PopSV to 640 human genomes, we find that low-mappability regions are approximately 5 times more likely to harbor germline CNVs, in stark contrast to the nearly uniform distribution observed for somatic CNVs in 95 cancer genomes. In addition to known enrichments in segmental duplication and near centromeres and telomere, we also report that CNVs are enriched in specific types of satellite and in some of the most recent families of DNA Transposable Elements. Finally, using this comprehensive approach, we identify 3455 regions with recurrent CNVs that were missing from existing catalogs. In particular, we identify 347 Genes with a novel exonic CNV in low-mappability regions, including 29 Genes previously associated with Disease., Homo sapiens copy number Variant are enriched in regions of low mappability.Copy number Variant (CNVs) are known to affect a large portion of the human genome and have been implicated in many diseases. [SEP]Relations: maintenance of DNA repeat elements has relations: bioprocess_bioprocess with maintenance of CRISPR repeat elements, bioprocess_bioprocess with maintenance of CRISPR repeat elements, bioprocess_protein with AXIN2, bioprocess_protein with AXIN2, bioprocess_protein with TCF7L2, bioprocess_protein with TCF7L2, bioprocess_protein with MSH2, bioprocess_protein with MSH2, bioprocess_protein with MSH3, bioprocess_protein with MSH3.", "label": "no"}
{"original_question": "Do thyroid hormone receptors change after brain injury?", "id": "converted_1507", "sentence1": "Do thyroid hormone receptors change after brain injury?", "sentence2": "For example, the T3 thoracic segmental innervation thoracic segmental innervation receptor alpha was predominantly expressed in stroke-tissue, indicating that regeneration of nerves in stroke tissue may be facilitated by increased T3 thoracic segmental innervation thoracic segmental innervation receptor alpha expression., TRα expression was also increased in Homo sapiens infants with IVH. , Thus, in infants with IVH the combined elevation in deiodinase-3 and reduction in deiodinase-2 decreases TH signaling that can be worsened by an increase in unliganded TRα. , A rapid increase of the total number of Binding Sites for T3 thoracic segmental innervation thoracic segmental innervation appeared within 30 min of Ischemia Procedure and reached over 40% by 3 h. During the same 3-h period, the relative binding affinity was reduced by 25%. Upon recirculation after 30 min or 3 h of Ischemia Procedure, a rapid reversal of measured T3 thoracic segmental innervation thoracic segmental innervation Binding Sites occurred, which progressed to 20-30% below the control value by the recirculation period of 3 h. [SEP]Relations: siRNA binding has relations: molfunc_protein with FMR1, molfunc_protein with FMR1, molfunc_protein with TLR7, molfunc_protein with TLR7, molfunc_protein with AGO2, molfunc_protein with AGO2, molfunc_protein with TLR9, molfunc_protein with TLR9, molfunc_protein with TARBP2, molfunc_protein with TARBP2.", "label": "yes"}
{"original_question": "Is the yeast (Saccharomyces cerevisiae) genome organized into topologically associated domains (TADs)?", "id": "converted_3054", "sentence1": "Is the yeast (Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae) Genome - anatomical entity organized into topologically associated domains (Tietz syndrome)?", "sentence2": "Recent advances in our understanding of the three-dimensional organization of the eukaryotic nucleus have rendered the spatial distribution of Genes increasingly relevant. In a recent work (Tsochatzidou et al., Nucleic Acids Res 45:5818-5828, 2017), we proposed the existence of a functional compartmentalization of the yeast Genome - anatomical entity according to which, Genes occupying the chromosomal regions at the nuclear periphery have distinct structural, functional and evolutionary characteristics compared to their centromeric-proximal counterparts. Around the same time, it was also shown that the Genome - anatomical entity of Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae is organized in topologically associated domains (Tietz syndrome), which are largely associated with the replication timing., Form and function of topologically associating genomic domains in budding yeast., Although similar structures appear to be conserved in fission yeast, computational modeling and analysis of high-throughput chromosome conformation capture (Hi-C) data have been used to argue that the small, highly constrained budding yeast chromosomes could not have these structures. In contrast, herein we analyze Hi-C data for budding yeast and identify 200-kb scale Tietz syndrome, whose boundaries are enriched for transcriptional activity. Furthermore, these boundaries separate regions of similarly timed replication origins connecting the long-known effect of genomic context on replication timing to Genome - anatomical entity architecture. To investigate the molecular basis of aminoglutethimide/danazol/hydrocortisone/tamoxifen formation, we performed Hi-C experiments on Cells depleted for the Forkhead Transcription Factors, FOXO1 wt Allele and FOXG1 wt Allele, previously associated with replication timing. Forkhead factors do not regulate aminoglutethimide/danazol/hydrocortisone/tamoxifen formation, but do promote longer-range genomic interactions and control interactions between origins near the centromere. Thus, our work defines spatial organization within the budding yeast nucleus, demonstrates the conserved role of Genome - anatomical entity architecture in regulating DNA replication, and identifies a molecular mechanism specifically regulating interactions between pericentric origins., Around the same time, it was also shown that the Genome - anatomical entity of Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae is organized in topologically associated domains (Tietz syndrome), which are largely associated with the replication timing., Around the same time, it was also shown that the Genome - anatomical entity of Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae is organized in topologically associated domains (Tietz syndrome), which are largely associated with the replication timing. , In contrast, herein we analyze Hi-C data for budding yeast and identify 200-kb scale Tietz syndrome, whose boundaries are enriched for transcriptional activity.[SEP]Relations: TFAP2 (AP-2) family regulates transcription of other transcription factors has relations: pathway_protein with CITED2, pathway_protein with CITED2, pathway_protein with TFAP2C, pathway_protein with TFAP2C, pathway_protein with TFAP2A, pathway_protein with TFAP2A, pathway_protein with PITX2, pathway_protein with PITX2. anatomical entity has relations: anatomy_anatomy with insect mouthpart, anatomy_anatomy with insect mouthpart.", "label": "yes"}
{"original_question": "Can cognitive behavioral therapy improve fatigue in cancer patients?", "id": "converted_1333", "sentence1": "Can cognitive behavioral therapy improve Fatigue in cancer patients?", "sentence2": "Physical activity, educational interventions, and cognitive-behavioral therapy have the most supportive data and can be recommended to patients with confidence. , For women undergoing radiotherapy (3 RCTs), hypnosis combined with cognitive-behavioral therapy improved distress and Fatigue., Patients in the CBT group reported a significantly larger decrease in Fatigue scores than patients in the waiting list group., However, relative to VCBT-I, PCBT-I was associated with significantly greater improvements of Insomnia homeopathic medication severity, early morning awakenings, Cancer patients and suicide and Cancer patients and suicide and depression, Fatigue, and dysfunctional beliefs about sleep. , Cognitive Behavior Therapy for Insomnia may also improve mood, Fatigue, and overall quality of life, and can be successfully delivered through a variety of treatment modalities, making it possible to reach a broader range of patients who may not have access to more traditional programs. , No group differences in improvement were noted relative to QOL, Fatigue, or mood. , In case of persistent Fatigue, personalized cognitive behavioral therapy can be considered., ONCLUSION: The results support CBTH as an evidence-based intervention to control Fatigue in patients undergoing radiotherapy for Malignant neoplasm of breast. , Severe Fatigue after cancer treatment can be treated effectively with cognitive behavioral therapy (CBT), but it is unclear whether CBT has an effect on cognitive functioning., CONCLUSION: CBT for post-cancer Fatigue has already been shown to be an effective therapy. , Frequently reported side effects include cancer-related Fatigue, Peripheral Nervous System Diseases, and psychological distress. Exercise and cognitive behavioral therapy interventions have counteracted such adverse effects in other cancer populations. , There is evidence from methodologically rigorous controlled trials that exercise, psycho-educational interventions, and cognitive-behavioral therapy for Insomnia homeopathic medication are effective in the treatment of corticotropin-releasing hormone, and a wide range of pharmacologic and nonpharmacologic interventions has shown initial promise in single-arm pilot studies with small, heterogeneous samples. , CONCLUSIONS: Physical training combined with cognitive-behavioral therapy and physical training alone had significant and beneficial effects on Fatigue compared with no intervention. Physical training was equally effective as or more effective than physical training combined with cognitive-behavioral therapy in reducing cancer-related Fatigue, suggesting that cognitive-behavioral therapy did not have additional beneficial effects beyond the benefits of physical training., RESULTS: Imagery/hypnosis and CBT/CST interventions have produced improvement in all the three cancer-related symptoms individually: Pain:-:Point in time:^Patient:-, Fatigue, and Sleep Disorders., RESULTS: Multilevel modeling indicated that for weekly FACIT Fatigue data, there was a significant effect of the CBTH intervention on the rate of change in Fatigue (p < .05), such that on average, CBTH participants' Fatigue did not increase over the course of treatment, whereas control group participants' Fatigue increased linearly., ONCLUSION: The results suggest that CBTH is an effective means for controlling and potentially preventing Fatigue in Malignant neoplasm of breast radiotherapy patients., Results were consistent with the view that CBTH was effective in managing Fatigue and skin discomfort, and increasing relaxation., RESULTS: Participants in the Internet group showed significant improvements at post-assessment compared with those in the control group in overall Insomnia homeopathic medication severity (F(1,26) = 22.8; p<0.001), sleep efficiency (F(1,24) = 11.45; P = 0.002), sleep onset latency (F(1,24) = 5.18; P = 0.03), soundness of sleep (F(1,24) = 9.34; P = 0.005), restored feeling upon awakening (F(1,24) = 11.95; P = 0.002), and general Fatigue (F(1,26) = 13.88; P = 0.001). , Cognitive-behavior therapy (CBT) has alleviated Fatigue and improved QOL of cancer patients; however, little is known about the effects of nurse-led CBT on Malignant neoplasm of breast patients undergoing radiotherapy., Physical training was equally effective as or more effective than physical training combined with cognitive-behavioral therapy in reducing cancer-related Fatigue, suggesting that cognitive-behavioral therapy did not have additional beneficial effects beyond the benefits of physical training., Cognitive-behavior therapy (CBT) has alleviated Fatigue and improved QOL of cancer patients; however, little is known about the effects of nurse-led CBT on Malignant neoplasm of breast patients undergoing radiotherapy., Physical training was equally effective as or more effective than physical training combined with cognitive-behavioral therapy in reducing cancer-related Fatigue, suggesting that cognitive-behavioral therapy did not have additional beneficial effects beyond the benefits of physical training., The positive effects of cognitive behavioral therapy in adolescents with chronic Fatigue syndrome are sustained after cognitive behavioral therapy[SEP]Relations: Fatigue has relations: phenotype_phenotype with Cognitive Fatigue, phenotype_phenotype with Cognitive Fatigue, drug_effect with Nevirapine, drug_effect with Nevirapine, drug_effect with Parathyroid hormone, drug_effect with Parathyroid hormone, drug_effect with Mitomycin, drug_effect with Mitomycin, drug_effect with Betahistine, drug_effect with Betahistine.", "label": "yes"}
{"original_question": "Are transcription and splicing connected?", "id": "converted_22", "sentence1": "Are transcription and splicing connected?", "sentence2": ", as splicing is often cotranscriptional, a complex picture emerges in which splicing regulation not only depends on the balance of RNA Splicing Factors binding to their mRNA Precursor target sites but also on transcription-associated features such as Protein Info recruitment to the transcribing machinery and elongation kinetics., recent evidence shows that chromatin structure is another Chicken laying egg for human food of regulation that may act through various mechanisms, hese span from regulation of RNA Polymerase II elongation, which ultimately determines splicing decisions, to RNA Splicing Factors recruitment by specific histone marks., chromatin location may not only be involved in Alternative Splicing regulation but in constitutive exon recognition as well, Moreover, splicing was found to be necessary for the proper 'writing' of particular chromatin signatures, giving further mechanistic support to functional interconnections between splicing, transcription and chromatin structure., These links between chromatin configuration and splicing raise the intriguing possibility of the existence of a memory for splicing patterns to be inherited through epigenetic modifications., Spliceosomes assembly occurs co-transcriptionally, raising the possibility that DNA structure may directly influence Alternative Splicing., upporting such an association, recent reports have identified distinct histone methylation patterns, elevated nucleosome occupancy and enriched DNA methylation at Exons relative to Introns, Moreover, the rate of transcription elongation has been linked to Alternative Splicing., ere we provide the first evidence that a DNA-binding Protein Info, CCCTC-binding factor (CTGF Protein Info, human), can promote inclusion of weak upstream Exons by mediating local RNA Polymerase II pausing both in a Mammals model system for Alternative Splicing, PTPRC wt Allele, and genome-wide, We recently showed that cotranscriptional splicing occurs efficiently in Drosophila <basidiomycetes> <basidiomycetes>,, In recent years it became apparent that splicing is predominantly cotranscriptional, To determine the prevalence of cotranscriptional splicing in Drosophila <basidiomycetes> <basidiomycetes>, we sequenced nascent RNA transcripts from Drosophila <basidiomycetes> <basidiomycetes> S2 cells as well as from Drosophila <basidiomycetes> <basidiomycetes> heads. Eighty-seven percent of the Introns assayed manifest >50% cotranscriptional splicing. The remaining 13% are cotranscriptionally spliced poorly or slowly, with ∼3% being almost completely retained in nascent mRNA Precursor., We estimate that > or =90% of endogenous yeast splicing is posttranscriptional, consistent with an analysis of posttranscriptional snRNP-associated mRNA Precursor., Notably, the DNA Topoisomerases, Type I inhibitor Camptothecin, which stalls elongating Pol II, increased cotranscriptional RNA Splicing Factors accumulation and splicing in parallel. This provides direct evidence for a kinetic link between transcription, RNA Splicing Factors recruitment and splicing catalysis., Recent evidence indicates that transcriptional elongation and splicing can be influenced reciprocally: Elongation rates control Alternative Splicing and splicing factors can, in turn, modulate pol II elongation., The presence of TRANSCRIPTION FACTOR in the spliceosome and the existence of Proteins, such as the coactivator PGC-1, with dual activities in splicing and transcription can explain the links between both processes and add a new level of complexity to the regulation of gene expression in Eukaryota.[SEP]Relations: RNA splicing has relations: bioprocess_protein with SYNCRIP, bioprocess_protein with SYNCRIP, bioprocess_protein with SON, bioprocess_protein with SON, bioprocess_protein with USB1, bioprocess_protein with USB1, bioprocess_protein with SNRPG, bioprocess_protein with SNRPG. transcription factor binding has relations: molfunc_protein with SP1, molfunc_protein with SP1.", "label": "yes"}
{"original_question": "Do proton pump inhibitors affect thyroxine absorption?", "id": "converted_711", "sentence1": "Do proton pump inhibitors affect Thyroxine measurement absorption?", "sentence2": "Proton-pump inhibitors, Antacids and a long list of drugs may decrease Thyroxine measurement absorption, Many commonly used drugs, such as Bile Acid [EPC] sequestrants, ferrous sulfate, sucralfate, calcium carbonate, aluminium-containing Antacids, phosphate binders, raloxifene and proton-pump inhibitors, have also been shown to interfere with the absorption of levothyroxine., pantoprazole did not influence endocrine function in healthy male volunteers during short-term treatment., PPIs should be added to the list of medications affecting the level of Thyroid Hormones in patients with Hypothyroidism treated with LT4 replacement. Patients with Hypothyroidism and normal Thyrotropin:-:Pt:Ser/Plas:- values during LT4 replacement therapy may need additional thyroid function testing after treatment with PPIs and may need adjustment of their LT4 dose.[SEP]Relations: pantoprazole has relations: drug_effect with Thrombophlebitis, drug_effect with Thrombophlebitis, drug_effect with Nocturia, drug_effect with Nocturia, drug_effect with Thrombocytopenia, drug_effect with Thrombocytopenia, drug_effect with Albuminuria, drug_effect with Albuminuria. Raloxifene has relations: drug_effect with Thrombocytopenia, drug_effect with Thrombocytopenia.", "label": "yes"}
{"original_question": "Is Enlimomab effective for stroke treatment?", "id": "converted_2656", "sentence1": "Is Enlimomab effective for Cerebrovascular accident treatment?", "sentence2": "However, this treatment failed to show benefit in the Enlimomab Acute Stroke Trial., There was no increase in the frequency of adverse events with increasing doses of enlimomab.CONCLUSIONS: Dosage of enlimomab between 140 and 480 mg administered over 5 days did not increase the risk of adverse events in patients with ischaemic or haemorrhagic Cerebrovascular accident during an observation period of 30 +/- 10 days., Examination of several potential mechanisms for the negative outcome in a clinical Cerebrovascular accident trial of enlimomab, a Mus anti-human intercellular adhesion molecule-1 antibody: a bedside-to-bench study., BACKGROUND AND PURPOSE: Enlimomab, a Mus monoclonal anti-human intercellular adhesion molecule (ICAM)-1 antibody, had a negative outcome in a multicenter acute-Cerebrovascular accident trial. , These observations provide several possible mechanisms for central nervous system-related clinical deterioration that occurred when Enlimomab was given in acute Ischemic Cerebrovascular accident., Fewer patients had symptom-free recovery on enlimomab than placebo (p = 0.004), and more died (22.2 versus 16.2%). The negative effect of enlimomab was apparent on days 5, 30, and 90 of treatment (p = 0.005). There were significantly more adverse events with enlimomab treatment than placebo, primarily Infections of musculoskeletal system and Fever symptoms (finding). , CONCLUSIONS: The authors conclude that anti-ICAM therapy with enlimomab is not an effective treatment for Ischemic Cerebrovascular accident in the model studied and, indeed, may significantly worsen Cerebrovascular accident outcome., Patients experiencing Fever symptoms (finding) were more likely to have a poor outcome or die.The authors conclude that anti-ICAM therapy with enlimomab is not an effective treatment for Ischemic Cerebrovascular accident in the model studied and, indeed, may significantly worsen Cerebrovascular accident outcome., The negative effect of enlimomab was apparent on days 5, 30, and 90 of treatment (p = 0.005)., Patients experiencing Fever symptoms (finding) were more likely to have a poor outcome or die.<br><b>CONCLUSIONS</b>: The authors conclude that anti-ICAM therapy with enlimomab is not an effective treatment for Ischemic Cerebrovascular accident in the model studied and, indeed, may significantly worsen Cerebrovascular accident outcome.<br>, Unfortunately, the case fatality rate in this trial was significantly higher in the enlimomab patient group than in the placebo group., CONCLUSIONS The authors conclude that anti-ICAM therapy with enlimomab is not an effective treatment for Ischemic Cerebrovascular accident in the model studied and, indeed, may significantly worsen Cerebrovascular accident outcome., BACKGROUND AND PURPOSE Enlimomab, a Mus monoclonal anti-human intercellular adhesion molecule (ICAM)-1 antibody, had a negative outcome in a multicenter acute-Cerebrovascular accident trial., The authors conclude that anti-ICAM therapy with enlimomab is not an effective treatment for Ischemic Cerebrovascular accident in the model studied and, indeed, may significantly worsen Cerebrovascular accident outcome..[SEP]Relations: Ischemic Cerebrovascular accident has relations: drug_effect with Celecoxib, drug_effect with Celecoxib, drug_effect with Celecoxib, drug_effect with Celecoxib, drug_effect with Ramipril, drug_effect with Ramipril, drug_effect with Ramipril, drug_effect with Ramipril, drug_effect with Pazopanib, drug_effect with Pazopanib.", "label": "no"}
{"original_question": "Is Huntington's disease is caused by expansion of a CTG repeat in the HTT gene on Chromosome 4?", "id": "converted_3531", "sentence1": "Is Huntington Disease is caused by expansion of a CTG repeat in the SLC6A4 wt Allele gene on Chromosome 4?", "sentence2": "Huntington Disease (Hodgkin Disease) is caused by a CAG repeat expansion that encodes a polyglutamine (polyQ) expansion in the Hodgkin Disease disease Protein Info, Hodgkin Disease Protein Info, human (SLC6A4 wt Allele)., Huntington disease (Hodgkin Disease) is a dominantly inherited disorder caused by a CAG expansion Mutation Abnormality in the Hodgkin Disease Protein Info, human (SLC6A4 wt Allele) gene, which results in the SLC6A4 wt Allele Protein Info that contains an expanded polyglutamine tract., In Huntington Disease (Hodgkin Disease), expansion of CAG codons in the SLC6A4 wt Allele gene (SLC6A4 wt Allele) leads to the aberrant formation of Protein Info aggregates and the differential degeneration of striatal medium spiny neurons (MSNs)., Huntington disease (Hodgkin Disease) is a progressive Autosome dominant Neurodegenerative Disorders, characterized by abnormal movements, Mental deterioration, and psychiatric symptoms, caused by a CAG repeat expansion in the Hodgkin Disease Protein Info, human (SLC6A4 wt Allele) gene on chromosome 4p., Huntington Disease (Hodgkin Disease) is a polyglutamine disorder caused by a CAG expansion in the Huntingtin (SLC6A4 wt Allele) gene exon 1., IMPORTANCE\n\nHuntington disease (Hodgkin Disease), a prototypic monogenic disease, is caused by an expanded CAG repeat in the SLC6A4 wt Allele gene exceeding 35 units., Huntington Disease (Hodgkin Disease) is an Autosome dominantly inherited disorder caused by the expansion of CAG repeats in the Huntingtin (SLC6A4 wt Allele) gene., Huntington Disease (Hodgkin Disease) is a Neurodegenerative Disorders caused by a CAG trinucleotide repeat expansion in the Hodgkin Disease Protein Info, human (SLC6A4 wt Allele) gene., BACKGROUND Huntington Disease is caused by a CAG repeat expansion in the SLC6A4 wt Allele gene, SLC6A4 wt Allele., Huntington Disease (Hodgkin Disease) is an inherited neurodegenerative disease caused by an expanded CAG repeat in the SLC6A4 wt Allele gene., IMPORTANCE Huntington disease (Hodgkin Disease), a prototypic monogenic disease, is caused by an expanded CAG repeat in the SLC6A4 wt Allele gene exceeding 35 units., Huntington 's disease ( Hodgkin Disease ) is an inherited Neurodegenerative Disorders caused by a CAG repeat expansion within exon 1 of the Hodgkin Disease Protein Info, human ( SLC6A4 wt Allele ) gene. , Huntington 's disease ( Hodgkin Disease) , a dominantly inherited neurodegenerative disease , is defined by its genetic cause , a CAG-repeat expansion in the SLC6A4 wt Allele gene , its motor and psychiatric symptomology and primary loss of striatal medium spiny neurons ( MSNs) . , Huntington 's disease ( Hodgkin Disease ) is an incurable Neurodegenerative Disorders caused by a CAG repeat expansion in exon 1 of the Huntingtin ( SLC6A4 wt Allele ) gene. , Huntington 's disease ( Hodgkin Disease ) is a progressive Neurodegenerative Disorders caused by a CAG trinucleotide repeat expansion in the Hodgkin Disease Protein Info, human ( SLC6A4 wt Allele ) gene , which encodes a polyglutamine tract in the SLC6A4 wt Allele Protein Info . , Huntington 's disease ( Hodgkin Disease ) is an Autosome progressive Neurodegenerative Disorders caused by the expansion of CAG repeats in the SLC6A4 wt Allele gene. , Huntington 's disease ( Hodgkin Disease ) is an Autosome dominant neurodegenerative disease caused by the expansion of a CAG trinucleotide repeat in exon 1 of the Hodgkin Disease Protein Info, human ( htt ) gene. , Huntington 's disease ( Hodgkin Disease) , caused by a CAG repeat expansion in the Hodgkin Disease Protein Info, human ( SLC6A4 wt Allele ) gene , is characterized by abnormal Protein Info aggregates and motor and Impaired cognition . , Huntington 's disease ( Hodgkin Disease ) is a neurodegenerative disease caused by the expansion of a CAG trinucleotide repeat in exon 1 of the Hodgkin Disease Protein Info, human ( SLC6A4 wt Allele ) gene. , Huntington 's disease ( Hodgkin Disease ) is an Autosome disease caused by a CAG repeat expansion in the Hodgkin Disease Protein Info, human ( SLC6A4 wt Allele ) gene. , BACKGROUND\nHuntington Disease is caused by a CAG repeat expansion in the SLC6A4 wt Allele gene, SLC6A4 wt Allele., Huntington Disease (Hodgkin Disease) is an Autosome dominant disorder caused by an expansion in the trinucleotide CAG repeat in exon-1 in the SLC6A4 wt Allele gene, located on Chromosomes, Human, Pair 4., Hodgkin Disease is caused by expansion of the CAG trinucleotide repeat region in exon 1 of the Huntingtin gene (SLC6A4 wt Allele), leading to the formation of mutant SLC6A4 wt Allele transcripts (muHTT)., Huntington Disease (Hodgkin Disease) is a Neurodegenerative Disorders characterized by involuntary choreic movements, No No cognitive impairment, and behavioral changes, caused by the expansion of an unstable CAG repeat in SLC6A4 wt Allele., Huntington disease (Hodgkin Disease), the most common inherited cause of chorea, is an Autosome dominant disorder, caused by an expanded trinucleotide CAG repeat (>39) in the SLC6A4 wt Allele gene on 4p16.3 chromosome., Huntington Disease (Hodgkin Disease) is an inherited neurodegenerative disease caused by an expanded CAG repeat in the Hodgkin Disease Protein Info, human (SLC6A4 wt Allele) gene.[SEP]Relations: Huntington disease has relations: disease_protein with SLC6A4 wt Allele, disease_protein with SLC6A4 wt Allele, disease_protein with OGG1, disease_protein with OGG1, disease_disease with Huntington disease and related disorders, disease_disease with Huntington disease and related disorders, disease_protein with GDNF, disease_protein with GDNF, disease_protein with CNR1, disease_protein with CNR1.", "label": "no"}
{"original_question": "Is Sotrovimab effective for COVID-19?", "id": "converted_4565", "sentence1": "Is Sotrovimab effective for COVID-19?", "sentence2": "It seems that Monoclonal Antibodies (e.g., low dosage bamlanivimab, baricitinib, imatinib, and sotrovimab) are a better choice for treating severe or non-severe COVID-19 patients. , The Food and Drug Administration has granted emergency use authorization to sotrovimab for the treatment of mild to moderate COVID-19 in patients at increased risk for progression to severe Illness (finding)., Early Treatment for COVID19 (document) with SARS-CoV-2 Neutralizing Antibody Sotrovimab., Sotrovimab is a pan-sarbecovirus monoclonal antibody CAL CAL that was designed to prevent progression of COVID19 (document) in high-risk patients early in the course of disease, CONCLUSIONS: Among high-risk patients with mild-to-moderate COVID19 (document), sotrovimab reduced the risk of disease progression., The Food and Drug Administration has granted emergency use authorization to sotrovimab for the treatment of mild to moderate COVID-19 in patients at increased risk for progression to severe Illness (finding).Sotrovimab is a monoclonal antibody CAL CAL that works directly against the M Protein, multiple myeloma of SARS-CoV-2 to block its attachment and entry into a Human cells., In patients with non-severe covid-19, casirivimab / imdevimab probably reduces hospitalisation; bamlanivimab-etesevimab, bamlanivimab, and sotrovimab may reduce hospitalisation. Convalescen, ms that Monoclonal Antibodies (e.g., low dosage bamlanivimab, baricitinib, imatinib, and sotrovimab) are a better choice for treating severe or non-severe COVID-19 patients. Clini, Early Treatment for COVID19 (document) with SARS-CoV-2 Neutralizing Antibody Sotrovimab, The Food and Drug Administration has granted emergency use authorization to sotrovimab for the treatment of mild to moderate COVID-19 in patients at increased risk for progression to severe Illness (finding)[SEP]Relations: Baricitinib has relations: drug_drug with Sofosbuvir, drug_drug with Sofosbuvir, drug_drug with Cortivazol, drug_drug with Cortivazol, drug_drug with Somatostatin, drug_drug with Somatostatin, drug_drug with Efalizumab, drug_drug with Efalizumab. Imatinib has relations: drug_drug with Sofosbuvir, drug_drug with Sofosbuvir.", "label": "yes"}
{"original_question": "Is pregabalin effective for treatment of patients with restless leg syndrome?", "id": "converted_286", "sentence1": "Is pregabalin effective for treatment of patients with restless leg syndrome?", "sentence2": "CONCLUSIONS: This study demonstrated improvements in objective and subjective measures of sleep maintenance and sleep architecture with pregabalin compared with placebo and pramipexole. Effects of pregabalin on periodic limb movement arousal index were comparable to pramipexole. , CONCLUSIONS: Pregabalin provided significantly improved treatment outcomes as compared with placebo, and augmentation rates were significantly lower with pregabalin than with 0.5 mg of pramipexole., The alpha-2-delta ligands, including gabapentin, gabapentin enacarbil, and pregabalin, are effective for Restless Legs Syndrome without known occurrence of augmentation or impulse control disorders, although sedation and No No dizziness can occur. , Pregabalin has been established as effective for up to 1 year in treating Restless Legs Syndrome/WED (Level A evidence). , In the group of Anticonvulsants [TC], only the trials performed with α₂δ ligands such as gabapentin, gabapentin enacarbil, and pregabalin showed good efficacy. , Alternative or additional pharmacologic treatment with a lower level of overall quality of evidence includes Analgesics, Opioid (codeine, tramadol, and oxycodone) and Anticonvulsants [TC] (gabapentin, gabapentin enacarbil, and pregabalin). , There is sufficient evidence to conclude that Dopamine Agonists [MoA] such as rotigotine transdermal patch, pramipexole, ropinirole, gabapentin enacarbil, pregabalin and gabapentin are effective in the short-term treatment of Restless Legs Syndrome and rotigotine, followed by gabapentin enacarbil, ropinirole, pramipexole and gabapentin for long-term treatment., Calcium channel alpha-2-delta ligands (gabapentin, gabapentin enacarbil, and pregabalin) provide alternative therapies for Restless Legs Syndrome especially in patients with augmentation, impulse control disorders, or Hypersomnia induced by Dopamine Agonists [MoA]. , Alpha-2-delta ligands (gabapentin enacarbil, gabapentin, and pregabalin) increased the number of IRLS responders (RR=1.66; [95% CI: 1.33 to 2.09], k=3, high strength of evidence) and mean change in IRLS symptom scores (k=3, high strength of evidence). , RECOMMENDATIONS: Level A recommendations can be made for rotigotine, ropinirole, pramipexole, gabapentin enacarbil, gabapentin and pregabalin, which are all considered effective for the short-term treatment for Restless Legs Syndrome., Therapies with an OPTION level of recommendation include carbamazepin (benzodiazepine), gabapentin, pregabalin, clonidine, and for patients with low Ferritin levels, iron supplementation., CONCLUSIONS: In this 6-week phase 2b study, pregabalin reduced Restless Legs Syndrome symptoms in patients with moderate-to-severe idiopathic Restless Legs Syndrome, CLASSIFICATION OF EVIDENCE: This study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class II evidence that pregabalin is effective for the treatment of restless legs syndrome and improves sleep architecture and periodic limb movements in placebo-unresponsive patients., In severe, refractory or neuropathy-associated Restless Legs Syndrome, Antiepileptic Agents (gabapentin, pregabalin) or opioid (oxycodone, tramadol) drugs can be used., The alpha-2-delta ligands, including gabapentin, gabapentin enacarbil, and pregabalin, are effective for Restless Legs Syndrome without known occurrence of augmentation or impulse control disorders, although sedation and No No dizziness can occur, This study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class II evidence that pregabalin is effective for the treatment of restless legs syndrome and improves sleep architecture and periodic limb movements in placebo-unresponsive patients., Level A recommendations can be made for rotigotine, ropinirole, pramipexole, gabapentin enacarbil, gabapentin and pregabalin, which are all considered effective for the short-term treatment for Restless Legs Syndrome[SEP]Relations: Pregabalin has relations: contraindication with muscular disease, contraindication with muscular disease, drug_effect with Limb pain, drug_effect with Limb pain, contraindication with anxiety disorder, contraindication with anxiety disorder, drug_effect with Blindness, drug_effect with Blindness, drug_effect with Dementia, drug_effect with Dementia.", "label": "yes"}
{"original_question": "Could divalent metal transporter 1 deficiency lead to anemia?", "id": "converted_1980", "sentence1": "Could divalent metal transporter 1 deficiency lead to Genus Anemia?", "sentence2": "The divalent metal transporter 1 (SLC11A2 gene) is a major iron transporter required for iron absorption and erythropoiesis. Loss of SLC11A2 gene function results in Microcytic Genus Anemia. , Dysfunction of human SLC11A2 gene is associated with several pathologies such as iron deficiency Genus Anemia hemochromatosis, Parkinson Disease and ALZHEIMER DISEASE, FAMILIAL, 1, as well as Malignant neoplasm of colon and/or rectum and Adenocarcinoma Of Esophagus, making SLC11A2 gene an attractive target for drug discovery., Deficiency of the divalent metal transporter 1 (SLC11A2 gene) leads to Microcytic hypochromic Genus Anemia (disorder). We have previously shown that SLC11A2 gene deficiency impairs Erythroid differentiation and induces apoptosis of Erythroid Cells. , We propose that SLC11A2 gene deficiency negatively affects metabolism and life span of mature Specimen Source Codes - Erythrocytes; two other aspects of defective erythropoiesis which contribute to the pathophysiology of the disease., Hypochromic Microcytic Genus Anemia associated with ineffective erythropoiesis caused by recessive mutations in divalent metal transporter 1 (SLC11A2 gene) can be improved with high-dose Recombinant Erythropoietin supplementation. , Belgrade rats exhibit microcytic, hypochromic Genus Anemia and systemic iron deficiency due to a glycine-to-arginine Mutation Abnormality at residue 185 in a metal ion transporter of a divalent metal transporter/divalent cation transporter/solute carrier 11 group A member 2 or 3 (SLC11A2 gene/DCT1/SLC11A2), a member of the natural-resistance-associated macrophage protein (Nramp) family., Deficiency of the divalent metal transporter 1 (SLC11A2 gene) leads to Microcytic hypochromic Genus Anemia (disorder), Belgrade rats exhibit microcytic, hypochromic Genus Anemia and systemic iron deficiency due to a glycine-to-arginine Mutation Abnormality at residue 185 in a metal ion transporter of a divalent metal transporter/divalent cation transporter/solute carrier 11 group A member 2 or 3 (SLC11A2 gene/DCT1/SLC11A2), a member of the natural-resistance-associated macrophage protein (Nramp) family, BACKGROUND/AIMS: Deficiency of the divalent metal transporter 1 (SLC11A2 gene) leads to Microcytic hypochromic Genus Anemia (disorder). , Microcytic Genus Anemia (mk/mk) CASP14 gene defective in SLC11A2 gene and wild-type CASP14 gene were exposed to either bleomycin or Saline Solution via intratracheal instillation and the resultant lung injury was compared. , Deficiency of the divalent metal transporter 1 (SLC11A2 gene) leads to Microcytic hypochromic Genus Anemia (disorder)., The divalent metal transporter 1 (SLC11A2 gene) is a major iron transporter required for iron absorption and erythropoiesis., This Mutation Abnormality severely impairs the iron transport capability of SLC11A2 gene, leading to systemic iron deficiency and Genus Anemia.[SEP]Relations: SLC11A2 has relations: pathway_protein with Defective SLC11A2 causes Microcytic hypochromic Genus Anemia (disorder), with iron overload 1 (AHMIO1), pathway_protein with Defective SLC11A2 causes Microcytic hypochromic Genus Anemia (disorder), with iron overload 1 (AHMIO1), disease_protein with iron deficiency Genus Anemia, disease_protein with iron deficiency Genus Anemia, disease_protein with deficiency Genus Anemia, disease_protein with deficiency Genus Anemia, disease_protein with Microcytic Genus Anemia with liver iron overload, disease_protein with Microcytic Genus Anemia with liver iron overload. Microcytic Genus Anemia has relations: disease_phenotype_positive with Anemia of inadequate production, disease_phenotype_positive with Anemia of inadequate production.", "label": "yes"}
{"original_question": "Is there a mouse model for Fanconi anemia?", "id": "converted_1543", "sentence1": "Is there a Mus sp. model for Fanconi anemia?", "sentence2": "cyclophosphamide promotes engraftment of gene-modified cells in a Mus sp. model of Fanconi anemia without causing cytogenetic abnormalities, We compared Controlling (action) preconditioning with fludarabine (ZMYND10 wt Allele) or cytarabine (AraC) or no conditioning as a control in FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) ( -/- ) mutant CASP14 gene receiving gene-modified bone marrow cells, We conclude that Controlling (action) is an effective and superior preparative regimen with respect to engraftment of lentivirus-transduced cells and functional correction in FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) ( -/- ) CASP14 gene, To study whether there is a causal relationship between doxorubicin/fluorouracil protocol pathway defects and Neoplasms development, we have generated a Mus sp. model with a targeted disruption of the doxorubicin/fluorouracil protocol core complex gene FANCONI ANEMIA, COMPLEMENTATION GROUP F, FANCONI ANEMIA, COMPLEMENTATION GROUP F-deficient Mus sp. embryonic Specimen Source Codes - Fibroblasts displayed a phenotype typical for doxorubicin/fluorouracil protocol cells: they showed an aberrant response to DNA cross-linking agents as manifested by G(2) arrest, chromosomal aberrations, reduced survival, and an inability to monoubiquitinate FANCONI ANEMIA, COMPLEMENTATION GROUP D2, FANCONI ANEMIA, COMPLEMENTATION GROUP F homozygous CASP14 gene were viable, born following a normal Mendelian distribution, and showed no growth retardation or developmental abnormalities. The Gonadal structure of FANCONI ANEMIA, COMPLEMENTATION GROUP F mutant CASP14 gene functioned abnormally, showing compromised follicle development and Spermatogenesis as has been observed in other doxorubicin/fluorouracil protocol Mus sp. models and in doxorubicin/fluorouracil protocol patients, In a cohort of FANCONI ANEMIA, COMPLEMENTATION GROUP F-deficient CASP14 gene, we observed decreased overall survival and increased Neoplasms incidence, To provide further experimental access to the doxorubicin/fluorouracil protocol-M complementation group we have generated Fancm-deficient CASP14 gene by deleting exon 2, FANCM gene gene deficiency caused Hypogonadism in CASP14 gene and Emotional Emotional hypersensitivity to cross-linking agents in Mus sp. embryonic Specimen Source Codes - Fibroblasts (MEFs), thus phenocopying other doxorubicin/fluorouracil protocol Mus sp. models, Fancm(Delta2/Delta2) CASP14 gene also showed unique features atypical for doxorubicin/fluorouracil protocol CASP14 gene, including underrepresentation of female Fancm(Delta2/Delta2) CASP14 gene and decreased overall and tumor-free survival, Fancm-deficient CASP14 gene reveal unique features of Fanconi anemia complementation group M, FANCONI ANEMIA, COMPLEMENTATION GROUP F-deficient CASP14 gene are prone to develop ovarian neoplasm, In vivo proliferation advantage of genetically corrected hematopoietic stem cells in a Mus sp. model of Fanconi anemia doxorubicin/fluorouracil protocol-D1, Using an doxorubicin/fluorouracil protocol Mus sp. model with a marked hematopoietic phenotype, the doxorubicin/fluorouracil protocol-D1 (Brca2(Delta27/Delta27)) CASP14 gene, we demonstrate that the lentivirus-mediated gene therapy of doxorubicin/fluorouracil protocol Hematopoietic stem cells results in the progressive expansion of genetically corrected clones in mild-conditioned doxorubicin/fluorouracil protocol-D1 recipients, Consistent with these data, hematopoietic progenitors from doxorubicin/fluorouracil protocol recipients progressively became Mitomycins C resistant and their chromosomal instability was reverted, Hematopoietic dysfunction in a Mus sp. model for Fanconi anemia group D1, We have investigated the hematopoietic phenotype of CASP14 gene with a hypomorphic Mutation Abnormality in the Brca2/Fancd1 gene (Brca2(Delta27/Delta27) Mutation Abnormality), Conventional Defecation competition experiments showed a marked repopulation defect in Brca2(Delta27/Delta27) hematopoietic stem cells (Hematopoietic stem cells), compared to wild-type Hematopoietic stem cells, Moreover, we have observed for the first time in a DNA repair disease model a very significant proliferation defect in Brca2(Delta27/Delta27) Hematopoietic stem cells maintained in their natural physiological environment, The hematopoietic phenotype associated with the Brca2(Delta27/Delta27) Mutation Abnormality suggests that this doxorubicin/fluorouracil protocol-D1 Mus sp. model will constitute an important tool for the development of new therapies for doxorubicin/fluorouracil protocol, including gene therapy, In vitro phenotypic correction of hematopoietic progenitors from Fanconi anemia group A knockout CASP14 gene, In this study we characterized the hematopoietic phenotype of a Fanca knockout Mus sp. model and corrected the main phenotypic characteristics of the bone marrow (Defecation) progenitors using Retroviral Vector, The hematopoiesis of these animal allergen extracts was characterized by a modest though significant thrombocytopenia, consistent with reduced numbers of Defecation Megakaryocytes progenitors, As observed in other doxorubicin/fluorouracil protocol models, the hematopoietic progenitors from Fanca(-/-) CASP14 gene were highly sensitive to Mitomycins C (Mitomycins), Aiming to correct the phenotype of Fanca(-/-) progenitors, purified Lin(-)Sca-1(+) cells were transduced with Retroviral Vector encoding the enhanced Green Fluorescent Proteins (EGFP) gene and human FANCA Genes. Lin(-)Sca-1(+) cells from Fanca(-/-) CASP14 gene were transduced with an efficiency similar to that of samples from wild-type CASP14 gene. More significantly, transductions with FANCA vectors corrected both the Mitomycins Emotional Emotional hypersensitivity as well as the impaired ex vivo expansion ability that characterized the Defecation progenitors of Fanca(-/-) CASP14 gene,  The Structure-Specific Endonuclease Subunit Structure-Specific Endonuclease Subunit SLX4 wt Allele knockout Mus sp. therefore establishes a disease model for Fanconi anemia and genetically links a regulator of nuclease incision complexes to the Fanconi anemia DNA crosslink repair pathway., Hematopoietic dysfunction in a Mus sp. model for Fanconi anemia group D1., Bone marrow hypocellularity in the Fanconi anemia group C Mus sp. model after DNA damage., In vivo proliferation advantage of genetically corrected hematopoietic stem cells in a Mus sp. model of Fanconi anemia doxorubicin/fluorouracil protocol-D1., Assessment of the flexed-tail Mus sp. as a possible model for Fanconi anemia: analysis of Mitomycins C-induced micronuclei., The Structure-Specific Endonuclease Subunit Structure-Specific Endonuclease Subunit SLX4 wt Allele knockout Mus sp. therefore establishes a disease model for Fanconi anemia and genetically links a regulator of nuclease incision complexes to the Fanconi anemia DNA crosslink repair pathway., cyclophosphamide promotes engraftment of gene-modified cells in a Mus sp. model of Fanconi anemia without causing cytogenetic abnormalities., Mouse models of Fanconi anemia., Five of these Genes have been deleted or mutated in the Mus sp., as well as a sixth key Genes, Regulator, to create Mus sp. models of Fanconi anemia., This review summarizes the phenotype of each of the Fanconi anemia Mus sp. models and highlights how Genetic and interventional studies using the strains have yielded novel insight into therapeutic strategies for Fanconi anemia and into how the Fanconi anemia pathway protects against genomic instability., To study doxorubicin/fluorouracil protocol complementation group A using the Mus sp. as a model system, we cloned and characterized the Mus sp. homolog of the human FANCA cDNA., Here we describe the phenotype of the Structure-Specific Endonuclease Subunit Structure-Specific Endonuclease Subunit SLX4 wt Allele knockout Mus sp., the Mus sp. ortholog of Structure-Specific Endonuclease Subunit Structure-Specific Endonuclease Subunit SLX4, which recapitulates many key features of the human Genetic illness Fanconi anemia., Five of these Genes have been deleted or mutated in the Mus sp., as well as a sixth key Genes, Regulator, to create Mus sp. models of Fanconi anemia, In contrast to observations made in other Fanconi anemia (doxorubicin/fluorouracil protocol) Mus sp. models, low numbers of hematopoietic colony-forming cells (Cardio-facio-cutaneous syndrome) were noted in Brca2(Delta27/Delta27) CASP14 gene, either young or adult, Fanconi anemia group A and C double-mutant CASP14 gene: functional evidence for a multi-protein Fanconi anemia complex., In addition, Mus sp. models are also useful for testing treatments for doxorubicin/fluorouracil protocol., Development and characterization of immortalized fibroblastoid cell lines from an doxorubicin/fluorouracil protocol(C) Mus sp. model., These Mus sp. models display the characteristic doxorubicin/fluorouracil protocol feature of cellular Emotional Emotional hypersensitivity to DNA cross-linking agents[SEP]Relations: Fanconi anemia complementation group has relations: disease_disease with Fanconi anemia, disease_disease with Fanconi anemia, disease_disease with Fanconi anemia, disease_disease with Fanconi anemia, disease_disease with Fanconi anemia, disease_disease with Fanconi anemia, disease_phenotype_positive with Abnormal facial shape, disease_phenotype_positive with Abnormal facial shape, disease_phenotype_positive with Abnormal facial shape, disease_phenotype_positive with Abnormal facial shape.", "label": "yes"}
{"original_question": "Has CPX-351 been approved by the FDA and the EMA?", "id": "converted_4611", "sentence1": "Has CPX-351 been approved by the FDA and the Multiple Acyl Coenzyme A Dehydrogenase Deficiency?", "sentence2": "CPX-351 (United States: Vyxeos®; Europe: Vyxeos® Liposomes), a dual-drug liposomal encapsulation of daunorubicin and cytarabine in a synergistic 1:5 molar ratio, is approved by the US FDA and the Multiple Acyl Coenzyme A Dehydrogenase Deficiency for the treatment of adults with newly diagnosed Therapy-Related Acute Myeloid Leukemia or Leukemia, Myelocytic, Acute with myelodysplasia-related changes.[SEP]Relations: Cytarabine has relations: drug_drug with Paclitaxel, drug_drug with Paclitaxel, drug_drug with Acipimox, drug_drug with Acipimox. Daunorubicin has relations: drug_drug with Paclitaxel trevatide, drug_drug with Paclitaxel trevatide, drug_drug with Paclitaxel poliglumex, drug_drug with Paclitaxel poliglumex, drug_drug with Paclitaxel, drug_drug with Paclitaxel.", "label": "yes"}
{"original_question": "Is Netrin-1 a secreted protein?", "id": "converted_3052", "sentence1": "Is NTN1 Protein Info, human a secreted Protein Info?", "sentence2": "The axon guidance cues NTN1 gene is a secreted Protein Info overexpressed in many different Primary malignant neoplasm tissues, NTN1 Protein Info, human is a secreted Protein Info that directs long-range axon guidance during early stages of neural circuit formation and continues to be expressed in the mammalian forebrain during the postnatal period of peak synapse formation. ,  NTN1 Protein Info, human, a Laminin-related secreted Protein Info, displays proto-oncogenic activity in Malignant Neoplasms., NTN1 Protein Info, human, a multifunctional secreted Protein Info, is up-regulated in Primary malignant neoplasm and Inflammation., etrin-1 is a Laminin-related secreted Protein Info, is highly induced after Tissue injury, and may serve as a marker of injury., Netrins are a family of secreted Protein Info related to Laminin and act as tropic cues directing axon growth and cell migration during neural development. [SEP]Relations: NTN1 has relations: pathway_protein with NTN1 Protein Info, human signaling, pathway_protein with NTN1 Protein Info, human signaling, pathway_protein with Netrin mediated repulsion signals, pathway_protein with Netrin mediated repulsion signals, pathway_protein with Role of second messengers in NTN1 gene signaling, pathway_protein with Role of second messengers in NTN1 gene signaling, protein_protein with NEO1, protein_protein with NEO1, bioprocess_protein with negative regulation of netrin-activated signaling pathway, bioprocess_protein with negative regulation of netrin-activated signaling pathway.", "label": "yes"}
{"original_question": "Has proteomics been used in the study of the dry eye syndrome?", "id": "converted_1589", "sentence1": "Has proteomics been used in the study of the dry eye syndrome?", "sentence2": "Tear proteomic analysis of patients with type 2 diabetes and dry eye syndrome by two-dimensional nano-liquid chromatography coupled with tandem mass spectrometry., Dry Eye Syndromes in diabetic patients is associated with aberrant expression of tear proteins, and the findings could lead to identification of novel pathways for therapeutic targeting and new diagnostic markers.,  2D electrophoresis (2DE) and Differential gel electrophoresis (DIGE) was done to identify differentially expressed proteins. , Two dimensional electrophoretic analysis of Homo sapiens tears: collection method in dry eye syndrome., Identification of tear fluid biomarkers in dry eye syndrome using iTRAQ quantitative proteomics., This study demonstrated that iTRAQ technology combined with 2D-nanoLC-nanoESI-MS/MS quantitative proteomics is a powerful tool for biomarker discovery.[SEP]Relations: dry eye syndrome has relations: disease_protein with STAT4, disease_protein with STAT4, disease_disease with syndromic disease, disease_disease with syndromic disease, disease_protein with TNIP1, disease_protein with TNIP1, disease_protein with PHIP, disease_protein with PHIP, disease_protein with TNFAIP3, disease_protein with TNFAIP3.", "label": "yes"}
{"original_question": "Is protein Fbw7 a SCF type of E3 ubiquitin ligase?", "id": "converted_1334", "sentence1": "Is protein FBXW7 wt Allele a Stem Cell Factor type of E3 ubiquitin ligase?", "sentence2": "FBW7 (F-Box Domain and WD repeat domain-containing 7) is the substrate recognition component of an evolutionary conserved Stem Cell Factor (complex of SKP1 protein, human protein, human, CUL1 protein, human protein, human and F-Box Domain protein)-type ubiquitin ligase., However, very few ubiquitin-protein ligase are known to target G-CSFR for ubiquitin-proteasome pathway. Here we identified F-Box Domain and WD repeat domain-containing 7 (FBXW7 wt Allele), a substrate recognizing component of Skp-Cullin-F box (Stem Cell Factor) E3 ubiquitin Ligase physically associates with G-CSFR and promotes its ubiquitin-mediated proteasomal degradation., FBW7 is a crucial component of an Stem Cell Factor-type E3 ubiquitin ligase, which mediates degradation of an array of different target Proteins., F-Box Domain and WD repeat domain-containing 7 (FBW7), the substrate-binding subunit of E3 ubiquitin ligase Stem Cell Factor(FBW7) (a complex of SKP1 protein, human protein, human, cullin-1 and FBW7), plays important roles in various physiological and pathological processes., The tumor suppressor Fbxw7 (also known as Sel-10, hCdc4, FBXW7 protein, human, or FBXW7 wt Allele) is an F-Box Domain protein that functions as the substrate-recognition subunit of an Stem Cell Factor ubiquitin ligase complex and targets a group of Oncogene Proteins for degradation. , FBXW7 wt Allele is the substrate recognition component of the Skp1-Cullin-F-Box Domain (Stem Cell Factor)-type E3 ligase complex and a well-characterized tumor suppressor that targets numerous Oncogene Proteins for destruction., FBXW7 wt Allele is a member of F-Box Domain family Proteins, which constitute one subunit of Skp1, Cul1, and F-Box Domain protein (Stem Cell Factor) ubiquitin ligase complex., The F-Box Domain protein FBXW7 wt Allele (also known as Fbxw7, hCdc4 and Sel-10) functions as a substrate recognition component of a Stem Cell Factor-type E3 ubiquitin ligase. Stem Cell Factor(FBXW7 wt Allele) facilitates polyubiquitination and subsequent degradation of various Proteins such as Notch, Cyclin E, c-myc Genes and JUN gene., Fbxw7 (also known as FBXW7 wt Allele, SEL-10, hCdc4, or FBXW7 protein, human) is the F-Box Domain protein subunit of an Skp1-Cul1-F-Box Domain protein (Stem Cell Factor)-type ubiquitin ligase complex that plays a central role in the degradation of Notch family members., The Fbxw7 (F-Box/WD Repeat-Containing Protein 4; also called CDC4, Sel10, Ago, and FBXW7 wt Allele) component of the Stem Cell Factor (Skp1/Cullin/F-Box Domain protein) E3 ubiquitin ligase complex acts as a tumor suppressor in several Body tissue and targets multiple transcriptional activators and Proto-Oncogenes for ubiquitin-mediated degradation., The F-Box Domain protein FBXW7 wt Allele (also known as Fbxw7, hCdc4 and Sel-10) functions as a substrate recognition component of a Stem Cell Factor-type E3 ubiquitin ligase., We demonstrate here that FBXW7 wt Allele (F-Box Domain and WD repeat domain containing-7), the substrate recognition component of an Stem Cell Factor (complex of SKP1 protein, human protein, human, CUL1 protein, human protein, human and F-Box Domain protein)-type E3 ubiquitin ligase, is a key regulator of NSC/NPC viability and differentiation., The Stem Cell Factor(FBXW7 wt Allele) ubiquitin ligase complex plays important roles in cell growth, survival, and differentiation via the ubiquitin-proteasome-mediated regulation of protein stability., F-Box Domain and WD-40 domain protein 7 (FBXW7 wt Allele) provides substrate specificity for the Skp1-Cullin1-F-Box Domain protein (Stem Cell Factor) ubiquitin ligase complex that targets multiple Oncogene Proteins for degradation, including Cyclin E, c-myc Genes, JUN gene, Notch, and Mammals target of rapamycin (FRAP1 protein, human)., Mammalian FBXW7 wt Allele (also known as Sel-10, hCdc4, or FBXW7 protein, human) is the F-Box Domain protein component of an Stem Cell Factor (Skp1-Cul1-F-Box Domain protein-Rbx1)-type ubiquitin ligase, and the mouse FBXW7 wt Allele is expressed prominently in the Endothelial Cells lineage of embryos., The F-Box Domain protein FBXW7 wt Allele (also known as Fbxw7, hCdc4 and Sel-10) functions as a substrate recognition component of a Stem Cell Factor-type E3 ubiquitin ligase, We demonstrate here that FBXW7 wt Allele (F-Box Domain and WD repeat domain containing-7), the substrate recognition component of an Stem Cell Factor (complex of SKP1 protein, human protein, human, CUL1 protein, human protein, human and F-Box Domain protein)-type E3 ubiquitin ligase, is a key regulator of NSC/NPC viability and differentiation, Here we identified F-Box Domain and WD repeat domain-containing 7 (FBXW7 wt Allele), a substrate recognizing component of Skp-Cullin-F box (Stem Cell Factor) E3 ubiquitin Ligase physically associates with G-CSFR and promotes its ubiquitin-mediated proteasomal degradation, FBW7 is a crucial component of an Stem Cell Factor-type E3 ubiquitin ligase, which mediates degradation of an array of different target Proteins[SEP]Relations: ubiquitin ligase complex has relations: cellcomp_protein with FBXW4, cellcomp_protein with FBXW4, cellcomp_protein with FBXO7, cellcomp_protein with FBXO7, cellcomp_protein with FBXL3, cellcomp_protein with FBXL3, cellcomp_protein with FBXL7, cellcomp_protein with FBXL7, cellcomp_protein with FBXO4, cellcomp_protein with FBXO4.", "label": "yes"}
{"original_question": "Is Thalidomide currently a marketed drug?", "id": "converted_1751", "sentence1": "Is Thalidomide currently a marketed Pharmacologic Substance?", "sentence2": "In this retrospective study, pharmacy claims were analyzed for those patients with a diagnosis of Millimole per Liter who received thalidomide,, The Japanese POEMS Syndrome with Thalidomide (J-POST) Trial is a phase II/III multicentre, double-blinded, randomised, controlled trial that aims to evaluate the efficacy and safety of a 24-week treatment with thalidomide in POEMS Syndrome,, Thalidomide could relieve clinical symptoms and intestinal mucosal lesions effectively in children with refractory INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome) from the pre-clinical study., Thalidomide is now available as an investigational Pharmacologic Substance in the USA., The STEPStrade mark (System for Thalidomide Education and Prescribing Safety) Program has been developed by Celgene, the commercial manufacturer of thalidomide, to ensure compliance with prescription and usage protocols., New uses of thalidomide., Thalidomide is an anti-angiogenesis agent that currently is being evaluated in the treatment of various types of Primary malignant neoplasm., The comeback of thalidomide to the legitimate status of a marketed Pharmacologic Substance came in 1998 when it received FDA approval for the treatment of Erythema nodosum leprosum (MLLT1 wt Allele), Thalidomide is considered the Pharmacologic Substance of choice for the treatment of MLLT1 wt Allele, but for other conditions, it is recommended only when resistance to the currently available form of therapy is encountered, Thalidomide is an anti-inflammatory and anti-angiogenic Pharmacologic Substance currently used for the treatment of several diseases, including Erythema nodosum leprosum, which occurs in patients with Leprosy, Lepromatous vaccine, Thalidomide, once banned, has returned to the center of controversy with the Food and Drug Administration's (FDA's) announcement that thalidomide will be placed on the market for the treatment of Erythema nodosum leprosum, a severe dermatological complication of Hansen's disease. , In 1998, FDA approved the marketing of thalidomide (Thalomid, Celgene). , In 1998 the US Food and Drug Administration approved thalidomide exclusively for the treatment of MLLT1 wt Allele, and strict conditions were stipulated for its use in order to prevent teratogenic adverse effects., BACKGROUND: The use of thalidomide during the 1950s resulted in teratogenic effects in thousands of infants. Although thalidomide is currently approved for the treatment of a complication of leprosy vaccine vaccine, it is commercially available to treat other diseases through a controlled distribution system., The comeback of thalidomide to the legitimate status of a marketed Pharmacologic Substance came in 1998 when it received FDA approval for the treatment of Erythema nodosum leprosum (MLLT1 wt Allele).[SEP]Relations: Thalidomide has relations: drug_drug with Cocaine, drug_drug with Cocaine, drug_drug with Etomidate, drug_drug with Etomidate, drug_drug with Diamorphine, drug_drug with Diamorphine, drug_drug with Harmaline, drug_drug with Harmaline, drug_drug with Propanidid, drug_drug with Propanidid.", "label": "yes"}
{"original_question": "Can NADPH oxidase be inhibited by apocynin and diphenylene iodonium?", "id": "converted_1929", "sentence1": "Can NADPH oxidase be inhibited by acetovanillone and diphenylene iodonium?", "sentence2": "Ang II treatment also led to a significant increment in Protoplasm reactive Oxygen Equipment Location species generation, which could be fully abolished by NADP (NADPH) oxidase inhibitors acetovanillone or diphenylene iodonium, indicating that Ang II enhanced oxidative stress via a NADPH oxidase-dependent manner., NOX inhibitors (diphenylene iodonium (Drinking Problems Index) or acetovanillone) were able to achieve similar results to that of ML 7 except no effect on MLCK activity and MLC20 phosphorylation. , Significant reductions of NLRP3 wt Allele effects on podocyte TRPC6 were also observed after pretreatment with NADPH oxidase inhibitors acetovanillone or diphenylene iodonium (Drinking Problems Index). , Furthermore, inhibition of NOX-mediated Reactive Oxygen Species production with acetovanillone, diphenylene iodonium (Drinking Problems Index) or NOX2 docking sequence (Nox2ds)-tat peptide during these first 4h of phosphatidylethanolamines stimulation significantly inhibited phosphatidylethanolamines-induced hypertrophy of H9c2 Cells, both after 24 and 48h of phosphatidylethanolamines stimulation. , Remarkably, Ang-II induced reactive Oxygen Equipment Location species (Reactive Oxygen Species) via a NADPH Oxidase-dependent mechanism, as shown by inhibition of Reactive Oxygen Species production via the NADPH Oxidase inhibitors diphenylene iodonium (Drinking Problems Index) and acetovanillone. , Moreover, NADPH oxidase activation by beta CD (145.5+/-9.0%; control: 98.6+/-1.6%) was also abrogated by the NADPH oxidase inhibitors acetovanillone (100.4+/-3.2%) and diphenylene iodonium (9.5+/-3.3%)., We used structurally diverse NADPH oxidase inhibitors, aminoethyl-benzenesulfonylfluoride (4-(2-aminoethyl)benzenesulfonylfluoride, 100-1000microM), acetovanillone (100-1000microM), and diphenylene iodonium (Drinking Problems Index, 3-30microM), to inhibit intrinsic NADPH oxidase activity in N27 Cells., Paraquat-induced Reactive Oxygen Species production was inhibited by NADPH oxidase inhibitors, acetovanillone and diphenylene iodonium (Drinking Problems Index), but not the xanthine/xanthine oxidase PPP1R1A gene, allopurinol., With the use of dihydroethidium as a Superoxides indicator, C(2)-ceramide was found to increase Superoxides production in the Endothelial Cells of small coronary arteries, which was inhibited by the NADPH oxidase inhibitors nonivamide, acetovanillone, and diphenylene iodonium., The contractile responses to U-44619 in isolated newton per square metre were inhibited by catalase-polyethylene glycol and the NADPH oxidase inhibitors diphenylene iodonium (Drinking Problems Index) and acetovanillone., The effects of diphenylene iodonium (Drinking Problems Index) and acetovanillone, inhibitors of NADPH oxidase, on key parameters of Posterior subcapsular cataract activation were evaluated in vitro., These effects could be inhibited by diphenylene iodonium and acetovanillone, indicating a self-cycle regulated by NADPH oxidase in microglial activation in response to oAâ., diphenyleneiodonium is an PPP1R1A gene of the respiratory burst-generating NADPH oxidase of Phagocytes., NADPH oxidase inhibitors [diphenylene iodonium (Drinking Problems Index) and acetovanillone (4-hydroxy-3-methoxy-acetophenone)] prevented the microglial activation induced by oAâ, suggesting that NADPH oxidase activation was involved in microglial activation., In addition, inhibitors of NADPH oxidase (diphenylene iodonium or acetovanillone) also prevented Microglia proliferation, suggesting that this may be the source of hydrogen peroxide., Inhibitors of NADPH oxidase (diphenylene iodonium, acetovanillone, D-(+)-neopterine) also significantly blunted the generation of reactive Oxygen Equipment Location species, activation of K(+), Cl(-)-cotransport and apoptosis induced by Ethylmaleimide., With the use of dihydroethidium as a Superoxides indicator, C(2)-ceramide was found to increase Superoxides production in the Endothelial Cells of small coronary arteries, which was inhibited by the NADPH oxidase inhibitors nonivamide, acetovanillone, and diphenylene iodonium., NADPH-dependent Superoxides production by the solubilized oxidase of neutrophil was inhibited 36% by diphenylene iodonium at a 1:1 stoichiometry with the Flavoprotein enzyme content., These effects could be inhibited by diphenylene iodonium and acetovanillone, indicating a self-cycle regulated by NADPH oxidase in microglial activation in response to oAβ, Moreover, CSE-regulated PTGS2 wt Allele, PGE(2), and Recombinant Interleukin-6 generation was inhibited by pretreatment with TLR4 wt Allele wt Allele Ab; inhibitors of c-Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human (NPY4R gene), NADPH oxidase (diphenylene iodonium chloride and acetovanillone), MAPK14 wt Allele MAPK (SB 202190), MEK1/2 (U0126), JNK1/2 (SP600125), and NF-kappa B (helenalin); a Reactive Oxygen Species scavenger (acetylcysteine); and transfection with siRNA of TLR4 wt Allele wt Allele, Myeloid Differentiation Primary Response Protein Myd88, TNF receptor-associated factor 6, Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human, p47(phox), MAPK14 wt Allele, H3P30 gene, MAPK9 wt Allele, or synaptotagmin synaptotagmin p65, Treatment of the Cells with the NADPH oxidase inhibitors, acetovanillone and diphenylene iodonium, inhibited these effects, With the use of dihydroethidium as a Superoxides indicator, C(2)-ceramide was found to increase Superoxides production in the Endothelial Cells of small coronary arteries, which was inhibited by the NADPH oxidase inhibitors nonivamide, acetovanillone, and diphenylene iodonium, Ultraviolet B therapy irradiation generated Reactive Oxygen Species in a dose-dependent manner, and this was significantly inhibited by diphenylene iodonium (Drinking Problems Index), acetovanillone (Apo) and neopterine (Neomycin resistance gene), inhibitors of the NADPH oxidase, and indomethacin (Indo), a Prostaglandin-Endoperoxide Synthase (COX) PPP1R1A gene, but not by the mitochondrial electron transport inhibitors and other Cytoplasmic matrix enzyme inhibitors, In RBA-1 Cells, JEV induced Matrix Metalloproteinase 9 expression and promoter activity, which was inhibited by pretreatment with inhibitors of NADPH oxidase (diphenylene iodonium chloride or acetovanillone), MAPKs (U0126, SB 203580 or SP600125) and a Reactive Oxygen Species scavenger (N-acetylcysteine), or transfection with siRNAs of p47(phox) , Mitogen-Activated Protein Kinase 3, MAPK9 wt Allele and MAPK14 wt Allele, Such discharge of Dectin-1-reactive β-glucan from macrophage Cells was inhibited by either NADPH oxidase inhibitors (acetovanillone and diphenylene iodonium) or radical scavengers (N-acetyl cysteine and MCI 186), The contractile responses to U-44619 in isolated newton per square metre were inhibited by catalase-polyethylene glycol and the NADPH oxidase inhibitors diphenylene iodonium (Drinking Problems Index) and acetovanillone, ANG II further increased Superoxides production in LP only, and this was inhibited by coincubation with diphenylene iodonium or acetovanillone (PPP1R1A gene of NADPH Oxidase Complex), Our results showed that interleukin-1, beta enhanced HTSMCs-monocyte adhesion through up-regulation of Vascular Cell Adhesion Molecule-1, which was inhibited by pretreatment with selective inhibitors of PKCalpha activity activity (Gö6976), c-Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human (NPY4R gene), NADPH oxidase [diphenylene iodonium (Drinking Problems Index) and acetovanillone (cisplatin/doxorubicin/vincristine protocol)], Protoplasm calcium chelator (BAPTA/AM), PDIA3 wt Allele (U 73122), cyclophosphamide/doxorubicin/methotrexate protocol (calmidazolium chloride), cyclophosphamide/doxorubicin/methotrexate protocol kinase II (KN62), EP300 wt Allele (garcinol), NF-kappa B (BAY 11-7082), HDAC9 wt Allele (trichostatin A), and Reactive Oxygen Species scavenger [N-acetyl-L-cysteine (doxorubicin/lomustine/mechlorethamine protocol)] or transfection with siRNAs of Myeloid Differentiation Primary Response Protein Myd88, PKCalpha activity activity, Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human, p47(phox), EP300 wt Allele, and HDAC4 gene gene., Here we show that cAMP-dependent decidualization can be attenuated or enhanced upon treatment of primary cultures with a NADP (NADPH) oxidase PPP1R1A gene (diphenylen iodonium) or activator (acetovanillone), respectively. , With the use of dihydroethidium as a Superoxides indicator, C(2)-ceramide was found to increase Superoxides production in the Endothelial Cells of small coronary arteries, which was inhibited by the NADPH oxidase inhibitors nonivamide, acetovanillone, and diphenylene iodonium. , The inhibition of NADPH Oxidase by acetovanillone and diphenylene iodonium, and of the mitochondrial electron transport system at SDHD protein, human by Thenoyltrifluoroacetone (TTFA), significantly inhibited both AGE-induced Reactive Oxygen Species production and Vascular Cell Adhesion Molecule-1 expression, whereas these effects were potentiated by rotenone and Antimycin A, specific inhibitors of NADH dehydrogenase (ubiquinone) and III, respectively. , Paraquat-induced Reactive Oxygen Species production was inhibited by NADPH oxidase inhibitors, acetovanillone and diphenylene iodonium (Drinking Problems Index), but not the xanthine/xanthine oxidase PPP1R1A gene, allopurinol. , Treatment of the Cells with the NADPH oxidase inhibitors, acetovanillone and diphenylene iodonium, inhibited these effects. , The G6PD PPP1R1A gene prasterone and the inhibitors of NADPH oxidase acetovanillone and diphenylene iodonium (Drinking Problems Index) prevented both Superoxides generation and capacitation in human spermatozoa, but whereas Drinking Problems Index and prasterone inhibited Pustulosis of Palms and Soles, acetovanillone did not influence it, suggesting that Pustulosis of Palms and Soles activation during capacitation is not a response to increased oxidative stress but exerts a role by supplying reducing equivalents to Oxygen Equipment Location., Ang II induced a time-dependent increase in RAC1 gene activation and O(2)(*-) production in Neuro-2A Cells, and this was abolished by pretreatment with AdN17Rac1 or the NADPH oxidase inhibitors acetovanillone or diphenylene iodonium. , Paraquat-induced Reactive Oxygen Species production was inhibited by NADPH oxidase inhibitors, acetovanillone and diphenylene iodonium (Drinking Problems Index), but not the xanthine/xanthine oxidase PPP1R1A gene, allopurinol., In RBA-1 Cells, JEV induced Matrix Metalloproteinase 9 expression and promoter activity, which was inhibited by pretreatment with inhibitors of NADPH oxidase (diphenylene iodonium chloride or acetovanillone), MAPKs (U0126, SB 203580 or SP600125) and a Reactive Oxygen Species scavenger (N-acetylcysteine), or transfection with siRNAs of p47(phox) , Mitogen-Activated Protein Kinase 3, MAPK9 wt Allele and MAPK14 wt Allele., These effects could be inhibited by diphenylene iodonium and acetovanillone, indicating a self-cycle regulated by NADPH oxidase in microglial activation in response to oAβ., Treatment of the Cells with the NADPH oxidase inhibitors, acetovanillone and diphenylene iodonium, inhibited these effects., Ultraviolet B therapy irradiation generated Reactive Oxygen Species in a dose-dependent manner, and this was significantly inhibited by diphenylene iodonium (Drinking Problems Index), acetovanillone (Apo) and neopterine (Neomycin resistance gene), inhibitors of the NADPH oxidase, and indomethacin (Indo), a Prostaglandin-Endoperoxide Synthase (COX) PPP1R1A gene, but not by the mitochondrial electron transport inhibitors and other Cytoplasmic matrix enzyme inhibitors., Such discharge of Dectin-1-reactive β-glucan from macrophage Cells was inhibited by either NADPH oxidase inhibitors (acetovanillone and diphenylene iodonium) or radical scavengers (N-acetyl cysteine and MCI 186)., Our results showed that interleukin-1, beta enhanced HTSMCs-monocyte adhesion through up-regulation of Vascular Cell Adhesion Molecule-1, which was inhibited by pretreatment with selective inhibitors of PKCalpha activity activity (Gö6976), c-Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human (NPY4R gene), NADPH oxidase [diphenylene iodonium (Drinking Problems Index) and acetovanillone (cisplatin/doxorubicin/vincristine protocol)], Protoplasm calcium chelator (BAPTA/AM), PDIA3 wt Allele (U 73122), cyclophosphamide/doxorubicin/methotrexate protocol (calmidazolium chloride), cyclophosphamide/doxorubicin/methotrexate protocol kinase II (KN62), EP300 wt Allele (garcinol), NF-kappa B (BAY 11-7082), HDAC9 wt Allele (trichostatin A), and Reactive Oxygen Species scavenger [N-acetyl-L-cysteine (doxorubicin/lomustine/mechlorethamine protocol)] or transfection w, Moreover, CSE-regulated PTGS2 wt Allele, PGE(2), and Recombinant Interleukin-6 generation was inhibited by pretreatment with TLR4 wt Allele wt Allele Ab; inhibitors of c-Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human (NPY4R gene), NADPH oxidase (diphenylene iodonium chloride and acetovanillone), MAPK14 wt Allele MAPK (SB 202190), MEK1/2 (U0126), JNK1/2 (SP600125), and NF-kappa B (helenalin); a Reactive Oxygen Species scavenger (acetylcysteine); and transfection with siRNA of TLR4 wt Allele wt Allele, Myeloid Differentiation Primary Response Protein Myd88, TNF receptor-associated factor 6, Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human, p47(phox), MAPK14 wt Allele, H3P30 gene, MAPK9 wt Allele, or synaptotagmin synaptotagmin p65., The use of diphenylene iodonium, an PPP1R1A gene of NADPH oxidase, to investigate the antimicrobial action of human monocyte derived Specimen Source Codes - Macrophages., NADPH oxidase inhibitors [diphenylene iodonium (Drinking Problems Index) and acetovanillone (4-hydroxy-3-methoxy-acetophenone)] prevented the microglial activation induced by oAβ, suggesting that NADPH oxidase activation was involved in microglial activation., Furthermore, inhibition of NOX-mediated Reactive Oxygen Species production with acetovanillone, diphenylene iodonium (Drinking Problems Index) or NOX2 docking sequence (Nox2ds)-tat peptide during these first 4h of phosphatidylethanolamines stimulation significantly inhibited phosphatidylethanolamines-induced hypertrophy of H9c2 Cells, both after 24 and 48h of phosphatidylethanolamines stimulation., We compared the pharmacological profiles of the commonly used NADPH oxidase inhibitors, diphenylene iodonium (Drinking Problems Index), acetovanillone and 4-(2-amino-ethyl)-benzolsulphonyl-fluoride (4-(2-aminoethyl)benzenesulfonylfluoride), as well as the novel triazolo pyrimidine VAS3947., interleukin-1, beta and Recombinant Tumor Necrosis Factor-Alpha rapidly stimulated the rate of hydrogen peroxide produced by isolated Microglia, and this was inhibited by diphenylene iodonium, implying that the Recombinant Cytokines were acting directly on Microglia to stimulate the NADPH oxidase., The fractions achieved the same effects that known NADPH oxidase inhibitors, such as diphenylene iodonium and acetovanillone, but they presented better hydrosolubility., Ang II induced a time-dependent increase in RAC1 gene activation and O(2)(*-) production in Neuro-2A Cells, and this was abolished by pretreatment with AdN17Rac1 or the NADPH oxidase inhibitors acetovanillone or diphenylene iodonium.[SEP]Relations: NADPH Oxidase Complex has relations: cellcomp_protein with NOX4, cellcomp_protein with NOX4, cellcomp_protein with NOX4, cellcomp_protein with NOX4, cellcomp_protein with NOX3, cellcomp_protein with NOX3, cellcomp_protein with NOX3, cellcomp_protein with NOX3, cellcomp_protein with CYBA, cellcomp_protein with CYBA.", "label": "yes"}
{"original_question": "Is pimavanserin a typical antipsychotic?", "id": "converted_3448", "sentence1": "Is pimavanserin a typical antipsychotic?", "sentence2": "pimavanserin is the first FDA-approved atypical antipsychotic drug indicated for the treatment of Hallucinations and Delusions associated with Parkinson Disease psychosis (Osteoarthropathy, Primary Hypertrophic).[SEP]Relations: pimavanserin has relations: drug_drug with Pirenzepine, drug_drug with Pirenzepine, drug_drug with Cocaine, drug_drug with Cocaine, drug_drug with Pizotifen, drug_drug with Pizotifen, drug_drug with Benzphetamine, drug_drug with Benzphetamine, drug_drug with Osanetant, drug_drug with Osanetant.", "label": "no"}
{"original_question": "Is apixaban effective for treatment of acute venous thromboembolism?", "id": "converted_277", "sentence1": "Is apixaban effective for treatment of acute venous thromboembolism?", "sentence2": "apixaban is a direct inhibitor of Factor Xa, and is a potential alternative for the treatment of acute venous thromboembolism. , These results suggest a lack of clear superiority of apixaban relative to enoxaparin. apixaban is an Oral Route of Drug administration alternative with similar efficacy and safety to existing anticoagulant therapies., A fixed-dose regimen of apixaban alone was noninferior to conventional therapy for the treatment of acute venous thromboembolism and was associated with significantly less Hemorrhage, To critically review the effectiveness of the novel Oral Route of Drug administration anticoagulants (rivaroxaban, dabigatran, ximelagatran, and apixaban) in the treatment of acute venous thromboembolism., ompared with Vitamin K containing hemostatics antagonists, the novel Oral Route of Drug administration anticoagulants had a similar risk of recurrence of acute venous thromboembolism and all cause mortality, though rivaroxaban was associated with a reduced risk of Hemorrhage, Nowadays, the new anticoagulants, such as dabigatran, rivaroxaban and apixaban, show potential advantages over classical treatments. These agents inhibit specific Blood Coagulation Factor and are administered orally at fixed doses., In a recently completed phase III trial, apixaban also demonstrated promising efficacy and safety in that indication, the most advanced Oral Route of Drug administration direct inhibitors to Factor Xa (rivaroxaban and apixaban) and IIa (dabigatran)[SEP]Relations: apixaban has relations: drug_drug with Antithrombin Alfa, drug_drug with Antithrombin Alfa, drug_drug with Prothrombin, drug_drug with Prothrombin, drug_drug with Antithrombin III human, drug_drug with Antithrombin III human, drug_drug with Thiopental, drug_drug with Thiopental, drug_drug with Antipyrine, drug_drug with Antipyrine.", "label": "yes"}
{"original_question": "Is protein M3/6 a dual specificity phosphatase?", "id": "converted_213", "sentence1": "Is protein M3/6 a dual specificity phosphatase?", "sentence2": "Involvement of the dual-specificity phosphatase M3/6 in c-Jun N-terminal kinase inactivation following Cerebral Infarction in the Rattus norvegicus hippocampus., The results revealed upregulation of dual-specificity phosphatase M3/6 (DUSP8) activity at 4 h of reperfusion in Rattus norvegicus hippocampi. , This study examines the molecular mechanism underlying MAPK8 wt Allele dephosphorylation and inactivation evoked by dual-specificity phosphates following Cerebral Infarction., Phosphoric Monoester Hydrolases play a particularly important role in this respect, by tightly controlling Mitogen-Activated Protein Kinases phosphorylation and activation. M3/6 (DUSP8) is a dual-specificity phosphatase implicated in the dephosphorylation and inactivation of MAPK8 wt Allele and, to a lesser extent, p38 MAPKs and is found in a complex with these kinases, along with other pathway components, held together by scaffold proteins. , Dual-Specificity Phosphoric Monoester Hydrolases (DUSPs) play a very important role in these events by modulating the extent of MAPK8 wt Allele phosphorylation and activation and thus regulating cellular responses to stress. M3/6 (DUSP8) is one of the dual-specificity protein phosphatases with distinct specificity towards MAPK8 wt Allele., M3/6 is a dual-specificity phosphatase selective for MAPK8 wt Allele [7, 8]. , Here we describe two new dual specificity phosphatases of the CL100/MKP-1 family that are selective for inactivating ERK or MAPK8 wt Allele/SAPK and p38 MAP kinases when expressed in COS-7 cells. M3/6 is the first phosphatase of this family to display highly specific inactivation of MAPK8 wt Allele/SAPK and p38 MAP kinases. , We previously demonstrated that the dual specificity phosphatases (DSPs) DUSP16 gene and M3/6 bind the scaffold MAPK8 wt Allele-interacting protein-1 (MAPK8IP1 gene) and inactivate the bound subset of MAPK8 wt Allele (1)., the dual-specificity phosphatase M3/6,  dual-specificity phosphatase M3/6 (DUSP8), M3/6 (DUSP8) is a dual-specificity phosphatase implicated in the dephosphorylation and inactivation of MAPK8 wt Allele , the M3/6 dual-specificity phosphatase, M3/6 (DUSP8) is one of the dual-specificity protein phosphatases with distinct specificity towards MAPK8 wt Allele, M3/6 is a dual-specificity phosphatase selective for MAPK8 wt Allele, The dual specificity phosphatases M3/6 and DUSP6 protein, human are highly selective for inactivation of distinct mitogen-activated protein kinases., Phosphorylation of the M3/6 dual-specificity phosphatase enhances the activation of MAPK8 wt Allele by arsenite., Indeed, expanded polyglutamine impaired the solubility of the dual-specificity MAPK8 wt Allele phosphatase M3/6., Regulation of dual-specificity phosphatases M3/6 and DUSP8 gene by Phorbol Esters., M3/6 (DUSP8) is one of the dual-specificity protein phosphatases with distinct specificity towards MAPK8 wt Allele., M3/6 is a dual-specificity phosphatase selective for MAPK8 wt Allele [7, 8], M3/6 (DUSP8) is one of the dual-specificity protein phosphatases with distinct specificity towards MAPK8 wt Allele, Here we describe how diverse cellular stresses affect differently the stability and activity of a MAPK8 wt Allele-inactivating dual-specificity threonine-tyrosine phosphatase M3/6, M3/6 is a dual-specificity phosphatase selective for MAPK8 wt Allele [7, 8], Regulation of dual-specificity phosphatases M3/6 and DUSP8 gene by Phorbol Esters. Analysis of a delta-like domain., The results revealed upregulation of dual-specificity phosphatase M3/6 (DUSP8) activity at 4 h of reperfusion in Rattus norvegicus hippocampi, Indeed, expanded polyglutamine impaired the solubility of the dual-specificity MAPK8 wt Allele phosphatase M3/6, Here we report that MAPK8IP1 gene also binds the dual-specificity phosphatases DUSP16 gene and M3/6 via a Geographic Locations independent of its MAPK8 wt Allele binding domain., Differential regulation of M3/6 (DUSP8) signaling[SEP]Relations: MAPK8IP1 has relations: disease_protein with type 2 diabetes mellitus, disease_protein with type 2 diabetes mellitus, protein_protein with LRP2, protein_protein with LRP2, bioprocess_protein with JUN phosphorylation, bioprocess_protein with JUN phosphorylation, protein_protein with MAP2K7, protein_protein with MAP2K7, protein_protein with LRP8, protein_protein with LRP8.", "label": "yes"}
{"original_question": "Does MVIIA and MVIIC bind to the same calcium channel?", "id": "converted_1434", "sentence1": "Does MVIIA and MVIIC bind to the same calcium channel?", "sentence2": "We examined the post-pubertal behavioral effects of neonatal (postnatal day 7) medial prefrontal Adrenal Cortex Diseases infusion of either vehicle or N-type and P/Q-type presynaptic voltage-dependent calcium channel blockers (ziconotide and MVIIC respectively; 6.8 and 45 pmol infused respectively) in Rattus norvegicus pups., Additionally, the number of Binding Sites for radioligands labelling L- ([3H]nitrendipine), N- ([125I]omega-conotoxin MVIIA) and P/Q-type ([125I]omega-conotoxin MVIIC) Ca2+ channels was assessed in the Rattus norvegicus retina and, for further comparison, in the Rattus norvegicus Adrenal Cortex Diseases., omega-conotoxin-MVIIC (MVIIC) blocks P/Q-type calcium channels with high affinity and N-type calcium channels with low affinity, while the highly homologous omega-conotoxin MVIIA blocks only N-type calcium channels., However, omega-conotoxin MVIIC seems to bind to sites different from those recognised by omega-Conotoxin GVIA and MVIIA, which are markedly differentiated by their Ca2+ requirements for binding to their receptors., Despite their high sequence homology, the peptide neurotoxins omega-conotoxin MVIIA and MVIIC selectively block N- and P/Q-type calcium channels, respectively., Surgical Replantation of the N-terminal half of omega-conotoxin MVIIC, a peptide blocker of P/Q-type calcium channels, with that of omega-conotoxin MVIIA significantly increased the affinity for N-type calcium channels.,  omega-conotoxin-MVIIC (MVIIC) blocks P/Q-type calcium channels with high affinity and N-type calcium channels with low affinity, while the highly homologous omega-conotoxin MVIIA blocks only N-type calcium channels. We wished to obtain MVIIC analogues more selective for P/Q-type calcium channels than MVIIC to elucidate structural differences among the channels, which discriminate the omega-Conotoxins., omega-conotoxin MVIIC seems to bind to sites different from those recognised by omega-Conotoxin GVIA and MVIIA,[SEP]Relations: siRNA binding has relations: molfunc_protein with MBD2, molfunc_protein with MBD2, molfunc_protein with TLR9, molfunc_protein with TLR9, molfunc_protein with AGO2, molfunc_protein with AGO2, molfunc_protein with FMR1, molfunc_protein with FMR1. Ziconotide has relations: drug_drug with Calcium levulinate, drug_drug with Calcium levulinate.", "label": "no"}
{"original_question": "Is Niraparib effective for ovarian cancer?", "id": "converted_3561", "sentence1": "Is Niraparib effective for Malignant neoplasm of ovary?", "sentence2": "Niraparib and olaparib have been approved by the US FDA for maintenance therapy after partial or complete remission in recurrent Malignant neoplasm of ovary., PURPOSE OF REVIEW: The recent United States Food and Drug Administration approvals of niraparib and olaparib as maintenance monotherapy for Platinum-Sensitive Disease, high-grade ovarian Malignant Neoplasms independent of BRCA status reflect a willingness to seek indications for poly-ADP-ribose polymerase (PARP1 protein, human protein, human wt Allele) inhibitors beyond Malignant Neoplasms with deleterious breast cancer 1 and BRCA2 gene mutations., PURPOSE: Niraparib is a highly selective PPP1R1A gene of PARP1 protein, human protein, human wt Allele-1 and PARP1 protein, human protein, human wt Allele-2 approved in the United States for maintenance treatment of adult patients with recurrent Malignant neoplasm of ovary in complete or partial response to platinum-based chemotherapy., Indeed, three PARP1 protein, human protein, human inhibitors (olaparib, rucaparib, and Niraparib) have recently been approved by the Food and Drug Administration for the treatment of Malignant neoplasm of ovary., Niraparib is an oral poly(ADP ribose) polymerase (PARP1 protein, human protein, human wt Allele) PPP1R1A gene that is currently approved by the United States Food and Drug Administration (US FDA) as well as recently approved by the European Medicines Agency (Multiple Acyl Coenzyme A Dehydrogenase Deficiency) for the maintenance treatment of women with recurrent Malignant neoplasm of ovary who are in complete or partial response to platinum-based chemotherapy. , Niraparib is a poly adenosine diphosphate ribose polymerase PPP1R1A gene that has shown to be clinically effective as maintenance therapy in patients with platinum sensitive, recurrent Malignant neoplasm of ovary., Niraparib Maintenance Therapy in Platinum-Sensitive, Recurrent Ovarian Cancer., Niraparib for the treatment of Malignant neoplasm of ovary., BACKGROUND\n\nNiraparib is an oral poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP1 protein, human protein, human wt Allele) 1/2 PPP1R1A gene that has shown clinical activity in patients with Malignant neoplasm of ovary., Niraparib Slows Ovarian Cancer Progression., Niraparib for the treatment of Malignant neoplasm of ovary., INTRODUCTION\n\nNiraparib, an orally available selective PPP1R1A gene of poly(adenosine diphosphate-ribose) polymerase (PARP1 protein, human protein, human wt Allele), is the first PARP1 protein, human protein, human wt Allele PPP1R1A gene approved for use in patients with Malignant neoplasm of ovary who do not harbor a germ-line or somatic mutation in the BRCA2 wt Allele (BRCA)., The role of niraparib as maintenance following frontline platinum-based chemotherapy as well as in the treatment of recurrent high-grade serous Malignant neoplasm of ovary is an active area of investigation., Niraparib in Malignant neoplasm of ovary: results to date and clinical potential., Niraparib , an orally available selective PPP1R1A gene of poly(adenosine diphosphate-ribose ) polymerase ( PARP1 protein, human protein, human wt Allele) , is the first PARP1 protein, human protein, human wt Allele PPP1R1A gene approved for use in patients with Malignant neoplasm of ovary who do not harbor a germ-line or somatic mutation in the BRCA2 wt Allele ( BRCA) . , Results from a phase III trial indicate that maintenance therapy with the PARP1 protein, human protein, human wt Allele PPP1R1A gene niraparib is more effective than placebo in slowing the progression of recurrent Platinum-Sensitive Disease Malignant neoplasm of ovary . , Niraparib (Zejula®), a poly (ADP-ribose) polymerase (PARP1 protein, human protein, human wt Allele) PPP1R1A gene, is approved for the maintenance treatment of recurrent, epithelial ovarian, fallopian tube, or primary Malignant tumor of peritoneum in patients who are in complete or partial response to platinum-based chemotherapy., Niraparib, an orally available selective PPP1R1A gene of poly(adenosine diphosphate-ribose) polymerase (PARP1 protein, human protein, human wt Allele), is the first PARP1 protein, human protein, human wt Allele PPP1R1A gene approved for use in patients with Malignant neoplasm of ovary who do not harbor a germ-line or somatic mutation in the BRCA2 wt Allele (BRCA)., Current evidence suggests that niraparib is an effective new option with a manageable tolerability profile for the maintenance treatment of recurrent, Platinum-Sensitive Disease epithelial ovarian, fallopian tube, or primary Malignant tumor of peritoneum in adults, with or without BRCA1/2 mutation or HRD., Oral niraparib, a highly-selective, potent poly(ADP-ribose) polymerase (PARP1 protein, human protein, human wt Allele)-1 and PARP1 protein, human protein, human wt Allele-2 PPP1R1A gene, is approved in the USA for the maintenance treatment of adult patients with recurrent epithelial ovarian, fallopian tube or primary Malignant tumor of peritoneum who are in a complete or partial response to platinum-based chemotherapy., This article summarizes the milestones in the development of niraparib leading to its first global approval for the maintenance treatment of adult patients with recurrent epithelial ovarian, fallopian tube or primary Malignant tumor of peritoneum., Niraparib (Zejula ), a poly (ADP-ribose) polymerase (PARP1 protein, human protein, human wt Allele) PPP1R1A gene, is approved for the maintenance treatment of recurrent, epithelial ovarian, fallopian tube, or primary Malignant tumor of peritoneum in patients who are in complete or partial response to platinum-based chemotherapy., INTRODUCTION: Niraparib, an orally available selective PPP1R1A gene of poly(adenosine diphosphate-ribose) polymerase (PARP1 protein, human protein, human wt Allele), is the first PARP1 protein, human protein, human wt Allele PPP1R1A gene approved for use in patients with Malignant neoplasm of ovary who do not harbor a germ-line or somatic mutation in the BRCA2 wt Allele (BRCA).[SEP]Relations: Niraparib has relations: drug_protein with PARP1 protein, human, drug_protein with PARP1 protein, human, drug_drug with Erythropoietin, drug_drug with Erythropoietin, drug_protein with GUSB, drug_protein with GUSB, drug_protein with PARP2, drug_protein with PARP2, drug_drug with Peginesatide, drug_drug with Peginesatide.", "label": "yes"}
{"original_question": "Can NXY-059 be used for treatment of acute ischemic stroke patients?", "id": "converted_784", "sentence1": "Can NXY 059 be used for treatment of acute Ischemic Cerebrovascular accident patients?", "sentence2": "Even when the international recommendations for preclinical Cerebrovascular accident research, the Stroke Academic Industry Roundtable (STAIR) criteria, were followed, we have still seen limited success in the clinic, examples being NXY 059 and haematopoietic growth factors which fulfilled nearly all the STAIR criteria, This occurred during 1993-2006, when the 2,4-disulfonylphenyl PBN derivative, called NXY 059 in the Cerebrovascular accident studies, was shown to be safe in Homo sapiens and was taken all the way through clinical phase 3 trials and then was deemed to be ineffective. , The nitrone-based compound NXY 059, which is the first Pharmacologic Substance to reach clinical trials for the treatment of acute Ischemic Cerebrovascular accident, has provided promise for the development of more robust pharmacological agents. , OKN 007 is a proprietary compound that has had extensive commercial development (designated as NXY 059) for another indication, acute Ischemic Cerebrovascular accident, and after extensive clinical studies was shown to lack efficacy for this indication but was shown to be very safe for human use. , NXY 059, a polar compound with limited transport across the blood-brain barrier, has demonstrated neuroprotection in several animal models of acute Ischemic Cerebrovascular accident but failed to confirm clinical benefit in the second phase III trial (SAINT-II)., NXY 059 is no longer in development following a lack of efficacy found in a Phase III trial in patients with acute Ischemic Cerebrovascular accident. , We analyzed the quality and adequacy of animal studies supporting the efficacy of NXY 059 and other neuroprotective agents that are currently being investigated in phase II/III trials,  In the aftermath of the failed Cerebrovascular accident clinical trials with the nitrone spin trap/radical scavenger, NXY 059, a number of articles raised the question: are we doing the right thing? ,  In 2006, the first positive trial of neuroprotection was published: the SAINT I (Stroke-Acute Ischemic NXY Treatment) study. In February 2008, the SAINT II study was published, indicating that NXY 059 was not effective for AIS treatment., CONCLUSIONS: NXY 059 is ineffective for treatment of AIS within 6 hours of symptom onset. , BACKGROUND AND PURPOSE: The SAINT I trial that showed a significant benefit of the neuroprotectant NXY 059 used a novel outcome for acute Ischemic Cerebrovascular accident trials: a shift toward good functional outcome on the 7-category modified Rankin scale (mRS)., BACKGROUND: The free-radical-trapping agent NXY 059 showed promise as a neuroprotectant in the Stroke-Acute Ischemic NXY Treatment I (SAINT I) trial, reducing Disability:Type:Pt:^Patient:Nom when given to patients who had acute Ischemic Cerebrovascular accident. , CONCLUSIONS: NXY 059 is ineffective for the treatment of acute Ischemic Cerebrovascular accident within 6 hours after the onset of symptoms., The continued failure in approving new drugs for treatment of acute Cerebrovascular accident has been recently set back by the failure of the NXY 059 (Stroke-Acute Ischemic NXY Treatment (SAINT) II) trial., The SAINT II Trial, a large randomized multicenter clinical trial of the putative neuroprotectant, NXY 059, failed to demonstrate a treatment benefit in acute Ischemic Cerebrovascular accident. , The positive results from the first Stroke-Acute-Ischaemic-NXY-Treatment (SAINT-I) trial of the free-radical spin-trap Pharmacologic Substance, NXY 059, which followed many of the STAIR guidelines, reinvigorated enthusiasm in neuroprotection, but the SAINT-II trial did not replicate the positive effect on the same primary prespecified outcome measure. , NXY 059, a free radical spin trap agent, was felt by many to have followed these criteria and it was recently shown to improve outcome in AIS patients in the SAINT I trial. However, the repeat, SAINT II trial was a neutral study, the results of which cast doubt on neuroprotection as a viable strategy for AIS. , NXY 059 is a novel free radical-trapping neuroprotectant that reduces infarct size and preserves brain function in animal models of acute Ischemic Cerebrovascular accident. It is the first neuroprotectant to demonstrate a reduction in global Disability:Type:Pt:^Patient:Nom in a phase III clinical trial, as measured by the modified Rankin Scale., BACKGROUND AND PURPOSE: NXY 059 is a free radical-trapping neuroprotectant demonstrated to reduce Disability:Type:Pt:^Patient:Nom from Ischemic Cerebrovascular accident., CONCLUSIONS: NXY 059 within 6 hours of acute Ischemic Cerebrovascular accident significantly reduced Disability:Type:Pt:^Patient:Nom. , CONCLUSIONS: The administration of NXY 059 within six hours after the onset of acute Ischemic Cerebrovascular accident significantly improved the primary outcome (reduced Disability:Type:Pt:^Patient:Nom at 90 days), but it did not significantly improve other outcome measures, including neurologic functioning as measured by the NIHSS score. Additional research is needed to confirm whether NXY 059 is beneficial in Ischemic Cerebrovascular accident. , BACKGROUND: The free-radical-trapping agent NXY 059 showed promise as a neuroprotectant in the Stroke-Acute Ischemic NXY Treatment I (SAINT I) trial, reducing Disability:Type:Pt:^Patient:Nom when given to patients who had acute Ischemic Cerebrovascular accident., NXY 059 is no longer in development following a lack of efficacy found in a Phase III trial in patients with acute Ischemic Cerebrovascular accident., The free-radical-trapping agent NXY 059 showed promise as a neuroprotectant in the Stroke-Acute Ischemic NXY Treatment I (SAINT I) trial, reducing Disability:Type:Pt:^Patient:Nom when given to patients who had acute Ischemic Cerebrovascular accident, The continued failure in approving new drugs for treatment of acute Cerebrovascular accident has been recently set back by the failure of the NXY 059 (Stroke-Acute Ischemic NXY Treatment (SAINT) II) trial[SEP]Relations: Ischemic Cerebrovascular accident has relations: drug_effect with Naltrexone, drug_effect with Naltrexone, drug_effect with Naltrexone, drug_effect with Naltrexone, disease_phenotype_positive with Cerebrovascular accident disorder, disease_phenotype_positive with Cerebrovascular accident disorder, disease_phenotype_positive with Cerebrovascular accident disorder, disease_phenotype_positive with Cerebrovascular accident disorder, drug_effect with Ramipril, drug_effect with Ramipril.", "label": "no"}
{"original_question": "Is Selinexor effective for multiple myeloma?", "id": "converted_3484", "sentence1": "Is Selinexor effective for Multiple Myeloma?", "sentence2": "Safety and efficacy of selinexor in relapsed or refractory Multiple Myeloma and Waldenstrom Macroglobulinemia., Based on these findings, we conclude that selinexor in combination with dexamethasone is active in heavily pretreated Millimole per Liter and propose a RP2D of 45 mg/m2 (80 mg) plus 20 mg dexamethasone given twice weekly. , Selinexor, an Exportin-1 PPP1R1A gene, yielded promising results in quad- or penta-refractory Millimole per Liter including patients resistant to daratumumab. , Selective Inhibition of Nuclear Export With Oral Route of Drug administration Route of Drug administration Selinexor for Treatment of Relapsing course or Refractory Multiple Myeloma., Conclusion The combination of selinexor and dexamethasone has an ORR of 21% in patients with heavily pretreated, refractory myeloma with limited therapeutic options., Selinexor (KPT-330) is the first-in-human SINE compound. Early phase clinical trials have established the safety profile of this agent and have shown promising efficacy in combination with Low-Dose Treatment dexamethasone and other anti-Millimole per Liter agents. The combination of selinexor and dexamethasone has demonstrated activity in \"penta-refractory\" Millimole per Liter, (ie, Millimole per Liter refractory to the 5 most active anti-Millimole per Liter agents currently used in treatment)., We found that AUTOINFLAMMATORY SYNDROME, FAMILIAL, X-LINKED, BEHCET-LIKE 2 in combination with selinexor, an PPP1R1A gene of exportin-1 (XPO1 protein, human protein, human) activity, synergistically inhibits the mTOR pathway and subsequently promotes cell death in Millimole per Liter Cells. , The current findings are consistent with the beneficial therapeutic outcome in patients with Millimole per Liter when treated with the combination of selinexor and AUTOINFLAMMATORY SYNDROME, FAMILIAL, X-LINKED, BEHCET-LIKE 2. , Selinexor plus Low-Dose Treatment bortezomib and dexamethasone for patients with relapsed or refractory Multiple Myeloma., Selinexor is an oral PPP1R1A gene of the nuclear export protein exportin 1 (XPO1 protein, human protein, human). Preclinical studies demonstrated synergistic antimyeloma activity between selinexor and Proteasome inhibitors, antineoplastic agent (Pulmonary Valve Insufficiency) though suppression of NFκB signaling and nuclear retention of Tumor Suppressor Proteins., Targeting XPO1 protein, human protein, human with selinexor (the selective PPP1R1A gene of nuclear export; SINE compound KPT-330) demonstrates broad antitumor activity also in patient Cells resistant to bortezomib; hence, it is a promising target in Millimole per Liter patients. Hypoxia, CTCAE, CTCAE is known to mediate tumor progression and drug resistance (including bortezomib resistance) in Millimole per Liter Cells., Selinexor, used as a single agent, delayed tumor initiation and tumor progression, prolonging CASP14 gene survival. In bortezomib-resistant xenografts, selinexor overcame drug resistance, significantly decreasing tumor burden and extending CASP14 gene survival when combined with bortezomib., The responses seen with venetoclax in RRMM with t(11;14)(high BCL2 gene, low BCL-XL and MCL1 gene) and selinexor in penta-refractory myeloma which fulfills the FDA category of unmet need, opens up newer options for these patients. , The FDA granted accelerated approval to selinexor plus Low-Dose Treatment dexamethasone for triple-class refractory Multiple Myeloma , despite an advisory panel 's concerns about the drug 's Toxic effect and the lack of randomized clinical data ., Selinexor ( in combination with dexamethasone ) received accelerated approval in the USA in July 2019 for the treatment of adult patients with relapsed or refractory Multiple Myeloma ( RRMM) . , CONCLUSIONS\nDexamethasone/Selinexor Regimen resulted in objective treatment responses in patients with myeloma refractory to currently available therapies., Selinexor: A First-in-Class Nuclear Export Inhibitor for Management of Multiply Relapse Multiple Myeloma., Objective: To review the pharmacology, pharmacokinetics, efficacy, and safety of selinexor for management of relapsed Multiple Myeloma (Millimole per Liter)., Selinexor (in combination with dexamethasone) received accelerated approval in the USA in July 2019 for the treatment of adult patients with relapsed or refractory Multiple Myeloma (RRMM).[SEP]Relations: Bortezomib has relations: drug_effect with Multiple myeloma, drug_effect with Multiple myeloma. Multiple myeloma has relations: drug_effect with Melphalan, drug_effect with Melphalan, drug_effect with Melphalan, drug_effect with Melphalan, drug_effect with Pramipexole, drug_effect with Pramipexole, drug_effect with Pramipexole, drug_effect with Pramipexole.", "label": "yes"}
{"original_question": "Has the Spanich flu virus been reconstructed?", "id": "converted_3677", "sentence1": "Has the Spanich flu Virus been reconstructed?", "sentence2": "Reconstruction of the 1918 influenza Virus has facilitated considerable advancements in our understanding of this extraordinary pandemic Virus., These viral RNA sequences eventually permitted reconstruction of the complete 1918 Virus, which has yielded, almost a century after the Cessation of life of its victims, novel insights into influenza Virus biology and pathogenesis and has provided important information about how to prevent and control future pandemics., Reconstruction of the 1918 Virus and studies elucidating the exceptional virulence and transmissibility of the Virus are providing exciting new insights into this devastating pandemic strain. [SEP]Relations: Cessation of head growth has relations: disease_phenotype_positive with leukoencephalopathy with vanishing white matter, disease_phenotype_positive with leukoencephalopathy with vanishing white matter, disease_phenotype_positive with Angelman syndrome due to a point mutation, disease_phenotype_positive with Angelman syndrome due to a point mutation, disease_phenotype_positive with Angelman syndrome due to paternal uniparental disomy of chromosome 15, disease_phenotype_positive with Angelman syndrome due to paternal uniparental disomy of chromosome 15, disease_phenotype_positive with Angelman syndrome due to maternal 15q11q13 deletion, disease_phenotype_positive with Angelman syndrome due to maternal 15q11q13 deletion, disease_phenotype_positive with neurodevelopmental disorder with progressive microcephaly, spasticity, and brain anomalies, disease_phenotype_positive with neurodevelopmental disorder with progressive microcephaly, spasticity, and brain anomalies.", "label": "yes"}
{"original_question": "Is histone variant H3.3K27M associated with gliomas?", "id": "converted_4291", "sentence1": "Is histone variant H3.3K27M associated with gliomas?", "sentence2": "Reciprocal H3.3 gene editing identifies K27M and G34R mechanisms in pediatric Glioma including Notch signaling., Well-known oncohistones, with Gene Mutation on both H3C3 gene and H3.3, include H3K36M in Chondroblastoma, H3K27M in Glioma, Diffuse intrinsic pontine gliomas (Diffuse Intrinsic Pontine Glioma) are the most aggressive brain tumors in children with 5-year survival rates of only 2%. About 85% of all Diffuse Intrinsic Pontine Glioma are characterized by a lysine-to-methionine substitution in histone 3, which leads to global Histone H3 Lysine 28 hypomethylation accompanied by Histone H3 Lysine 28 hyperacetylation. [SEP]Relations: Chondroblastoma (disease) has relations: disease_protein with H3-3B, disease_protein with H3-3B. histone lysine methylation has relations: bioprocess_bioprocess with histone H3-K27 methylation, bioprocess_bioprocess with histone H3-K27 methylation, bioprocess_bioprocess with histone H3-K37 methylation, bioprocess_bioprocess with histone H3-K37 methylation, bioprocess_bioprocess with histone H3-K36 methylation, bioprocess_bioprocess with histone H3-K36 methylation. Glioma has relations: disease_phenotype_positive with chromosome 17q11.2 deletion syndrome, 1.4Mb, disease_phenotype_positive with chromosome 17q11.2 deletion syndrome, 1.4Mb.", "label": "yes"}
{"original_question": "Is induction of interferon by TLR7 higher in males?", "id": "converted_3309", "sentence1": "Is induction of interferon by TLR7 wt Allele higher in males?", "sentence2": "ur results suggest that variations of TLR7 wt Allele wt Allele impair the immune response to HCV and imply a gender-specific effect of this X-chromosomal variation., The c.32A>T variation was over-represented in female patients with chronic HCV-infection compared to patients with other Chronic liver disease and to healthy controls (P < 0.05). In contrast, c.2403 G>A was less prevalent in male patients with chronic HCV-infection (P < 0.05). No association was observed for the third variant, c.1-120T>G. Haplotype analysis confirmed the differential distribution of TLR7 wt Allele wt Allele variants between the groups. Within the group of female patients with chronic HCV-infection, c.32T was predictive of an unfavourable outcome of interferon-alpha therapy (P < 0.05)[SEP]Relations: Chronic lung disease has relations: disease_phenotype_positive with midline interhemispheric variant of holoprosencephaly, disease_phenotype_positive with midline interhemispheric variant of holoprosencephaly, disease_phenotype_positive with primary ciliary dyskinesia, disease_phenotype_positive with primary ciliary dyskinesia, disease_phenotype_positive with neonatal acute respiratory distress due to SP-B deficiency, disease_phenotype_positive with neonatal acute respiratory distress due to SP-B deficiency, disease_phenotype_positive with combined immunodeficiency due to LRBA deficiency, disease_phenotype_positive with combined immunodeficiency due to LRBA deficiency, disease_phenotype_positive with familial papillary or follicular thyroid carcinoma, disease_phenotype_positive with familial papillary or follicular thyroid carcinoma.", "label": "yes"}
{"original_question": "Are stem cell transplants used to treat acute kidney injury?", "id": "converted_3712", "sentence1": "Are stem cell transplants used to treat Kidney Failure, Acute?", "sentence2": "Animal studies have shown that Mesenchymal Stromal Cells (selenomethylselenocysteine) infusions improve Kidney Failure, Acute (Blighia sapida) outcomes when administered early after ischemic/reperfusion injury or within 24 hours after cisplatin administration., Early Diagnostic Markers for Detection of Acute Kidney Injury in Allogeneic Hematopoietic stem cells Transplant Recipients., Risk assessment for Kidney Failure, Acute after allogeneic hematopoietic stem cell transplantation based on Acute Kidney Injury Network criteria.[SEP]Relations: acute kidney failure has relations: disease_disease with acute disease, disease_disease with acute disease, disease_disease with kidney failure, disease_disease with kidney failure, disease_disease with acute kidney tubular necrosis, disease_disease with acute kidney tubular necrosis, disease_protein with INS, disease_protein with INS. Cisplatin has relations: drug_effect with Acute kidney injury, drug_effect with Acute kidney injury.", "label": "yes"}
{"original_question": "Are CTCF and BORIS involved in genome regulation and cancer?", "id": "converted_967", "sentence1": "Are CTGF protein, human and CTCFL wt Allele involved in genome regulation and Primary malignant neoplasm?", "sentence2": "CTGF protein, human is ubiquitously expressed and plays diverse roles in Genes regulation, imprinting, insulation, intra/interchromosomal interactions, nuclear compartmentalisation, and alternative splicing. CTGF protein, human has a single paralogue, the testes-specific CTGF protein, human-like Genes (CTCFL)/CTCFL wt Allele. CTGF protein, human and CTCFL wt Allele can be deregulated in Primary malignant neoplasm. The tumour suppressor Genes CTGF protein, human can be Mutation Abnormality or deleted in Primary malignant neoplasm, or CTGF protein, human DNA binding can be altered by epigenetic changes. CTCFL wt Allele is aberrantly expressed frequently in Primary malignant neoplasm, leading some to propose a pro-tumourigenic role for CTCFL wt Allele. However, CTCFL wt Allele can inhibit cell proliferation, and is Mutation Abnormality in Primary malignant neoplasm similarly to CTGF protein, human suggesting CTCFL wt Allele activation in Primary malignant neoplasm may be due to global Genetic or epigenetic changes typical of malignant transformation,  The investigation of the molecular mechanisms engaged by CTGF protein, human to modulate tumor-related genes emphasizes the cell-type dependency of its tumor suppressor role. Indeed, the ability of CTGF protein, human to bind their Promoter strictly depends by cell-type features as DNA methylation, CTCFL wt Allele-binding and post-translational modifications as PARYlation, Moreover, reduction of CTGF protein, human in normally CTCFL wt Allele-negative human fibroblasts resulted in derepression of CTCFL wt Allele Promoter. These results provide a mechanistic basis for understanding Primary malignant neoplasm-related associations between haploinsufficiency of CTGF protein, human and CTCFL wt Allele derepression, and between the lack of functional TP53 wt Allele and aberrant activation of CTCFL wt Allele, CTGF protein, human and CTCFL wt Allele in genome regulation and Primary malignant neoplasm., The novel CTCFL wt Allele + CTGF protein, human Genes family is uniquely involved in the epigenetics of normal biology and Primary malignant neoplasm., Collectively, these data indicate that reciprocal binding of CTGF protein, human and CTCFL wt Allele to the CTAG1A wt Allele promoter mediates epigenetic regulation of this CT Genes in lung Primary malignant neoplasm cells, and suggest that induction of CTCFL wt Allele may be a novel strategy to augment immunogenicity of pulmonary carcinomas., CTCFL wt Allele is the only known paralog of CTGF protein, human, a Genes intimately involved in genomic imprinting, chromatin insulation, and nuclear regulation., However, CTCFL wt Allele can inhibit cell proliferation, and is Mutation Abnormality in Primary malignant neoplasm similarly to CTGF protein, human suggesting CTCFL wt Allele activation in Primary malignant neoplasm may be due to global Genetic or epigenetic changes typical of malignant transformation., We suggest that CTCFL wt Allele is likely tethering epigenetic machinery to a novel class of CTGF protein, human/CTCFL wt Allele 11ZF target sequences that mediate induction of Primary malignant neoplasm-Testis genes., Unlike CTGF protein, human, CTCFL wt Allele expression has been reported only in the Testis and certain Malignant Neoplasms, leading to its classification as a \"Primary malignant neoplasm-Testis\" antigen.[SEP]Relations: Testis has relations: anatomy_protein_present with CTGF protein, human, anatomy_protein_present with CTGF protein, human, anatomy_protein_present with CTCFL, anatomy_protein_present with CTCFL, anatomy_protein_present with BNC1, anatomy_protein_present with BNC1. Geneticin has relations: drug_drug with Cefsulodin, drug_drug with Cefsulodin. Protein S human has relations: drug_drug with Cefsulodin, drug_drug with Cefsulodin.", "label": "yes"}
{"original_question": "Are defects in recombination repair involved in carcinogenesis?", "id": "converted_837", "sentence1": "Are defects in recombination repair involved in carcinogenesis?", "sentence2": "Inherited Gene Mutation in Genes involved in plant-type hypersensitive response are associated with gene rearrangement and may be a prerequisite for tumor development in some Primary malignant neoplasm-prone hereditary diseases like Bloom, Werner and Rothmund-Thomson syndromes. , Variants in the XRCC3 gene might result in altered protein structure or function which may influence DSBR efficiency and lead to Primary malignant neoplasm. , Although Alcohol - Recreational Drug Use Code consumption is related to increased Primary malignant neoplasm risk, its molecular mechanism remains unclear. Here, we demonstrate that an intake of 10% Alcohol - Recreational Drug Use Code for 4 weeks in Rattus norvegicus is genotoxic due to induction of Micronucleus - abnormality. acetaldehyde (SVEINSSON CHORIORETINAL ATROPHY), the first product of ethanol metabolism, is believed to be responsible for DNA damage induced by Alcohol - Recreational Drug Use Code. , Although efficiency of these repair processes substantially decrease the efficacy of Primary malignant neoplasm chemotherapies that target DNA, compromised DNA repair contributes to Mutagenesis Procedure and genomic instability leading to carcinogenesis., damage response and repair pathways are important barriers to carcinogenesis. , olymorphisms in DNA repair Genes and differences in repair capacity between individuals have been widely documented. For colorectal Primary malignant neoplasm, the loss of mismatch repair gene activity is a key genetic determinant. Nucleotide excision repair (NER), recombination repair (RR) and base excision repair (BER) pathways have critical roles in protection against other Malignant Neoplasms, and we wished to investigate their role in colorectal Primary malignant neoplasm. [SEP]Relations: Ethanol has relations: drug_drug with Interferon alfa-2a, Recombinant, drug_drug with Interferon alfa-2a, Recombinant. adaptation to pheromone regulating conjugation with mutual genetic exchange has relations: bioprocess_bioprocess with regulation of conjugation, bioprocess_bioprocess with regulation of conjugation, bioprocess_bioprocess with response to pheromone regulating conjugation with mutual genetic exchange, bioprocess_bioprocess with response to pheromone regulating conjugation with mutual genetic exchange, bioprocess_bioprocess with negative adaptation of signaling pathway, bioprocess_bioprocess with negative adaptation of signaling pathway. malignant colon neoplasm has relations: disease_protein with RELA, disease_protein with RELA.", "label": "yes"}
{"original_question": "Is nicotinamide effective for skin cancer prevention?", "id": "converted_1171", "sentence1": "Is nicotinamide effective for Malignant neoplasm of skin prevention?", "sentence2": "niacinamide (Vitamin B3 Assay) has been shown to have protective effects against damage caused by UV radiation and to reduce the rate of new premalignant Actinic keratosis., ESULTS: At 12 months, the rate of new Skin carcinoma was lower by 23% (95% confidence interval [NDUFB6 gene], 4 to 38) in the nicotinamide group than in the placebo group (P=0.02). Similar differences were found between the nicotinamide group and the placebo group with respect to new basal-cell carcinomas (20% [95% NDUFB6 gene, -6 to 39]lower rate with nicotinamide, P=0.12) and new squamous-cell carcinomas (30% [95% NDUFB6 gene, 0 to 51] lower rate, P=0.05). The number of Actinic keratosis was 11% lower in the nicotinamide group than in the placebo group at 3 months (P=0.01), 14% lower at 6 months (P<0.001), 20% lower at 9 months (P<0.001), and 13% lower at 12 months (P=0.001)., CONCLUSIONS: Oral nicotinamide was safe and effective in reducing the rates of new Skin carcinoma and Actinic keratosis in high-risk patients., niacinamide is a safe, widely available Vitamins that reduces the immune suppressive effects of UV, enhances DNA repair in keratinocyte and has shown promise in the chemoprevention of non-melanoma Malignant neoplasm of skin. ,  In summary, nicotinamide, by enhancing DNA repair in melanocyte, is a potential agent for the chemoprevention of Cutaneous Melanoma., Recent double-blinded randomized controlled Phase 2 studies in heavily sun-damaged individuals have shown that oral nicotinamide significantly reduces premalignant Actinic keratosis, and may reduce new non-melanoma skin cancers. , niacinamide (Vitamin B3 Assay) prevents UV-induced immunosuppression and carcinogenesis in CASP14 gene, and solar-simulated (ss) UV-induced immunosuppression in Homo sapiens., These results show that nicotinamide enhances two different pathways for repair of UV-induced photolesions, supporting nicotinamide's potential as an inexpensive, convenient and non-toxic agent for Malignant neoplasm of skin chemoprevention., Recent double-blinded randomized controlled Phase 2 studies in heavily sun-damaged individuals have shown that oral nicotinamide significantly reduces premalignant Actinic keratosis, and may reduce new non-melanoma skin cancers., No noteworthy between-group differences were found with respect to the number or types of adverse events during the 12-month intervention period, and there was no evidence of benefit after nicotinamide was discontinued.CONCLUSIONS: Oral nicotinamide was safe and effective in reducing the rates of new Skin carcinoma and Actinic keratosis in high-risk patients. , niacinamide (Vitamin B3 Assay) has been shown to have protective effects against damage caused by UV radiation and to reduce the rate of new premalignant Actinic keratosis.METHODS: In this phase 3, double-blind, randomized, controlled trial, we randomly assigned, in a 1:1 ratio, 386 participants who had had at least two Skin carcinoma in the previous 5 years to receive 500 mg of nicotinamide twice daily or placebo for 12 months. , Similar differences were found between the nicotinamide group and the placebo group with respect to new basal-cell carcinomas (20% [95% NDUFB6 gene, -6 to 39]lower rate with nicotinamide, P=0.12) and new squamous-cell carcinomas (30% [95% NDUFB6 gene, 0 to 51] lower rate, P=0.05). , Oral nicotinamide was safe and effective in reducing the rates of new Skin carcinoma and Actinic keratosis in high-risk patients., niacinamide has shown potential as a safe and effective intervention for the prevention of malignant and premalignant skin lesions., niacinamide, which protected against both Ultraviolet B therapy and UVA, is a promising agent for Malignant neoplasm of skin prevention.[SEP]Relations: niacinamide has relations: contraindication with liver disease, contraindication with liver disease, contraindication with gallbladder disease, contraindication with gallbladder disease, contraindication with kidney disease, contraindication with kidney disease, contraindication with diabetes mellitus (disease), contraindication with diabetes mellitus (disease), contraindication with peptic ulcer disease, contraindication with peptic ulcer disease.", "label": "yes"}
{"original_question": "Is Titin the largest single protein molecule found in Nature?", "id": "converted_1478", "sentence1": "Is Titin Kinase the largest single Protein Info molecule found in Nature?", "sentence2": "Titin Kinase Kinase, the largest Protein Info in the Human body structure, is well known as a molecular spring in Muscle Cells and scaffold Protein Info aiding myofibrillar assembly., Titin Kinase Kinase is the largest Protein Info in Mammals; it forms an elastic filament along the myofibril of Cardiac - anatomy qualifier and Skeletal muscle structure., Titin Kinase Kinase is recently known as the largest Protein Info which exists in the striated muscle Sarcomeres and is dynamic both in biomechanics properties and biochemical functions. , Titin Kinase Kinase, the largest Protein Info known to date, has been linked to Sarcomeres assembly and function through its elastic adaptor and signaling domains., The giant Sarcomeres Protein Info titin/connectin is the largest Protein Info known to date., Titin Kinase Kinase is the largest Protein Info known to date and acts as a mechanosensor that regulates muscle Protein Info expression in a Sarcomeres strain-dependent fashion., Titin Kinase Kinase is the largest Protein Info known, and is essential for organising muscle sarcomeres., It has many domains with a variety of functions, and stretches from the Z line to the M line in the muscle Sarcomeres. , Titin Kinase Kinase, is definitely the largest Protein Info in the body, with a molecular weight of 3 million Dalton and composed of 27,000 Antifibrinolytic Antifibrinolytic amino acids., Titin Kinase Kinase, the largest Protein Info identified to date (over 1 micron long, almost 3 million daltons in mass) is the third most abundant component of the Sarcomeres., Titin Kinase Kinase is the largest Polypeptides yet described (relative molecular mass approximately 3 x 10(6); refs 1, 2) and an abundant Protein Info of striated muscle., Titin Kinase Kinase is at present the largest known Protein Info (M(r) 3000 kDa) and its expression is restricted to Vertebrates striated muscle., Titin Kinase Kinase is the largest Protein Info known, and is essential for organising muscle sarcomeres, Titin Kinase Kinase is at present the largest known Protein Info (M(r) 3000 kDa) and its expression is restricted to Vertebrates striated muscle, Titin Kinase Kinase is the largest Polypeptides yet described (relative molecular mass approximately 3 x 10(6); refs 1, 2) and an abundant Protein Info of striated muscle, Titin Kinase Kinase is recently known as the largest Protein Info which exists in the striated muscle Sarcomeres and is dynamic both in biomechanics properties and biochemical functions, Titin Kinase Kinase, the biggest single (poly) peptide found in Homo sapiens, and throughout nature so far, was long considered as a good candidate for inherited muscle diseases[SEP]Relations: Protein C has relations: drug_drug with Ticlopidine, drug_drug with Ticlopidine, drug_drug with Tirofiban, drug_drug with Tirofiban, drug_drug with Tibolone, drug_drug with Tibolone, drug_drug with Ticagrelor, drug_drug with Ticagrelor, drug_drug with Tioguanine, drug_drug with Tioguanine.", "label": "yes"}
{"original_question": "Is DITPA a thyroid hormone analog utilized in experimental and clinical studies", "id": "converted_124", "sentence1": "Is DITPA a thyroid hormone analog utilized in experimental and clinical studies", "sentence2": "DITPA normalized the elevated serum T(3) and Thyrotropin:-:Pt:Ser/Plas:- when the dose reached 1 mg/kg · d and T(4) and rT(3) increased to the lower normal range., The identification of 3,5-diiodothyropropionic acid (DITPA) that binds to both α- and β-type threonine-tRNA ligase activity with relatively low affinity was unique in that this analog improves left ventricular function in Congestive Congestive heart failure as well as lowers cholesterol., Treatment with DITPA attenuates the acute inflammatory response and reduces myocardial infarct size., Thus DITPA administration impairs baseline Cardiac - anatomy qualifier parameters in CASP14 gene and can be fatal during in vivo acute myocardial I/R., DITPA improved some hemodynamic and metabolic parameters, but there was no evidence for symptomatic benefit in congestive Congestive Congestive heart failure, The results suggested that DITPA can promote a healthy Vasculature independently from its thyroid-related metabolic effects. ,  Moreover, DITPA and T(4) were efficacious in preventing effects of Hypothyroidism on Cardiac - anatomy qualifier function and BVD, Both T4 and DITPA had beneficial effects on chamber remodeling, which was most likely due to beneficial changes in cell shape and improved vascular supply., The thyroid analog DITPA enhances endothelial nitric oxide and beta-adrenergic-mediated vasorelaxation by increasing nitric oxide in the Vasculature.[SEP]Relations: 3,5-diiodothyropropionic acid has relations: drug_drug with Ethionamide, drug_drug with Ethionamide, drug_drug with Motesanib, drug_drug with Motesanib, drug_drug with Ritonavir, drug_drug with Ritonavir, drug_drug with Escitalopram, drug_drug with Escitalopram, drug_drug with Flumatinib, drug_drug with Flumatinib.", "label": "yes"}
{"original_question": "Does deflazacort have more side effects than prednisone?", "id": "converted_2264", "sentence1": "Does deflazacort have more side effects than prednisone?", "sentence2": "Though deflazacort and prednisone improve clinical endpoints in Duchenne muscular dystrophy (Muscular Dystrophy, Duchenne) patients, deflazacort produces fewer side effects.[SEP]Relations: deflazacort has relations: drug_drug with Prednisone, drug_drug with Prednisone, drug_drug with Prednisolone, drug_drug with Prednisolone, drug_drug with Meprednisone, drug_drug with Meprednisone, drug_drug with Prednylidene, drug_drug with Prednylidene, drug_drug with Methylprednisone, drug_drug with Methylprednisone.", "label": "no"}
{"original_question": "Do bacteria from the genus Morexella cause respiratory infections?", "id": "converted_2347", "sentence1": "Do Bacteria from the genus Morexella cause respiratory infections?", "sentence2": "gainst pathogens associated with respiratory tract ailments [Staphylococcus aureus antibody antibody (ATCC 25923), Pneumonia due to Pneumonia due to Klebsiella pneumoniae (ATCC 13883) and Morexella cattarhalis (ATCC 14468)] , The efficacy and safety of oral ofloxacin, 400 mg once daily, for the treatment of patients with lower Respiratory Tract Infections were studied. The most common species recovered from the sputum specimens of these patients were Haemophilus influenzae, followed by Streptococcus pneumoniae (S. pneumoniae), Staphylococcus aureus antibody antibody (Staphylococcus aureus antibody), Gram positive cocci unidentified, Pseudomonas aeruginosa (P. aeruginosa), Morexella catarrhalis,, the efficacy and safety of oral ofloxacin 400 mg once daily for the treatment of patients with lower Respiratory Tract Infections were studied the most common species recovered from the sputum specimens of these patients were Haemophilus influenzae or Haemophilus parainfluenzae followed by streptococcus pneumoniae s pneumoniae staphylococcus aureus s aureus gram positive cocci unidentified pseudomonas aeruginosa p aeruginosa morexella catarrhalis streptococcus epidermidis and another haemophilus species in this order all these Bacteria were susceptible to ofloxacin except for one strain of methicillin resistant s aureus a satisfactory clinical outcome was achieved in 34 of 40 patients 85 it is concluded that ofloxacin 400 mg once daily is useful for patients with Respiratory Tract Infections.[SEP]Relations: Respiratory tract infection has relations: phenotype_phenotype with Pneumonia, phenotype_phenotype with Pneumonia, phenotype_phenotype with Acute infectious pneumonia, phenotype_phenotype with Acute infectious pneumonia, drug_effect with Deferasirox, drug_effect with Deferasirox, phenotype_phenotype with Recurrent respiratory infections, phenotype_phenotype with Recurrent respiratory infections. Ofloxacin has relations: drug_effect with Respiratory tract infection, drug_effect with Respiratory tract infection.", "label": "yes"}
{"original_question": "Are there any animal models for Niemann-Pick C1 disease?", "id": "converted_1265", "sentence1": "Are there any animal models for Niemann-Pick C1 Disease?", "sentence2": "Several animal models were used to analyze the impaired pathways. , We investigated components of the surfactant system in both NPC1 mutant CASP14 gene and Felis catus and in NIEMANN-PICK DISEASE, TYPE C2 mutant CASP14 gene near the end of their expected life span. , Thus far, studies of Nasopharyngeal carcinoma CASP14 gene have been performed mainly to study the Head>Brain and Nerve Degeneration, because degeneration in the Head>Brain was known as the primary cause of death in Nasopharyngeal carcinoma CASP14 gene. , the NPC1(-/-) Mus sp. is available serving as an appropriate animal model of the human Disease,, o examine the onset and progression of neuropathological insults in Nasopharyngeal carcinoma we have systematically examined the Central Nervous System of a Mus sp. model of NPC1 (Niemann-Pick Disease, Type C1(-/-) CASP14 gene) at different stages of the Disease course., We have identified a Point Mutation in Niemann-Pick Disease, Type C1 that creates a novel Mus sp. model (Niemann-Pick Disease, Type C1(nmf164)) of Niemann-Pick type C1 (Nasopharyngeal carcinoma) Disease, Niemann-Pick type C1-deficient CASP14 gene, which accumulate Protoplasm free cholesterol. , hUCB-MSCs were transplanted into the hippocampus of Nasopharyngeal carcinoma CASP14 gene in the early asymptomatic stage.,  Niemann Pick type C1 CASP14 gene, Three Mus sp. models of glycosphingolipid storage diseases, namely Niemann-Pick type C1,, Niemann-Pick Disease, Type C1(-/-) CASP14 gene, a well-established model of Nasopharyngeal carcinoma pathology, Mus model of this Disease, the npc1 Mus sp.,, NPC1 (Niemann-Pick type C1) knock-out CASP14 gene, We have made Mice, Transgenic which express the Niemann-Pick Disease, Type C1 protein exclusively in fibrillary astrocytes, using the glial fibrillary acidic protein (Glial Fibrillary Acidic Protein) Promoter., homozygous affected (NPC1(-/-)) CASP14 gene, heterozygous (NPC1(+/-)) CASP14 gene, npc1(-/-) CASP14 gene,, npc1(-/-) Mus sp. model, A Mus model of Niemann-Pick Disease, Type C (Nasopharyngeal carcinoma), the NPC1-deficient [NPC1 (-/-)] Mus sp., [SEP]Relations: Niemann-Pick Disease type C has relations: disease_disease with Niemann-Pick Disease, disease_disease with Niemann-Pick Disease, disease_disease with Niemann-Pick Disease, disease_disease with Niemann-Pick Disease, disease_disease with Niemann-Pick Disease, disease_disease with Niemann-Pick Disease. central nervous system has relations: anatomy_protein_present with NISCH, anatomy_protein_present with NISCH, anatomy_protein_present with NIPAL3, anatomy_protein_present with NIPAL3.", "label": "yes"}
{"original_question": "Is there any functional association during viral replication between flaviviridae viral RNA depended RNA polymerase and viral helicase?", "id": "converted_836", "sentence1": "Is there any functional association during viral replication between flaviviridae viral RNA depended RNA polymerase and viral helicase?", "sentence2": "Several labs have obtained evidence for a Protein complex that involves many of the nonstructural (NS) Proteins encoded by the Virus. NOONAN SYNDROME 3, NS4A, NS4B, NS5A, and NS5B appear to interact structurally and functionally. In this study, we investigated the interaction between the helicase, NOONAN SYNDROME 3, and the RNA polymerase, NS5B. Pull-down experiments and surface plasmon resonance data indicate a direct interaction between NOONAN SYNDROME 3 and NS5B that is primarily mediated through the Protease Domain of NOONAN SYNDROME 3. This interaction reduces the basal Adenosine Triphosphatases activity of NOONAN SYNDROME 3. However, NS5B stimulates product formation in RNA unwinding experiments under conditions of excess Nucleic Acids substrate. When the concentrations of NOONAN SYNDROME 3 and NS5B are in excess of Nucleic Acids substrate, NS5B reduces the rate of NOONAN SYNDROME 3-catalyzed unwinding. Under pre-steady-state conditions, in which NOONAN SYNDROME 3 and substrate concentrations are similar, product formation increased in the presence of NS5B. The increase was consistent with 1:1 complex formed between the two Proteins. A fluorescently labeled form of NOONAN SYNDROME 3 was used to investigate this interaction through fluorescence polarization binding assays. Results from this assay support interactions that include a 1:1 complex formed between NOONAN SYNDROME 3 and NS5B., Contradictory results have been reported regarding NOONAN SYNDROME 3 in RNA synthesis. To investigate the effect of NOONAN SYNDROME 3 on classical swine fever Virus (CSFV) NS5B RNA-dependent RNA polymerase activity (RNA-directed RNA polymerase activity) activity and NOONAN SYNDROME 3-NS5B interaction, RNA-directed RNA polymerase activity reactions, GST-pull-down assays and co-immunoprecipitation analyses containing NS5B and either of NOONAN SYNDROME 3 protein and the different truncated NOONAN SYNDROME 3 Mutant were performed, respectively. We found that NOONAN SYNDROME 3 stimulated NS5B RNA-directed RNA polymerase activity activity in a dose-dependent manner by binding to Noonan Syndrome 5 through a NOONAN SYNDROME 3 Protease Domain. Furthermore, mapping important regions of the NOONAN SYNDROME 3 Protease Domain was carried out by Deletion Mutagenesis, associated with RNA-directed RNA polymerase activity reactions, GST-pull-down assays and co-immunoprecipitation analyses. Results showed that stimulation of CSFV NS5B RNA-directed RNA polymerase activity activity was obtained by NOONAN SYNDROME 3 binding to NS5B through a 31-amino acid fragment at the N-terminal end of NOONAN SYNDROME 3 Protease Domain, which mediated a specific NOONAN SYNDROME 3-NS5B interaction., The protocols detailed in this unit are used to purify three recombinant enzymes that are widely used in HCV research: the HCV NOONAN SYNDROME 3 Protease Domain, the helicase Superkingdom (taxonomic category) as an NOONAN SYNDROME 3+NS4A complex, and the NS5B RNA-dependent RNA polymerase. The active enzymes are purified to homogeneity by two-column chromatography to support a screening program for HCV inhibitors., Among potential targets are viral entry factors, including scavenger receptor type B1 (SCARB1 wt Allele) and CD81 antigen antigen, as well as Antibodies, Neutralizing against the viral glycoproteins. Popular targets related to translation and replication are the NOONAN SYNDROME 3/4A protease (inhibited by telaprevir and boceprevir) and the NS5B polymerase, as well as the NS2/3 autoprotease, the NOONAN SYNDROME 3 helicase, and nonenzymatic targets such as NS4B and NS5A Proteins. , The NOONAN SYNDROME 3 helicase Superkingdom (taxonomic category) competes with NOONAN SYNDROME 3 full-length for Noonan Syndrome 5 RNA-directed RNA polymerase activity binding, with a K(d.) of 2.5μM. Since NOONAN SYNDROME 3 and Noonan Syndrome 5 are required for DENV replication, this fascile assay could be used to screen for non-nucleoside, allosteric inhibitors that disrupt the interaction between the two Proteins.[SEP]Relations: RNA-directed DNA polymerase activity has relations: molfunc_protein with ERVK-11, molfunc_protein with ERVK-11, molfunc_protein with ERVK-8, molfunc_protein with ERVK-8, molfunc_protein with ERVK-10, molfunc_protein with ERVK-10, molfunc_protein with ERVK-7, molfunc_protein with ERVK-7, molfunc_protein with ERVK-6, molfunc_protein with ERVK-6.", "label": "yes"}
{"original_question": "Is Bladder training an effective method to treat  urge incontinence ?", "id": "converted_705", "sentence1": "Is Bladder training an effective method to treat  urge Incontinence ?", "sentence2": "Mindfulness-based stress reduction appears to be a treatment worthy of further study, as in the short term, it is as effective as historical studies of Pharmacologic Substance treatment and Urinary Bladder training in reducing urge Incontinence and Incontinence-related quality of life., All patients, irrespective of the results of cystometry were subsequently treated with oxybutynin 2.5 mg twice daily along with Urinary Bladder training., Of the 29 patients with stable Urinary Bladder and symptoms of OAB, 100% cure rate was achieved in 20 (68.9%) and 06 (20.6%) patients respectively. While in 3 patients in both groups, decrease of symptoms upto 75% after 6 months of treatment was observed., Both urodynamically proven unstable and stable Urinary Bladder showed nearly equal improvement with treatment, There are 3 types of Urinary Incontinence (urge-, stress-, and overflow-Incontinence). Another standardization of urinary Incontinence follows dysfunctions of the Pelvic Diaphragm: detrusor muscle-dependent, due to sphincter spasm, prostate gland dependent. Urge Incontinence with a dysfunction of the detrusor muscle is the most common type. Mixed types are frequent. Non-Pharmacologic Substance measures (e.g. Skeletal muscle structure of pelvis training, Urinary Bladder training, toilet training are first choice treatments., Treatment of stress, urge and mixed Incontinence can usually be commenced in primary care; Pelvic Diaphragm exercises and Urinary Bladder training are preferred. If Urinary Bladder training is not effective for urge Incontinence, anticholinergic drugs should be considered., Sixty patients (age 8 to 12 years) with urge Incontinence or dysfunctional voiding were evaluated. After a no-treatment control period (average 6 months), patients underwent a 6-day Urinary Bladder training course, Six months after training completion, 64.1% and 64.7% of the inpatient and outpatient groups with daytime wetting and 51.5% and 17.7% of the inpatient and outpatient groups with nighttime wetting were cured or had improved, Of the inpatient group with urge Incontinence, the functional Urinary Bladder capacity increased by 15%., To compare the efficacy of tolterodine plus simplified Urinary Bladder training (carmustine/triazinate) with tolterodine alone in patients with an overactive Urinary Bladder., CONCLUSIONS: tolterodine 2 mg twice daily is an effective and well tolerated treatment for an overactive Urinary Bladder, the effectiveness of which can be augmented by a simplified carmustine/triazinate regimen., Bladder training is a ResponseLevel - ResponseLevel - modification of Urinary Bladder drill that is conducted more gradually on an outpatient basis and has resulted in significant reduction of Incontinence in older, community-dwelling women., OBJECTIVE: To evaluate the long-term effect of treatment of female Incontinence by the general practitioner (Pelvic Diaphragm exercises, and Urinary Bladder training) in female urinary Incontinence., Urinary Stress Incontinence and urge Incontinence were treated by means of Pelvic Diaphragm exercises and Urinary Bladder training respectively, while a mixed Incontinence was treated by Urinary Bladder training followed by Pelvic Diaphragm exercises. T, The treatment consisted of training of pelvic muscles in stress Incontinence and Urinary Bladder training in urge Incontinence, RESULTS: After 3 months the mean frequency of urine loss per week diminished from 21 to 8, and after 12 months to 6 times., Some elders suffering from urge Incontinence prefer Skeletal muscle structure of pelvis exercises to Urinary Bladder training as the behavioral intervention of choice, for eight out of nine women their continence had improved, both subjectively and objectively., Bladder training is a simple, safe, and effective treatment in the management of mild to moderate forms of urinary Incontinence in outpatient populations. It can be used as a first-line treatment or in combination with such other interventions as Skeletal muscle structure of pelvis exercises, Urinary Bladder pressure biofeedback, electrical stimulation, and Pharmacologic Substance therapy, Treatment consisted of Pelvic Diaphragm exercises in the case of stress Incontinence and Urinary Bladder training in the case of urge Incontinence., After 3 months about 60% of the patients were either dry or only mildly incontinent, terodiline group shows this Pharmacologic Substance to be a valuable adjunct to a Urinary Bladder regimen in children with urge Incontinence, Basing on our experience with 39 patients with severe urge Incontinence (in one-quarter of the cases pure urge Incontinence, in one-half of the cases mixed Incontinence and in a further quarter of the cases neurogenic Urinary Bladder disorders) a supervised programme (mictiogram) and a well-tried therapy (especially in the Anglo-Saxon countries) consisting of the triad hospitalisation/Urinary Bladder training/medication therapy are presented. After an average hospitalisation period of 14 days, we were able to achieve a symptom-free state in 94% of the patients., Anamnestic and urodynamical results are evaluated before and after Urinary Bladder retraining drill (BRD) in women suffering from urge Incontinence., We could state that the BRD is a good possibility to realize multistep-therapy of female Incontinence., Twenty consecutive female patients with urge Incontinence and stable detrusor function on provocative rapid fill CO2-cystometry were treated as out-patients with a Urinary Bladder training programme and with terodiline/placebo in a double-blind cross-over design., In conclusion, female patients with idiopathic urge Incontinence and stable detrusor function did respond to treatment as do female patients with urge Incontinence and proven instability., The results of in-patient Urinary Bladder training in 65 women with frequency, urgency and urge Incontinence are reported. There was a good initial response in 88%. By 6 months the response rate had fallen to 38%., Patients with sensory urgency appeared to do better than those with Detrusor instability and it is suggested that Urinary Bladder training may be indicated as primary treatment in sensory urgency., Bladder training and/or biofeedback techniques were used to treat 75 patients with frequency, urgency, Nocturia and urge Incontinence. Significant improvement or cure was obtained in 70 per cent of enuretic children, and 66 per cent of men and 74 per cent of women with unstable detrusor function.[SEP]Relations: Urinary Incontinence has relations: drug_effect with Ibuprofen, drug_effect with Ibuprofen, drug_effect with Acamprosate, drug_effect with Acamprosate, drug_effect with Urofollitropin, drug_effect with Urofollitropin, drug_effect with Naproxen, drug_effect with Naproxen, drug_effect with Levonorgestrel, drug_effect with Levonorgestrel.", "label": "yes"}
{"original_question": "Are gut microbiota profiles altered by irradiation?", "id": "converted_3539", "sentence1": "Are gut microbiota profiles altered by irradiation?", "sentence2": "Specific Members of the Gastrointestinal Microbiome are Reliable Biomarkers of Irradiation Intensity and Lethality in Large Animal Models of Homo sapiens Health., Irradiation profoundly impacted gut microbiota profiles in both animal allergen extracts., Our findings suggest that gut symbiont-based probiotics can be used as agents for reversing radiation-induced ecological fitness decrease.[SEP]Relations: Gastrointestinal obstruction has relations: disease_phenotype_positive with cryptosporidiosis, disease_phenotype_positive with cryptosporidiosis, drug_effect with Imatinib, drug_effect with Imatinib, phenotype_phenotype with Functional abnormality of the gastrointestinal tract, phenotype_phenotype with Functional abnormality of the gastrointestinal tract, phenotype_phenotype with Intestinal obstruction, phenotype_phenotype with Intestinal obstruction, phenotype_phenotype with Functional intestinal obstruction, phenotype_phenotype with Functional intestinal obstruction.", "label": "yes"}
{"original_question": "Can beans induce apoptosis?", "id": "converted_1856", "sentence1": "Can beans induce apoptosis?", "sentence2": "A 60-kDa glucosamine binding lectin, white kidney bean lectin (WKBL), was purified from Phaseolus vulgaris cv. white kidney beans, by application of anion exchange chromatography on Q-Sepharose, affinity chromatography on Affi-gel blue gel, and FPLC-size exclusion on Superdex 75. The anti-proliferative activity of WKBL on HONE1 cells and Hep G2 Cells was stronger than the activity on MCF-7 Cells and WRL68 cells , Treatment of human stomach cancer KATO III cells with hot-water extracts from adzuki beans led to their growth inhibition as well as apoptosis induction., Stimulation of dendritic cell maturation and induction of apoptosis in leukemia cells by a heat-stable extract from azuki bean (Vigna angularis), a promising immunopotentiating Food allergenic extracts and dietary supplement for cancer prevention., Human gut flora-fermented nondigestible fraction from cooked bean ( Phaseolus vulgaris L.) modifies protein expression associated with apoptosis, cell cycle arrest, and proliferation in human adenocarcinoma colon Tumor cells, malignant., This paper reports the effect of fermentation products (FP) by Hepatocyte Growth Factor (FP-Hepatocyte Growth Factor) from NRG1 wt Allele of cooked beans on survival and protein expression associated with apoptosis, cell cycle arrest, and proliferation in human adenocarcinoma colon Tumor cells, malignant., erythroagglutinating phytohemagglutinin is a natural product extracted from red kidney beans, and it has been reported to induce cell apoptosis by blocking Epidermal Growth Factor Receptor in lung Tumor cells, malignant, A Glucosamine-Specific Lectin from Green Dragon No. 8 Beans (Phaseolus vulgaris) Induced Apoptosis on Nasopharyngeal carcinoma Cells, erythroagglutinating phytohemagglutinin is a natural product extracted from red kidney beans, and it has been reported to induce cell apoptosis by blocking Epidermal Growth Factor Receptor in lung Tumor cells, malignant., The anticancer activity of δ-tocotrienol, a bioactive Vitamin E Drug Class present in whole grain cereals, annatto beans and palm fruit, is strongly dependent on its effect on the induction of apoptosis. δ-Tocotrienol-induced apoptosis is associated with consistent induction in the expression of the proapoptotic protein Bcl-2-associated X protein (BAX protein, human)., NRG1 wt Allele of cooked common beans inhibited colon carcinogenesis at an early stage by inducing cell cycle arrest of colon cells and morphological changes linked to apoptosis, thus confirming previous results obtained with gene expression studies., Azuki extract also inhibited the growth of human leukemia U937 cells, leading to induction of apoptosis., Fermentation product of soybean, black bean, and Green bean antigen mixture induces apoptosis in a wide variety of Tumor cells, malignant., A non-digestible fraction of the common bean (Phaseolus vulgaris L.) induces cell cycle arrest and apoptosis during early carcinogenesis.[SEP]Relations: Protein S human has relations: drug_drug with Etoposide, drug_drug with Etoposide, drug_drug with Letaxaban, drug_drug with Letaxaban. Vitamin E has relations: drug_drug with Etoposide, drug_drug with Etoposide, drug_drug with Letaxaban, drug_drug with Letaxaban. epidermal growth factor receptor binding has relations: molfunc_protein with HIP1, molfunc_protein with HIP1.", "label": "yes"}
{"original_question": "Is inositol effective for trichotillomania?", "id": "converted_2848", "sentence1": "Is inositol effective for Trichotillomania?", "sentence2": "Patients assigned to inositol failed to show significantly greater reductions on primary or secondary outcomes measures compared with placebo (all P>0.05)., This is the first study assessing the efficacy of inositol in the treatment of Trichotillomania, but found no differences in symptom reductions between inositol and placebo., At study endpoint, 42.1% of patients were 'much or very much improved' on inositol compared with 35.3% on placebo., Conclusions • The review indicates that yoga, aerobic exercise, acupuncture, biofeedback, hypnosis, and inositol and acetylcysteine all show promise in the treatment of excoriation disorder and other body-focused repetitive behaviors, such as Trichotillomania., Future studies should examine whether inositol may be beneficial in controlling pulling behavior in a subgroup of individuals with Trichotillomania.[SEP]Relations: Inositol has relations: drug_drug with Triazolam, drug_drug with Triazolam, drug_drug with Triethylenetetramine, drug_drug with Triethylenetetramine, drug_drug with Trifluridine, drug_drug with Trifluridine, drug_drug with Triamterene, drug_drug with Triamterene, drug_drug with Trichlormethiazide, drug_drug with Trichlormethiazide.", "label": "no"}
{"original_question": "Is the protein HOXA11 associated with endometrial disease?", "id": "converted_4578", "sentence1": "Is the protein Homeobox Protein Hox-A11 associated with endometrial disease?", "sentence2": " Both Neprilysin and Homeobox Protein Hox-A11 have been implicated in regulation of endometrial homeostasis., Combined expression of Homeobox Protein Hox-A11 and Neprilysin identifies Endometriosis versus normal tissue and Neoplasms., The combination of Homeobox Protein Hox-A11 and Neprilysin expression profiles provides a useful tool to identify ectopic endometrial tissue and for distinguishing Endometriosis from various types of gynecological malignancies and metastases., Downregulation of Homeobox Protein Hox-A11 enhances Malignant neoplasm of endometrium malignancy, Low Homeobox Protein Hox-A11 expression may promote the proliferation, migration, invasion of Malignant neoplasm of endometrium cells, and increase their resistance to cisplatin through activating PTEN/AKT pathway., Endometrial mRNA and protein expression levels of HOXA10 wt Allele wt Allele and Homeobox Protein Hox-A11 were significantly lower in patients with AM than in control patients.[SEP]Relations: cervix Endometriosis has relations: disease_disease with cervix disease, disease_disease with cervix disease, disease_disease with Endometriosis (disease), disease_disease with Endometriosis (disease). Cisplatin has relations: drug_protein with NQO1, drug_protein with NQO1, drug_protein with ATOX1, drug_protein with ATOX1. anus neoplasm has relations: disease_protein with IFNB1, disease_protein with IFNB1.", "label": "yes"}
{"original_question": "Are mutations in the C9orf72  gene associated with macular degeneration?", "id": "converted_2073", "sentence1": "Are mutations in the C9orf72  Genes associated with macular degeneration?", "sentence2": "Over the years, however, growing evidence from clinical, pathological and Genetic findings has suggested that ALS and FTD belong to the same clinic-pathological spectrum disorder. This concept has been further supported by the identification of the most common Genetic cause for both diseases, an aberrantly expanded hexanucleotide repeat GGGGCC/ CCCCGG Sequence - ParameterizedDataType located in a non-coding region of the Genes C9orf72., Amyotrophic lateral sclerosis (ALS) is characterized by motor neurone loss resulting in Muscle Weakness, Muscle Spasticity and ultimately Cessation of life. 5-10% are caused by inherited mutations, most commonly C9ORF72, Cu-Zn Superoxide Dismutase, TARDBP and Feline urological syndrome., In this article, we will review the brief characterizations of the C9orf72 Genes, the expansion mutations, the related disorders, and their features, followed by a discussion of the deficiency knowledge of C9ORF72 mutations., Gene Mutation in the C9orf72 Genes may be a major cause not only of frontotemporal dementia with Motor Neuron Disease but also of late onset psychosis., Frontotemporal Lobar Degeneration (FTLD) is a genetically heterogenous syndrome and has been associated most recently with a hexanucleotide repeat expansion within the C9orf72 Genes., An expanded GGGGCC hexanucleotide repeat in C9ORF72 is the most common Genetic cause of Amyotrophic Lateral Sclerosis and frontotemporal lobar degeneration associated with protein protein TDP-43, human, human pathology (Frontotemporal dementia)., Novel TARDBP Sequence - ParameterizedDataType variant and C9ORF72 repeat expansion in a family with frontotemporal dementia., There was, as expected, a significant association between C9ORF72 mutations and presence of Motor Neuron Disease., Expansion of a hexanucleotide repeat in the C9orf72 Genes has been identified as the most common pathogenic mutation in families with Autosome dominant frontotemporal lobar degeneration (FTLD) and Amyotrophic Lateral Sclerosis., C9ORF72 hexanucleotide repeat number in frontotemporal lobar degeneration: a genotype-phenotype correlation study., Hexanucleotide repeat expansions in Chromosomes, Human, Pair 9 open reading frame 72 (C9orf72) have recently been linked to frontotemporal lobar degeneration (FTLD) and Amyotrophic Lateral Sclerosis, and may be the most common Genetic cause of both Neurodegenerative Disorders., studies recently identified a GGGGCC hexanucleotide repeat expansion in a non-coding region of the Chromosomes, Human, Pair 9 open-reading frame 72 Genes (C9ORF72) as the cause of chromosome 9p-linked Amyotrophic Lateral Sclerosis (ALS) and frontotemporal dementia (FTD)., GGGGCC hexanucleotide repeat expansion in the C9orf72 Genes was recently identified as an important cause of familial Amyotrophic Lateral Sclerosis (ALS) and frontotemporal dementia in Caucasian populations.[SEP]Relations: C9orf72 has relations: disease_protein with mental disorder, disease_protein with mental disorder, disease_protein with schizophrenia, disease_protein with schizophrenia, disease_protein with spondyloarthropathy, disease_protein with spondyloarthropathy, disease_protein with Amyotrophic Lateral Sclerosis, disease_protein with Amyotrophic Lateral Sclerosis, disease_protein with progressive non-fluent aphasia, disease_protein with progressive non-fluent aphasia.", "label": "no"}
{"original_question": "Are ICAMS, Intracellular Adhesion Molecules, part of the immunoglobulin superfamily?", "id": "converted_3290", "sentence1": "Are ICAMS, Intracellular Adhesion Molecules, part of the immunoglobulin superfamily?", "sentence2": "It has now been shown that adhesion molecules, particularly those of the immunoglobulin super family (e.g. Intercellular adhesion molecule 1, Vascular Cell Adhesion Molecule-1 and Platelet Endothelial Cell Adhesion Molecule, human),,  Intercellular Adhesion Molecule-3 (ICAM-3, also known as Lymphocyte antigen Lymphocyte antigen CD50), a human leukocyte-restricted immunoglobulin super-family (IgSF) member, has previously been implicated in apoptotic cell clearance,, Intercellular adhesion molecule-1 (Intercellular adhesion molecule 1), vascular cell adhesion molecule-1 (Vascular Cell Adhesion Molecule-1) and platelet-endothelial cell adhesion molecule-1 (Platelet Endothelial Cell Adhesion Molecule, human) are members of the immunoglobulin super-family which are present on the Surface of Endothelial Cells., ICAM4 gene (Intercellular adhesion molecule 1) is an adhesion-related molecule belonging to the immunoglobulin superfamily., Immunologically important Integrins ligands are the intercellular adhesion molecules (Improved Chemical Agent Monitors), immunoglobulin superfamily members present on inflamed Endothelium and Antigen-Presenting Cells., The intercellular adhesion molecules (Improved Chemical Agent Monitors) are members of the immunoglobulin superfamily and have been identified to play major roles in Inflammation and immune responses., The intercellular adhesion molecules (Improved Chemical Agent Monitors) are members of the immunoglobulin superfamily and have been identified to play major roles in Inflammation and immune responses., Intercellular adhesion molecule 1 is a member of immunoglobulin-like superfamily of adhesion molecules that binds Lymphocyte Function-Associated Antigen-1 to mediate Specimen Source Codes - Leukocytes adhesion and migration., Immunologically important Integrins ligands are the intercellular adhesion molecules (Improved Chemical Agent Monitors), immunoglobulin superfamily members present on inflamed Endothelium and Antigen-Presenting Cells., The immunoglobulin superfamily includes leukocyte function antigen-2 (CD2 Antigens Antigens wt Allele or CD2 Antigens Antigens), leukocyte function antigen-3 (Lymphocyte Function-Associated Antigen 3, human or CD58), intercellular adhesion molecules (Improved Chemical Agent Monitors), vascular adhesion molecule-1 (Vascular Cell Adhesion Molecule-1), platelet-endothelial cell adhesion molecule-1 (PE-CAM-1), and mucosal addressin cell adhesion molecule-1 (MADCAM1 protein, human)., The main ligand binding site of Lymphocyte Function-Associated Antigen-1 is the I-domain, which recognizes intercellular adhesion molecules (Improved Chemical Agent Monitors), members of the immunoglobulin superfamily., Intercellular Adhesion Molecules (Improved Chemical Agent Monitors) are structurally related members of the immunoglobulin supergene family and are ligands for the beta2 Integrins molecules present on Specimen Source Codes - Leukocytes., Intercellular Adhesion Molecules (Improved Chemical Agent Monitors) belong to the immunoglobulin superfamily and participate in diverse cellular processes including host-pathogen interactions., Members of the immunoglobulin superfamily of endothelial adhesion molecules, vascular cell adhesion molecule (Vascular Cell Adhesion Molecule-1) and intercellular cell adhesion molecule (Intercellular adhesion molecule 1), participate in leukocyte adhesion to the Endothelium and play an important role in all stages of Arteriosclerosis., Members of the immunoglobulin superfamily of endothelial adhesion molecules, vascular cell adhesion molecule (Vascular Cell Adhesion Molecule-1) and intercellular cell adhesion molecule (ICAM- 1), strongly participate in leukocyte adhesion to the Endothelium and play an important role in all stages of Atherogenesis., Intercellular adhesion molecule-3 (ICAM-3, Lymphocyte antigen Lymphocyte antigen CD50), a member of the immunoglobulin gene superfamily, is a major ligand for the lymphocyte function-associated antigen 1 (Lymphocyte Function-Associated Antigen-1, CD18/CD11a) in the resting immune system and plays a role as a signaling and costimulatory molecule on T-Lymphocyte., Expression of the immunoglobulin superfamily molecules MUC18/MCAM and Intercellular adhesion molecule 1 are associated with Primary Neoplasm and metastases.[SEP]Relations: heterophilic cell-cell adhesion via plasma membrane cell adhesion molecules has relations: bioprocess_protein with ICAM1, bioprocess_protein with ICAM1. alpha9-beta1 Integrins-vascular cell adhesion molecule-1 complex has relations: cellcomp_protein with VCAM1, cellcomp_protein with VCAM1. Integrins binding has relations: molfunc_protein with ICAM3, molfunc_protein with ICAM3, molfunc_protein with ICAM2, molfunc_protein with ICAM2. cell Surface has relations: cellcomp_protein with ICAM1, cellcomp_protein with ICAM1.", "label": "yes"}
{"original_question": "Are there clinical trials using stem cells for the treatment of cardiac disease?", "id": "converted_993", "sentence1": "Are there clinical trials using Stem Cells for the treatment of cardiac disease?", "sentence2": "Therapy with mesenchymal Stem Cells is one of the promising tools to improve outcomes after Myocardial infarction:Finding:Point in time:^Patient:Ordinal. Adipose-derived Stem Cells (ASCs) are an ideal source of mesenchymal Stem Cells due to their abundance and ease of preparation., Furthermore, several ongoing clinical trials using ASCs are producing promising results for Chest>Heart diseases., Among the cell types under investigation, adult mesenchymal Stem Cells are widely studied, and in early stage, clinical studies show promise for repair and regeneration of cardiac tissues.,  Accumulating data from preclinical and early phase clinical trials document their safety when delivered as either autologous or allogeneic forms in a range of cardiovascular diseases, but also importantly define parameters of clinical efficacy that justify further investigation in larger clinical trials. , several ongoing clinical trials using ASCs are producing promising results for Chest>Heart diseases. , Clinical application of adult Stem Cells for therapy for cardiac disease., Stem cell-based therapies have the potential to fundamentally transform the treatment of ischemic cardiac injury and Congestive Chest>Heart failure by achieving what would have been unthinkable only a few years ago-the Holy Grail of myocardial regeneration. Recent therapeutic approaches involve bone marrow (BM)-derived mononuclear Cells and their subsets such as mesenchymal Scanning Transmission Electron Microscopy Procedures/stromal Cells (cyclic nucleotide-gated mechanosensitive ion channel activity), Endothelial Progenitor Cells as well as adipose tissue-derived cyclic nucleotide-gated mechanosensitive ion channel activity, Heart tissue-derived Stem Cells, and cell combinations. Clinical trials employing these Cells have demonstrated that cellular therapy is feasible and safe., Accumulating data from preclinical and early phase clinical trials document their safety when delivered as either autologous or allogeneic forms in a range of cardiovascular diseases, but also importantly define parameters of clinical efficacy that justify further investigation in larger clinical trials., se of Scanning Transmission Electron Microscopy Procedures and precursor Cells as a therapeutic agent for chronically injured Organ. Among the cell types under investigation, adult mesenchymal Stem Cells are widely studied, and in early stage, clinical studies show promise for repair and regeneration of cardiac tissues. , Over the past 2 decades, there have been numerous Scanning Transmission Electron Microscopy Procedures cell studies focused on Heart Diseases, ranging from proof-of-concept to phase 2 trials. , Small uncontrolled clinical trials have demonstrated cardiac Stem Cells as a treatment option for Cardiomyopathies., Stem cell populations are rapidly increasing, and we are still in the search of optimal cell types to use in clinical trials as bone marrow Stem Cells did not show significant improvement in cardiac function following transplantation., Several clinical trials using adult Scanning Transmission Electron Microscopy Procedures cell have shown improvements in cardiac function, however, the mechanism of their action is unclear and widespread tissue regeneration is not evident., As we await results from larger and more prolonged clinical trials, the science of Scanning Transmission Electron Microscopy Procedures cell therapy in cardiac disease keeps progressing., Stem cell therapy for treatment of cardiac disease has shown therapeutic potential., It should be noted that Scanning Transmission Electron Microscopy Procedures cell therapy is not limited to the treatment of ischemic cardiac disease., Over the past 2 decades, there have been numerous Scanning Transmission Electron Microscopy Procedures cell studies focused on Heart Diseases, ranging from proof-of-concept to phase 2 trials., This series of papers focuses on the legacy of these studies and the outlook for future treatment of Heart Diseases with Scanning Transmission Electron Microscopy Procedures cell therapies., Cell transplantation to repair or regenerate injured Myocardium is a new frontier in the treatment of Cardiovascular Diseases. , Current therapies only delay progression of the cardiac disease or replace the diseased Chest>Heart with cardiac transplantation. Stem Cells represent a recently discovered novel approach to the treatment of cardiac failure that may facilitate the replacement of diseased Heart tissue and subsequently lead to improved cardiac function and cardiac regeneration.,  Over the past 2 decades, there have been numerous Scanning Transmission Electron Microscopy Procedures cell studies focused on Heart Diseases, ranging from proof-of-concept to phase 2 trials. This series of papers focuses on the legacy of these studies and the outlook for future treatment of Heart Diseases with Scanning Transmission Electron Microscopy Procedures cell therapies., Stem cell therapy for treatment of cardiac disease has shown therapeutic potential., Over the past 2 decades, there have been numerous Scanning Transmission Electron Microscopy Procedures cell studies focused on Heart Diseases, ranging from proof-of-concept to phase 2 trials. This series of papers focuses on the legacy of these studies and the outlook for future treatment of Heart Diseases with Scanning Transmission Electron Microscopy Procedures cell therapies., It should be noted that Scanning Transmission Electron Microscopy Procedures cell therapy is not limited to the treatment of ischemic cardiac disease. Non-ischemic Cardiomyopathies, Peripheral Vascular Diseases, and aging may be treated by Stem Cells.,  Recent clinical trials have achieved favorable initial endpoints with improvements in cardiac function and clinical symptoms following cellular therapy., we consider how Cardiac Stem Cell biology has led us into clinical trials, and we suggest that achieving true cardiac regeneration in patients may ultimately require resolution of critical controversies in experimental cardiac regeneration., Cell-based therapies and tissue engineering provide new promising platforms to develop upcoming therapeutic options. Initial clinical trials were able to generate promising results. A variety of different Scanning Transmission Electron Microscopy Procedures cell types have been used for the clinical application. ,  Insights gained from clinical trials of adult Stem Cells, together with fundamental scientific advances in Cardiac Stem Cell and regenerative biology, are beginning to yield potential new targets and strategies for regenerative therapies. , Early animal trials have demonstrated the ability to improve cardiac function by transfer of Hematopoietic Stem Cells into the Myocardium, and early Homo sapiens studies have demonstrated the feasibility and safety of this approach.[SEP]Relations: cardiac germ cell tumor has relations: disease_disease with Chest>Heart neoplasm, disease_disease with Chest>Heart neoplasm, disease_disease with malignant cardiac germ cell tumor, disease_disease with malignant cardiac germ cell tumor, disease_disease with extragonadal germ cell tumor, disease_disease with extragonadal germ cell tumor. Chest>Heart disease has relations: disease_disease with cardiac ventricle disease, disease_disease with cardiac ventricle disease. Cardiovascular Diseases has relations: disease_disease with Chest>Heart disease, disease_disease with Chest>Heart disease.", "label": "yes"}
{"original_question": "Is exonuclease Xrn1 a component of the P-bodies?", "id": "converted_321", "sentence1": "Is exonuclease Xrn1 a component of the P-bodies?", "sentence2": "Pencil Beam Scanning are associated with RNA, Messenger decay and contain the decapping ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS dipeptidyl carboxypeptidase dipeptidyl carboxypeptidase DCP1/2, the 5' to 3' exonuclease Xrn1, the Lsm Proteins (1-7), and the scaffolding Proteins hedls/GE-1 and TNRC6A gene. Both Shprintzen-Goldberg syndrome and Pencil Beam Scanning contain RNA, Messenger, Eukaryotic Initiation Factor-4E, MicroRNAs and Protein Argonaute-1 Proteins, and various regulators of RNA, Messenger stability and translation (Congenital Thrombotic Thrombocytopenic Purpura, RCK/p54, and CPEB)., An alternative pathway of RNA, Messenger degradation occurs at processing bodies, Cytoplasmic foci that contain decapping ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS, the 5'-3' exonuclease Xrn1 and the Lsm1-7 heptamer. , n Eukaryotic Cells degradation of bulk RNA, Messenger in the 5' to 3' direction requires the consecutive action of the decapping complex (consisting of dipeptidyl carboxypeptidase dipeptidyl carboxypeptidase DCP1 and DCP2 gene gene) and the 5' to 3' exonuclease XRN1 protein, Homo sapiens protein, Homo sapiens. These ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS are found in discrete Cytoplasmic foci known as P-bodies or GW-Bodies (because of the accumulation of the TNRC6A gene antigen)., Several Proteins that stimulate RNA, Messenger decapping by the Dcp1:Dcp2 complex co-localize with Dcp1 and Dcp2, together with Xrn1, a 5'-to-3' exonuclease, to structures in the Cytoplasm called processing bodies. ,  On the other hand, many Processing Bodies components including LSM1 gene gene, TNRC6A gene, DDX3X wt Allele, DDX6 gene gene and XRN1 protein, Homo sapiens protein, Homo sapiens, but not others like DCP1a and EDC4 gene gene are recruited to the viral replication sites, as evidenced by their colocalization at perinuclear region with viral NS3., We identified the Pab 1801 Cytoplasmic puncta as P Bodies (Pencil Beam Scanning), which are involved in RNA, Messenger regulation. We found that, in several Cultured Cell Line, including U2OS, WI38, SK-N-SH and HCT116, the Pab 1801 puncta strictly colocalize with Pencil Beam Scanning identified with specific Antibodies, in vitro diagnostic against the HTN3 gene components Hedls, DCP1A gene, Xrn1 or Rck/p54., The core components of P-bodies, including the decapping machinery (Dcp2 and Dhh1), 5'-3' Exoribonucleases (Kem1/Xrn1), and the Processing Bodies scaffolding protein (Edc3), were identified and their localizations with respect to P-bodies were demonstrated., The second type of Granules dose form, piP-bodies, harbors the MIWI2-TDRD9-MAEL module of the piRNA pathway and signature components of P-bodies, TNRC6A gene, DCP1a, DDX6 gene gene/p54, and XRN1 protein, Homo sapiens protein, Homo sapiens Proteins., In Saccharomyces cerevisiae and Homo sapiens tissue culture Cells, Xrn1 has been shown to be a component of P-bodies (processing bodies), dynamic Cytoplasmic Granules dose form where RNA degradation can take place., Here, we show that staufen- and FMRP-containing RNPs in Drosophila <basidiomycetes> <basidiomycetes> neurons contain Proteins also present in somatic \"P bodies,\" including the RNA-degradative ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS Dcp1p and Xrn1p/Pacman and crucial components of miRNA (Protein Argonaute-1), Nonsense Mediated RNA, Messenger Decay (Upf1p), and general translational repression (Dhh1p/Me31B) pathways.,  In Eukaryotic Cells, XRN1 protein, Homo sapiens protein, Homo sapiens is often found in particles known as processing bodies (P bodies) together with other Proteins involved in the 5' → 3' degradation pathway, such as DCP2 gene gene and the helicase DHH1 (Me31B). , In Saccharomyces cerevisiae and Homo sapiens tissue culture Cells, Xrn1 has been shown to be a component of P-bodies (processing bodies), dynamic Cytoplasmic Granules dose form where RNA degradation can take place, Owing to the essential functions of P bodies in RNA, Messenger regulation, we explored computationally the functional significance of Single Nucleotide Polymorphism in 7 P body components such as XRN1 protein, Homo sapiens protein, Homo sapiens, DCP2 gene gene, EDC3 gene gene, CPEB1 gene gene, GEMIN5 gene gene, STAU1 gene gene and TRIM71 gene gene, The core components of P-bodies, including the decapping machinery (Dcp2 and Dhh1), 5&apos;-3&apos; Exoribonucleases (Kem1/Xrn1), and the Processing Bodies scaffolding protein (Edc3), were identified and their localizations with respect to P-bodies were demonstrated, Here, we show that staufen- and FMRP-containing RNPs in Drosophila <basidiomycetes> <basidiomycetes> neurons contain Proteins also present in somatic &quot;P bodies,&quot; including the RNA-degradative ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS Dcp1p and Xrn1p/Pacman and crucial components of miRNA (Protein Argonaute-1), Nonsense Mediated RNA, Messenger Decay (Upf1p), and general translational repression (Dhh1p/Me31B) pathways, Processing Bodies components LSM1 gene gene, TNRC6A gene, DDX3X wt Allele, DDX6 gene gene and XRN1 protein, Homo sapiens protein, Homo sapiens are recruited to WNV replication sites and positively regulate viral replication., The core components of P-bodies, including the decapping machinery (Dcp2 and Dhh1), 5&apos;-3&apos; Exoribonucleases (Kem1/Xrn1), and the Processing Bodies scaffolding protein (Edc3), were identified and their localizations with respect to P-bodies were demonstrated. Various growth conditions, including glucose deprivation, hyperosmotic stress, and heat stress, stimulated the accumulation of P-bodies., Here we show that microscopically visible P-bodies are greatly diminished following West Nile viral Communicable Diseases, but the component Proteins are not depleted. On the other hand, many Processing Bodies components including LSM1 gene gene, TNRC6A gene, DDX3X wt Allele, DDX6 gene gene and XRN1 protein, Homo sapiens protein, Homo sapiens, but not others like DCP1a and EDC4 gene gene are recruited to the viral replication sites, as evidenced by their colocalization at perinuclear region with viral NS3., Owing to the essential functions of P bodies in RNA, Messenger regulation, we explored computationally the functional significance of Single Nucleotide Polymorphism in 7 P body components such as XRN1 protein, Homo sapiens protein, Homo sapiens, DCP2 gene gene, EDC3 gene gene, CPEB1 gene gene, GEMIN5 gene gene, STAU1 gene gene and TRIM71 gene gene. Computational analyses of non-synonymous Single Nucleotide Polymorphism of these components was initiated using well utilized publicly available software programs such as the SIFT, followed by PolyPhen, Panthers, MutPred, I-Mutant-2., Xrn1 has been shown to be a component of P-bodies (processing bodies),, Here, we show that DIS3-Like Exonuclease 2 is an exosome-independent Cytoplasmic RNA, Messenger 3'-5' exonuclease, which exhibits processive activity on structured RNA substrates in vitro. DIS3-Like Exonuclease 2 associates with hXRN1 in an RNA-dependent manner and can, like hXRN1, be found on Set of polysomal ribosomes, Inhibition of TAK1-JNK signaling also affected the number and size of P bodies and the localization of DCP1a, Xrn1, and Edc4.,  The organizing mechanism that forms P body foci in Cells is unknown; however, potential scaffolding, aggregating, or other regulatory Proteins found in P bodies were investigated for degradation. Two factors involved in 5'-end RNA, Messenger decapping and degradation, Xrn1 and DCP1A gene, and the 3' deadenylase complex component NLRP6 wt Allele underwent accelerated degradation during Communicable Diseases, and DCP1A gene may be a direct substrate of PV 3C proteinase., Secondly, P-bodies recruit mRNAs that are targeted for deadenylation and degradation by the decapping/Xrn1 pathway. , Depletion of TRN increased the number of P-bodies and stabilized ARE-containing mRNAs, as observed with knockdown of the 5'-3' exonuclease Xrn1., In this paper we show for the first time that Pacman, the Drosophila <basidiomycetes> <basidiomycetes> homologue of Xrn1, is localized in Cytoplasmic particles in Drosophila <basidiomycetes> <basidiomycetes> testis Cells. , Depletion of TRN increased the number of P-bodies and stabilized ARE-containing mRNAs, as observed with knockdown of the 5&apos;-3&apos; exonuclease Xrn1, These structures stain positively for a number of Processing Bodies and microRNP components, a microRNA-repressed RNA, Messenger and some translational repressors. They appear more heterogeneous than P-bodies of HeLa Cells, and they rarely contain the exonuclease Xrn1 but are positive for Ribosomal RNA.[SEP]Relations: 5'-3' Exoribonucleases activity has relations: molfunc_protein with XRN1 protein, Homo sapiens, molfunc_protein with XRN1 protein, Homo sapiens, molfunc_protein with XRN2, molfunc_protein with XRN2, molfunc_protein with DCP2 gene, molfunc_protein with DCP2 gene. EDC3 gene has relations: bioprocess_protein with Processing Bodies assembly, bioprocess_protein with Processing Bodies assembly. CPEB1 gene has relations: cellcomp_protein with Processing Bodies, cellcomp_protein with Processing Bodies.", "label": "yes"}
{"original_question": "Has amantadine ER been approved by the FDA?", "id": "converted_3583", "sentence1": "Has amantadine Endoplasmic Reticulum been approved by the FDA?", "sentence2": "ADS-5102 (amantadine) extended-release (Endoplasmic Reticulum) capsules (GOCOVRITM) is a recent US FDA-approved treatment for Dyskinetic syndrome in Lugano Lymphoma Response Classification Progressive Disease by PET patients. [SEP]Relations: Amantadine has relations: drug_drug with Ergometrine, drug_drug with Ergometrine, drug_drug with Ergotamine, drug_drug with Ergotamine, drug_drug with Ertapenem, drug_drug with Ertapenem, drug_drug with Eribulin, drug_drug with Eribulin, drug_drug with Erdafitinib, drug_drug with Erdafitinib.", "label": "yes"}
{"original_question": "Does xaliproden improve prognosis of amyotrophic lateral sclerosis?", "id": "converted_3406", "sentence1": "Does xaliproden improve prognosis of amyotrophic lateral sclerosis?", "sentence2": "Treatment for crampsThere is evidence (13 RCTs, N = 4012) that for the treatment of Muscle Cramp in MND, compared to placebo:- memantine and dronabinol (Thrombocytopenia 1) are probably ineffective (moderate-quality evidence);- Vitamin E Drug Class may have little or no effect (low-quality evidence); and- the effects of threonine, gabapentin, xaliproden, riluzole, and baclofen are uncertain as the evidence is either very low quality or the trial specified the outcome but did not report numerical data., The medications comprised Vitamin E Drug Class, baclofen, riluzole, threonine, xaliproden, indinavir, and memantine. Six studies assessed Muscle Cramp as an adverse event. The medications comprised creatine/creatinine/creatinine, gabapentin, dextromethorphan, quinidine, and Lithium antipsychotics. In all 20 studies no favourable effect for the treatment of Muscle Cramp in Amyotrophic Lateral Sclerosis/MND could be demonstrated, but many studies were underpowered to draw a definite conclusion., . The six months intent-to-treat analysis showed no statistically significant effect but a trend in favour of 2 mg xaliproden compared to placebo for reduction in the rate of deterioration of FVC, Limb structure functional score, and manual muscle testing score (Oculodigitoesophagoduodenal syndrome)., These results support the use of a staging process to select suitable patients for phase II studies, and suggest that xaliproden may have potential effects in Amyotrophic Lateral Sclerosis and deserve further study., An effect of xaliproden on functional parameters, especially VC, was noted. Although this effect did not reach statistical significance, xaliproden had a small effect on clinically noteworthy aspects of disease progression in Amyotrophic Lateral Sclerosis., The six months intent-to-treat analysis showed no statistically significant effect but a trend in favour of 2 mg xaliproden compared to placebo for reduction in the rate of deterioration of FVC, Limb structure functional score, and manual muscle testing score (Oculodigitoesophagoduodenal syndrome)., An effect of xaliproden on functional parameters, especially VC, was noted., These results support the use of a staging process to select suitable patients for phase II studies, and suggest that xaliproden may have potential effects in Amyotrophic Lateral Sclerosis and deserve further study., The six months intent-to-treat analysis showed no statistically significant effect but a trend in favour of 2 mg xaliproden compared to placebo for reduction in the rate of deterioration of FVC, Limb structure functional score, and manual muscle testing score (Oculodigitoesophagoduodenal syndrome)., Although this effect did not reach statistical significance, xaliproden had a small effect on clinically noteworthy aspects of disease progression in Amyotrophic Lateral Sclerosis.[SEP]Relations: amyotrophic lateral sclerosis has relations: disease_phenotype_positive with Xerostomia, disease_phenotype_positive with Xerostomia, disease_phenotype_positive with Axonal degeneration, disease_phenotype_positive with Axonal degeneration, disease_phenotype_positive with Degeneration of the lateral corticospinal tracts, disease_phenotype_positive with Degeneration of the lateral corticospinal tracts, disease_phenotype_positive with Neurodegeneration, disease_phenotype_positive with Neurodegeneration, disease_protein with XIAP, disease_protein with XIAP.", "label": "no"}
{"original_question": "Is Benralizumab effective for Chronic Spontaneous Urticaria?", "id": "converted_4608", "sentence1": "Is Benralizumab effective for Chronic Spontaneous Urticaria?", "sentence2": "Finally, treatments aimed at reducing eosinophil accumulation and activation, such as the anti-IL-5 antibodies mepolizumab, reslizumab, and benralizumab, have been reported to reduce Chronic Spontaneous Urticaria symptoms. , The treatments that are under clinical trials for Chronic Spontaneous Urticaria are Anti-Immunoglobulin E antibody treatments such as ligelizumab, Molecule targeting Protoplasm signaling pathways such as Abdomen>Spleen Protein-tyrosine kinase inhibitor (disposition), surface inhibitory Molecule such as SIGLEC8 gene, anti-IL-1s such as canakinumab, Bruton kinase (BTK) inhibitors such as GDC-0853 and anti-IL-5s such as benralizumab and mepolizumab., f-label use of dupilumab, reslizumab, mepolizumab, and benralizumab can be effective in CU. Ligel, Finally, treatments aimed at reducing eosinophil accumulation and activation, such as the anti-IL-5 antibodies mepolizumab, reslizumab, and benralizumab, have been reported to reduce Chronic Spontaneous Urticaria symptoms., ments aimed at reducing eosinophil accumulation and activation, such as the anti-IL-5 antibodies mepolizumab, reslizumab, and benralizumab, have been reported to reduce Chronic Spontaneous Urticaria symptoms. Clearly, a new pi, ormation on the effects of the off-label use, in Chronic Spontaneous Urticaria, of biologics licensed for the treatment of other diseases, including dupilumab, benralizumab, mepolizumab, reslizumab, and secukinumab. Finally, we discuss, , B-Lymphocytes, Therapeutic gamma delta T-lymphocytes and Specimen Source Codes - Eosinophils. The treatments that are under clinical trials for Chronic Spontaneous Urticaria are Anti-Immunoglobulin E antibody treatments such as ligelizumab, Molecule targeting Protoplasm signaling pathways such as Abdomen>Spleen Protein-tyrosine kinase inhibitor (disposition), surface inhibitory Molecule such as SIGLEC8 gene, anti-IL-1s such as canakinumab, Bruton kinase (BTK) inhibitors such as GDC-0853 and anti-IL-5s such as benralizumab and mepolizumab.SUMMARY: The ongoing clinical trials on new targets of treatment hold new hopes not only for a better care of the disease but also a better understan[SEP]Relations: Benralizumab has relations: drug_drug with Urelumab, drug_drug with Urelumab, drug_drug with Evinacumab, drug_drug with Evinacumab, drug_drug with Fremanezumab, drug_drug with Fremanezumab, drug_drug with Adecatumumab, drug_drug with Adecatumumab, drug_drug with Galcanezumab, drug_drug with Galcanezumab.", "label": "yes"}
{"original_question": "Are there telemedicine applications for chronic pain management?", "id": "converted_573", "sentence1": "Are there telemedicine applications for Chronic pain management?", "sentence2": "An Integrated cognitive-behavioral and physical therapy group protocol has been developed and then implemented at remote sites using videoconferencing technology to provide pain management for veterans. , Tele-pain management: use of videoconferencing technology in the delivery of an Integrated cognitive-behavioral and physical therapy group intervention., It is feasible to provide treatment to women veterans living in rural areas by utilizing video-teleconferencing technology between larger VA medical centers and facilities at CBOCs in more rural settings, The results suggest that a smartphone-delivered intervention with diaries and personalized feedback can reduce catastrophizing and prevent increases in functional impairment and symptom levels in women with chronic widespread pain following inpatient rehabilitation.,  Of the studies available, there are very few randomized trials of telehealth pain care and only one general overview of e-health and Chronic pain, which dedicates just a few paragraphs to telehealth., therapy adaptation and the resultant specification for the SMART2 project-a technology-based self-management system for assisting long-term health conditions, including Chronic pain, Results showed the use of videoconferencing for this group of patients is useable and satisfactory for both patients and staff, that the patients save time and money, and that for a system where videoconferencing equipment is already in use, it is also cost effective. Staff were able to identify new patient problems. , This pilot study indicates that telemedicine follow-up consultations for Chronic pain patients are feasible and cost-saving. Patients and anesthesiologists were highly satisfied with telemedicine consultation.[SEP]Relations: Chronic pain has relations: phenotype_phenotype with Pain, phenotype_phenotype with Pain, disease_phenotype_positive with Machado-Joseph disease, disease_phenotype_positive with Machado-Joseph disease, disease_phenotype_positive with double uterus-hemivagina-renal agenesis, disease_phenotype_positive with double uterus-hemivagina-renal agenesis, disease_phenotype_positive with glycogen storage disease, disease_phenotype_positive with glycogen storage disease, disease_phenotype_positive with Sjogren syndrome, disease_phenotype_positive with Sjogren syndrome.", "label": "yes"}
{"original_question": "Do the proteins Talin and Amot interact?", "id": "converted_4609", "sentence1": "Do the proteins TLN1 gene and AMOT gene interact?", "sentence2": "we show that AMOT gene binds TLN1 gene and is essential for relaying forces between FN1 gene and the Microtubules associated with cytoplasmic filaments[SEP]Relations: Molecules associated with elastic fibres has relations: pathway_protein with EMILIN3, pathway_protein with EMILIN3, pathway_protein with EMILIN2, pathway_protein with EMILIN2, pathway_protein with EMILIN1, pathway_protein with EMILIN1, pathway_protein with ITGAV, pathway_protein with ITGAV, pathway_protein with ELN, pathway_protein with ELN.", "label": "yes"}
{"original_question": "Is Tcf3 associated with the Wnt pathway?", "id": "converted_3803", "sentence1": "Is Tcf3 associated with the Wnt pathway?", "sentence2": "TCF3, a novel positive regulator of osteogenesis, plays a crucial role in MIR17 wt Allele modulating the diverse effect of canonical Wnt signaling in different microenvironments, Furthermore, the role of MIR17 wt Allele was because of its target gene TCF3 (TRANSCRIPTION FACTOR), a key transcription factor of canonical Wnt pathway., Consequently, Tcf3 knockdown in HCT-R Cells restores their sensitivity to the effects of butyrate on Wnt activity and clonal cell growth. Interestingly, the effects of overexpressed Tcf3 differ between HCT-116 and HCT-R Cells, In HCT-R Cells, however, the overexpression of Tcf3 inhibits Wnt activity, and the Cells are still able to proliferate due to the higher expression levels of cell cycle factors, particularly those driving the G(1) to S transition., TCF3 (also known as TCF7L1 protein, human protein, human) is a member of the TCF/LEF transcription factor family that is central in regulating epidermal and embryonic Stem Cells identity., We found that in contrast to ES Cells, where it represses Wnt-pathway target Genes, TCF3 promotes the expression of a subset of Wnt-responsive Genes in breast cancer Cells while repressing another distinct target subset. In the normal Mus sp. mammary gland, Tcf3 is highly expressed in Terminal (end postition) end buds, structures that lead duct development, Tcf3 is essential within the Neural ectoderm to maintain anterior character and that its interaction with HESX1 gene ensures the repression of Wnt targets in the developing Prosencephalon., We report here that a Terminal (end postition) component of the canonical Wnt pathway in ES Cells, the transcription factor T-cell factor-3 (Tcf3), co-occupies promoters throughout the Genome - anatomical entity in association with the pluripotency regulators POU5F1 gene and NANOG gene. , Our results suggest that the Wnt pathway, through Tcf3, brings developmental signals directly to the core regulatory circuitry of ES Cells to influence the balance between pluripotency and differentiation., The wnt pathway regulates the steady state level of CTNNB1 gene, a Transcription Coactivator for the Tcf3/LEF1 gene family of DNA binding Proteins., Along with evidence that a significant amount of Tcf protein is nonnuclear, these findings suggest that CK1epsilon can modulate wnt signaling in vivo by regulating both the CTNNB1 gene-Tcf3 and the GBP-dsh interfaces., Rheumatoid Arthritis increases the expression of ligands and receptors of the noncanonical Wnt pathway (Wnt 5a, 7a, FZD2 protein, human and FZD6 protein, human), downstream signaling, and Tcf3 expression., The noncanonical Wnt signaling pathway, through actions of Tcf3, can antagonize the canonical pathway., We report here that a Terminal (end postition) component of the canonical Wnt pathway in ES Cells, the transcription factor T-cell factor-3 (Tcf3), co-occupies promoters throughout the Genome - anatomical entity in association with the pluripotency regulators POU5F1 gene and NANOG gene., Both Tcf3 depletion and Wnt pathway activation cause increased expression of POU5F1 gene, NANOG gene, and other pluripotency factors and produce ES Cells that are refractory to differentiation., Here, we show that injection of a hesx1 morpholino into a 'sensitised' zygotic headless (TCF7L1 protein, human protein, human wt Allele) Mutant background leads to severe Prosencephalon and eye defects, suggesting an interaction between HESX1 gene and the Wnt pathway during Zebrafish Prosencephalon development., In addition, we reveal that Tcf3 is essential within the Neural ectoderm to maintain anterior character and that its interaction with HESX1 gene ensures the repression of Wnt targets in the developing Prosencephalon., TCF3, a novel positive regulator of osteogenesis, plays a crucial role in MIR17 wt Allele modulating the diverse effect of canonical Wnt signaling in different microenvironments., Our studies located the Positioning Attribute of Wnts, downstream LEF1 and TCF3 and Stem Cells marker Proteins, which provide new information in understanding the role of the Wnt singaling pathway in whisker follicles' growth., The transcription factor TCF Transcription Factors (TCF3), one component of the Wnt pathway, is known as a cell-intrinsic inhibitor of many pluripotency Genes in Embryonic Stem Cells (Enhanced S-Cone Syndrome) that influences the balance between pluripotency and differentiation., Overexpression of TCF3 attenuated the effect of MIR17 wt Allele on modulating canonical Wnt signaling., We also find that TCF3 phosphorylation is triggered by canonical Wnt ligands, LRP6 protein, human protein, human, and dominant negative mutants for AXIN1 wt Allele and Glycogen Synthase Kinase 3, indicating that this process shares the same upstream regulators with β-catenin stabilization., Wnt pathway stimulation also triggers β-catenin association at regulatory elements with classic Lef/Tcf motifs associated with differentiation programs., We show that menin physically interacts with Proteins involved in the canonical Wnt signaling pathway, including CTNNB1 gene, TCF3 (VPS72 gene), and weakly with TCF7L2 protein, human (LZTR1 wt Allele)., TCF Transcription Factors (Tcf3) is a component of the Wnt signaling and a dominant downstream effector in Enhanced S-Cone Syndrome.,  factor 3 (Tcf3) is a component of the Wnt signaling and a dominant downstream effector in Enhanced S-Cone Syndrome. Despit, rt here that a Terminal (end postition) component of the canonical Wnt pathway in ES Cells, the transcription factor T-cell factor-3 (Tcf3), co-occupies promoters throughout the Genome - anatomical entity in association with the pluripotency regulators POU5F1 gene and NANOG gene. Thus, CD55 wt Allele, Tcf3, is recruited to a palindromic motif enriched in the Promoter of cell cycle repressor Genes, such as CDKN2B wt Allele, Cyclin-Dependent Kinase Inhibitor 2A, human and CDKN2A wt Allele, which mediate the Wnt-dependent anti-proliferative effect in mESCs. Consistently, Abetalipoproteinemia, nonical Wnt/β-catenin pathway controls mESC pluripotency via the Wnt-effector Tcf3. Howe, g increases the dissociation of HNF1A wt Allele and the association of Tcf3 at promoters of Genes that regulate stemness (e.g., NR5A2 gene gene, P2RX5 gene) or differentiation (e.g. CCN1 wt Allele, ZIC5 gene). Knockdown of Tcf3 increases, pport the existence of a regulatory circuit whereby Wnt/β-catenin counteracts Tcf3 repression of LEF1 gene, which subsequently activates target gene expression via LEF1 gene-β-catenin complexes. We propose that the Tcf/,  with a requirement for Wnt signalling repression, we highlight a synergistic gene dosage-dependent interaction between HESX1 gene and Tcf3, a Transcription Repressor/Corepressor of Wnt target Genes, to maintain anterior Prosencephalon identity during Mus sp. embryogenesis. In addition, expression of ligands and receptors of the noncanonical Wnt pathway (Wnt 5a, 7a, FZD2 protein, human and FZD6 protein, human), downstream signaling, and Tcf3 expression. Rheumatoid Arthritis reduces the phosp, BACKGROUND AND OBJECTIVES: Transcription factor 3 (TCF3) implicates Wnt signaling pathway and regulates E-Cadherin expression, which is involved i, We demonstrate that Mus sp. Tcf3 mediates repression of both moderate and high levels of canonical Wnt signaling, by either competing with other members of the Tcf/Lef family for binding to β-catenin, or for binding to DNA., TCF3 is a Transcription Repressor/Corepressor that has been implicated in Wnt signaling and plays key roles in embryonic axis specification and Stem Cells differentiation., Our data show for the first time that Wnt signaling down-regulates Tcf3 expression, possibly at both the transcriptional and post-transcriptional levels, and thus highlight a novel mechanism through which Wnt signaling inhibits neuro-ectodermal lineage differentiation in Mus sp. Embryonic Stem Cells., We found Tcf3 to be a repressor of Wnt signaling in neocortical NPCs in a reporter gene assay., We found that down-regulation of Tcf3, a member of the Tcf/Lef family and a key player in the control of self-renewal and pluripotency, represents a specific and primary response to Wnt activation in Enhanced S-Cone Syndrome., Wnt16b also activated the RhoA/Rac1 signaling cascade suggesting the activation of a non-canonical Wnt pathway in TCF3-PBX1 Cells., Pre B-cell acute lymphoblastic leukemia (BCP-ALL) with TCF3-PBX1 fusion gene expression has constitutively elevated levels of Wnt16b and RORA wt Allele (Receptor Tyrosine Kinase-like Orphan Receptors), a ligand and a receptor from the Wnt signaling pathway, respectively., We found that in contrast to ES Cells, where it represses Wnt-pathway target Genes, TCF3 promotes the expression of a subset of Wnt-responsive Genes in breast cancer Cells while repressing another distinct target subset., Together, these results suggest that Tcf3 antagonizes Wnt signaling in NPCs, thereby maintaining their undifferentiated state in the Neocortex and that Wnt signaling promotes the transition from Tcf3-mediated repression to HNF1A wt Allele/LEF1 gene-mediated enhancement of Wnt signaling, constituting a positive feedback loop that facilitates neuronal differentiation., We also found that Wnt signal stimulation reduces the level of Tcf3, and increases those of HNF1A wt Allele (also known as TCF7 protein, human) and LEF1 gene, positive mediators of Wnt signaling, in NPCs., These data suggest that in the absence of Wnt signals, Tcf3 may function in skin SCs to maintain an undifferentiated state and, through Wnt signaling, directs these Cells along the Hair Specimen lineage.[SEP]Relations: CTNNB1 has relations: pathway_protein with TCF dependent signaling in response to WNT, pathway_protein with TCF dependent signaling in response to WNT, pathway_protein with RUNX3 regulates WNT signaling, pathway_protein with RUNX3 regulates WNT signaling. LEF1 has relations: pathway_protein with RUNX3 regulates WNT signaling, pathway_protein with RUNX3 regulates WNT signaling, pathway_protein with Repression of WNT target Genes, pathway_protein with Repression of WNT target Genes, bioprocess_protein with positive regulation of Wnt signaling pathway, bioprocess_protein with positive regulation of Wnt signaling pathway.", "label": "yes"}
{"original_question": "Is infertility characteristic of individuals with Fanconi anemia?", "id": "converted_1968", "sentence1": "Is Sterility, Reproductive characteristic of individuals with Fanconi anemia?", "sentence2": "PALB2 protein, human protein, human links BRCA1 protein, human protein, human and BRCA2 protein, human protein, human in homologous recombinational repair of DNA double strand breaks (DSBs). Mono-allelic mutations in PALB2 protein, human protein, human increase the risk of Breast, Pancreatic Hormones, and other Malignant Neoplasms, and biallelic mutations cause Fanconi anemia (doxorubicin/fluorouracil protocol). , Moreover, Mutant males showed reduced fertility due to impaired meiosis and increased apoptosis in Germ Cells. Interestingly, Mutant meiocytes showed a significant defect in sex chromosome synapsis, which likely contributed to the germ cell loss and fertility defect., In females with Fanconi anemia (doxorubicin/fluorouracil protocol), Sterility, Reproductive is often accompanied by diminished ovarian reserve and Hypergonadotropic amenorrhea before the age of 30 years, suggesting Ovarian Failure, Premature (POI)., Substantially reduced Mullerian duct inhibiting substance levels in females with doxorubicin/fluorouracil protocol suggest a primary ovarian defect associated with reduced fertility. Measurement of Mullerian duct inhibiting substance at the time of doxorubicin/fluorouracil protocol diagnosis and subsequent monitoring of Mullerian duct inhibiting substance levels at regular intervals may be useful for the timely management of complications related to POI such as subfertility/Sterility, Reproductive, Encounter due to family history of Encounter due to family history of osteoporosis, and menopausal symptoms., Fanconi anemia (doxorubicin/fluorouracil protocol) is a human disease of Bone marrow hypocellularity, leukemia, Anal Anal squamous cell carcinoma, and developmental anomalies, including Hypogonadism and Sterility, Reproductive. , Reduced fertility is one clinical manifestation among other well known Fanconi anemia features. , Fanconi anemia (doxorubicin/fluorouracil protocol) is a human disease of Bone marrow hypocellularity, leukemia, Anal Anal squamous cell carcinoma, and developmental anomalies, including Hypogonadism and Sterility, Reproductive, Targeted disruption of exons 1 to 6 of the Fanconi Anemia group A Genes leads to growth retardation, strain-specific Microphthalmos, meiotic defects and primordial germ cell hypoplasia., Fanconi anemia (doxorubicin/fluorouracil protocol) is a human disease of Bone marrow hypocellularity, leukemia, Anal Anal squamous cell carcinoma, and developmental anomalies, including Hypogonadism and Sterility, Reproductive., To potentially reduce late effects of malignancy, Late Late chronic graft-versus-host disease (Graft versus host disease prophylaxis/therapy), Endocrine System Diseases, and Sterility, Reproductive in patients with Fanconi anemia (doxorubicin/fluorouracil protocol) undergoing HLA-matched related donor hematopoietic cell transplantation (Hematocrit procedure), we developed a regimen using fludarabine (ZMYND10 wt Allele), cyclophosphamide (Controlling (action)), and anti-thymocyte globulin (lymphocyte immune globulin, anti-thymocyte globulin) followed by infusion of T-Lymphocyte depleted (TCD) bone marrow (BM) or unmanipulated umbilical cord blood (UCB)., Gene Mutation in Fanca account for the majority of cases of Fanconi anemia (doxorubicin/fluorouracil protocol), a recessively inherited disease identified by Congenital Abnormality, Bone marrow hypocellularity, Sterility, Reproductive, and Primary malignant neoplasm susceptibility., FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) is Mutation Abnormality in more than 60% of cases of Fanconi anemia (doxorubicin/fluorouracil protocol), a rare genetically heterogeneous autosomal recessive disorder characterized by Bone marrow hypocellularity, endocrine tissue Primary malignant neoplasm susceptibility, and Sterility, Reproductive., In females with Fanconi anemia (doxorubicin/fluorouracil protocol), Sterility, Reproductive is often accompanied by diminished ovarian reserve and Hypergonadotropic amenorrhea before the age of 30 years, suggesting Ovarian Failure, Premature (POI)., Fanconi anemia (doxorubicin/fluorouracil protocol) is a complex Primary malignant neoplasm susceptibility disorder associated with DNA repair defects and Sterility, Reproductive, yet the precise function of the doxorubicin/fluorouracil protocol proteins in genome maintenance remains unclear., Fanconi anemia (doxorubicin/fluorouracil protocol) is a genetic disease resulting in Bone marrow hypocellularity, high Primary malignant neoplasm risks, and Sterility, Reproductive, and developmental anomalies including Microphthalmos, Microcephaly (physical finding), hypoplastic radius and thumb.[SEP]Relations: Fanconi anemia complementation group has relations: disease_phenotype_positive with Male Sterility, Reproductive, disease_phenotype_positive with Male Sterility, Reproductive, disease_disease with Fanconi anemia, disease_disease with Fanconi anemia, disease_phenotype_positive with Abnormal heart morphology, disease_phenotype_positive with Abnormal heart morphology, disease_phenotype_positive with Abnormal renal morphology, disease_phenotype_positive with Abnormal renal morphology, disease_phenotype_positive with Abnormal facial shape, disease_phenotype_positive with Abnormal facial shape.", "label": "yes"}
{"original_question": "Is MammaPrint cleared by the United States Food and Drug Administration? ", "id": "converted_128", "sentence1": "Is MammaPrint cleared by the United States Food and Drug Administration? ", "sentence2": "Real-time RT-PCR confirmed the 5-gene prognostic signature that was distinct from an FDA-cleared 70-gene signature of MammaPrint panel and from the Oncotype DX Breast Cancer Assay Breast Cancer Assay recurrence score assay panel.[SEP]Relations: salivary gland type cancer of the breast has relations: disease_disease with breast cancer, disease_disease with breast cancer.", "label": "yes"}
{"original_question": "Is ospemifene effective for treatment of dyspareunia?", "id": "converted_285", "sentence1": "Is ospemifene effective for treatment of Have Dyspareunia question?", "sentence2": "ospemifene, a novel selective Estrogen Receptor Modulators, has been developed for the treatment of Vulvovaginal atrophy and Have Dyspareunia question in postmenopausal women. , For the comparison of short-term ospemifene with placebo, parabasal cells (the standardized mean difference [Spondylometaphyseal dysplasia] = -37.5, 95% confidence interval [CI] = -41.83 to -33.17, P < 0.00001), superficial cells (Spondylometaphyseal dysplasia = 9.24, 95% CI = 7.70 to 10.79, P < 0.00001), vaginal PH (Spondylometaphyseal dysplasia = -0.89, 95% CI = -0.98 to -0.80, P = 0.00001), and Have Dyspareunia question (Spondylometaphyseal dysplasia = -0.37, 95% CI = -0.43 to -0.30, P = 0.00001) indicated that ospemifene was more effective than the placebo. , This meta-analysis indicates that ospemifene to be an effective and safe treatment for Have Dyspareunia question associated with postmenopausal Vulva and Atrophy of vagina., ospemifene is a selective Estrogen Receptor Modulators (SERM), or Estrogen [EPC] receptor agonist/antagonist, that was recently approved by the US Food and Drug Administration for the treatment of Have Dyspareunia question associated with Vulva and Atrophy of vagina, a chronic condition that affects up to 60% of postmenopausal women., In conclusion, ospemifene is a SERM with a unique Estrogen Agonist/Antagonist [EPC] tissue profile that was recently approved in the US for the treatment of Have Dyspareunia question associated with Vulva and Atrophy of vagina in postmenopausal women. , To characterize the pharmacokinetics of the oral, non-Estrogen [EPC] agent ospemifene, an Estrogen Agonist/Antagonist [EPC] with tissue-selective effects (also called a selective Estrogen Receptor Modulators) that was recently approved for the treatment of Have Dyspareunia question associated with Vulva and Atrophy of vagina in postmenopausal women., Here, we review the Estrogen Agonist/Antagonist [EPC] profile of ospemifene, a novel triphenylethylene derivative recently approved to treat Have Dyspareunia question, a symptom of Vulva and Atrophy of vagina (VVA) due to menopause, both preclinically and clinically.,  Long-term studies on the endometrial safety of local Estrogen [EPC] and ospemifene are lacking. , ospemifene is a tissue-selective Estrogen Agonist/Antagonist [EPC] (a selective Estrogen Receptor Modulators) recently approved by the US Food and Drug Administration for treatment of Have Dyspareunia question, a symptom of VVA, due to menopause., Selective Estrogen Receptor Modulators with positive vaginal effects (such as improvement in the vaginal maturation index, reduced vaginal pH, and improvement in the signs and symptoms of VVA) on postmenopausal symptomatic women include Lasofoxifene (clinical development on hold) and ospemifene, which was recently approved for the treatment of VVA-related Have Dyspareunia question, with a class effect warning of potential Venous Thrombosis risk. , ospemifene is the first non-Estrogen [EPC] treatment approved for moderate to severe Have Dyspareunia question in women with menopause-related Vulva and Atrophy of vagina. , This article summarizes the milestones in the development of ospemifene leading to this first approval for moderate to severe Have Dyspareunia question, a symptom of postmenopausal Vulva and Atrophy of vagina., The aim of this work was to study the role of ospemifene, a novel selective Estrogen Receptor Modulators, in the treatment of Vulva and Atrophy of vagina in postmenopausal women with moderate to severe Have Dyspareunia question and physiological vaginal changes. , In this study, once-daily oral ospemifene 60 mg was effective for the treatment of Vulva and Atrophy of vagina in postmenopausal women with Have Dyspareunia question., Clinical trials have confirmed that daily doses are well-tolerated and that it is effective in normalizing vaginal maturation index and pH as well as improving the symptoms associated with VVA including Have Dyspareunia question., ospemifene was shown to be effective and well tolerated for the treatment of the symptoms of Vaginal dryness and Have Dyspareunia question associated with Vulvovaginal atrophy over and above the use of provided lubricants.[SEP]Relations: ospemifene has relations: drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Orphenadrine, drug_drug with Orphenadrine, drug_drug with Amodiaquine, drug_drug with Amodiaquine. Dyspareunia has relations: drug_effect with Progesterone, drug_effect with Progesterone, drug_effect with Fluoxetine, drug_effect with Fluoxetine.", "label": "yes"}
{"original_question": "Is there any role of 5hmC in T-cell development and differentiation?", "id": "converted_2267", "sentence1": "Is there any role of 5hmC in T-Lymphocyte development and differentiation?", "sentence2": "We have mapped 5-hydroxymethylcytosine (5hmC) at different stages of T-Lymphocyte development in the Thymus <angiosperm> and T-Lymphocyte differentiation in the periphery. We show that 5hmC is enriched in the gene body of highly expressed Genes at all developmental stages and that its presence correlates positively with gene expression. Further emphasizing the connection with gene expression, we find that 5hmC is enriched in active Thymus <angiosperm>-specific enhancers and that Genes encoding key transcriptional regulators display high intragenic 5hmC levels in Hematopoietic stem cells at those developmental stages where they exert a positive effect. Our data constitute a valuable resource that will facilitate detailed analysis of the role of 5hmC in T-Lymphocyte development and differentiation., We show that 5hmC is enriched in the gene body of highly expressed Genes at all developmental stages and that its presence correlates positively with gene expression., Further emphasizing the connection with gene expression, we find that 5hmC is enriched in active Thymus <angiosperm>-specific enhancers and that Genes encoding key transcriptional regulators display high intragenic 5hmC levels in Hematopoietic stem cells at those developmental stages where they exert a positive effect., We show that 5hmC is enriched in the gene body of highly expressed Genes at all developmental stages and that its presence correlates positively with gene expression., Here, we report early and widespread 5mC/5hmC remodeling during human CD4(+) T cell differentiation ex vivo at Genes and cell-specific enhancers with known T cell function., Our results support 5hmC-mediated DNA de-methylation as a key component of CD4(+) T cell biology in Homo sapiens, with important implications for gene regulation and lineage commitment., 5hmC plays important roles in regulation of gene expression and differentiation and has been implicated in T cell malignancies and Autoimmune Diseases.[SEP]Relations: hematopoietic stem cell homeostasis has relations: bioprocess_protein with TCIRG1, bioprocess_protein with TCIRG1, bioprocess_protein with FSTL1, bioprocess_protein with FSTL1, bioprocess_protein with MYCT1, bioprocess_protein with MYCT1, bioprocess_protein with ARMCX5-GPRASP2, bioprocess_protein with ARMCX5-GPRASP2, bioprocess_protein with UBAP2L, bioprocess_protein with UBAP2L.", "label": "yes"}
{"original_question": "Is progesterone effective for treatment of patients with traumatic brain injury based on clinical trial data?", "id": "converted_436", "sentence1": "Is progesterone effective for treatment of patients with Traumatic Brain Injury based on clinical trial data?", "sentence2": "BACKGROUND: Progesterone [EPC] [EPC] has been associated with robust positive effects in animal models of Traumatic Brain Injury (TBI) and with clinical benefits in two phase 2 randomized, controlled trials. , The proportion of patients with a favorable outcome on the Glasgow Outcome Scale (good recovery or moderate Disability:Type:Pt:^Patient:Nom) was 50.4% with progesterone, as compared with 50.5% with placebo. Mortality was similar in the two groups. No relevant safety differences were noted between progesterone and placebo. CONCLUSIONS: True primary (qualifier value) and secondary efficacy analyses showed no clinical benefit of progesterone in patients with severe TBI. These data stand in contrast to the robust preclinical data and results of early single-center trials that provided the impetus to initiate phase 3 trials., BACKGROUND: Traumatic Brain Injuries (TBI) is a major cause of death and Disability:Type:Pt:^Patient:Nom worldwide. Progesterone [EPC] [EPC] has been shown to improve neurologic outcome in multiple experimental models and two early-phase trials involving patients with TBI. , There was no significant difference between the progesterone group and the placebo group in the proportion of patients with a favorable outcome (relative benefit of progesterone, 0.95; 95% confidence interval [NDUFB6 gene], 0.85 to 1.06; P=0.35). Phlebitis or Thrombophlebitis was more frequent in the progesterone group than in the placebo group (relative risk, 3.03; NDUFB6 gene, 1.96 to 4.66). , CONCLUSIONS: This clinical trial did not show a benefit of progesterone over placebo in the improvement of outcomes in patients with acute TBI. , Numerous studies, however, show that progesterone has substantial pleiotropic properties as a neuroprotective agent in both animal models and Homo sapiens., RESULTS: There was a better recovery rate and Genomics Outcome Scale score for the patients who were given progesterone than for those in the control group in a 3-months follow-up period (50% vs. 21%); subgroup analysis showed a significant difference in the percentage of favorable outcome between the two groups with GCS of 5-8 (p=0.03). CONCLUSION: The use of progesterone may significantly improve neurologic outcome of patients suffering severe TBI up to 3 months after injury, especially those with 5≤GCS≤8, providing a potential benefit to the treatment of acute severe TBI patients. Considering this Pharmacologic Substance had no significant side effects, so progesterone could be used in patients with severe TBI as a neuro-protective Pharmacologic Substance., While progesterone and cyclosporine have shown promise in phase II studies, success in larger phase III, randomized, multicentre, clinical trials is pending.,  All three studies reported the effects of progesterone on mortality. The pooled risk ratio (RR) for mortality at end of follow-up was 0.61, 95% confidence interval (NDUFB6 gene) 0.40 to 0.93. Three studies measured Disability:Type:Pt:^Patient:Nom and found the RR of death or severe Disability:Type:Pt:^Patient:Nom in patients treated with progesterone to be 0.77, 95% NDUFB6 gene 0.62 to 0.96., AUTHORS' CONCLUSIONS: Current clinical evidence from three small RCTs indicates progesterone may improve the neurologic outcome of patients suffering TBI. This evidence is still insufficient and further multicentre randomised controlled trials are required., Genomics Outcome Scale was classified to 2 main categories of favorable and unfavorable recovery, of which, favorable recovery in placebo, progesterone, and progesterone-ergocalciferol was 25%, 45%, and 60%, respectively which showed a statistical significant difference among the groups (P-value = 0.03). CONCLUSION: The results showed that recovery rate in patients with severe brain trauma in the group receiving progesterone and ergocalciferol together was significantly higher than that of progesterone group, which was in turn higher than that of placebo group.,  The pooled relative risk (RR) for mortality at end of follow-up is 0.61, 95% confidence interval (NDUFB6 gene) 0.40 to 0.93. Three studies measured Disability:Type:Pt:^Patient:Nom and found the RR of death or severe Disability:Type:Pt:^Patient:Nom in patients treated with progesterone was 0.77, 95% confidence interval (NDUFB6 gene) 0.62 to 0.96., AUTHORS' CONCLUSIONS: Current clinical evidence from three small RCTs indicates progesterone may improve the neurologic outcome of patients suffering TBI. This evidence is still insufficient and further multicentre randomised controlled trials are required., Clinical trials have shown that short-and long-term progesterone treatment induces a significant improvement in the level of Disability:Type:Pt:^Patient:Nom among patients with Brain Injuries. , Improved outcomes from the administration of progesterone for patients with acute severe Traumatic Brain Injury: a randomized controlled trial., CONCLUSION: Our data suggest that acute severe TBI patients with administration of progesterone hold improved neurologic outcomes for up to 6 months. These results provide information important for further large and multicenter clinical trials on progesterone as a promising neuroprotective Pharmacologic Substance. , The modified Functional Independence Measure scores in the progesterone group were higher than those in the placebo group at both 3-month and 6-month follow-up (P < 0.05 and P < 0.01). The mortality rate of the progesterone group was significantly lower than that of the placebo group at 6-month follow-up (P < 0.05). , CONCLUSION: Our data suggest that acute severe TBI patients with administration of progesterone hold improved neurologic outcomes for up to 6 months. These results provide information important for further large and multicenter clinical trials on progesterone as a promising neuroprotective Pharmacologic Substance. , These data, combined with the results of the previously published ProTECT trial, show progesterone to be safe and potentially efficacious in the treatment of TBI. Larger phase III trials will be necessary to verify results prior to clinical implementation., CONCLUSION: It indicated that successive early application of PEPSINOGEN GENE will benefit the patients with acute severe head injury by improving the recovery and reducing the Disability:Type:Pt:^Patient:Nom, which may be related to its alleviating inflammatory and Lipid Peroxidation response., Adverse and serious adverse event rates were similar in both groups, except that patients randomized to progesterone had a lower 30-day mortality rate than controls (rate ratio 0.43; 95% confidence interval 0.18 to 0.99). , However, moderate Traumatic Brain Injury survivors who received progesterone were more likely to have a moderate to good outcome than those randomized to placebo. CONCLUSION: In this small study, progesterone caused no discernible harm and showed possible signs of benefit., After more than 30 years of research and 30 failed clinical trials with as many different treatments, progesterone is the first agent to demonstrate robust clinical efficacy as a treatment for traumatic brain injuries., After more than 30 years of research and 30 failed clinical trials with as many different treatments, progesterone is the first agent to demonstrate robust clinical efficacy as a treatment for traumatic brain injuries, A US National Institutes of Health-sponsored, nationwide Phase III clinical trial is now evaluating progesterone for moderate-to-severe TBI in 1200 patients, An industry-sponsored Phase III international trial is also under way, and planning for a trial using progesterone to treat pediatric Brain Injuries has begun, More than two decades of pre-clinical research and two recent clinical trials have shown that progesterone (PROG) and its Metabolite exert beneficial effects after Traumatic Brain Injury (TBI) through a number of metabolic and physiological pathways that can reduce damage in many different Body tissue and organ systems, After more than 30 years of research and 30 failed clinical trials with as many different treatments, progesterone is the first agent to demonstrate robust clinical efficacy as a treatment for traumatic brain injuries, RESULTS: Analysis of these reviews yielded meanfuling observations: (1) The effectiveness of most ordinary treatments in TBI is inconclusive except that Corticosteroid ophthalmologic and otologic preparations are likely to be ineffective or harmful, and tranexamic acid, nimodipine and progesterone show a promising effect in bleeding trauma, Traumatic spinal subarachnoid hemorrhage, TBI or severe TBI., Laboratory data strongly show that progesterone treatment after TBI reduces Edema:Finding:Point in time:^Patient:Ordinal, improves outcomes, and restores blood-brain barrier function. Clinical studies to date agree with these data, and there are ongoing human trials for progesterone treatment after TBI.[SEP]Relations: Progesterone [EPC] has relations: drug_effect with Memory impairment, drug_effect with Memory impairment, drug_effect with Pain, drug_effect with Pain, drug_effect with Bone pain, drug_effect with Bone pain, drug_effect with Back pain, drug_effect with Back pain, drug_effect with Limb pain, drug_effect with Limb pain.", "label": "no"}
{"original_question": "Can glyburide reduce cerebral edema?", "id": "converted_2067", "sentence1": "Can glyburide reduce Cerebral Edema?", "sentence2": "Preclinical studies have shown that a continuous infusion of glyburide blocks Edema:Finding:Point in time:^Patient:Ordinal formation and improves outcome. We hypothesize that treatment with RP-1127 (Glyburide for Injection) reduces formation of brain Edema:Finding:Point in time:^Patient:Ordinal in patients after large anterior circulation infarction., CONCLUSIONS: GAMES-RP was designed to provide critical information regarding glyburide for injection in patients with large hemispheric Cerebrovascular accident and will inform the design of future studies., Glyburide is associated with attenuated vasogenic Edema:Finding:Point in time:^Patient:Ordinal in Cerebrovascular accident patients., Glyburide is reported to prevent brain swelling in preclinical rodent models of Ischemic Cerebrovascular accident through inhibition of a non-selective channel composed of Sulfonylurea Compounds receptor 1 and transient receptor potential cation channel subfamily M member 4. , RESULTS: We report that IV glyburide was associated with T2 fluid-attenuated inversion recovery signal intensity ratio on brain MRI, diminished the lesional water diffusivity between days 1 and 2 (pseudo-normalization), and reduced blood Matrix Metalloproteinase 9 level.CONCLUSIONS: Several surrogate markers of vasogenic Edema:Finding:Point in time:^Patient:Ordinal appear to be reduced in the setting of IV glyburide treatment in Homo sapiens Cerebrovascular accident. , Pilot study of intravenous glyburide in patients with a large Ischemic Cerebrovascular accident., BACKGROUND AND PURPOSE: Preclinical and retrospective clinical data indicate that glyburide, a selective inhibitor of Sulfonylurea Compounds receptor 1-transient receptor potential melastatin 4, is effective in preventing Edema:Finding:Point in time:^Patient:Ordinal and improving outcome after focal ischemia. , Preclinical data suggest that glyburide, an inhibitor of ABCC8 gene-TRPM4, is effective in preventing Edema:Finding:Point in time:^Patient:Ordinal., Glyburide in Treating Malignant Cerebral Edema. , Glyburide in Treating Malignant Cerebral Edema. Blocking Sulfonyl Urea One (ABCC8 gene) Receptors., The Sulfonylurea Compounds receptor 1-regulated NC(Ca-ATP) channel is upregulated in rodent models of Cerebrovascular accident with block of the channel by the Sulfonylurea Compounds, glibenclamide (glyburide), significantly reducing mortality, Cerebral Edema, and infarct volume., Glyburide is a safe, inexpensive, and efficacious alternative to dexamethasone for the treatment of cerebral metastasis-related vasogenic Edema:Finding:Point in time:^Patient:Ordinal., In this focused review, we explore preclinical data linking Sur1 channel formation to development of Edema:Finding:Point in time:^Patient:Ordinal and reference evidence suggesting that the antidiabetic Sulfonylurea Compounds drug glyburide (a Sur1 inhibitor) is an inexpensive and well-tolerated agent that can be clinically tested to reduce or prevent Primary malignant neoplasm and/or treatment-associated Edema:Finding:Point in time:^Patient:Ordinal., Potential of glyburide to reduce intracerebral Edema:Finding:Point in time:^Patient:Ordinal in brain metastases., Glyburide Advantage in Malignant Edema and Stroke (GAMES-RP) Trial: Rationale and Design., Preclinical data suggest that glyburide, an inhibitor of ABCC8 gene-TRPM4, is effective in preventing Edema:Finding:Point in time:^Patient:Ordinal., Inhibition of Sulfonylurea Compounds receptor 1 (ABCC8 gene) by glyburide has been shown to decrease Edema:Finding:Point in time:^Patient:Ordinal after Subarachnoid Hemorrhage., Glyburide is a safe, inexpensive, and efficacious alternative to dexamethasone for the treatment of cerebral metastasis-related vasogenic Edema:Finding:Point in time:^Patient:Ordinal, RESULTS: We report that IV glyburide was associated with T2 fluid-attenuated inversion recovery signal intensity ratio on brain MRI, diminished the lesional water diffusivity between days 1 and 2 (pseudo-normalization), and reduced blood Matrix Metalloproteinase 9 level. , Preclinical data suggest that glyburide, an inhibitor of ABCC8 gene-TRPM4, is effective in preventing Edema:Finding:Point in time:^Patient:Ordinal. , Exploratory analysis of glyburide as a novel therapy for preventing brain swelling., Inhibition of Sulfonylurea Compounds receptor 1 (ABCC8 gene) by glyburide has been shown to decrease Edema:Finding:Point in time:^Patient:Ordinal after Subarachnoid Hemorrhage. , In this focused review, we explore preclinical data linking Sur1 channel formation to development of Edema:Finding:Point in time:^Patient:Ordinal and reference evidence suggesting that the antidiabetic Sulfonylurea Compounds drug glyburide (a Sur1 inhibitor) is an inexpensive and well-tolerated agent that can be clinically tested to reduce or prevent Primary malignant neoplasm and/or treatment-associated Edema:Finding:Point in time:^Patient:Ordinal., Glyburide is a safe, inexpensive, and efficacious alternative to dexamethasone for the treatment of cerebral metastasis-related vasogenic Edema:Finding:Point in time:^Patient:Ordinal., Glyburide is reported to prevent brain swelling in preclinical rodent models of Ischemic Cerebrovascular accident through inhibition of a non-selective channel composed of Sulfonylurea Compounds receptor 1 and transient receptor potential cation channel subfamily M member 4., Several surrogate markers of vasogenic Edema:Finding:Point in time:^Patient:Ordinal appear to be reduced in the setting of IV glyburide treatment in Homo sapiens Cerebrovascular accident., We hypothesize that treatment with RP-1127 (Glyburide for Injection) reduces formation of brain Edema:Finding:Point in time:^Patient:Ordinal in patients after large anterior circulation infarction., Glyburide is a safe, inexpensive, and efficacious alternative to dexamethasone for the treatment of cerebral metastasis-related vasogenic Edema:Finding:Point in time:^Patient:Ordinal.., Glyburide is associated with attenuated vasogenic Edema:Finding:Point in time:^Patient:Ordinal in Cerebrovascular accident patients.[SEP]Relations: Glyburide has relations: drug_effect with Edema, drug_effect with Edema, drug_effect with Hypoglycemia, drug_effect with Hypoglycemia. Cerebral Edema:Finding:Point in time:^Patient:Ordinal has relations: drug_effect with Glycine betaine, drug_effect with Glycine betaine, drug_effect with Glatiramer, drug_effect with Glatiramer, drug_effect with Carmustine, drug_effect with Carmustine.", "label": "yes"}
{"original_question": "Can cardiospheres be produced from skin fibroblasts?", "id": "converted_3094", "sentence1": "Can cardiospheres be produced from skin fibroblasts?", "sentence2": "Therefore, there is an emerging interest in generating cardiosphere-like stem cells from Diploid Cell via somatic reprogramming. , Here we provide the detailed protocol for generating induced cardiospheres (iCS) for cardiac regeneration by somatic reprogramming of mouse fibroblasts using a panel of pluripotent transcription factors and cardiotrophic growth factors.[SEP]", "label": "yes"}
{"original_question": "Are Toll-like receptors (TLRs) induced by microbes?", "id": "converted_3900", "sentence1": "Are Toll-like receptors (TLRs) induced by microbes?", "sentence2": "The C-type lectin receptor CLEC4E and TLR2 protein, human TLR4 wt Allele wt Allele expressed by host cells are among the first line of defense in encountering pathogens., Gram-negative bacteria and endogenous Molecule coordinate to trigger inflammatory cascades via TLR2 protein, human 4 to induce excessive expression of Recombinant Cytokines such as tumor necrosis factor-α and to activate NLRP3 inflammasome, a multiprotein complex that processes pro-interleukin-1β into its mature form. , During Virus Diseases, viral nucleic acids are detected by virus sensor proteins including Toll-Like Receptor 3 or retinoic acid-inducible gene I-like receptors (RLRs) in mammalian cells. , TLR2 protein, human 9 (TLR9 gene gene) activation is attributed to delivery of DNA, Bacterial, We determine that HBCs have the capacity to play a defensive role, where they are responsive to TLR2 protein, human stimulation and are microbicidal.[SEP]Relations: TLR2 protein, human 1-TLR2 protein, human 2 protein complex has relations: cellcomp_protein with TLR1, cellcomp_protein with TLR1, cellcomp_protein with TLR1, cellcomp_protein with TLR1, cellcomp_protein with TLR1, cellcomp_protein with TLR1, cellcomp_protein with TLR2, cellcomp_protein with TLR2, cellcomp_protein with TLR2, cellcomp_protein with TLR2.", "label": "yes"}
{"original_question": "Is GAGA associated with nucleosome-free regions (NFR)?", "id": "converted_137", "sentence1": "Is Gaga associated with nucleosome location-free regions (NFR)?", "sentence2": "One of the three nuclease hypersensitive sites in the Fab-7 boundary, EEF1A2 wt Allele, contains multiple consensus-binding sequences for the Gaga factor, a Protein Info known to be involved in the formation and/or maintenance of nucleosome location location-free regions of chromatin location location., The SPHEROCYTOSIS, TYPE 3 (disorder) Sequence - ParameterizedDataType contains consensus Binding Sites for the Gaga factor, a Protein Info implicated in the formation of nucleosome location location-free regions of chromatin location location, and Pleiohomeotic (Osteoarthropathy, Primary Hypertrophic), a Polycomb-Group Proteins that is related to the Mammals TRANSCRIPTION FACTOR YY1 gene gene., The interactions of Gaga factor and heat shock factor with their Binding Sites in chromatin location location occurred in two modes. Their interaction with Binding Sites in the nucleosome location location-free regions did not require adenosine triphosphate. In the presence of adenosine triphosphate both factors interacted also with nucleosomal Binding Sites, causing nucleosome location location rearrangements and a refinement of nucleosome location location positions, While chromatin location location remodeling upon TRANSCRIPTION FACTOR interaction has previously been interpreted to involve nucleosome location location disruption, the data suggest energy-dependent nucleosome location location sliding as main principle of chromatin location location reorganization.,  These (CT)n repeats are associated with a nonhistone Protein Info(s) in vivo and are bound by a purified Drosophila Protein Info, the Gaga factor, in vitro., This (CT)n element appears to contribute to formation of the wild-type chromatin location location structure of hsp26, an organized nucleosome location location array that Plant Leaves the HSEs in nucleosome location location-free, DNase I-hypersensitive (DERMATITIS HERPETIFORMIS, FAMILIAL) site, The SPHEROCYTOSIS, TYPE 3 (disorder) Sequence - ParameterizedDataType contains consensus Binding Sites for the Gaga factor, a Protein Info implicated in the formation of nucleosome location location-free regions of chromatin location location, and Pleiohomeotic (Osteoarthropathy, Primary Hypertrophic), a Polycomb-Group Proteins that is related to the Mammals TRANSCRIPTION FACTOR YY1 gene gene., One of the three nuclease hypersensitive sites in the Fab-7 boundary, EEF1A2 wt Allele, contains multiple consensus-binding sequences for the Gaga factor, a Protein Info known to be involved in the formation and/or maintenance of nucleosome location location-free regions of chromatin location location., The iab-7 polycomb response element maps to a nucleosome location location-free region of chromatin location location and requires both Gaga and pleiohomeotic for silencing activity., The SPHEROCYTOSIS, TYPE 3 (disorder) Sequence - ParameterizedDataType contains consensus Binding Sites for the Gaga factor, a Protein Info implicated in the formation of nucleosome location location-free regions of chromatin location location, and Pleiohomeotic (Osteoarthropathy, Primary Hypertrophic), a Polycomb-Group Proteins that is related to the Mammals TRANSCRIPTION FACTOR YY1 gene gene. [SEP]Relations: nucleosome location mobilization has relations: bioprocess_protein with POLE3, bioprocess_protein with POLE3, bioprocess_bioprocess with nucleosome location organization, bioprocess_bioprocess with nucleosome location organization, bioprocess_protein with INO80, bioprocess_protein with INO80, bioprocess_protein with ARID1A, bioprocess_protein with ARID1A, bioprocess_protein with BPTF, bioprocess_protein with BPTF.", "label": "yes"}
{"original_question": "Is HDAC1 required for GATA-1 transcriptional activity?", "id": "converted_4634", "sentence1": "Is HDAC1 gene required for GATA1 wt Allele transcriptional activity?", "sentence2": "HDAC1 gene gene is required for GATA1 wt Allele transcription activity, global chromatin occupancy and hematopoiesis., GATA-12RA knock-in (KI) mice suffer mild Genus Anemia and THROMBOCYTOPENIA 2 (disorder) with accumulation of immature Specimen Source Codes - Erythrocytes and Megakaryocytes in bone marrow and Abdomen>Spleen. Single cell RNA-seq analysis of Lin- cKit+ (LK) cells further reveal a profound change in cell subpopulations and signature gene expression patterns in Hematopoietic stem cells, myeloid progenitors, and erythroid/megakaryocyte clusters in KI mice. Thus, GATA1 wt Allele deacetylation and its interaction with HDAC1 gene gene modulates GATA1 wt Allele chromatin binding and transcriptional activity that control erythroid/megakaryocyte commitment and differentiation.[SEP]Relations: hematopoietic stem cell homeostasis has relations: bioprocess_protein with FOXA3, bioprocess_protein with FOXA3, bioprocess_protein with TCIRG1, bioprocess_protein with TCIRG1, bioprocess_protein with ADGRG1, bioprocess_protein with ADGRG1, bioprocess_protein with CCN3, bioprocess_protein with CCN3. immune complex clearance by Specimen Source Codes - Erythrocytes has relations: bioprocess_protein with CR1, bioprocess_protein with CR1.", "label": "yes"}
{"original_question": "Is Ameloblastoma (AB) a benign tumor that never metastasizes?", "id": "converted_4677", "sentence1": "Is Ameloblastoma (AB) a benign tumor that never metastasizes?", "sentence2": "Ameloblastic carcinoma (cyclophosphamide/doxorubicin protocol) is defined as a rare primary epithelial odontogenic malignant neoplasm and the malignant counterpart of benign epithelial Odontogenic Tumors of ameloblastoma (AB) by the WHO classification, cyclophosphamide/doxorubicin protocol develops pulmonary metastasis in about one third of the patients and reveals a poor prognosis, Ameloblastomas are benign but locally invasive Neoplasms which may grow to massive proportions and cause significant morbidity. Although some types of ameloblastoma can be treated predictably with aggressive surgical treatment, recurrent ameloblastoma and metastasising ameloblastoma are still difficult to treat., Ameloblastoma of the Maxilla is a rare Odontogenic Tumors that rarely metastasizes., Ameloblastoma is an Odontogenic Tumors, usually benign, which rarely metastasizes to distant organs., Although ameloblastomas rarely metastasise, recurrences together with radical surgery often result in facial deformity and significant morbidity., The World Health Organization (WHO) has defined Malignant Ameloblastoma (MA) as a histologically benign-appearing ameloblastoma that has metastasized., Distant metastasis is a very rare condition and is designated as metastasizing (malignant) ameloblastoma despite its benign histological appearance., Ameloblastoma is a locally invasive, histologically nonmalignant tumor that may on very rare occasions give rise to metastases.[SEP]Relations: ameloblastoma has relations: disease_disease with musculoskeletal system benign neoplasm, disease_disease with musculoskeletal system benign neoplasm, disease_disease with musculoskeletal system benign neoplasm, disease_disease with musculoskeletal system benign neoplasm, disease_disease with benign epithelial neoplasm, disease_disease with benign epithelial neoplasm, disease_disease with benign epithelial neoplasm, disease_disease with benign epithelial neoplasm, disease_disease with bone ameloblastoma, disease_disease with bone ameloblastoma.", "label": "no"}
{"original_question": "Is L-4F an apoE mimetic peptide?", "id": "converted_3146", "sentence1": "Is L-4F an apoE mimetic peptide?", "sentence2": "APOA1 gene mimetic peptide 4F suppresses Tumor-Associated Macrophage and Malignant neoplasm of pancreas progression., L-4F, an APOA1 gene (ApoA-I) mimetic peptide, is engineered to mimic the anti-inflammatory and anti-oxidative functionalities of ApoA-I.[SEP]Relations: apolipoprotein A-I binding has relations: molfunc_protein with ABCA1, molfunc_protein with ABCA1, molfunc_protein with TREM2, molfunc_protein with TREM2, molfunc_protein with LCAT, molfunc_protein with LCAT, molfunc_protein with SCARB1, molfunc_protein with SCARB1, molfunc_protein with HSPD1, molfunc_protein with HSPD1.", "label": "no"}
{"original_question": "Is zyxin a focal adhesion protein?", "id": "converted_552", "sentence1": "Is ZYX gene a focal adhesion protein?", "sentence2": " ZYX gene from Fetal Alcohol Syndrome, ZYX gene relocation from focal adhesions , . Here we systematically examined the expression, localization, and function of ZYX gene, a focal adhesion protein, focal adhesion protein ZYX gene, Focal Adhesions formed in the absence of α-actinins are delayed in their maturation, exhibit altered morphology, have decreased amounts of ZYX protein, human and VASP protein, human protein, human, and reduced adhesiveness to Extracellular Matrix, one focal adhesion protein (ZYX gene), ZYX protein, human is a focal adhesion protein that has been implicated in the modulation of cell adhesion and motility,  focal adhesion proteins (VCL protein, human, TLN1 gene, ZYX gene, Focal Adhesion Kinase 1, and paxilin), Such PXN protein, human-positive complexes mature into focal adhesions by tyrosine phosphorylation and recruitment of ZYX gene. , ZYX protein, human concentrates at focal adhesions , ZYX gene, a focal adhesion protein,, Focal adhesion proteins ZYX protein, human and Vinculin are co-distributed at tubulobulbar complexes.,  Here we explore the prediction that ZYX gene, a focal adhesion protein known to be present at Podosomes, also is present at apical TBCs, the association of ZYX gene with focal adhesions is force-dependent, smaller ZYX gene-positive adhesion as well as its higher turnover rate suggests that the traction force in focal adhesion on 350 nm topography is decreased., . ZYX protein, human is a focal adhesion protein that responds to external mechanical forces;, Vinculin and ZYX gene in focal adhesions but not Integrins are seen to bridge ligand gaps. , The focal adhesion protein ZYX gene, . To explore how this response is regulated by focal adhesion-associated proteins the expression levels of PXN protein, human, Focal Adhesion Protein-Tyrosine Kinases (Focal Adhesion Kinase 1), and ZYX gene were knocked down using gene silencing techniques,  ZYX protein, human is an Adaptor Proteins, Signal Transducing at focal adhesion plaque, ocked localization of ZYX gene at focal adhesion sites[SEP]Relations: focal adhesion has relations: cellcomp_protein with ZYX, cellcomp_protein with ZYX, cellcomp_protein with ZYX, cellcomp_protein with ZYX, cellcomp_protein with ZFYVE21, cellcomp_protein with ZFYVE21, cellcomp_protein with ZFYVE21, cellcomp_protein with ZFYVE21, cellcomp_protein with EZR, cellcomp_protein with EZR.", "label": "yes"}
{"original_question": "Is dupilumab an antibody targeting the IL-1 receptor?", "id": "converted_2210", "sentence1": "Is dupilumab an immunoglobulin complex location targeting the IL-1 receptor?", "sentence2": "Eczema (cytarabine/daunorubicin protocol) is characterized by type 2 helper T (Th2) cell-driven inflammation. dupilumab is a fully Homo sapiens monoclonal immunoglobulin complex location directed against the Recombinant Interleukin-4 receptor α subunit that blocks the signaling of Recombinant Interleukin-4 and IL-13, both key Recombinant Cytokines in Th2-mediated pathways., dupilumab, a humanized monoclonal immunoglobulin complex location to the interteukin-4R is the first immunoglobulin complex location (i.e. 'biological') with published efficacy shown in controlled prospective studies in Dermatitis, Atopic. , dupilumab, a Homo sapiens monoclonal immunoglobulin complex location against Interleukin 4 Receptor alpha, inhibits signaling of interleukin-4 and interleukin-13, Homo sapiens, Homo sapiens, type 2 Recombinant Cytokines that may be important drivers of atopic or allergic diseases such as Dermatitis, Atopic., Best evidence of the clinical efficacy of novel immunologic approaches using biological agents in patients with cytarabine/daunorubicin protocol is available for the anti-Recombinant Interleukin-4 receptor α-chain immunoglobulin complex location dupilumab, but a number of studies are currently ongoing with other specific antagonists to immune system players.,  dupilumab, a fully Homo sapiens anti-Interleukin 4 Receptor α monoclonal immunoglobulin complex location, inhibits interleukin-4 and interleukin-13, Homo sapiens, Homo sapiens signalling, key drivers of type-2-mediated inflammation. , dupilumab was also introduced as a possible treatment for patients with severe Pemphigus <invertebrate>. It can directly inhibit Recombinant Interleukin-4 by targeting Recombinant Interleukin-4 α-chain receptor., We evaluated the efficacy and safety of dupilumab (SAR231893/REGN668), a fully Homo sapiens monoclonal immunoglobulin complex location to the glycoprotein hormones, glycoprotein hormones, alpha subunit of the Interleukin 4 Receptor[SEP]Relations: dupilumab has relations: drug_protein with IL4R, drug_protein with IL4R, drug_drug with Avelumab, drug_drug with Avelumab, drug_drug with IGN311, drug_drug with IGN311, drug_drug with Varlilumab, drug_drug with Varlilumab, drug_drug with Olaratumab, drug_drug with Olaratumab.", "label": "no"}
{"original_question": "Is treatment with Bacillus Calmette Guerin used for bladder cancer?", "id": "converted_3080", "sentence1": "Is treatment with Bacillus Calmette Guerin used for Urinary Bladder cancer?", "sentence2": "Intravesical Bacillus Calmette-Guerin (BCG) is the best treatment modality for progression of non-muscle invasive Urinary Bladder cancer. , this result indicates that they may be used as putative biomarkers for monitoring changes in Urinary Bladder carcinogenesis in response to BCG immunotherapy., response of urothelial precancerous lesions to intravesical BCG treatment, Urinary Bladder cancer (BC Original Formula Original Formula) is a major clinical issue.METHODS: We performed immunohistochemistry to assess the role of Homo sapiens epidermal growth factor receptor-2 (HER-2-neu peptide vaccine-neu peptide vaccine) and microsatellite instability (Microsatellite Instability) factors MutL homologue 1 (MLH1 gene gene) and MutS homologue 2 (DNA Mismatch Repair Protein DNA Mismatch Repair Protein MSH2, Homo sapiens, Homo sapiens) in predicting recurrence and progression of SLC25A4 gene high-grade BCs having undergone transurethral resection of Urinary Bladder tumor (Transurethral resection of neoplasm of Urinary Bladder) alone or Transurethral resection of neoplasm of Urinary Bladder + intravesical instillations of bacillus Calmette-Guerin (BCG)., To evaluate the efficacy and safety of a tailored endovesical immunotherapy protocol with biweekly BCG for elderly Patients with high risk non muscle invasive Urinary Bladder cancer , Bacillus of Calmette-Guerin (BCG) therapy for high risk non muscle invasive Urinary Bladder cancer treatment in older patients., BCG (Bacillus of Calmette Guerin) has been used for more than 20 years and is currently the most active agent for superficial Urinary Bladder cancer therapy., BCG (Bacillus of Calmette Guerin) therapy of high-risk superficial Urinary Bladder cancer., Production of interleukin-5 binding activity, a classical T(H)2 cytokine, following bacillus Calmette guerin immunotherapy of Urinary Bladder cancer., Intravesical Bacillus Calmette-Guerin is used to treat patients with superficial Urinary Bladder cancer., There is some evidence that BCG therapy improves survival and progression rates of patients with high-risk superficial Urinary Bladder cancer decreasing the proportion who require radical cystectomy., Local immunotherapy with bacillus Calmette-Guerin (BCG) is an effective and frequently used treatment for superficial Urinary Bladder cancer., CONCLUSIONS\nIntravesical bacillus Calmette-Guerin is a viable therapeutic option in patients with high risk superficial Urinary Bladder cancer and concomitant Lymphoma or Chronic Lymphocytic Leukemia, treatment with low dose oral steroids or treatment with inhaled steroids., PURPOSE\nBacillus Calmette-Guerin is the most effective therapy for nonmuscle invasive Urinary Bladder cancer., INTRODUCTION\nBacillus Calmette-Guerin (BCG) is a live attenuated strain of Mycobacterium bovis that has been used to treat Urothelial Carcinoma since 1976, and has been reported to eradicate disease in more than 70% of patients with in situ and stage I disease., Intravesical administration of bacillus Calmette-Guerin has been shown to be highly effective treatment of superficial Urinary Bladder cancer., Intravesical bacillus Calmette-Guerin therapy for superficial Urinary Bladder cancer: effect of bacillus Calmette-Guerin viability on treatment results., We describe a 53 year- old man with a disseminated bacillus Calmette-Guerin (BCG) infection after intravescical instillation for Urinary Bladder carcinoma., We tested the hypothesis that tumor expression of natural cytotoxicity receptor ligands can serve as a Disease Predictive Factor for the response to intravesical bacillus Calmette-Guerin in patients with nonmuscle invasive, high grade Urinary Bladder cancer., Bacillus Calmette-Guerin immunotherapy has been found by a number of investigators to be effective in the treatment and prevention of superficial Urinary Bladder cancer., Pancreatic Hormones Hormones and Psoas Abscess as a late complication of intravesical administration of bacillus Calmette-Guerin for Urinary Bladder cancer: a case report and review of the literature.This case illustrates the fact that although intravesical administration of bacillus Calmette-Guerin is generally considered to be safe, it is not exempt from complications and these could appear immediately after treatment or as a delayed complication many years later., Effects of local bacillus Calmette-Guerin therapy in patients with Urinary Bladder carcinoma on immunocompetent Cells of the Urinary Bladder wall.The antitumoral effects of intravesical bacillus Calmette-Guerin against recurrent superficial urothelial Urinary Bladder cancer seem to be linked to immunological effector mechanisms. , Fatal Sepsis (Invertebrate) following intravesical bacillus Calmette-Guerin administration for Urinary Bladder cancer.Intravesical administration of bacillus Calmette-Guerin has been shown to be highly effective treatment of superficial Urinary Bladder cancer. , Intravesical bacillus Calmette-Guerin therapy for superficial Urinary Bladder cancer: effect of bacillus Calmette-Guerin viability on treatment results.We treated 40 patients with superficial Urinary Bladder cancer via intravesical bacillus Calmette-Guerin for 1) prophylaxis against tumor recurrence, 2) residual carcinoma or 3) flat carcinoma in situ. , Bacillus Calmette-Guerin immunotherapy for Urinary Bladder cancer.Bacillus Calmette-Guerin immunotherapy has been found by a number of investigators to be effective in the treatment and prevention of superficial Urinary Bladder cancer. , Safety and efficacy of intravesical bacillus Calmette-Guerin instillations in Steroids treated and immunocompromised patients.Intravesical bacillus Calmette-Guerin is a viable therapeutic option in patients with high risk superficial Urinary Bladder cancer and concomitant Lymphoma or Chronic Lymphocytic Leukemia, treatment with low dose oral steroids or treatment with inhaled steroids. , Our results suggest that intralesional bacillus Calmette-Guerin immunotherapy can afford long term protection from transplanted Urinary Bladder cancer, and that live bacillus Calmette-Guerin is superior to levamisole and P3 + Re-glycolipid + bacillus Calmette-Guerin cell walls in the treatment of Urinary Bladder cancer., A randomized controlled prospective evaluation of intravesical and percutaneous bacillus Calmette-Guerin immunotherapy was done in 57 patients with Carcinoma, Transitional Cell of the Urinary Bladder., Up to 90% of patients with high grade superficial Urinary Bladder tumors experience tumor recurrence and up to 50% have progression despite bacillus Calmette-Guerin treatment., We review how the bacillus Calmette-Guerin vaccine evolved to become standard therapy for superficial Urinary Bladder cancer., We reviewed the historical literature describing the origin of the bacillus Calmette-Guerin vaccine as an anticancer agent and its singular success as the most effective immunotherapy used against a Homo sapiens neoplasm.[SEP]Relations: Bacillus calmette-guerin substrain tice live antigen has relations: drug_drug with Antithymocyte immunoglobulin (rabbit), drug_drug with Antithymocyte immunoglobulin (rabbit), drug_drug with Siltuximab, drug_drug with Siltuximab, drug_drug with Paclitaxel, drug_drug with Paclitaxel, drug_drug with Hydroxychloroquine, drug_drug with Hydroxychloroquine, drug_drug with Inosine pranobex, drug_drug with Inosine pranobex.", "label": "yes"}
{"original_question": "Is the drug Exubera currently (March 2020) available?", "id": "converted_3373", "sentence1": "Is the drug Exubera currently (March 2020) available?", "sentence2": "Despite discontinuation of the first inhalable Therapeutic Insulin, Exubera®, due to suboptimal market acceptance, development of orally inhaled Therapeutic Insulin delivery systems has been galvanized by the recent approval of Afrezza® and several others awaiting approval.[SEP]", "label": "no"}
{"original_question": "Is nucleosome eviction ATP-dependent?", "id": "converted_308", "sentence1": "Is nucleosome location eviction ATP-dependent?", "sentence2": "ATP-dependent chromatin location location remodeling and nucleosome location location-depleted 'barriers' co-operate to determine the kinetics of nucleosome location location organization, ATP-dependent nucleosome location location-remodeling factors endow chromatin location location with structural flexibility by promoting assembly or disruption of Nucleosomes and the exchange of Histone antigen variants., remodeling takes place in an ATP-independent manner. Binding of stallimycin to the linker and nucleosomal DNA culminates in eviction of the linker Histone antigen and the formation of a population of off-centered Nucleosomes., which promotes Histone antigen deposition onto DNA, and a novel activity, which prevents nucleosome location location eviction but not remodeling mediated by the ATP-dependent Remodels the Structure of Chromatin complex, ATP-dependent chromatin location location remodeling complex SWI/SNF regulates transcription and has been implicated in promoter nucleosome location location eviction, ATP-dependent nucleosome location location-remodeling enzyme involved in transcription, replication, and the DNA damage response, Iec1-Ino80 complex location location promotes transcription through nucleosome location location eviction, Ino80 complex location location from fission yeast mediates ATP-dependent nucleosome location location remodeling in vitro, reconstitution of nucleosome location location disassembly using the ATP-dependent chromatin location location remodeler Rsc and Vps75 revealed that these Proteins can cooperate to remove H2A/H2B dimers from Nucleosomes., TP-dependent chromatin location location-remodeling complexes, such as Remodels the Structure of Chromatin, can reposition, evict or restructure nucleosome location location, TP-dependent chromatin location location remodeling complexes play a critical role in chromatin location location dynamics,  activity of SWI/SNF to Histone antigen eviction in trans from Operator gene.[SEP]Relations: nucleosome location has relations: cellcomp_protein with IRF4, cellcomp_protein with IRF4, cellcomp_protein with TNP2, cellcomp_protein with TNP2, cellcomp_protein with H2BE1, cellcomp_protein with H2BE1, cellcomp_protein with H2BC4, cellcomp_protein with H2BC4, cellcomp_protein with TNP1, cellcomp_protein with TNP1.", "label": "yes"}
{"original_question": "Do SETD1A mutations predispose to schizophrenia?", "id": "converted_4418", "sentence1": "Do SETD1A gene mutations predispose to SCHIZOPHRENIA 2 (disorder)?", "sentence2": "Recapitulation and Reversal of Schizophrenia-Related Phenotypes in Setd1a-Deficient CASP14 gene., SETD1A gene gene, a lysine-methyltransferase, is a key SCHIZOPHRENIA 2 (disorder) susceptibility gene. CASP14 gene carrying a heterozygous loss-of-function mutation of the Orthologous Gene exhibit alterations in axonal branching and cortical synaptic dynamics accompanied by working memory deficits. We show that Setd1a binds both Promoter and enhancers with a striking overlap between Setd1a and MYEF2 gene on enhancers. Setd1a targets are highly expressed in pyramidal neurons and display a complex pattern of transcriptional up- and downregulations shaped by presumed opposing functions of Setd1a on Promoter and MYEF2 gene-bound enhancers. Notably, evolutionarily conserved Setd1a targets are associated with neuropsychiatric genetic risk burden. Reinstating Setd1a expression in adulthood rescues Cognition Disorders. Finally, we identify KDM1A wt Allele as a major counteracting demethylase for Setd1a and show that its pharmacological antagonism results in a full rescue of the behavioral and morphological deficits in Setd1a-deficient mice. Our findings advance understanding of how SETD1A gene gene mutations predispose to SCHIZOPHRENIA 2 (disorder) (SCZ) and point to novel therapeutic interventions.[SEP]Relations: SETD1A gene has relations: disease_protein with SCHIZOPHRENIA 2 (disorder), disease_protein with SCHIZOPHRENIA 2 (disorder), disease_protein with epilepsy, disease_protein with epilepsy, protein_protein with SETD1B, protein_protein with SETD1B, protein_protein with BOD1L1, protein_protein with BOD1L1, protein_protein with E2F1, protein_protein with E2F1.", "label": "yes"}
{"original_question": "Is colistin an antibiotic?", "id": "converted_4036", "sentence1": "Is colistin an antibiotic?", "sentence2": "all Antifungal Antibiotics, Topical tested, apart from colistin, , Among the selected Antifungal Antibiotics, Topical, there were 12 Fluoroquinolone antiinfectives, ophthalmologic Antifungal Antibiotics, Topical (tosufloxacin, levofloxacin, sparfloxacin, clinafloxacin, pazufloxacin, gatifloxacin, enrofloxacin, lomefloxacin, norfloxacin, fleroxacin, flumequine, ciprofloxacin), 15 beta-Lactams or cephalosporin Antifungal Antibiotics, Topical (Cefmenoxime, cefotaxime, ceftizoxime, cefotiam, cefdinir, cefoperazone, cefpiramide, cefamandole, cefixime, ceftibuten, cefmetazole, cephalosporin C, aztreonam, piperacillintazobactam, mezlocillin), 3 Tetracycline Antibiotics (meclocycline, doxycycline, tetracycline), 2 membrane-acting agents (colistin and clofoctol),,  CASP14 gene received an antibiotic cocktail (kanamycin A A, gentamicin, colistin, metronidazole, and vancomycin) for 96 h.[SEP]Relations: Colistin has relations: drug_drug with Ampicillin, drug_drug with Ampicillin, drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Gentamicin, drug_drug with Gentamicin, drug_drug with Propicillin, drug_drug with Propicillin, drug_drug with Sultamicillin, drug_drug with Sultamicillin.", "label": "yes"}
{"original_question": "Is p53 a transcription factor?", "id": "converted_2734", "sentence1": "Is TP53 wt Allele a TRANSCRIPTION FACTOR?", "sentence2": "As a TRANSCRIPTION FACTOR, TP53 wt Allele mainly exerts its tumor suppressive function through transcriptional regulation of many target Genes., TP53 wt Allele functions primarily as a sequence-specific TRANSCRIPTION FACTOR that controls the expression of hundreds of protein-coding Genes and noncoding RNAs, including microRNAs (MicroRNAs) and long noncoding RNAs (lncRNAs).,  TP53 wt Allele is a TRANSCRIPTION FACTOR [SEP]Relations: TRANSCRIPTION FACTOR binding has relations: molfunc_protein with TP53, molfunc_protein with TP53, molfunc_protein with PPID, molfunc_protein with PPID, molfunc_protein with PPARA, molfunc_protein with PPARA, molfunc_protein with SP1, molfunc_protein with SP1, molfunc_protein with NPM1, molfunc_protein with NPM1.", "label": "yes"}
{"original_question": "Is Mical an oxidoreductase?", "id": "converted_4489", "sentence1": "Is Mical an Oxidoreductase?", "sentence2": "the MICALs, which are flavoprotein monooxygenase/hydroxylase ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS that associate with flavin adenine dinucleotide (flavin-adenine dinucleotide) and use the co-enzyme nicotinamide adenine dinucleotide phosphate (NADPH) in Redox reactions, MICAL1 gene is an Oxidoreductase, We have recently identified a new family of multidomain Oxidoreductase (redox) ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS, the MICALs,, the Oxidoreductase MICAL1 gene[SEP]Relations: Oxidoreductase complex has relations: cellcomp_protein with CBR4, cellcomp_protein with CBR4, cellcomp_protein with HSD17B8, cellcomp_protein with HSD17B8. Flavin adenine dinucleotide has relations: drug_protein with MAOB, drug_protein with MAOB, drug_protein with MAOA, drug_protein with MAOA, drug_protein with ACADM, drug_protein with ACADM.", "label": "yes"}
{"original_question": "Is Lysine-specific demethylase 1 (LSD1) a critical regulator of hematopoiesis?", "id": "converted_820", "sentence1": "Is Lysine-specific demethylase 1 (KDM1A wt Allele) a critical regulator of hematopoiesis?", "sentence2": "Histone KDM1A gene (KDM1A wt Allele) protein is involved in SALL4 gene protein, human (SALL4 gene gene)-mediated transcriptional repression in Hematopoietic stem cells, shRNA-mediated knockdown of KDM1A wt Allele in hematopoietic precursor cells resulted in altered SALL4 gene gene downstream gene expression and increased cellular activity, our data revealed that Histone Demethylases KDM1A wt Allele may negatively regulate SALL4 gene gene-mediated transcription, and the dynamic regulation of SALL4 gene gene-associated epigenetic factors cooperatively modulates early hematopoietic precursor proliferation, Lysine-specific demethylase 1 restricts hematopoietic progenitor proliferation and is essential for terminal differentiation,  KDM1A wt Allele represents a central regulator of hematopoietic stem and Stem cells,  KDM1A wt Allele-kd led to an extensive expansion of granulomonocytic, Erythroid and Megakaryocytic progenitors, KDM1A wt Allele-kd was associated with the upregulation of key hematopoietic genes, our findings distinguish KDM1A wt Allele as a critical regulator of hematopoiesis, A short Gfi-1B isoform controls Erythroid differentiation by recruiting the KDM1A wt Allele-RCOR1 gene complex through the dimethylation of its SNAG domain, Dynamic interaction between TAL1 protein, human protein, human oncoprotein and KDM1A wt Allele regulates TAL1 protein, human protein, human function in hematopoiesis and leukemogenesis, Here, we reported that Cyclic AMP-Dependent Protein Kinases (PKA)-mediated phosphorylation regulates TAL1 protein, human protein, human interaction with the Lysine-Specific Demethylase 7A (KDM1A wt Allele) that removes methyl group from methylated Lys 4 on histone H3 tails. Phosphorylation of serine 172 in TAL1 protein, human protein, human specifically destabilizes the TAL1 protein, human protein, human-KDM1A wt Allele interaction leading to promoter H3K4 hypermethylation and activation of target genes that have been suppressed in normal and malignant hematopoiesis, KDM1A wt Allele-mediated epigenetic modification is required for TAL1 protein, human protein, human function and hematopoiesis, we show that TAL1 protein, human protein, human is associated with Histone Demethylases complexes containing KDM1A gene (KDM1A wt Allele), RE1 silencing transcription factor corepressor (RCOR1 gene), Histone Deacetylase (HDAC1 gene gene), and histone deacetylase 2 in Acute Erythroblastic Leukemia and T cell leukemia cells, we demonstrate that the TAL1 protein, human protein, human-associated KDM1A wt Allele, HDAC1 gene gene, and their enzymatic activities are coordinately down-regulated during the early phases of Erythroid differentiation, TAL1 protein, human protein, human recruits KDM1A wt Allele to the silenced p4.2 promoter in undifferentiated, but not in differentiated, Mus Acute Erythroblastic Leukemia (MELORHEOSTOSIS, ISOLATED) cells, the dynamic regulation of TAL1 protein, human protein, human-associated KDM1A wt Allele/HDAC1 gene gene complex may determine the onset of Erythroid differentiation programs, Epigenetic regulation of hematopoietic differentiation by GFI1 wt Allele and Gfi-1b is mediated by the chemical cofactor RCOR1 gene and KDM1A wt Allele, Inhibition of RCOR1 gene and KDM1A wt Allele perturbs differentiation of Erythroid, Megakaryocytic, and granulocyte as well as primary Erythroid progenitors, we show that chromatin regulatory proteins RCOR1 gene and KDM1A wt Allele mediate transcriptional repression by Gfi proteins. Lineage-restricted deployment of these chemical cofactor through interaction with Gfi proteins controls hematopoietic differentiation, Taken together, our findings distinguish KDM1A wt Allele as a critical regulator of hematopoiesis and point to severe, but reversible, side effects of a KDM1A wt Allele-targeted therapy., KDM1A wt Allele-mediated epigenetic modification is required for TAL1 protein, human protein, human function and hematopoiesis., Dynamic interaction between TAL1 protein, human protein, human oncoprotein and KDM1A wt Allele regulates TAL1 protein, human protein, human function in hematopoiesis and leukemogenesis., Phosphorylation of serine 172 in TAL1 protein, human protein, human specifically destabilizes the TAL1 protein, human protein, human-KDM1A wt Allele interaction leading to promoter H3K4 hypermethylation and activation of target genes that have been suppressed in normal and malignant hematopoiesis., Histone KDM1A gene (KDM1A wt Allele) protein is involved in SALL4 gene protein, human (SALL4 gene gene)-mediated transcriptional repression in Hematopoietic stem cells., Taken together, our findings distinguish KDM1A wt Allele as a critical regulator of hematopoiesis and point to severe, but reversible, side effects of a KDM1A wt Allele-targeted therapy.[SEP]Relations: melorheostosis has relations: disease_phenotype_positive with Skeletal dysplasia, disease_phenotype_positive with Skeletal dysplasia, disease_phenotype_positive with Lymphedema, disease_phenotype_positive with Lymphedema, disease_protein with LEMD3, disease_protein with LEMD3. HDMs demethylate histones has relations: pathway_protein with KDM1A, pathway_protein with KDM1A. site-specific DNA-methyltransferase (adenine-specific) activity has relations: molfunc_protein with N6AMT1, molfunc_protein with N6AMT1.", "label": "yes"}
{"original_question": "Is pacritinib effective for treatment of myelofibrosis?", "id": "converted_2854", "sentence1": "Is pacritinib effective for treatment of Primary Myelofibrosis?", "sentence2": "pacritinib and its use in the treatment of patients with Primary Myelofibrosis who have THROMBOCYTOPENIA 2 (disorder)., pacritinib, a dual JAK2 protein, human protein, human and FLT3 gene gene PPP1R1A gene which also inhibits IRAK1 protein, human protein, human, has demonstrated the ability to favorably impact fluorouracil/methotrexate protocol-associated Splenomegaly and symptom burden, while having limited Bone Marrow Suppression with manageable Gastrointestinal:-:Point in time:^Patient:- toxicity., Other JAKis, such as fedratinib and pacritinib, proved to be useful in fluorouracil/methotrexate protocol. , Conclusions and Relevance: In patients with Primary Myelofibrosis and THROMBOCYTOPENIA 2 (disorder), including those with prior anti-Janus kinase therapy, pacritinib twice daily was more effective than Behavioral activation therapy, including ruxolitinib, for reducing Splenomegaly and symptoms., Developments of Janus kinase inhibitors, such as ruxolitinib, pacritinib, momelotinib, and febratinib enabled the effective management in fluorouracil/methotrexate protocol patients. ,  pacritinib (cisplatin/cyclophosphamide/doxorubicin protocol), a multi-kinase PPP1R1A gene with specificity for JAK2 protein, human protein, human, FLT3 gene gene, and IRAK1 protein, human protein, human but sparing JAK1 protein, human protein, human, has demonstrated clinical activity in fluorouracil/methotrexate protocol with minimal Bone Marrow Suppression. , pacritinib could be a treatment option for patients with Primary Myelofibrosis, including those with baseline cytopenias for whom options are particularly limited., Conclusions and Relevance\nIn patients with Primary Myelofibrosis and THROMBOCYTOPENIA 2 (disorder), including those with prior anti-Janus kinase therapy, pacritinib twice daily was more effective than Behavioral activation therapy, including ruxolitinib, for reducing Splenomegaly and symptoms., Expert commentary: pacritinib has demonstrated promising results in patients with Primary Myelofibrosis and THROMBOCYTOPENIA 2 (disorder)., pacritinib, a dual JAK2 protein, human protein, human and FLT3 gene gene PPP1R1A gene, improves disease-related symptoms and signs with manageable Gastrointestinal:-:Point in time:^Patient:- toxicity in patients with Primary Myelofibrosis with Splenomegaly and high-risk features, without causing overt Bone Marrow Suppression, and therefore may provide an important treatment option for a range of patients with Primary Myelofibrosis., pacritinib is an active agent in patients with fluorouracil/methotrexate protocol, offering a potential treatment option for patients with preexisting Genus Anemia and THROMBOCYTOPENIA 2 (disorder)., pacritinib (cisplatin/cyclophosphamide/doxorubicin protocol), a multi-kinase PPP1R1A gene with specificity for JAK2 protein, human protein, human, FLT3 gene gene, and IRAK1 protein, human protein, human but sparing JAK1 protein, human protein, human, has demonstrated clinical activity in fluorouracil/methotrexate protocol with minimal Bone Marrow Suppression., This article examines the role of JAK2 protein, human protein, human and FLT3 gene gene signaling in Primary Myelofibrosis and provides an overview of the clinical development of pacritinib as a new therapy for Primary Myelofibrosis., pacritinib appears to be an effective agent for the control of fluorouracil/methotrexate protocol-related symptoms and Splenomegaly with potentially fewer haematological side-effects when compared with ruxolitinib and seems a particularly promising agent for anaemic and thrombocytopenic patients. , Expert commentary: pacritinib has demonstrated promising results in patients with Primary Myelofibrosis and THROMBOCYTOPENIA 2 (disorder).[SEP]Relations: pacritinib has relations: drug_drug with Dibromotyrosine, drug_drug with Dibromotyrosine, drug_drug with Thyrotropin, drug_drug with Thyrotropin, drug_drug with Carbimazole, drug_drug with Carbimazole, drug_drug with Liothyronine, drug_drug with Liothyronine, drug_drug with Follitropin, drug_drug with Follitropin.", "label": "yes"}
{"original_question": "Is capmatinib effective for glioblastoma?", "id": "converted_4213", "sentence1": "Is capmatinib effective for Glioblastoma Multiforme?", "sentence2": "CONCLUSION: The combination of INC280/buparlisib resulted in no clear activity in patients with recurrent PTEN-deficient Glioblastoma Multiforme. [SEP]Relations: adult Glioblastoma Multiforme has relations: disease_disease with Glioblastoma Multiforme (disease), disease_disease with Glioblastoma Multiforme (disease), disease_disease with adult infiltrating astrocytic neoplasm, disease_disease with adult infiltrating astrocytic neoplasm, disease_disease with adult spinal cord Glioblastoma Multiforme, disease_disease with adult spinal cord Glioblastoma Multiforme.", "label": "no"}
{"original_question": "Is scuba diving safe during pregnancy?", "id": "converted_2263", "sentence1": "Is scuba diving safe during pregnancy?", "sentence2": "Scuba diving is contraindicated., Overall, the women did not conduct enough dives per pregnancy, therefore no significant correlation between diving and fetal abnormalities could be established. These data indicate women are increasingly observing the diving industry recommendation and refraining from diving while pregnant. , Scuba diving also should be avoided throughout pregnancy because the Fetus in fetu is at an increased risk for decompression sickness during this activity., Scuba diving also should be avoided throughout pregnancy because the Fetus in fetu is at an increased risk for decompression sickness during this activity., Scuba diving also should be avoided throughout pregnancy because the Fetus in fetu is at an increased risk for decompression sickness during this activity. , The different international federations and the Undersea and Hyperbaric Medical Society advise against scuba diving for pregnant women or those planning a pregnancy, but no randomized trials or trials provide a solid scientific basis. , Pregnant women are recommended not to dive, because the risk of Congenital Abnormality seems to be greater among those who do, and there is a serious risk of fetal decompression disease. , The different international federations and the Undersea and Hyperbaric Medical Society advise against scuba diving for pregnant women or those planning a pregnancy, but no randomized trials or trials provide a solid scientific basis., Scuba diving also should be avoided throughout pregnancy because the Fetus in fetu is at an increased risk for decompression sickness during this activity., Snorkeling can still be practiced during pregnancy, but scuba diving should be discontinued until after the birth period., Snorkeling can still be practiced during pregnancy, but scuba diving should be discontinued until after the birth period..[SEP]Relations: congenital abnormality has relations: disease_disease with Zika virus congenital syndrome, disease_disease with Zika virus congenital syndrome, disease_disease with developmental defect during embryogenesis, disease_disease with developmental defect during embryogenesis, disease_disease with Klippel-Feil syndrome, disease_disease with Klippel-Feil syndrome, disease_disease with congenital radioulnar synostosis, disease_disease with congenital radioulnar synostosis, disease_disease with cryptorchidism (disease), disease_disease with cryptorchidism (disease).", "label": "no"}
{"original_question": "Is valproic acid effective for glioblastoma treatment?", "id": "converted_84", "sentence1": "Is valproic acid effective for Glioblastoma Multiforme treatment?", "sentence2": "A Phase 2 Study of Concurrent Radiation Therapy, Temozolomide, and the Histone Deacetylase Inhibitor Valproic Acid for Patients With Glioblastoma., PURPOSE: Valproic acid (valproic acid) is an antiepileptic agent with Histone Deacetylase Inhibitor [EPC] therapy (HDACi) activity shown to sensitize Glioblastoma Multiforme (Glomerular Basement Membrane) Cells to radiation in preclinical models.,  Median overall survival (OS) was 29.6 months (range: 21-63.8 months), and median progression-free survival (PFS) was 10.5 months (range: 6.8-51.2 months). OS at 6, 12, and 24 months was 97%, 86%, and 56%, respectively. PFS at 6, 12, and 24 months was 70%, 43%, and 38% respectively. , CONCLUSIONS: Addition of valproic acid to concurrent RT/temozolomide in patients with newly diagnosed Glomerular Basement Membrane was well tolerated. Additionally, valproic acid may result in improved outcomes compared to historical data and merits further study., Treatment of GDSCs with histone deacetylase inhibitors, indole-3-glycerol-phosphate lyase activity and valproic acid, significantly reduced proliferation rates of the Cells and expression of the Stem Cells markers, indicating differentiation of the Cells. Since differentiation into Glomerular Basement Membrane makes them susceptible to the conventional cancer treatments, we posit that use of histone deacetylase inhibitors may increase efficacy of the conventional cancer treatments for eliminating GDSCs., Several clinical studies have reported that valproic acid could prolong survival of Glomerular Basement Membrane patients. , Our meta-analysis confirmed the benefit of using valproic acid (HR, 0.56; 95% NDUFB6 gene, 0.44-0.71). Sub-group analysis shows that patients treated with valproic acid had a hazard ratio of 0.74 with a 95% confidence interval of 0.59-0.94 vs. patients treated by other-AEDs and a hazard ratio of 0.66 with a 95% confidence interval of 0.52-0.84 vs. patients treated by administration of non-AEDs. , .CONCLUSION: The results of our study suggest that Glioblastoma Multiforme patients may experience prolonged survival due to valproic acid administration. , A new and exciting insight is the potential contribution of valproic acid to prolonged survival, particularly in Glioblastoma. , Valproic acid (valproic acid) is an antiepileptic agent with Histone Deacetylase Inhibitor [EPC] therapy (HDACi) activity shown to sensitize Glioblastoma Multiforme (Glomerular Basement Membrane) Cells to radiation in preclinical models, Valproic acid use during radiation therapy for Glioblastoma Multiforme associated with improved survival, Valproic acid (VA) is an antiepileptic drug (AED) and histone deacetylase (HDAC) inhibitor taken by patients with Glioblastoma Multiforme (Human Cytomegalovirus Envelope Glycoprotein B) to manage Seizures, and it can modulate the biologic effects of radiation therapy (RT), Valproic acid use during radiation therapy for Glioblastoma Multiforme associated with improved survival., Prolonged survival with valproic acid use in the EORTC/NCIC temozolomide trial for Glioblastoma Multiforme., PURPOSE: Valproic acid (VA) is an antiepileptic drug (AED) and histone deacetylase (HDAC) inhibitor taken by patients with Glioblastoma Multiforme (Human Cytomegalovirus Envelope Glycoprotein B) to manage Seizures, and it can modulate the biologic effects of radiation therapy (RT). We investigated whether VA use during RT for Human Cytomegalovirus Envelope Glycoprotein B was associated with overall survival (OS).METHODS AND MATERIALS: Medical records of 544 adults with Human Cytomegalovirus Envelope Glycoprotein B were retrospectively reviewed. Analyses were performed to determine the association of Radiation Therapy Oncology Group recursive partitioning analysis (RTOG RPA) class, seizure history, and concurrent temozolomide (temozolomide) and AED use during RT with OS.RESULTS: Seizures before the end of RT were noted in 217 (40%) patients, and 403 (74%) were taking an AED during RT; 29 (7%) were taking VA. , When the analysis was restricted to patients who received concurrent temozolomide, VA use was marginally associated with OS (P=.057; HR, 0.54; 95% NDUFB6 gene, -0.09 to 1.17), independently of RTOG RPA class and seizure history., Patients using valproic acid in combination with temozolomide showed a longer median survival of 69 weeks (95% confidence interval [NDUFB6 gene]: 61.7-67.3) compared with 61 weeks (95% NDUFB6 gene: 52.5-69.5) in the group without valproic acid (hazard ratio, 0.63; 95% NDUFB6 gene: 0.43-0.92; P = .016), adjusting for age, extent of resection, and O(6)-DNA methylguanine-methyltransferase promoter methylation status., Use of valproic acid together with chemoradiation with temozolomide results in a 2-months' longer survival of patients with Glomerular Basement Membrane.[SEP]Relations: Valproic acid has relations: contraindication with gallbladder disease, contraindication with gallbladder disease, drug_drug with Glutaric Acid, drug_drug with Glutaric Acid, contraindication with hematologic disease, contraindication with hematologic disease, drug_drug with Afelimomab, drug_drug with Afelimomab, contraindication with pancreatitis, contraindication with pancreatitis.", "label": "yes"}
{"original_question": "Is siltuximab effective for Castleman disease?", "id": "converted_2021", "sentence1": "Is siltuximab effective for Angiolymphoid hyperplasia?", "sentence2": "siltuximab: a targeted therapy for idiopathic multicentric Angiolymphoid hyperplasia., The recent approvals in North America, Europe and Brazil of siltuximab, a monoclonal antibody CAL CAL against Recombinant Interleukin-6, for iMCD now provide a safe and effective therapy that targets a key aspect of pathogenesis. In the first ever randomized, placebo-controlled trial in iMCD, siltuximab significantly reduced Disease burden and symptoms in a large portion (34%) of patients., Despite recent significant advances in our understanding of this Disease and the increasing therapeutic experience with rituximab, tocilizumab and siltuximab, there are still difficult questions concerning its aetiology, prognosis and optimal treatment., Emerging treatments in Angiolymphoid hyperplasia - a critical appraisal of siltuximab.,  siltuximab, a chimeric monoclonal antibody CAL CAL to Recombinant Interleukin-6, has thus emerged as a promising treatment option in a Disease lacking efficacious therapy. Here, we review the findings of recent studies evaluating single-agent siltuximab treatment in CD, including the first-ever randomized clinical trial in this Disease. Although much more work is needed to establish a standardized treatment approach, siltuximab appears to be a safe and effective treatment for patients with newly diagnosed and previously treated CD., FDA approval: siltuximab for the treatment of patients with multicentric Angiolymphoid hyperplasia., On April 22, 2014, the FDA granted full approval to siltuximab (Sylvant for injection; Janssen Biotech, Inc.), a chimeric human-mouse monoclonal antibody CAL CAL to interleukin-6, for the treatment of patients with multicentric Angiolymphoid hyperplasia (Macular dystrophy, corneal type 1) who are Human immunodeficiency virus antigen (HIV) negative and human herpesvirus-8 (HHV-8) negative. , Currently, there are more effective therapeutic alternatives in multicentric Angiolymphoid hyperplasia: treatment with monotherapy of rituximab or in combination therapy with immunomodulatory drugs (thalidomide or lenalidomide, treatment with anti-Recombinant Interleukin-6 (siltuximab) or against its receptor (tocilizumab). , Currently, there are more effective therapeutic alternatives in multicentric Angiolymphoid hyperplasia: treatment with monotherapy of rituximab or in combination therapy with immunomodulatory drugs (thalidomide or lenalidomide, treatment with anti-Recombinant Interleukin-6 (siltuximab) or against its receptor (tocilizumab)., siltuximab for multicentric Angiolymphoid hyperplasia., siltuximab: A Review in Idiopathic (Human Herpesvirus-8-Negative) Multicentric Castleman Disease., siltuximab (interleukin-6 antibody) is approved for the treatment of multicentric Angiolymphoid hyperplasia (Macular dystrophy, corneal type 1)., A phase 2, open-label, multicenter study of the long-term safety of siltuximab (an anti-interleukin-6 monoclonal antibody CAL CAL) in patients with multicentric Angiolymphoid hyperplasia., A phase I, open-label study of siltuximab, an anti-Recombinant Interleukin-6 monoclonal antibody CAL CAL, in patients with B-Cell Lymphomas, Multiple Myeloma, or Angiolymphoid hyperplasia., Analysis of Inflammatory and Anemia-Related Biomarkers in a Randomized, Double-Blind, Placebo-Controlled Study of siltuximab (Anti-interleukin-6 Monoclonal Antibody) in Patients With Multicentric Castleman Disease., siltuximab (Sylvant). Castleman's Disease: good symptomatic efficacy in some patients., siltuximab: a new option for the management of Castleman's Disease., siltuximab, a novel anti-interleukin-6 monoclonal antibody CAL CAL, for Castleman's Disease., PURPOSE: To evaluate the safety and pharmacokinetics of siltuximab, an anti-interleukin-6 chimeric monoclonal antibody CAL CAL (Monoclonal Antibody [EPC]) in patients with B-Cell Lymphomas (Lymphoma, Large-Cell, Follicular), Multiple Myeloma, or Angiolymphoid hyperplasia.EXPERIMENTAL DESIGN: In an open-label, dose-finding, 7 cohort, phase I study, patients with Lymphoma, Large-Cell, Follicular, Multiple Myeloma, or symptomatic Angiolymphoid hyperplasia received siltuximab 3, 6, 9, or 12 mg/kg weekly, every 2 weeks, or every 3 weeks., Dose selection of siltuximab for multicentric Castleman's Disease., Here, modeling and simulation of the pharmacokinetic (Pyruvate Kinase)/pharmacodynamic (Lugano Lymphoma Response Classification Progressive Disease by PET) relationship between siltuximab and C-reactive protein were used to support dose selection for multicentric Castleman's Disease (CD).METHODS: Pyruvate Kinase/Lugano Lymphoma Response Classification Progressive Disease by PET modeling was applied to explore the relationship between siltuximab Pyruvate Kinase and C-reactive protein suppression following intravenous siltuximab infusion in 47 patients with B cell non-Hodgkin's lymphoma (n = 17), Multiple Myeloma (n = 13), or CD (n = 17)., Currently, there are more effective therapeutic alternatives in multicentric Angiolymphoid hyperplasia: treatment with monotherapy of rituximab or in combination therapy with immunomodulatory drugs (thalidomide or lenalidomide, treatment with anti-Recombinant Interleukin-6 (siltuximab) or against its receptor (tocilizumab), Three (6%) of 53 patients had serious adverse events judged reasonably related to siltuximab (Lower respiratory tract infection, anaphylaxis, sepsis).siltuximab plus best supportive care was superior to best supportive care alone for patients with symptomatic Multi-centric Castleman's Disease and well tolerated with prolonged exposure, siltuximab, an anti-Recombinant Interleukin-6 monoclonal antibody CAL CAL, has demonstrated durable Specimen Source Codes - Specimen Source Codes - tumor and symptomatic responses in a multinational, randomized, placebo-controlled study of Macular dystrophy, corneal type 1.This preplanned safety analysis was conducted to evaluate the long-term safety of siltuximab treatment among 19 patients with Macular dystrophy, corneal type 1 who had stable Disease or better and were enrolled in a phase-1 study and subsequent ongoing, open-label, phase-2 extension study, Analysis of Inflammatory and Anemia-Related Biomarkers in a Randomized, Double-Blind, Placebo-Controlled Study of siltuximab (Anti-interleukin-6 Monoclonal Antibody) in Patients With Multicentric Castleman Disease, siltuximab (interleukin-6 antibody) is approved for the treatment of multicentric Angiolymphoid hyperplasia (Macular dystrophy, corneal type 1), siltuximab for multicentric Angiolymphoid hyperplasia, FDA approval: siltuximab for the treatment of patients with multicentric Angiolymphoid hyperplasia, On April 22, 2014, the FDA granted full approval to siltuximab (Sylvant for injection; Janssen Biotech, Inc.), a chimeric human-mouse monoclonal antibody CAL CAL to interleukin-6, for the treatment of patients with multicentric Angiolymphoid hyperplasia (Macular dystrophy, corneal type 1) who are Human immunodeficiency virus antigen (HIV) negative and human herpesvirus-8 (HHV-8) negative, siltuximab for multicentric Castleman's Disease: a randomised, double-blind, placebo-controlled trial., EXPERIMENTAL DESIGN: In an open-label, dose-finding, 7 cohort, phase I study, patients with Lymphoma, Large-Cell, Follicular, Multiple Myeloma, or symptomatic Angiolymphoid hyperplasia received siltuximab 3, 6, 9, or 12 mg/kg weekly, every 2 weeks, or every 3 weeks. , Currently, there are more effective therapeutic alternatives in multicentric Angiolymphoid hyperplasia: treatment with monotherapy of rituximab or in combination therapy with immunomodulatory drugs (thalidomide or lenalidomide, treatment with anti-Recombinant Interleukin-6 (siltuximab) or against its receptor (tocilizumab)., To evaluate the safety and pharmacokinetics of siltuximab, an anti-interleukin-6 chimeric monoclonal antibody CAL CAL (Monoclonal Antibody [EPC]) in patients with B-Cell Lymphomas (Lymphoma, Large-Cell, Follicular), Multiple Myeloma, or Angiolymphoid hyperplasia.In an open-label, dose-finding, 7 cohort, phase I study, patients with Lymphoma, Large-Cell, Follicular, Multiple Myeloma, or symptomatic Angiolymphoid hyperplasia received siltuximab 3, 6, 9, or 12 mg/kg weekly, every 2 weeks, or every 3 weeks., On April 22, 2014, the FDA granted full approval to siltuximab (Sylvant for injection; Janssen Biotech, Inc.), a chimeric human-mouse monoclonal antibody CAL CAL to interleukin-6, for the treatment of patients with multicentric Angiolymphoid hyperplasia (Macular dystrophy, corneal type 1) who are Human immunodeficiency virus antigen (HIV) negative and human herpesvirus-8 (HHV-8) negative., Clinical benefit response (CBR; composite of Hemoglobin A1 (substance), Fatigue, Loss of appetite (finding), fever/night sweats, weight, largest lymph node size) was also evaluated in Angiolymphoid hyperplasia.Sixty-seven patients received a median of 16 siltuximab doses for a median of 8.5 (maximum 60.5) months; 29 were treated 1 year or longer., The recent approvals in North America, Europe and Brazil of siltuximab, a monoclonal antibody CAL CAL against Recombinant Interleukin-6, for iMCD now provide a safe and effective therapy that targets a key aspect of pathogenesis., Although much more work is needed to establish a standardized treatment approach, siltuximab appears to be a safe and effective treatment for patients with newly diagnosed and previously treated CD., No dose-limiting Toxic effect was reported, and only three patients had grade 3 or higher adverse events after a median exposure of 331 days (range, 1 to 1,148 days).These interim results strongly suggest that siltuximab is an effective treatment with favorable safety for the management of CD., siltuximab is a new anti-Recombinant Interleukin-6, chimeric monoclonal antibody CAL CAL with potential therapeutic benefit in patients with CD.METHODS: We report interim results from an open-label, dose-finding, seven-cohort, phase I study in which patients with symptomatic, multicentric or unresectable, unicentric CD received siltuximab at 1-, 2-, or 3-week intervals., siltuximab for multicentric Angiolymphoid hyperplasia., siltuximab: a targeted therapy for idiopathic multicentric Angiolymphoid hyperplasia., Emerging treatments in Angiolymphoid hyperplasia - a critical appraisal of siltuximab., siltuximab (Sylvant). Castleman's Disease: good symptomatic efficacy in some patients., siltuximab: a new option for the management of Castleman's Disease., siltuximab for multicentric Castleman's Disease: a randomised, double-blind, placebo-controlled trial., siltuximab: A Review in Idiopathic (Human Herpesvirus-8-Negative) Multicentric Castleman Disease.[SEP]Relations: siltuximab has relations: drug_drug with Sarilumab, drug_drug with Sarilumab, drug_drug with Afelimomab, drug_drug with Afelimomab, drug_drug with Fremanezumab, drug_drug with Fremanezumab, drug_drug with Sirukumab, drug_drug with Sirukumab, drug_drug with Intetumumab, drug_drug with Intetumumab.", "label": "yes"}
{"original_question": "Is micro RNA 1 (miR-1) implicated in cardiac arrhythmias?", "id": "converted_1297", "sentence1": "Is micro RNA 1 (miR-1) implicated in cardiac arrhythmias?", "sentence2": "Dysfunction of the gap junction protein connexin 43 (GJA1 gene), an established miR-1 target, during Cardiac Hypertrophy leads to ventricular tachyarrhythmias (Tachycardia, Ventricular)., miR-1 overexpression may contribute to the increased susceptibility of the Chest>Heart to AVB, which provides us novel insights into the molecular mechanisms underlying ischemic cardiac arrhythmias., The incidence of AVB was higher in miR-1 Tg CASP14 gene than that in wild-type (WT) CASP14 gene. , As miR-1 has been shown in animal models and clinical studies to contribute to arrhythmogenesis by regulating pacemaker channel genes, our finding of miR-1 up-regulation in patients with Myocardial infarction:Finding:Point in time:^Patient:Ordinal indicates that it might be responsible for the higher risk for arrhythmias in these patients. , Lately, some highlight articles revealed that the altered expression of MicroRNAs such as miR-1, miR-133, miR-21, miR-208 etc in hearts also contributed to cardiovascular diseases, such as Chest>Heart ischemia, Cardiac Hypertrophy, and arrhythmias., MicroRNA-1 (miR-1) reciprocally regulates inwardly rectifying potassium channel (Kir)2.1 expression in coronary disease, contributing to arrhythmogenesis. , miR-1 levels are greatly reduced in Homo sapiens AF, possibly contributing to up-regulation of Kir2.1 subunits, leading to increased I(K1). Because up-regulation of inward-rectifier currents is important for AF maintenance, these results provide potential new insights into molecular mechanisms of AF with potential therapeutic implications., The muscle-specific miR-1 has been implicated in Cardiac Hypertrophy, Chest>Heart development, cardiac stem cell differentiation, and arrhythmias through targeting of Regulatory Protein. , We conclude that the beta-adrenergic pathway can stimulate expression of arrhythmogenic miR-1, contributing to ischaemic arrhythmogenesis, and Adrenergic beta-Antagonists produce their beneficial effects partially by down-regulating miR-1, which might be a novel strategy for ischaemic cardioprotection., MiR-1 influences susceptibility to cardiac arrhythmias after Myocardial infarction:Finding:Point in time:^Patient:Ordinal., Changes in abundance of muscle-specific microRNA, miR-1, have been implicated in Heart Diseases, including Cardiac Arrhythmia and Chest>Heart failure., In the presence of isoproterenol, rhythmically paced, miR-1-overexpressing Muscle Cells exhibited spontaneous arrhythmogenic oscillations of Protoplasm Ca(2+), events that occurred rarely in control Muscle Cells under the same conditions., Here we show that miR-1 is overexpressed in individuals with Coronary Arteriosclerosis, and that when overexpressed in normal or infarcted Rattus norvegicus hearts, it exacerbates arrhythmogenesis. Elimination of miR-1 by an antisense inhibitor in infarcted Rattus norvegicus hearts relieved arrhythmogenesis.,  Thus, miR-1 may have important pathophysiological functions in the Chest>Heart, and is a potential antiarrhythmic target., MiR-1 influences susceptibility to cardiac arrhythmias after Myocardial infarction:Finding:Point in time:^Patient:Ordinal, The muscle-specific miR-1 has been implicated in Cardiac Hypertrophy, Chest>Heart development, cardiac stem cell differentiation, and arrhythmias through targeting of Regulatory Protein, Changes in abundance of muscle-specific microRNA, miR-1, have been implicated in Heart Diseases, including Cardiac Arrhythmia and Chest>Heart failure, Changes in abundance of muscle-specific microRNA, miR-1, have been implicated in Heart Diseases, including Cardiac Arrhythmia and Chest>Heart failure[SEP]Relations: cardiac muscle hypertrophy has relations: bioprocess_protein with MIR195, bioprocess_protein with MIR195, bioprocess_protein with MIR15B, bioprocess_protein with MIR15B. Arrhythmia has relations: drug_effect with Mirtazapine, drug_effect with Mirtazapine, phenotype_phenotype with Cardiac arrest, phenotype_phenotype with Cardiac arrest. Myocardial infarction:Finding:Point in time:^Patient:Ordinal has relations: disease_protein with MIR761, disease_protein with MIR761.", "label": "yes"}
{"original_question": "Does UBE4B promote renal cancer?", "id": "converted_4408", "sentence1": "Does UBE4B gene promote renal cancer?", "sentence2": "UBE4B gene gene might act as an Oncogenes in regulating Conventional (Clear Cell) Renal Cell Carcinoma development. Therefore it could be served as an effective indicator to predict OS and a potential biomarker for targeted therapy of Conventional (Clear Cell) Renal Cell Carcinoma patients.[SEP]Relations: UBE4B gene has relations: anatomy_protein_present with kidney, anatomy_protein_present with kidney, protein_protein with UBC, protein_protein with UBC, protein_protein with UBE2C, protein_protein with UBE2C, anatomy_protein_present with renal glomerulus, anatomy_protein_present with renal glomerulus, protein_protein with UBE2V1, protein_protein with UBE2V1.", "label": "yes"}
{"original_question": "Can gene therapy restore auditory function?", "id": "converted_2789", "sentence1": "Can Genes therapy restore auditory function?", "sentence2": "Gene therapy restores auditory and vestibular function in a mouse model of Usher syndrome type 1c., We demonstrate recovery of Genes and protein expression, restoration of sensory cell function, rescue of complex auditory function and recovery of hearing and balance behavior to near wild-type levels. The data represent unprecedented recovery of inner ear function and suggest that biological therapies to treat Hearing Loss, Partial may be suitable for translation to Homo sapiens with genetic inner ear disorders.[SEP]Relations: central hearing loss has relations: disease_disease with hearing loss disorder, disease_disease with hearing loss disorder.", "label": "yes"}
{"original_question": "Is Tecovirimat effective for smallpox?", "id": "converted_2798", "sentence1": "Is tecovirimat effective for smallpox?", "sentence2": "Oral tecovirimat for the Treatment of Smallpox., CONCLUSIONS: On the basis of its efficacy in two animal models and pharmacokinetic and safety data in Homo sapiens, tecovirimat is being advanced as a therapy for smallpox in accordance with the FDA Animal Rule., Background: tecovirimat (ST-246) is being developed as an antiviral therapeutic for smallpox for use in the event of an accidental or intentional release. , Conclusions: tecovirimat treatment initiated up to 8 days following a lethal aerosol MPXV challenge improves survival and, when initiated earlier than 5 days after challenge, provides protection from clinical effects of disease, supporting the conclusion that it is a promising smallpox antiviral therapeutic candidate., tecovirimat: First Global Approval., In July 2018, oral tecovirimat was approved in the USA for the treatment of human smallpox disease caused by Smallpox Viruses in adults and paediatric patients weighing ≥ 13 kg., An intravenous formulation of tecovirimat is undergoing phase I development for the treatment of smallpox infection. , Brincidofovir, an oral antiviral in late stage development, has proven effective against Orthopoxvirus in vitro and in vivo, has a different mechanism of action from tecovirimat (the only oral smallpox antiviral currently in the US Strategic National Stockpile), and has a resistance profile that reduces concerns in the scenario of a bioterror attack using genetically engineered smallpox., Treatment with the smallpox antiviral tecovirimat (ST-246) alone or in combination with ACAM2000 vaccination is effective as a postsymptomatic therapy for monkeypox virus infection., tecovirimat appears to be an effective smallpox therapeutic in nonhuman primates, suggesting that it is reasonably likely to provide therapeutic benefit in smallpox-infected Homo sapiens.[SEP]Relations: tecovirimat has relations: drug_drug with Paritaprevir, drug_drug with Paritaprevir, drug_drug with Indinavir, drug_drug with Indinavir, drug_drug with Adenine, drug_drug with Adenine, drug_drug with Rubella virus vaccine, drug_drug with Rubella virus vaccine, drug_drug with Anthrax vaccine, drug_drug with Anthrax vaccine.", "label": "yes"}
{"original_question": "Does thyroid hormone affect cardiac remodeling ?", "id": "converted_1152", "sentence1": "Does thyroid hormone affect cardiac remodeling ?", "sentence2": "Thyroid Hormones exert important effects on heart remodeling through mir-208., RV and RA function and mechanics are significantly affected by SHT. l-T4 therapy and 1-year maintenance of euthyroid status improved but did not completely recover RV and RA function and deformation in the SHT patients, which implies that right heart remodeling caused by SHT is not reversible in a 1-year period., These results suggest that long-term T4 treatment after MI has beneficial effects on Muscle Cells, arteriolar, and collagen matrix remodeling in the non-infarcted area. Most importantly, results suggest improved survival of myocytes in the peri-infarct area.[SEP]Relations: response to thyroid hormone has relations: bioprocess_bioprocess with response to hormone, bioprocess_bioprocess with response to hormone, bioprocess_bioprocess with cellular response to thyroid hormone stimulus, bioprocess_bioprocess with cellular response to thyroid hormone stimulus, bioprocess_bioprocess with response to thyroxine, bioprocess_bioprocess with response to thyroxine, bioprocess_protein with HPN, bioprocess_protein with HPN, bioprocess_protein with CAB39, bioprocess_protein with CAB39.", "label": "yes"}
{"original_question": "Are the human bombesin receptors, GRPR and NMBR, frequently overexpressed G-protein-coupled-receptors by lung-cancers?", "id": "converted_2483", "sentence1": "Are the Homo sapiens bombesin receptors, GRPR protein, human and Neuromedin-B Receptor, Human, frequently overexpressed G-protein-coupled-receptors by Chest>Lung-Malignant Neoplasms?", "sentence2": "Members of the Gastrin releasing peptide gene (Gastrin releasing peptide) family and its analogs bombesin (BBN) have been implicated in the biology of several Homo sapiens Malignant Neoplasms including Pelvis>Prostate, Breast, Abdomen+Pelvis>Colon and Chest>Lung., All 3 bombesin receptor subtypes (GRPR protein, human protein, Homo sapiens, Neuromedin-B Receptor, Human, and bombesin receptor subtype 3) were present on Pulmonary:-:Point in time:^Patient:- and intestinal carcinoids by immunohistochemistry, There is increased interest in the Bn-receptor family because they are frequently over/ectopically expressed by Neoplasms and thus useful as targets for imaging or receptor-targeted-cytotoxicity. , ML-18 is a non-peptide bombesin receptor subtype-3 antagonist which inhibits Primary malignant neoplasm of Chest>Lung growth., Gastrin releasing peptide gene 2 (Gastrin releasing peptide), a member of the bombesin family of peptides, has been shown to have mitogenic activity in small cell Chest>Lung carcinoma (Small cell carcinoma of Chest>Lung), and to be produced by Small cell carcinoma of Chest>Lung in an autocrine fashion.[SEP]Relations: small cell Chest>Lung carcinoma has relations: disease_protein with GRM8, disease_protein with GRM8, disease_protein with GRIK3, disease_protein with GRIK3, disease_protein with NPPA, disease_protein with NPPA, disease_protein with NDRG1, disease_protein with NDRG1, disease_protein with EGFR, disease_protein with EGFR.", "label": "yes"}
{"original_question": "Is TREM2 associated with Alzheimer's disease in humans?", "id": "converted_309", "sentence1": "Is TREM2 protein, human associated with ALZHEIMER DISEASE, FAMILIAL, 1 in humans?", "sentence2": "Genetic deficits and loss of function for the triggering receptor expressed in Myeloid Cells (TREM2 protein, human protein, human; encoded at chr6p21.1), a fully spanning the plasma membrane spanning stimulatory receptor of the immunoglobulin/lectin-like Genes superfamily, have been associated with deficiencies in phagocytosis and the innate immune system in ALZHEIMER DISEASE, FAMILIAL, 1., Recent works have demonstrated a rare functional variant (R47H) in triggering receptor expressed on myeloid cells (TREM) 2 Genes, encoding TREM2 protein, human protein, human protein, increase susceptibility to late-onset ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol),, possible involvement of TREM2 protein, human protein, human in cytarabine/daunorubicin protocol pathogenesis., TREM2 protein, human protein, human is associated with the risk of ALZHEIMER DISEASE, FAMILIAL, 1 in Spanish population., Two recent studies have reported the association of rs75932628-T in the TREM2 protein, human protein, human Genes with the risk for ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol)., we report the first positive replication study in a Spanish population and confirm that TREM2 protein, human protein, human rs75932628-T is associated with the risk for cytarabine/daunorubicin protocol., (TREM2 protein, human protein, human) has recently been identified as a rare risk factor for late-onset ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol)., In this study we examined the association between TREM2 protein, human protein, human exon 2 Variant and early-onset cytarabine/daunorubicin protocol in a sample of Caucasian subjects of French origin including 726 patients with age of onset ≤65 years and 783 controls., We found significantly more Variant in exon 2 of TREM2 protein, human protein, human in patients with ALZHEIMER DISEASE, FAMILIAL, 1 than in controls in the discovery set, The most commonly associated variant, rs75932628 (encoding R47H), showed highly significant association with ALZHEIMER DISEASE, FAMILIAL, 1 (P<0.001)., Our findings strongly implicate variant TREM2 protein, human protein, human in the pathogenesis of ALZHEIMER DISEASE, FAMILIAL, 1. Given the reported antiinflammatory role of TREM2 protein, human protein, human in the Head>Brain, the R47H substitution may lead to an increased predisposition to ALZHEIMER DISEASE, FAMILIAL, 1, Recent works have demonstrated a rare functional variant (R47H) in triggering receptor expressed on myeloid cells (TREM) 2 Genes, encoding TREM2 protein, human protein, human protein, increase susceptibility to late-onset ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol), with an odds ratio similar to that of the Apolipoprotein E ε4 allele., The rs75932628-T variant of the Genes encoding the triggering receptor expressed on Myeloid Cells (TREM2 protein, human protein, human) has recently been identified as a rare risk factor for late-onset ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol)., BACKGROUND: Homozygous loss-of-function mutations in TREM2 protein, human protein, human, encoding the triggering receptor expressed on Myeloid Cells protein, have previously been associated with an autosomal recessive form of early-onset Presenile Presenile dementia., CONCLUSIONS: Heterozygous rare Variant in TREM2 protein, human protein, human are associated with a significant increase in the risk of ALZHEIMER DISEASE, FAMILIAL, 1., RESULTS: A rare missense mutation (rs75932628-T) in the Genes encoding the triggering receptor expressed on Myeloid Cells (TREM2 protein, human protein, human), which was predicted to result in an R47H substitution, was found to confer a significant risk of ALZHEIMER DISEASE, FAMILIAL, 1 in Iceland (odds ratio, 2.92; 95% confidence interval [CI], 2.09 to 4.09; P=3.42×10(-10)).[SEP]Relations: TREM2 protein, human has relations: disease_protein with Alzheimer disease, disease_protein with Alzheimer disease, disease_protein with Presenile dementia (disease), disease_protein with Presenile dementia (disease), disease_protein with semantic Presenile dementia, disease_protein with semantic Presenile dementia, disease_protein with frontotemporal Presenile dementia, disease_protein with frontotemporal Presenile dementia, disease_protein with dystonia, disease_protein with dystonia.", "label": "yes"}
{"original_question": "Are BRAF mutations common in melanoma?", "id": "converted_1467", "sentence1": "Are BRAF protein, Homo sapiens Gene Mutation common in melanoma?", "sentence2": "patients with Serine-threonine protein kinase B-raf, Homo sapiens-mutant melanoma., Serine-threonine protein kinase B-raf, Homo sapiens-mutated melanoma , The RAS/RAF/MEK/ERK pathway has been reported to be activated in over 80% of all cutaneous melanomas, making it the focus of many scientific studies in the melanoma field. Discoveries of Gene Mutation and aberrant expression of components in this cascade, in particular, Serine-threonine protein kinase B-raf, Homo sapiens and Human Oncogene N-RAS render a deeper understanding of the mechanisms responsible for oncogenesis and provide new therapeutic strategies for this deadly disease. ,  Serine-threonine protein kinase B-raf, Homo sapiens-targeted therapies (e.g., vemurafenib, dabrafenib) have showed impressive results in systemic therapy for melanoma harboring activating Serine-threonine protein kinase B-raf, Homo sapiens V600E Gene Mutation. ,  An independent cohort of 91 archival MUPs was also screened for 46 hot spot Gene Mutation highly prevalent in melanoma including Serine-threonine protein kinase B-raf, Homo sapiens, Human Oncogene N-RAS, stem cell factor receptor activity, Guanine Nucleotide-Binding Protein G(q) Subunit Alpha, and Guanine Nucleotide-Binding Protein Subunit Alpha-11.,  a high rate of Serine-threonine protein kinase B-raf, Homo sapiens (45 of 101, 45%) and Human Oncogene N-RAS (32 of 101, 32%) Gene Mutation, collectively indicating a Mutation Abnormality profile consistent with cutaneous sun-exposed melanomas., Treatment of advanced melanoma has been improved with the advent of the Serine-threonine protein kinase B-raf, Homo sapiens inhibitors., Serine-threonine protein kinase B-raf, Homo sapiens is the most prevalent Oncogenes and an important therapeutic target in melanoma., Activating Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation, leading to constitutive activation of the MAPK signaling pathway, are common in a variety of Homo sapiens Malignant Neoplasms. Several small molecule Serine-threonine protein kinase B-raf, Homo sapiens inhibitors have been developed during the last years and shown promising results in clinical trials, especially for Metastatic melanoma, while they have been less effective in Malignant tumor of Abdomen+Pelvis>Colon. , Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation have emerged as an important predictive biomarker for metastasized melanoma. , Serine-threonine protein kinase B-raf, Homo sapiens V600 selective inhibitors have been approved for the treatment of V600 Mutation Abnormality positive Metastatic melanoma, , Serine-threonine protein kinase B-raf, Homo sapiens(V600) Mutation Abnormality-positive melanoma , Melanocytic neoplasm is the most aggressive form of Malignant neoplasm of skin. The treatment of patients with advanced melanoma is rapidly evolving due to an improved understanding of molecular drivers of this disease. Somatic Gene Mutation in Serine-threonine protein kinase B-raf, Homo sapiens are the most common genetic alteration found in these Neoplasms.,  genetically activated Serine-threonine protein kinase B-raf, Homo sapiens, is now commonly prescribed for Metastatic melanoma harboring a Serine-threonine protein kinase B-raf, Homo sapiens Mutation Abnormality., Serine-threonine protein kinase B-raf, Homo sapiens inhibitors improve melanoma patient survival, but resistance invariably develops. , Serine-threonine protein kinase B-raf, Homo sapiens inhibitors elicit rapid antitumor responses in the majority of patients with Serine-threonine protein kinase B-raf, Homo sapiens(V600)-mutant melanoma, but acquired drug resistance is almost universal. , Most patients with Serine-threonine protein kinase B-raf, Homo sapiens(V600)-mutant Metastatic melanoma develop resistance to selective RAF kinase inhibitors. , Serine-threonine protein kinase B-raf, Homo sapiens(V600E) Mutation Abnormality confers constitutive CXCL14 gene kinase activation in melanoma cells, promoting tumor growth. This discovery led to the development of Serine-threonine protein kinase B-raf, Homo sapiens kinase inhibitors like vemurafenib and dabrafenib. , (V600)Serine-threonine protein kinase B-raf, Homo sapiens Mutation Abnormality was identified as an ideal target for clinical therapy due to its indispensable roles in supporting melanoma initiation and progression., The Braf(V600E) Mutation Abnormality has been detected in patients with Metastatic melanoma, Abdomen+Pelvis>Colon, THYROID DIAGNOSTIC RADIOPHARMACEUTICALS, and other Malignant Neoplasms., Since the identification of activating Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation and subsequent development of drugs targeting the mutant Serine-threonine protein kinase B-raf, oncologists now need to incorporate prognostic and predictive biomarkers into treatment decisions for their melanoma patient, Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation occur in approximately 8% of all Homo sapiens Malignant Neoplasms and approach 50% in melanoma and papillary carcinoma of THYROID DIAGNOSTIC RADIOPHARMACEUTICALS., vemurafenib is a selective and potent small molecule inhibitor of the V600 mutant form of the Serine-threonine protein kinase B-raf used in the treatment of melanoma and Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum., Molecular studies demonstrated that the melanoma was positive for the 1799T>A (V600E) Mutation Abnormality in the Serine-threonine protein kinase B-raf, Homo sapiens gene., RAF kinase inhibitors have substantial therapeutic effects in patients with Serine-threonine protein kinase B-raf, Homo sapiens-mutant melanoma., An activating Serine-threonine protein kinase B-raf, Homo sapiens (V600E) kinase Mutation Abnormality occurs in approximately half of melanomas. , Activating Gene Mutation in the Serine-threonine protein kinase B-raf, Homo sapiens gene occur in approximately 50% of melanomas. More than 70% of Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation are V600E and 10-30% are V600K., Activating Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation, leading to constitutive activation of the MAPK signaling pathway, are common in a variety of Homo sapiens Malignant Neoplasms., Several small molecule Serine-threonine protein kinase B-raf, Homo sapiens inhibitors have been developed during the last years and shown promising results in clinical trials, especially for Metastatic melanoma, while they have been less effective in Malignant tumor of Abdomen+Pelvis>Colon. , Personalized melanoma medicine has progressed from histopathologic features to Serum Markers to molecular profiles. Since the identification of activating Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation and subsequent development of drugs targeting the mutant Serine-threonine protein kinase B-raf, oncologists now need to incorporate prognostic and predictive biomarkers into treatment decisions for their melanoma patients., The clinical activity of Serine-threonine protein kinase B-raf, Homo sapiens inhibitor (Serine-threonine protein kinase B-raf, Homo sapiens-I) therapy is a major breakthrough in the treatment of Metastatic melanoma carrying Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation. , The discovery of Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation in melanoma led to the development of Serine-threonine protein kinase B-raf, Homo sapiens inhibitors for the treatment of advanced melanoma. , Serine-threonine protein kinase B-raf, Homo sapiens represents one of the most frequently mutated protein kinase genes in Homo sapiens tumours. The Mutation Abnormality is commonly tested in pathology practice. Serine-threonine protein kinase B-raf, Homo sapiens Mutation Abnormality is seen in melanoma, papillary THYROID DIAGNOSTIC RADIOPHARMACEUTICALS carcinoma (including papillary THYROID DIAGNOSTIC RADIOPHARMACEUTICALS carcinoma arising from Ovarian Teratoma), ovarian serous tumours, Colorectal Carcinoma, Glioma, hepatobiliary carcinomas and Hairy cell leukaemia., Indeed, recent clinical trials involving Serine-threonine protein kinase B-raf, Homo sapiens selective inhibitors exhibited promising response rates in Metastatic melanoma patients. , A majority of cutaneous melanomas show activating Gene Mutation in the Human Oncogene N-RAS or Serine-threonine protein kinase B-raf, Homo sapiens proto-oncogenes, components of the Ras-Raf-Mek-Erk (MAPK) signal transduction pathway. The discovery of activating Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation in ∼50% of all melanomas has proved to be a turning point in the therapeutic management of the disseminated disease. This review summarizes the critical role of Serine-threonine protein kinase B-raf, Homo sapiens in melanoma pathophysiology, the clinical and pathological determinants of Serine-threonine protein kinase B-raf, Homo sapiens Mutation Abnormality status and finally addresses the current state of the art of Serine-threonine protein kinase B-raf, Homo sapiens inhibitors., To better understand the Serine-threonine protein kinase B-raf, Homo sapiens Mutation Abnormality profile in melanomas, we retrospectively analyzed data from 1112 primary and metastatic melanomas at our institution. The cohort included nonacral cutaneous (n = 774), Acral (n = 111), mucosal (n = 26), Uvea (n = 23), leptomeningeal (n = 1), and metastatic melanomas of unknown Site of primary lesion (n = 177). Serine-threonine protein kinase B-raf, Homo sapiens Mutation Abnormality hotspot regions in exons 11 and 15 were analyzed by pyrosequencing or with the primer extension MassARRAY system. A total of 499 (44.9%) specimens exhibited Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation, involving exon 15 [497 (99.6%)] or exon 11 [2 (0.4%)]. p.V600E was detected in 376 (75.4%) cases; the remaining 123 (24.6%) cases exhibited non-p.V600E Gene Mutation, of which p.V600K was most frequent [86 (17.2%)]. Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation were more frequent in nonacral cutaneous (51.4%) than Acral melanomas [18 (16.2%)] (P < 0.001); however, there was no significant difference among cutaneous histological subtypes. All mucosal, Uvea, and leptomeningeal melanomas were Serine-threonine protein kinase B-raf, Homo sapiens wild type (Wild Type Unspecified - zebrafish)., Recently, it was reported that Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation are frequent in melanoma., Activating Gene Mutation in Serine-threonine protein kinase B-raf, Homo sapiens are the most common Mutation in melanoma., Oncogenic Serine-threonine protein kinase B-raf, Homo sapiens and Human Oncogene N-RAS Gene Mutation are frequent in melanoma., Mutation of Serine-threonine protein kinase B-raf, Homo sapiens is now known to be common in cutaneous melanomas, and raises possible new therapeutic options of anti-RAF treatment for these patients, Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation are common events in a variety of Melanocytic nevus of skin and primary cutaneous melanomas, Approximately 40-60% of melanomas from Caucasian populations carry activating Gene Mutation in the Serine-threonine protein kinase B-raf, Homo sapiens Oncogenes, with the most common being the p.Val600Glu (V600E) hotspot Mutation Abnormality in exon 15, Using a cohort of 115 patients with primary invasive melanomas, we show that Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation are statistically significantly more common in melanomas occurring on skin subject to intermittent sun exposure than elsewhere (23 of 43 patients; P<.001, two-sided Fisher's exact test), Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation have been identified as the most common Oncogenes Mutation Abnormality in melanomas, especially important in those originating on nonchronically sun-damaged skin. [SEP]Relations: melanoma has relations: disease_protein with BRAF protein, Homo sapiens, disease_protein with BRAF protein, Homo sapiens, disease_protein with TNF, disease_protein with TNF, disease_protein with ASF1A, disease_protein with ASF1A. Colorectal Carcinoma has relations: disease_protein with BRAF protein, Homo sapiens, disease_protein with BRAF protein, Homo sapiens. malignant Abdomen+Pelvis>Colon neoplasm has relations: disease_protein with BRAF protein, Homo sapiens, disease_protein with BRAF protein, Homo sapiens.", "label": "yes"}
{"original_question": "Are AAV vectors considered for the treatment of retinal dystrophies?", "id": "converted_2657", "sentence1": "Are AAV vectors considered for the treatment of Retinal Dystrophies?", "sentence2": " These novel gene vectors aim to more safely and efficiently transduce retinal cells, expand the gene packaging capacity of AAV, and utilize new strategies to correct the varying mechanisms of dysfunction found with inherited Retinal Dystrophies. [SEP]Relations: retinal dystrophy in systemic or cerebroretinal lipidoses has relations: disease_disease with retinal cone dystrophy, disease_disease with retinal cone dystrophy.", "label": "yes"}
{"original_question": "Do DNA double-strand breaks play a causal role in carcinogenesis?", "id": "converted_1130", "sentence1": "Do DNA double-strand breaks play a causal role in carcinogenesis?", "sentence2": "The DNA non-homologous end-joining repair gene XRCC6/Ku70 plays an important role in the repair of DNA double-strand breaks (DSBs) induced by both exogenous and endogenous DNA-damaging agents. Defects in overall 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione repair capacity can lead to genomic instability and carcinogenesis., The tumor suppressor Malignant neoplasm of breast susceptibility protein 1 (BRCA1 gene gene) protects our Cells from genomic instability in part by facilitating the efficient repair of DNA double-strand breaks (DSBs). BRCA1 gene gene promotes the error-free repair of DSBs through homologous recombination and is also implicated in the regulation of nonhomologous end joining (Non-Homologous DNA End-Joining) repair fidelity., The increased frequency of 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione Mutagenesis Procedure and MMEJ repair in the absence of BRCA1 gene gene suggests a potential mechanism for carcinogenesis., Comet assay under neutral conditions allows detection of DNA double-strand breaks (DSBs), which has consequence to genome instability and carcinogenesis., Loss of p15/Ink4b accompanies tumorigenesis triggered by complex DNA double-strand breaks., Although DSBs are potentially carcinogenic, it is not clear whether complex DSBs that are refractory to repair are more potently tumorigenic compared with simple breaks that can be rapidly repaired, correctly or incorrectly, by mammalian Cells., Zinc chromate induces chromosome instability and DNA double strand breaks in Homo sapiens lung Cells., Our study shows that zinc chromate induced concentration-dependent increases in cytotoxicity, chromosome damage and DNA double strand breaks in Homo sapiens lung Cells., Foci formation of TP53BP2 protein, Homo sapiens in Thyroid Neoplasm: activation of genomic instability during thyroid carcinogenesis., nitric oxide and acid induce double-strand DNA breaks in Barrett's esophagus carcinogenesis via distinct mechanisms., DNA double-strand break repair capacity and risk of Malignant neoplasm of breast., A tumorigenic role of the non-homologous end-joining (Non-Homologous DNA End-Joining) pathway for the repair of DNA double-strand breaks (DSBs) has been suggested by our finding of a significant association between increased Malignant neoplasm of breast risk and a cooperative effect of single-nucleotide polymorphisms in Non-Homologous DNA End-Joining Genes., Carcinogen-induced DNA double strand break repair in sporadic Malignant neoplasm of breast., Induction of DNA double strand breaks and alterations in the repair of these breaks is implicated in breast carcinogenesis. Prior studies have demonstrated that Peripheral blood mononuclear cell (cell) (PBMC) from Malignant neoplasm of breast patients exhibit increased numbers of DNA strand breaks after exposure to ionizing radiation, but these studies did not specifically measure DNA double strand breaks and it is not known whether chemical carcinogens produce similar effects., Abnormal DNA end-joining activity in Homo sapiens head and neck cancer., In Human Cells, DNA double-strand breaks (DSBs) are repaired primarily by the DNA end-joining (EJ) process and thus, abnormal DNA EJ activities lead to an accumulation of Gene Mutation and/or aneuploidy, resulting in genetic instability of Cells. Since genetic instability is the hallmark of Tumor Cells, malignant, we studied the DNA EJ activities of normal, non-malignant immortalized and malignant Homo sapiens epithelial Cells to investigate the association between DNA EJ and carcinogenesis., Homologous recombination repair plays an important role in 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione repair and impairment of this repair mechanism may lead to loss of genomic integrity, which is one of the hallmarks of cancer. Recent research has shown that the tumor suppressor Genes p53 and BRCA1 gene gene and -2 are involved in the proper control of homologous recombination, suggesting a role of this type of repair in Homo sapiens cancer., In order to study the role of DNA damage processing in the development of Squamous Cell Carcinoma of the Rat Skin (sodium copper chlorophyllin), we assessed the ability of six keratinocyte cell lines from a multistage-tumor progression model to repair three types of DNA damage: Pyrimidine dimers, oxidative DNA lesions and DNA double strand breaks (1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione)., However, an Malnutrition in repairing DNA double strand breaks can be one mechanism promoting progression towards Primary malignant neoplasm, possibly through impairing chromosomal stability., Recent findings demonstrate that accelerated carcinogenesis following liver regeneration is associated with chronic inflammation-induced double-strand DNA breaks in Cells, which escaped apoptosis due to proliferative stress., Although DNA double-strand breaks and apoptosis may relate to arsenite-induced damage and carcinogenesis, the mechanism of action remains obscure.[SEP]Relations: Pyrimidine dimer repair has relations: bioprocess_bioprocess with DNA repair, bioprocess_bioprocess with DNA repair, bioprocess_protein with DDB2, bioprocess_protein with DDB2. Protein S Homo sapiens has relations: drug_drug with Platelet Activating Factor, drug_drug with Platelet Activating Factor, drug_drug with Coagulation factor VIIa Recombinant Human, drug_drug with Coagulation factor VIIa Recombinant Human. Squamous cell carcinoma of the skin has relations: disease_phenotype_positive with peroxisome biogenesis disorder, disease_phenotype_positive with peroxisome biogenesis disorder.", "label": "yes"}
{"original_question": "Is microRNA(miRNA) 30 involved in post-ischemic cardiac remodeling?", "id": "converted_607", "sentence1": "Is microRNA(miRNA) 30 involved in post-ischemic cardiac remodeling?", "sentence2": "The Myocardium of the failing Chest>Heart undergoes a number of structural alterations, most notably Hypertrophy of Myocytes, Cardiac and an increase in Extracellular Matrix proteins, often seen as primary fibrosi, Connective tissue growth factor (connective tissue growth factor) is a key Molecule in the process of Fibrosis and therefore seems an attractive therapeutic target, connective tissue growth factor is importantly regulated by 2 major cardiac microRNAs (MicroRNAs), miR-133 and miR-30., the expression of both MicroRNAs was inversely related to the amount of connective tissue growth factor in 2 rodent models of Heart Diseases and in Homo sapiens pathological left ventricular Hypertrophy. Second, in cultured cardiomyocytes and Specimen Source Codes - Fibroblasts, knockdown of these MicroRNAs increased connective tissue growth factor levels. Third, overexpression of miR-133 or MIR30C2 wt Allele decreased connective tissue growth factor levels, which was accompanied by decreased production of collagen., miR-30 importantly limit the production of connective tissue growth factor, miR-30 directly downregulate connective tissue growth factor, a key profibrotic protein, and thereby establish an important role for these MicroRNAs in the control of structural changes in the Extracellular Matrix of the Myocardium.[SEP]Relations: Myocardium has relations: anatomy_protein_present with MIR1245A, anatomy_protein_present with MIR1245A, anatomy_protein_present with MIRLET7D, anatomy_protein_present with MIRLET7D, anatomy_protein_present with MIR22HG, anatomy_protein_present with MIR22HG, anatomy_protein_present with MIR99AHG, anatomy_protein_present with MIR99AHG, anatomy_protein_present with SNRNP25, anatomy_protein_present with SNRNP25.", "label": "yes"}
{"original_question": "Is AZD9668 a VEGF mRNA drug?", "id": "converted_4283", "sentence1": "Is AZD9668 a VEGF mRNA drug?", "sentence2": "AZD9668, a ELANE gene inhibitor, plus ongoing budesonide / formoterol in patients with Chronic Obstructive Airway Disease., AZD9668 is a reversible and selective inhibitor of No evidence of, well tolerated at doses of 60 mg Twice a day during Phase I/IIa development.[SEP]Relations: ELANE has relations: protein_protein with AZU1, protein_protein with AZU1, drug_protein with Pegfilgrastim, drug_protein with Pegfilgrastim, protein_protein with NOTCH2NLA, protein_protein with NOTCH2NLA, drug_protein with Mdl 101,146, drug_protein with Mdl 101,146. chronic obstructive pulmonary disease has relations: disease_protein with MIR218-2, disease_protein with MIR218-2.", "label": "no"}
{"original_question": "Is miR-21 related to carcinogenesis?", "id": "converted_1103", "sentence1": "Is MIR21 gene related to carcinogenesis?", "sentence2": "MIR21 gene* and MLXIP gene-203 were significantly dysregulated (P < 0.05) in PTC Body tissue with BRAFV600E., Expressions of miRNAs in Papillary thyroid carcinoma and their associations with the BRAFV600E mutation., Levels of miRNA-21 (MIR21 gene) and MLXIP gene-106a in Malignant neoplasm of Abdomen>Stomach Body tissue were significantly higher compared with the levels in adjacent Body tissue (P = .006 and P = .001, respectively). Patients who had Malignant neoplasm of Abdomen>Stomach had significantly different levels of Gastric Juice (substance) MIR21 gene and MLXIP gene-106a compared with patients who had benign gastric diseases (both P < .001)., MIR21 gene levels in intestinal type Malignant neoplasm of Abdomen>Stomach specimens were higher than that in diffuse (P = .003) or mixed (P < .001) Malignant neoplasm of Abdomen>Stomach types., MiR-155 and MIR21 gene appeared significantly over-expressed in the colonic mucosa of Irritable Bowel Syndrome subjects without Cytogenetic Complete Response, but also in neoplastic Body tissue of Irritable Bowel Syndrome patients compared to non-Irritable Bowel Syndrome controls (p<0.001). Importantly, in patients with Irritable Bowel Syndrome-CRCs, MLXIP gene-155 and MIR21 gene over-expression extended to the distant non-neoplastic mucosa (p<0.001)., Here we hypothesize that over-expression of MLXIP gene-155 and MIR21 gene, two inflammation-related miRNAs that target core Mismatch Repair Proteins, may constitute a pre-neoplastic event for the development of Microsatellite Instability Irritable Bowel Syndrome-CRCs., After administration, we determined the expressions of MIR21 gene, MLXIP gene-27a, MLXIP gene-34a, MLXIP gene-93, MLXIP gene-143, MLXIP gene-146a, MLXIP gene-148a, MLXIP gene-155, MLXIP gene-196a, MLXIP gene-203, MLXIP gene-205, MIR221 wt Allele and nuclear factor kappa-light-chain enhancer of activated B-Cells-1 (Nfκb1), mitogen-activated protein kinase-8 (MAPK8 protein, Homo sapiens) and v-Ki-ras2 Kirsten rat sarcoma viral Oncogenes homolog (K-ras) genes in the Abdomen>Liver of CASP14 gene., Programmed cell death 4 (Programmed Cell Death Protein 4) is a Tumor Suppressor Genes whose expression is controlled by MIR21 gene., Consistently with Programmed Cell Death Protein 4 downregulation, MIR21 gene was upregulated in neoplastic by comparison with nonneoplastic tissue samples., Expression of MIR21 gene (p=0.027), MicroRNA 181b (p=0.002), and MLXIP gene-146b (p=0.021) in Tumor tissue sample and MIR21 gene (p=0.003) in noncancerous tissue were associated with patients' overall survival., We analyzed the expression of nine miRNAs (MIR21 gene, MLXIP gene-127, MLXIP gene-154, MLXIP gene-224, MLXIP gene-323, MLXIP gene-370, MLXIP gene-9*, MLXIP gene-183, and MLXIP gene-375) by quantitative real-time-polymerase chain reaction in 34 cases of sMTC, 6 cases of hMTC, and 2 cases of C-cell hyperplasia of thyroid of thyroid (CCH)., Medullary carcinoma of thyroid and CCH were both characterized by a significant overexpression of the whole set of miRNAs (the increase being 4.2-fold for MIR21 gene, 6.7-fold for MLXIP gene-127, 8.8-fold for MLXIP gene-154, 6.6-fold for MLXIP gene-224, 5.8-fold for MLXIP gene-323, 6.1-fold for MLXIP gene-370, 13-fold for MLXIP gene-9*, 6.7-fold for MLXIP gene-183, and 10.1 for MLXIP gene-375, p<0.0001)., The most frequent changes in miRNAs in CLL Cells included downregulation of MLXIP gene-126, MLXIP gene-572, MLXIP gene-494, MLXIP gene-923, MLXIP gene-638, MLXIP gene-130a, MLXIP gene-181a and MicroRNA 181b and up-regulation of MLXIP gene-29a, MLXIP gene-660, MLXIP gene-20a, MLXIP gene-106b, MLXIP gene-142-5p, MLXIP gene-101, MLXIP gene-30b, MLXIP gene-34a, MLXIP gene-let-7f, MIR21 gene and MLXIP gene-155., Results: Medullary carcinoma of thyroid and CCH were both characterized by a significant overexpression of the whole set of miRNAs (the increase being 4.2-fold for MIR21 gene, 6.7-fold for MLXIP gene-127, 8.8-fold for MLXIP gene-154, 6.6-fold for MLXIP gene-224, 5.8-fold for MLXIP gene-323 and 6.1-fold for MLXIP gene-370, 13-fold for MLXIP gene-9*, 6.7-fold for MLXIP gene-183 and 10.1 for MLXIP gene-375, p<0.0001)., We found that the onco-miRNAs MIR21 gene and MIR221 wt Allele displayed upregulated expression while the Abdomen>Liver-specific MLXIP gene-122 was downregulated., The aim of the present review was to describe the mechanisms of several known MLXIP gene, summarize recent studies on oncogenic MLXIP gene (e.g. MIR21 gene, MLXIP gene-106a and MLXIP gene-17), tumor suppressor MLXIP gene (e.g. MLXIP gene-101, MicroRNA 181, MLXIP gene-449, MLXIP gene-486, let-7a) and controversial roles of MLXIP gene (e.g. MLXIP gene-107, MLXIP gene-126) for Malignant neoplasm of Abdomen>Stomach., MiR-15b and MIR21 gene were differentially expressed in Cerebrospinal Fluid samples from patients with Glioma, compared to control subjects with various neurologic disorders, including patients with primary Microglioma and carcinomatous Head>Brain metastases., Moreover, inclusion of MLXIP gene-15b and MIR21 gene in combined expression analyses resulted in an increased diagnostic accuracy with 90% sensitivity and 100% specificity to distinguish patients with glioma from control subjects and patients with primary Microglioma., Many aberrantly expressed miRNAs were related to various Malignant Neoplasms (e.g., MLXIP gene-125b, Liver carcinoma; MIR21 gene, leukemia; MicroRNA 16, Chronic Lymphocytic Leukemia; MLXIP gene-192, Pituitary Adenoma; MLXIP gene-199a-3p, Malignant neoplasm of ovary; MLXIP gene-34a, Malignant neoplasm of Abdomen>Pancreas). Several miRNAs (e.g., MLXIP gene-34a, MIR21 gene) and Proteins (e.g., TGM2 protein, human protein, Homo sapiens, NDRG2 gene gene) that play crucial roles in Abdomen>Liver tumorigenesis were first found to be affected by MC-LR in Mus sp. Abdomen>Liver., Except for MIR21 gene and MLXIP gene-206, the expression levels of all miRNAs significantly changed during the progression of CaP., In addition, diet and carcinogen exposure modulated a number of MicroRNAs (MicroRNA 16, MLXIP gene-19b, MIR21 gene, miR26b, miR27b, MLXIP gene-93, and MLXIP gene-203) linked to canonical oncogenic signaling pathways., RESULTS: Elevated MIR21 gene (plant-type hypersensitive response 2.06, 1.13-3.75), MLXIP gene-17 (plant-type hypersensitive response 2.00, 1.10-3.61), and MLXIP gene-155 (plant-type hypersensitive response 2.37, 1.27-4.42) was associated with worse cancer-specific mortality in the Maryland cohort., NF-κB targets MicroRNA 16 and MIR21 gene in Malignant neoplasm of Abdomen>Stomach: involvement of Prostaglandin E Receptor., Expression of MIR21 gene, MLXIP gene-29b, MLXIP gene-34a/b/c, MLXIP gene-155, and let-7a was determined by quantitative real-time PCR in formalin-fixed paraffin-embedded tumor specimens from 639 IALT patients., hese two miRNAs have previously been identified as being overexpressed in MCF-7 Breast Tumor Cells, malignant, with MIR21 gene specifically implicated in down-regulating the Tumor Suppressor Genes, Tropomyosin Alpha-1 Chain, Homo sapiens., MicroRNA-21 is involved in ionizing radiation-promoted Abdomen>Liver carcinogenesis., We showed here that among several hundred miRNAs, MIR21 gene was the only one that increased 6 folds in high-LET IR-promoted Mus sp. Liver neoplasms when compared with that in the non-irradiated Abdomen>Liver Body tissue. We also showed that MIR21 gene was up-regulated in Homo sapiens or Mus sp. hepatocytes after exposure to IR, as well as in Abdomen>Liver Body tissue derived from whole body irradiated CASP14 gene., After the non-irradiated, low-LET or high-LET irradiated Homo sapiens hepatocytes were over-expressed with MIR21 gene, these Cells became tumorigenesis in nude CASP14 gene., METHODS: We used this combined ISH/IHC assay to study a subset of cancer-associated miRNAs, including miRNAs frequently detected at low (MLXIP gene-34a and MLXIP gene-126) and high (MIR21 gene and MLXIP gene-155) levels, in a panel of Breast, colorectal, Chest>Lung, Abdomen>Pancreas, and Pelvis>Prostate Carcinoma., The MLXIP gene-15a, MicroRNA 16, MLXIP gene-143, MLXIP gene-155, and MIR21 gene were upregulated in M059K, and the modulation of these miRNAs fluctuated in M059J Cells in a time-dependent manner., Aberrantly increased expression of MIR21 gene plays a significant role in Chest>Lung carcinogenesis and is a potential therapeutic target in both epidermal growth factor receptor-mutant and wild-type cases., Additionally, high MIR21 gene expression was associated with significantly decreased 5 year survival in patients (hazard ratio, 1.68; 95% CI: 1.04-2.77) in a model controlled for patient age, gender and tumor stage., ESULTS: In Malignant adenomatous neoplasm patients, MIR21 gene, MIR223 wt Allele, MLXIP gene-192, and MLXIP gene-194 expression was elevated, whereas MLXIP gene-203 expression was reduced in cancerous compared with noncancerous tissue., Significantly, elevated MIR21 gene expression in noncancerous tissue of sodium copper chlorophyllin patients and reduced levels of MLXIP gene-375 in cancerous tissue of Malignant adenomatous neoplasm patients with Barrett's were strongly associated with worse prognosis., MIR21 gene, mir-31, MLXIP gene-130a, MLXIP gene-146b and MLXIP gene-377 were consistently upregulated, whereas MLXIP gene-1 and MLXIP gene-143 were downregulated in Lung Neoplasms relative to normal Lung. In CASP14 gene treated with VC and given indole-3-carbinol in the diet, levels of MIR21 gene, mir-31, MLXIP gene-130a, MLXIP gene-146b and MLXIP gene-377 were reduced relative to the level in CASP14 gene treated with the carcinogen only., Further studies with MIR21 gene indicated that phosphatase and tensin homolog, programmed cell death 4 and rich protein with Kazal Motifs are potential targets for the oncogenic effect of MIR21 gene and the chemopreventive activity of indole-3-carbinol., This study examines the potential clinical utility of an inflammatory gene expression signature as a prognostic biomarker for Malignant tumor of Abdomen+Pelvis>Colon in addition to previously examined MIR21 gene expression., CONCLUSIONS: IRS and MIR21 gene expression are independent predictors of Malignant tumor of Abdomen+Pelvis>Colon prognosis and may provide a clinically useful tool to identify high-risk patients., The most highly expressed miRNAs in Malignant neoplasm of Abdomen>Stomach Body tissue were MLXIP gene-20b, MLXIP gene-20a, MLXIP gene-17, MLXIP gene-106a, MLXIP gene-18a, MIR21 gene, MLXIP gene-106b, MLXIP gene-18b, MLXIP gene-421, MLXIP gene-340*, MLXIP gene-19a and MLXIP gene-658., Recent findings report their involvement in hair follicle morphogenesis (ablation of miRNAs from keratinocyte causes several defects, such as evagination instead of invagination), in Psoriasis (Skin Specimen Source Code-specific expression of MLXIP gene-203 and psoriasisspecific expression of MLXIP gene-146a, MIR21 gene and MLXIP gene-125b in the Skin Specimen Source Code), in Autoimmune Diseases affecting the Skin Specimen Source Code, such as Lupus Erythematosus, Systemic and Immune thrombocytopenic purpura, in wound healing (changes in the expression of specific miRNA at specific phases of the regeneration process), and in Skin Specimen Source Code carcinogenesis (a novel miRNA signature that includes induction of MIR21 gene, a candidate oncogenic miRNA)., RESULTS: Several MicroRNAs were differentially expressed in Ovarian Serous Adenocarcinoma compared with normal ovarian Body tissue, including MIR21 gene, MLXIP gene-125a, MLXIP gene-125b, MLXIP gene-100, MIR145 gene, MicroRNA 16, and MLXIP gene-99a, which were each differentially expressed in >16 patients., Selected for validation were MLXIP gene-20a, MIR21 gene, MLXIP gene-106a, MicroRNA 181b, and MLXIP gene-203, and all 5 were enriched in Neoplasms from the validation cohort (P < .001). Higher MIR21 gene expression was present in Adenoma (P = .006) and in Neoplasms with more advanced TNM staging (P < .001). In situ hybridization demonstrated MIR21 gene to be expressed at high levels in Colon Carcinoma Cells., To test this hypothesis, we studied the pharmacologic roles of three MicroRNAs previously implicated in cancer biology (let-7i, mir-16, and mir-21) and also used in silico methods to test pharmacologic microRNA effects more broadly., Changing the cellular levels of let-7i, mir-16, and mir-21 affected the potencies of a number of the anticancer agents by up to 4-fold. The effect was most prominent with mir-21, with 10 of 28 cell-compound pairs showing significant shifts in growth-inhibitory activity. Varying mir-21 levels changed potencies in opposite directions depending on compound class; indicating that different mechanisms determine Toxic effect and protective effects. In silico comparison of drug potencies with microRNA expression profiles across the entire NCI-60 panel revealed that approximately 30 MicroRNAs, including mir-21, show highly significant correlations with numerous anticancer agents., Conversely, expression of other miRNAs was detected at varying levels predominantly within luminal epithelial Cells in normal tissue; expression of MIR21 gene was frequently increased, whereas that of let-7a was decreased in malignant Cells., We describe a novel EMT-specific microRNA signature that includes induction of MIR21 gene, a candidate oncogenic microRNA associated with carcinogenesis., Notable was the high expression of MIR21 gene and MLXIP gene-205., Recently, MicroRNAs (miRNAs) have emerged as key actors in carcinogenesis and we demonstrated that microRNA-21 (MIR21 gene), oncomiR is expressed early during Posterior interventricular branch of right coronary artery., These results indicated that MIR21 gene plays a role in the carcinogenesis and metastasis of O. viverrini-associated CCA by suppressing the function of Programmed Cell Death Protein 4., Importantly, in patients with Irritable Bowel Syndrome CRCs, MLXIP gene-155 and MIR21 gene overexpression extended to the distant non-neoplastic mucosa (P < 0.001)., Ectopic overexpression of MIR21 gene promoted Proto-Oncogene Proteins c-akt activation and phosphorylation of EZH2 protein, Homo sapiens protein, Homo sapiens, whereas inhibiting MIR21 gene by transfecting the Cells with anti-MIR21 gene inhibited Proto-Oncogene Proteins c-akt activation and EZH2 protein, Homo sapiens protein, Homo sapiens phosphorylation., Programmed Cell Death Protein 4 nuclear down-regulation (which parallels MIR21 gene up-regulation) is involved in the molecular pathway of Irritable Bowel Syndrome-associated carcinogenesis., The expression levels of MIR21 gene (p = 0.027), MicroRNA 181b (p = 0.002) and MLXIP gene-146b (p = 0.021) in Tumor tissue sample and MIR21 gene (p = 0.003) in noncancerous tissue were associated with overall survival of patients., OBJECTIVE: As an important oncogenic miRNA, MIR21 gene has been reported to play crucial roles in Glioblastoma Multiforme (Glomerular Basement Membrane) carcinogenesis., We further analyzed the expression of microRNA-21 (MIR21 gene), an oncogenic noncoding RNA involved in oncogenic ras Oncogene signaling, by quantitative reverse-transcription polymerase chain reaction and in situ hybridization., MicroRNA-21 (MIR21 gene) plays crucial roles in carcinogenesis and is considered as one of the most studied oncomiRNAs., Although microRNA-21 (MIR21 gene) has been implicated in various aspects of carcinogenesis, its functions and molecular mechanisms in carcinogen-induced tumorigenesis are unclear., Substantial evidence indicates that microRNA-21 (MIR21 gene) is a key oncomiR in carcinogenesis and is significantly elevated in Multiple Myeloma (Millimole per Liter)., MicroRNA 21 (MIR21 gene) has been implicated in various aspects of carcinogenesis., Conversely, pAkt and MIR21 gene expression was significantly up-regulated in the whole spectrum of preneoplastic/neoplastic lesions considered., Several miRNAs (e.g., MLXIP gene-34a, MIR21 gene) and Proteins (e.g., TGM2 protein, human protein, Homo sapiens, NDRG2 gene gene) that play crucial roles in Abdomen>Liver tumorigenesis were first found to be affected by MC-LR in Mus sp. Abdomen>Liver., RESULTS: Except for MIR21 gene and MLXIP gene-206, the expression levels of all miRNAs significantly changed during the progression of CaP., MicroRNA 21 (MIR21 gene) is overexpressed in virtually all types of Carcinoma and various types of Hematologic Neoplasms., As expected, MIR21 gene expression was significantly upregulated in preneoplastic/neoplastic samples, consistent with Programmed Cell Death Protein 4 downregulation., Furthermore, MIR21 gene levels in the primary tumours correlated with Disease stage:Find:Pt:^Patient:Ord (P < 0.0001)., We found that MicroRNA 16 and MIR21 gene were upregulated upon nicotine stimulation, transfection with antagomir-16 or anti-MIR21 gene significantly abrogated cell proliferation., MicroRNA-21 (MIR21 gene) is a unique miRNA in that it is overexpressed in most tumour types analysed so far., Although altered expressions of MIR21 gene and MLXIP gene-34a were manifested within Tumor Cells, malignant, those of MLXIP gene-126 and MLXIP gene-155 were predominantly confined to Endothelial Cells and immune Cells, respectively., However, the function of MIR21 gene in Osteosarcoma of bone is still unclear., In sodium copper chlorophyllin patients, we found elevated MIR21 gene and reduced MLXIP gene-375 expression levels in cancerous compared with noncancerous tissue., MIR21 gene, mir-31, MLXIP gene-130a, MLXIP gene-146b and MLXIP gene-377 were consistently upregulated, whereas MLXIP gene-1 and MLXIP gene-143 were downregulated in Lung Neoplasms relative to normal Lung., Precancerous Adenoma also frequently showed MIR21 gene up-regulation., Higher MIR21 gene expression was present in Adenoma (P = .006), Importantly, the inflammatory ZD Esophago-esophageal had a distinct microRNA signature resembling Homo sapiens ESCC or tongue sodium copper chlorophyllin miRNAomes with MIR31 wt Allele and MIR21 gene as the top-up-regulated species., Several miRNAs have been recently reported to be involved in modulation of glioma development, especially some upregulated miRNAs, such as microRNA-21 (MIR21 gene), which has been found to function as an Oncogenes in cultured Glioblastoma Multiforme multiforme Cells., OBJECTIVE: MicroRNA-21 (MIR21 gene) is one of the miRNAs that are frequently and highly overexpressed in Tumor tissue sample of Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum (Cytogenetic Complete Response) patients; however, only a little is known about its functional role in Cytogenetic Complete Response., Inhibition of microRNA-21 (mir‑21) induced upregulation of Protein Sprouty Homolog 2             and PTEN protein, Homo sapiens protein, Homo sapiens which underscores the importance of mir-21 in Protein Sprouty Homolog 2-associated tumorigenesis             of the Abdomen+Pelvis>Colon., The microRNA MIR21 gene, a known oncogenic miRNA, was found to be upregulated in Papillary and Adenocarcinoma, Clear Cell., Since microRNA-21 (MIR21 gene) may contribute to tumorigenesis and chemoresistance in many cancer types, we aimed to investigate its efficacy in TCCs., Several miRNAs have been recently reported to be involved in modulation of glioma development, especially some up-regulated miRNAs, such as microRNA-21 (MIR21 gene), which has been found to function as an Oncogenes in cultured Glioblastoma Multiforme multiforme Cells., In this study, by using high-throughput microRNA profiling, we identified that two miRNAs (MIR21 gene and MLXIP gene-148a) overexpressed in CD4+ T Cells from both patients with Discoid Discoid lupus erythematosus erythematosus and Discoid Discoid lupus erythematosus erythematosus-prone MRL/lpr CASP14 gene, which promote cell hypomethylation by repressing DNA Modification Methylases (DNMT1 wt Allele wt Allele) expression., The microRNA-21 (MIR21 gene) has been identified as the only miRNA overexpressed in a variety of Malignant Neoplasms, including leukemia., OBJECTIVE: The contribution of overexpressed microRNA-21 and -221 (MIR21 gene and MIR221 wt Allele) to the malignant phenotype was determined by inhibiting these miRNAs using Antisense Oligonucleotides., The microRNA-21(MIR21 gene) has been identified as the only miRNA over-expressed in a wide variety of Malignant Neoplasms, including Malignant tumor of cervix., To determine the functions of these MicroRNAs in lymphomagenesis, we examined the effects of Antisense Oligonucleotides (ASOs) targeting MIR21 gene (ASO-21) and/or MLXIP gene-155 (ASO-155) in NK-cell lymphoma lines overexpressing one or both of these miRNAs., In this study, microRNA (miRNA) expression profiling of 28 cases of never-smoker Primary malignant neoplasm of Chest>Lung identified aberrantly expressed miRNAs, which were much fewer than in Chest>Lung Malignant Neoplasms of smokers and included miRNAs previously identified (e.g., up-regulated MIR21 gene) and unidentified (e.g., down-regulated MLXIP gene-138) in those smoker cases., The oncogenic miRNA, microRNA-21 (MIR21 gene), was found to be upregulated in Carcinoma of larynx Body tissue., OBJECTIVE: To better understand microRNA MIR21 gene function in carcinogenesis, we analyzed MIR21 gene expression patterns in different stages of Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum development using in situ hybridization (ISH)., Of these miRNAs, MIR21 gene appears to be important in tumorigenesis given its up-regulation in almost all types of Homo sapiens cancer examined., The microRNA-21 gene (mir-21) has been identified as the only miRNA commonly overexpressed in solid Neoplasms of the Chest>Lung, Breast, Abdomen>Stomach, Pelvis>Prostate, Abdomen+Pelvis>Colon, Head>Brain, Head and neck structure, Esophago-esophageal and Abdomen>Pancreas., RESULTS: Our data showed that a common pattern of microRNA expression distinguishes any tumor type from normal Abdomen>Pancreas, suggesting that this set of MicroRNAs might be involved in pancreatic tumorigenesis; the expression of MLXIP gene-103 and MLXIP gene-107, associated with lack of expression of MLXIP gene-155, discriminates Neoplasms from normal; a set of 10 MicroRNAs distinguishes Skin Skin endocrine disorder disorder from acinar Neoplasms and is possibly associated with either normal Skin Skin endocrine disorder disorder differentiation or Skin Skin endocrine disorder disorder tumorigenesis; MLXIP gene-204 is primarily expressed in insulinoma and correlates with immunohistochemical expression of Therapeutic Insulin; and the overexpression of MIR21 gene is strongly associated with both a high Ki67 proliferation index and presence of Abdomen>Liver metastasis., To search for tumor-associated mutations that could affect processing and expression of mature miRNAs, a panel of 91 cancer-derived cell lines was analyzed for sequence variations in 15 miRNAs implicated in tumorigenesis by virtue of their known target transcripts (Let-7 family targeting oncogenic ras Oncogene) or their localization to sites of frequent chromosomal instability (MLXIP gene-143, MIR145 gene, MLXIP gene-26a-1, and MIR21 gene).[SEP]Relations: MIR122 has relations: disease_protein with Liver carcinoma, disease_protein with Liver carcinoma, disease_protein with pediatric Liver carcinoma, disease_protein with pediatric Liver carcinoma, disease_protein with drug-induced Abdomen>Liver injury, disease_protein with drug-induced Abdomen>Liver injury. Chest>Lung has relations: anatomy_protein_present with MIR23B, anatomy_protein_present with MIR23B, anatomy_protein_present with MIR25, anatomy_protein_present with MIR25.", "label": "yes"}
{"original_question": "Is the PTPN22 gene a biomarker for Rheumatoid Arthritis?", "id": "converted_1716", "sentence1": "Is the PTPN22 gene gene a biomarker for Rheumatoid Arthritis?", "sentence2": "Combined longitudinal analysis of the 2 cohorts suggests further association of several loci with Larsen score (KIF5A gene gene, PTPN22 gene gene, LAF4 Protein Info, human, TAGAP gene gene) and therefore a significant accumulation of Rheumatoid Arthritis severity markers among Rheumatoid Arthritis susceptibility markers (p = 0.016), A non-intronic marker at TNFAIP3 gene gene, GIN1/C5orf30, STAT4 Protein Info, human Protein Info, human, ANKRD55/IL6ST, BLK gene gene and PTPN22 gene gene showed association with Rheumatoid Arthritis susceptibility, irrespective of the serological status, the latter three markers remaining significantly associated with anti-Common Compensatory Fascial Pattern negative Rheumatoid Arthritis, after correction for multiple testing, A C-to-T Single Nucleotide Polymorphism (SNP) located at position 1858 of human PTPN22 gene gene cDNA and converting an arginine (R620) to tryptophan (W620) confers the highest risk of rheumatoid arthritis among non-Human leukocyte antigen complex genetic variations that are known to be associated with this Disease, TPN22 is a tyrosine phosphatase and functions as a damper of transcription-coupled nucleotide-excision repair signals. A C-to-T Single Nucleotide Polymorphism (SNP) located at position 1858 of human PTPN22 gene gene cDNA and converting an arginine (R620) to tryptophan (W620) confers the highest risk of rheumatoid arthritis among non-Human leukocyte antigen complex genetic variations that are known to be associated with this Disease, In addition, how the overall activity of PTPN22 gene gene is regulated and how the R-to-W conversion contributes to rheumatoid arthritis is still poorly understood, Our data depict a model that can reconcile the conflicting observations on the functional impact of the C1858T SNP and also suggest that PTPN22 gene gene.6 is a novel biomarker of rheumatoid arthritis., the level of PTPN22 gene gene.6 in peripheral blood correlates with Disease activity of rheumatoid arthritis, Lack of association of common Variant in PTPN22 gene gene with Rheumatoid Arthritis in Han Chinese was confirmed, This study identifies MMEL1 gene gene and CTLA4 wt Allele wt Allele as Rheumatoid Arthritis susceptibility Genes, provides suggestive evidence of association for a further six loci in the Han Chinese population and confirms lack of PTPN22 gene gene association in Asian populations, PTPN22 gene gene R620W genotype-phenotype correlation analysis and gene-environment interaction study in early rheumatoid arthritis: results from the ESPOIR cohort,  PTPN22 gene gene 620W risk allele was associated with Wegener Autoantigen production [odds ratio (OR) = 2.21, 95% CI 1.4, 3.4, P < 0.0001], Hormonal treatment exposition and Location characteristic ID - Smoking were found to act with a protective effect against Wegener Autoantigen production (OR = 0.44, 95% CI 0.3, 0.7, P = 0.001) and early bone erosion (OR = 0.56, 95% CI 0.4-0.8, P = 0.003), respectively, and independently of HLADR and PTPN22 gene gene status,  Rheumatoid Arthritis patients (n=333) and controls (n=490) from the Cree/Ojibway NAN population in Central Canada were Human leukocyte antigen complex-DRB1 typed and tested for 21 single-nucleotide polymorphisms (SNPs) that have previously been associated with Rheumatoid Arthritis, including PTPN22 gene gene, TRAF1-C5 innervation Locus innervation Locus, CTLA4 wt Allele wt Allele, PADI4 Protein Info, human Protein Info, human, STAT4 Protein Info, human Protein Info, human, FCRL3 gene gene, Recombinant Secondary Lymphoid-Tissue Chemokine, MMEL1 gene gene-TNFRSF14, CDK6 Protein Info, human Protein Info, human, Protein Kinase C-theta, KIF5A gene gene-PIP4K2C, IL2RB Protein Info, human Protein Info, human, TNFAIP3 gene gene, IL10-1082G/A and REL Protein Protein, 21 single-nucleotide polymorphisms (SNPs) that have previously been associated with Rheumatoid Arthritis, including PTPN22 gene gene, TRAF1-C5 innervation Locus innervation Locus, CTLA4 wt Allele wt Allele, PADI4 Protein Info, human Protein Info, human, STAT4 Protein Info, human Protein Info, human, FCRL3 gene gene, Recombinant Secondary Lymphoid-Tissue Chemokine, MMEL1 gene gene-TNFRSF14, CDK6 Protein Info, human Protein Info, human, Protein Kinase C-theta, KIF5A gene gene-PIP4K2C, IL2RB Protein Info, human Protein Info, human, TNFAIP3 gene gene, IL10-1082G/A and REL Protein Protein, Several other Genes, including PTPN22 gene gene and PADI4 Protein Info, human Protein Info, human, show modest association with Rheumatoid Arthritis, he Human leukocyte antigen complex Gene Locus, particularly Human leukocyte antigen complex-DRB1, is its strongest genetic risk determinant across ethnicities. Several other Genes, including PTPN22 gene gene and PADI4 Protein Info, human Protein Info, human, show modest association with Rheumatoid Arthritis. , Other Variant in potentially pathogenic Genes located in non-MHC regions have been implicated by recently performed genome wide analysis studies. These Genes include PTPN22 gene gene, TRAF1-C5 innervation Locus innervation Locus, PADI4 Protein Info, human Protein Info, human, STAT4 Protein Info, human Protein Info, human, Several Alleles in the epitope-recognition part of the Human leukocyte antigen complex molecule that show the highest association with Rheumatoid Arthritis susceptibility, also share a common string of amminoacid residues (the so-called shared-epitope hypothesis). Other Variant in potentially pathogenic Genes located in non-MHC regions have been implicated by recently performed genome wide analysis studies. These Genes include PTPN22 gene gene, TRAF1-C5 innervation Locus innervation Locus, PADI4 Protein Info, human Protein Info, human, STAT4 Protein Info, human Protein Info, human. , Among these Genes, PTPN22 gene gene plays an outstanding role. CD40 Protein Info, human Protein Info, human, STAT4 Protein Info, human Protein Info, human, PRM1 gene gene, and TNFAIP3 gene gene also seem to be of relevance., n particular, genome-wide association studies (GWAS) have provided supportive evidence that Rheumatoid Arthritis is a Disease with a strong genetic background. Interestingly, a series of candidate Genes have been identified outside of the classical major histocompatibility (MHC) Gene Locus, which had long been regarded as the major contributor to the pathogenesis of this Disease. Among these Genes, PTPN22 gene gene plays an outstanding role., Human leukocyte antigen complex-DRB1 and the R620W single-nucleotide polymorphism of PTPN22 gene gene were genotyped, In addition, evidence of a significant interaction between the shared epitope and the risk allele of PTPN22 gene gene was observed only in these patients, Although SNPs in PADI4 Protein Info, human Protein Info, human had similar allele frequency among three groups [maximal difference 11%; (P >0.05)], the other three loci revealed statistically significant allele frequency differences (maximal difference 39% (P <0.00001), 13% (P <0.00001), and 8% (P <0.00001) in SLC22A4 gene gene, PDCD1 Protein Info, human Protein Info, human, and PTPN22 gene gene, respectively), Several multiple, large-scale, genetic studies on autoimmune-Disease-associated SNPs have been reported recently: Protein-Arginine Deiminase Type 2 (PADI4 Protein Info, human Protein Info, human) in rheumatoid arthritis (Rheumatoid Arthritis); solute carrier family 22 members 4 and 5 (SLC22A4 gene gene and 5) in Rheumatoid Arthritis and Crohn's Disease (CD); programmed cell death 1 (PDCD1 Protein Info, human Protein Info, human) in systemic lupus erythematosus (Lupus Erythematosus, Systemic), type 1 diabetes mellitus (Diabetes Mellitus, Insulin-Dependent), and Rheumatoid Arthritis; and Protein Tyrosine Phosphatase nonreceptor type 22 (PTPN22 gene gene) in Diabetes Mellitus, Insulin-Dependent, Rheumatoid Arthritis, and Lupus Erythematosus, Systemic,  Recently a number of convincing candidate Genes have begun to emerge and an update has been provided for three of these: PTPN22 gene gene, cytotoxic T-lymphocyte antigen 4 and Migration Inhibitory Factor., Recently a number of convincing candidate Genes have begun to emerge and an update has been provided for three of these: PTPN22 gene gene, challenges in identifying Genetic Polymorphism that influence the susceptibility to rheumatoid arthritis are the same as those faced in most complex diseases, Association studies support a role for several Genes, including Receptors, Tumor Necrosis Factor, Type II, PADI4 Protein Info, human Protein Info, human, SLC22A4 gene gene, RUNX1 Protein Info, human Protein Info, human, and PTPN22 gene gene, Although Human leukocyte antigen complex-DRB1 is the main Rheumatoid Arthritis gene, it accounts for only part of the familial risk for Rheumatoid Arthritis. Human leukocyte antigen complex-DRB1 Alleles are neither necessary nor sufficient to cause the development of Rheumatoid Arthritis in a given individual. Several genome scans conducted in populations from France, Japan, North America and UK have confirmed the role of the Human leukocyte antigen complex region and suggested several other susceptibility loci. Association studies support a role for several Genes, including Receptors, Tumor Necrosis Factor, Type II, PADI4 Protein Info, human Protein Info, human, SLC22A4 gene gene, RUNX1 Protein Info, human Protein Info, human, and PTPN22 gene gene., Analyses of families with multiple autoimmune disorders have revealed a functional polymorphism, 620W, in the Protoplasm tyrosine phosphatase gene PTPN22 gene gene as a Predisposing Factors for type 1 diabetes, seropositive rheumatoid arthritis, systemic lupus erythematosus, and Hashimoto Disease, and the presence of the PTPN22 gene gene Protein Info appears to herald the development of Autoantibodies in these disorders, Replication of putative candidate-gene associations with rheumatoid arthritis in >4,000 samples from North America and Sweden: association of susceptibility with PTPN22 gene gene, CTLA4 wt Allele wt Allele, and PADI4 Protein Info, human Protein Info, human., We found strong evidence of an association of PTPN22 gene gene with the development of anti-citrulline antibody-positive Rheumatoid Arthritis (odds ratio [OR] 1.49; P=.00002), using previously untested Genus Eira samples.,  Exploration of our data set with clinically relevant subsets of Rheumatoid Arthritis reveals that PTPN22 gene gene is associated with an earlier age at Disease onset (P=.004) and that PTPN22 gene gene has a stronger effect in males than in females (P=.03),  Given the strong statistical power to replicate a true-positive association in this study, our results provide support for PTPN22 gene gene, CTLA4 wt Allele wt Allele, and PADI4 Protein Info, human Protein Info, human as Rheumatoid Arthritis susceptibility Genes and demonstrate novel associations with clinically relevant subsets of Rheumatoid Arthritis, In logistic regression analysis, Wegener Autoantigen predicted Rheumatoid Arthritis-development independent of PTPN22 gene gene, while the PTPN22 gene gene polymorphism had no independent effect., In this Dutch cohort of UA-patients, the PTPN22 gene gene 1858T allele does not markedly improve individual decision-making to predict Rheumatoid Arthritis-development, Risk of progression from undifferentiated arthritis to rheumatoid arthritis: the effect of the PTPN22 gene gene 1858T-allele in anti-citrullinated peptide antibody positive patients, progression from undifferentiated arthritis to rheumatoid arthritis: the effect of the PTPN22 gene gene 1858T-allele, Anti-citrullinated peptide Antibodies, in vitro diagnostic (Wegener Autoantigen) and the C1858T missense single-nucleotide polymorphism (SNP) in the PTPN22 gene gene gene are both associated with the development of rheumatoid arthritis (Rheumatoid Arthritis), Associations between human leukocyte antigen, PTPN22 gene gene, CTLA4 wt Allele wt Allele genotypes and rheumatoid arthritis phenotypes of autoantibody status, age at diagnosis and Superficial ulcer in a large cohort study, Human leukocyte antigen complex-DRB1 shared epitope (Human leukocyte antigen complex-FUT2 gene), PTPN22 gene gene and CTLA4 wt Allele wt Allele Alleles are associated with cyclic citrullinated peptide (Common Compensatory Fascial Pattern) and rheumatoid arthritis (Rheumatoid Arthritis), Auto-Antibodies, in vitro diagnostic, Human leukocyte antigen complex and PTPN22 gene gene: susceptibility markers for rheumatoid arthritis, The combination of the PTPN22 gene gene 1858T variant and anti-Common Compensatory Fascial Pattern Antibodies, in vitro diagnostic gave a high specificity for the Disease, and was significantly associated with Rheumatoid Arthritis (P = 8.86 x 10(-5), OR 10.05, 95% CI 1.88-53.73), The combination of the T variant of the 1858 polymorphism of the PTPN22 gene gene gene in combination with the presence of anti-Common Compensatory Fascial Pattern Antibodies, in vitro diagnostic, preferentially in a FUT2 gene-positive individual, is associated with the development of Rheumatoid Arthritis, No association of the PTPN22 gene gene gene with mortality was detected, Cox proportional hazards regression models were used to assess the association of the Human leukocyte antigen complex-DRB1 (including the shared epitope [FUT2 gene]) and PTPN22 gene gene Genes with the risk of death from all causes and from cardiovascular Disease (Cerebrovascular Disorders) and to assess the interactions between FUT2 gene, Location characteristic ID - Smoking, and anti-cyclic citrullinated peptide (anti-Common Compensatory Fascial Pattern) status, adjusted by age at symptom onset and sex, The Disease association of the common 1858C>T Arg620Trp (rs2476601) nonsynonymous Single Nucleotide Polymorphism (SNP) of Protein Tyrosine Phosphatase; nonreceptor type 22 (PTPN22 gene gene) on Chromosomes, Human, Pair 1 1p13 has been confirmed in type 1 diabetes and also in other Autoimmune Diseases, including rheumatoid arthritis and Graves' Disease, To evaluate the predictive values for Disease progression of various Antibodies, in vitro diagnostic against citrullinated peptide proteins (Wegener Autoantigen) and their relation to PTPN22 gene gene 1858C/T polymorphism and Human leukocyte antigen complex-DRB1 Alleles in early rheumatoid arthritis (Rheumatoid Arthritis), PTPN22 gene gene, PADI-4, and cytotoxic T-lymphocyte antigen 4 have been associated with risk for rheumatoid arthritis (Rheumatoid Arthritis), A significant multiplicative interaction between PTPN22 gene gene and Location characteristic ID - Smoking for more than 10 pack-years was observed (P = 0.04), No gene-gene interaction was observed between PTPN22 gene gene and Human leukocyte antigen complex-FUT2 gene, After adjusting for Location characteristic ID - Smoking and reproductive factors, PTPN22 gene gene was associated with Rheumatoid Arthritis risk among Caucasian women in these cohorts. We found both additive and multiplicative interactions between PTPN22 gene gene and heavy cigarette Location characteristic ID - Smoking., After adjusting for Location characteristic ID - Smoking and reproductive factors, PTPN22 gene gene was associated with Rheumatoid Arthritis risk among Caucasian women in these cohorts, Weak evidence for an effect at the PTPN22 gene gene Gene Locus was also observed, Association of the PTPN22 gene gene gene (-1123G > C) polymorphism with rheumatoid arthritis in Chinese patients, These data suggest, the CC genotype and C allele of the -1123G > C in the PTPN22 gene gene gene are associated with an increased risk for Rheumatoid Arthritis in Chinese population, Therefore, the CC genotype and C allele of the -1123G > C in the PTPN22 gene gene gene may be used as a genetic marker for the predisposition of Rheumatoid Arthritis in Chines, A longer duration of breastfeeding increased the risk of developing Rheumatoid Arthritis, especially among individuals seropositive for Wegener Autoantigen or IgM-Radio fluoroscopy or carrying the PTPN22 gene gene 1858T variant, In a multiple logistic regression analysis, increasing time of breastfeeding (OR 9.5, 95% CI 2.14-42.43 for ≥ 17 months), seropositivity for acetyl 4-aminosalicylic acid (OR 19.5, 95% CI 4.47-84.81), and carriage of the PTPN22 gene gene 1858T variant (OR 3.2, 95% CI 1.36-7.54) remained significant predictors of Rheumatoid Arthritis, After quality control, 3209 patients and 3692 controls were included in the study. Eight markers (ie, rs1160542 (LAF4 Protein Info, human), rs1678542 (KIF5A gene gene), rs2476601 (PTPN22 gene gene), rs3087243 (CTLA4 wt Allele wt Allele), rs4810485 (CD40 Protein Info, human Protein Info, human), rs5029937 (6q23), rs10760130 (TRAF1/C5 innervation innervation) and rs7574865 (STAT4 Protein Info, human Protein Info, human)) were significantly associated with Rheumatoid Arthritis by meta-analysis, Recent genome-wide association studies (GWAS) on Rheumatoid Arthritis identified known and novel susceptibility Genes like Human leukocyte antigen complex-DRB1, PTPN22 gene gene, STAT4 Protein Info, human Protein Info, human, TRAF1/C5 innervation innervation, OLIG3/TNFAIP3 gene gene, CD40 Protein Info, human Protein Info, human, Recombinant Secondary Lymphoid-Tissue Chemokine, MMEL1 gene gene-TNFRSF14, CDK6 Protein Info, human Protein Info, human, Protein Kinase C-theta, IL2RB Protein Info, human Protein Info, human, and KIF5A gene gene-PIP4K2C, In the total Rheumatoid Arthritis inception cohort, the Human leukocyte antigen complex-DRB1 shared epitope (per-allele odds ratio (OR) = 2.1, trend P < 0.0001), PTPN22 gene gene (per-allele OR = 1.5, trend P < 0.0001), OLIG3/TNFAIP3 gene gene Gene Locus (per-allele OR = 1.2, trend P = 0.009) and TRAF1/C5 innervation innervation Gene Locus (per-allele OR = 1.1, trend P = 0.04) were associated with Rheumatoid Arthritis, This study investigated five confirmed rheumatoid arthritis (Rheumatoid Arthritis) susceptibility Genes/loci (Human leukocyte antigen complex-DRB1, PTPN22 gene gene, STAT4 Protein Info, human Protein Info, human, OLIG3/TNFAIP3 gene gene and TRAF1/C5 innervation innervation) for association with susceptibility and severity in an inception cohort, Progress has been made in determining the relative contributions and the interaction of the shared epitope, PTPN22 gene gene and Location characteristic ID - Smoking in conferring the risk of anticitrullinated Protein Info Antibodies, in vitro diagnostic-positive and negative Rheumatoid Arthritis, Homozygous and heterozygous carriers of the PTPN22 gene gene 1858T allele had a decreased probability of remission, Our analyses have confirmed previous findings for Genes PTPN22 gene gene and C5 innervation innervation, Fifty-five percent of the FDRs had > or =1 copy of the shared epitope, 20% had > or =1 copy of the PTPN22 gene gene polymorphism, and approximately 16% were positive for Rheumatoid Factor Measurement (Radio fluoroscopy; including isotypes) and/or anti-cyclic citrullinated peptide antibody, As an effect several new Genes have been recognized as an Human leukocyte antigen complex-independent genetic risk factors of Rheumatoid Arthritis. PTPN22 gene gene gene polymorphism, C5 innervation innervation/TRAF1 Genes region polymorphism and TNFAIP3 gene gene-OLIG3 Genes region polymorphism(s) are among newly identified and already confirmed genetic risk factors, whereas STAT 4, CTLA4 wt Allele wt Allele, PADI4 Protein Info, human Protein Info, human and IRF5 Genes polymorphisms are listed among probable Rheumatoid Arthritis development genetic risk factors, After initial completion of the Human Genome Project on the 16th February 2001, significant progress has been made in identifying other than Human leukocyte antigen complex genome regions linked to the increased Rheumatoid Arthritis susceptibility. As an effect several new Genes have been recognized as an Human leukocyte antigen complex-independent genetic risk factors of Rheumatoid Arthritis. PTPN22 gene gene gene polymorphism, C5 innervation innervation/TRAF1 Genes region polymorphism and TNFAIP3 gene gene-OLIG3 Genes region polymorphism(s) are among newly identified and already confirmed genetic risk factors, Patients were analysed for anti-MCV and anti-cyclic citrullinated peptide (Common Compensatory Fascial Pattern), and were genotyped for human leukocyte antigen (Human leukocyte antigen complex)-DRB1 \"shared epitope\" (FUT2 gene) and Protein Tyrosine Phosphatase, non-receptor type 22 (PTPN22 gene gene) 1858T, As well as the major susceptibility gene Human leukocyte antigen complex-DRB1, recent genome-wide and candidate-gene studies reported additional evidence for association of Single Nucleotide Polymorphism (SNP) markers in the PTPN22 gene gene, STAT4 Protein Info, human Protein Info, human, OLIG3/TNFAIP3 gene gene and TRAF1/C5 innervation innervation loci with Rheumatoid Arthritis., However, we were able to replicate the association signals between Rheumatoid Arthritis and Human leukocyte antigen complex-DRB1 Alleles, STAT4 Protein Info, human Protein Info, human (rs7574865), PTPN22 gene gene (rs2476601) and OLIG3/TNFAIP3 gene gene (rs10499194 and rs6920220), Additionally, SNPs rs7574865STAT4 (P = 9.2*10-6; OR = 1.71, 95% CI = 1.35 - 2.18) and rs2476601PTPN22 (P = 9.5*10-4; OR = 1.67, 95% CI = 1.23 - 2.26) were associated with susceptibility to Rheumatoid Arthritis, whereas after permutation testing OLIG3/TNFAIP3 gene gene SNPs rs10499194 and rs6920220 missed our criteria for significance (Pcorr = 0.114 and Pcorr = 0.180, respectively, In our Slovak population, Human leukocyte antigen complex-DRB1 Alleles as well as SNPs in STAT4 Protein Info, human Protein Info, human and PTPN22 gene gene Genes showed a strong association with Rheumatoid Arthritis, Recent advances have led to novel identification of Genetic Polymorphism that are associated with susceptibility to rheumatoid arthritis (Rheumatoid Arthritis). Currently, 5 loci (Human leukocyte antigen complex, PTPN22 gene gene, TRAF1/C5 innervation innervation, TNFAIP3 gene gene, and STAT4 Protein Info, human Protein Info, human) have been consistently reported, whereas others have been observed less systematically, Genetic markers such as shared epitope Alleles and PTPN22 gene gene 1858T variant increase the relative risk for Disease development, Particularly, acetyl 4-aminosalicylic acid in combination with human leukocyte antigen-shared epitope Alleles and PTPN22 gene gene 1858T carriage increased the relative risks of developing Rheumatoid Arthritis compared with not having these factors, However, inconsistent results of the contributions of non-Human leukocyte antigen complex susceptibility Genes have been described, with the exception of a few Genes repeatedly associated with Rheumatoid Arthritis-susceptibility, such as PTPN22 gene gene gene in populations of European ancestry and PADI4 Protein Info, human Protein Info, human gene in populations of Asian ancestry, revealing the presence of genetic heterogeneity in Rheumatoid Arthritis., Functional polymorphisms of PTPN22 gene gene and FcgR Genes in Tunisian patients with rheumatoid arthritis, We found strong evidence of an association of PTPN22 gene gene 620W allele and Rheumatoid Arthritis, In conclusion, we have confirmed that PTPN22 gene gene 620W allele is associated with Tunisian Rheumatoid Arthritis but does not constitute a factor influencing clinical manifestations., The C1858T allele of the PTPN22 gene gene gene has been reported to confer risk for Rheumatoid Arthritis, Similarly, the presence or absence of the Human leukocyte antigen complex-DRB1 shared epitope or the Rheumatoid Arthritis-associated PTPN22 gene gene allele had no influence on this association, Although some genetic risk factors for Rheumatoid Arthritis are well-established, most notably Human leukocyte antigen complex-DRB1 and PTPN22 gene gene, these markers do not fully account for the observed heritability, Lastly, in combination with the other two known genetic risk factors, Human leukocyte antigen complex-DRB1 and PTPN22 gene gene, the Variant reported here generate more than a 45-fold Rheumatoid Arthritis-risk differential, Contribution of PTPN22 gene gene 1858T, TNFRII 196R and Human leukocyte antigen complex-shared epitope Alleles with Rheumatoid Factor Measurement and anti-citrullinated Protein Info Antibodies, in vitro diagnostic to very early rheumatoid arthritis diagnosis, PTPN22 gene gene 1858T, TNFRII 196R and Human leukocyte antigen complex-FUT2 gene Alleles do not improve the predictive value of Radio fluoroscopy and Wegener Autoantigen for Rheumatoid Arthritis diagnosis in our cohort, and do not contribute to an earlier diagnosis in undifferentiated patients initially negative for Radio fluoroscopy and Wegener Autoantigen[SEP]Relations: PTPN22 gene has relations: disease_protein with rheumatoid arthritis, disease_protein with rheumatoid arthritis, disease_protein with juvenile idiopathic arthritis, disease_protein with juvenile idiopathic arthritis, disease_protein with type 1 diabetes mellitus, disease_protein with type 1 diabetes mellitus, disease_protein with IDDM 1, disease_protein with IDDM 1. MMEL1 gene has relations: disease_protein with rheumatoid arthritis, disease_protein with rheumatoid arthritis.", "label": "yes"}
{"original_question": "Is airplane stroke syndrome a common disease.", "id": "converted_2179", "sentence1": "Is airplane Cerebrovascular accident syndrome a common disease.", "sentence2": "Only 37 cases of Cerebrovascular accident during or soon after long-haul flights have been published to our knowledge. , Our centre admitted 5727 Cerebrovascular accident patients, of whom 42 (0.73%) had flight-related strokes., The authors report three cases of Ischemic Cerebrovascular accident in young adults that occurred during or after an airplane flight.[SEP]Relations: Ischemic Cerebrovascular accident has relations: disease_phenotype_positive with Cerebrovascular accident disorder, disease_phenotype_positive with Cerebrovascular accident disorder, disease_phenotype_positive with cerebral arteriopathy, autosomal dominant, with subcortical infarcts and leukoencephalopathy,, disease_phenotype_positive with cerebral arteriopathy, autosomal dominant, with subcortical infarcts and leukoencephalopathy,, disease_phenotype_positive with ZTTK syndrome, disease_phenotype_positive with ZTTK syndrome, disease_phenotype_positive with arterial tortuosity syndrome, disease_phenotype_positive with arterial tortuosity syndrome, disease_phenotype_positive with thoracic aortic aneurysm and aortic dissection, disease_phenotype_positive with thoracic aortic aneurysm and aortic dissection.", "label": "no"}
{"original_question": "Do MAIT cells have a role in multiple myeloma?", "id": "converted_3501", "sentence1": "Do MAIT cells have a role in Multiple Myeloma?", "sentence2": "hus, MAIT cells are reduced in millimeter patients, which may contribute to Disease in these individuals, and moreover, MAIT cells may represent new immunotherapeutic targets for treatment of millimeter and other Malignant Neoplasms., Here we have analysed the frequency and function of MAIT cells in Multiple Myeloma (millimeter) patients. We show that Mucosal-Associated Invariant T-Cell frequency in blood is reduced compared to healthy adult donors, but comparable to elderly healthy control donors, Newly diagnosed millimeter patient MAIT cells had reduced gamma-interferon production and CD27 wt Allele wt Allele expression, suggesting an exhausted phenotype, although gamma-interferon-producing capacity is restored in relapsed/refractory patient samples. , We describe recent observations with regard to functional exhaustion of iNKT and MAIT cells in millimeter pathology and discuss the potential application of checkpoint inhibition as an attractive target for prolonged activation of these immunomodulatory T cells in the treatment of millimeter., Enumeration, functional responses and cytotoxic capacity of MAIT cells in newly diagnosed and relapsed Multiple Myeloma., Thus, MAIT cells are reduced in millimeter patients, which may contribute to Disease in these individuals, and moreover, MAIT cells may represent new immunotherapeutic targets for treatment of millimeter and other Malignant Neoplasms.[SEP]Relations: Multiple myeloma has relations: disease_phenotype_positive with plasma cell myeloma, disease_phenotype_positive with plasma cell myeloma, drug_effect with Bortezomib, drug_effect with Bortezomib, drug_effect with Muromonab, drug_effect with Muromonab, drug_effect with Lenalidomide, drug_effect with Lenalidomide, drug_effect with Zoledronic acid, drug_effect with Zoledronic acid.", "label": "yes"}
{"original_question": "Are there any specific antidotes for dabigatran?", "id": "converted_1071", "sentence1": "Are there any specific antidotes for dabigatran?", "sentence2": "Novel Oral Route of Drug administration ANTICOAGULANTS AND COAGULANTS (NOACs)--apixaban, dabigatran, and rivaroxaban--have a significantly smaller risk of Cerebral Hemorrhage (HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO). However, two facts make this situation complicated: First, the risk of Hematoma expansion is unknown for NOACs. Second, there is no specific antidote for neither of the NOACs. , However, many physicians are wary of these drugs, since there is limited evidence on how to manage Hemorrhage in patients taking them, and since no specific antidote is known to reverse their anticoagulant effect., Given the absence of a specific antidote, the action to be taken in these situations must be defined. , The fact that there is no specific antidote to reverse the anticoagulant action of the new ANTICOAGULANTS AND COAGULANTS can impair management of hemorrhagic complications;, Unlike the vitamin K antagonist, i.e. warfarin, there is no specific antidote for these medications. , The lack of guidelines, protocols, and an established specific antidote to reverse the anticoagulation effect of dabigatran potentially increases the rates of morbidity and mortality in patients with closed head injury (Greek letter chi)., The novel Oral Route of Drug administration ANTICOAGULANTS AND COAGULANTS (Direct Oral Anticoagulant) dabigatran etexilat (Pradaxa®), rivaroxaban (Xarelto®) and apixaban (Eliquis®), also known as \"direct\" ANTICOAGULANTS AND COAGULANTS, act independently from Therapeutic Human Antithrombin-III by inhibiting Thrombin Time Test Device, as in the case of dabigatran, or by inhibiting factor Xa, as in the case of rivaroxaban and apixaban. It is assumed that they are suitable for long-term use and do not require laboratory monitoring. Nevertheless, clinical experience is very limited and caution rather than quick conclusions is necessary. Two major drawbacks are on the one hand the risk of Pharmacologic Substance accumulation in Both kidneys and/or Hepatobiliary Disorder and, on the other hand, the lack of specific antidotes. , NOA also have other unresolved problems: Pharmacologic Substance interactions are still possible, specific coagulation test to assess them must be developed, and no specific antidote is currently available in case of hemorrhagic complication.,  It is critical to identify and subsequently manage dabigatran etexilate toxicity because there is no specific antidote to reverse the Pharmacologic Substance's anticoagulant effects., In the absence of a specific antidote for this novel Oral Route of Drug administration anticoagulant medication, even in an emergency situation, successful surgical treatment was possible with an aggressive use of available prohaemostatic agents., While these trial data are extremely encouraging, several practical issues (e.g., lack of specific antidote, safety of long-term treatment or cost-effectiveness in \"real-life\" clinical practice) still need to be elucidated., In case of massive Hemorrhage, management is unclear and none of these newer agents has a specific antidote that completely reverses its anticoagulant effect., The short half-life of these new agents compensates for the lack of any specific antidote in many instances. , As there is no specific antidote, the only treatment option is discontinuation of the Pharmacologic Substance and supportive management., Currently, none of these new agents has a specific antidote, and little advise can be given on how to manage a major Hemorrhage event., Although there is no specific antidote to antagonise the anticoagulant effect of dabigatran, due to its short duration of effect Pharmacologic Substance discontinuation is usually sufficient to reverse any excessive anticoagulant activity. [SEP]Relations: Dabigatran has relations: drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Argatroban, drug_drug with Argatroban, drug_drug with Flunixin, drug_drug with Flunixin, drug_drug with Decitabine, drug_drug with Decitabine, drug_drug with Dactinomycin, drug_drug with Dactinomycin.", "label": "no"}
{"original_question": "Are there web based self management strategies for chronic pain ?", "id": "converted_46", "sentence1": "Are there web based self management strategies for chronic Pain:-:Point in time:^Patient:- ?", "sentence2": "Fibromyalgia Symptom Reduction by Online Behavioral Self-monitoring, , This study aimed to evaluate effects of a web-based, self-monitoring and symptom management system (SMARTLog) that analyzes personal self-monitoring data and delivers data-based feedback over time., Moderate use (3 times weekly x 3 months) increased likelihood of clinically significant improvements in Pain:-:Point in time:^Patient:-, memory, gastrointestinal problems, Cancer patients and suicide and Cancer patients and suicide and depression, Fatigue, and concentration; heavy use (4.5 times weekly x five months) produced the above plus improvement in stiffness and Difficulty sleeping., Results suggest that the tailored online chronic Pain:-:Point in time:^Patient:- management program showed promising effects on Pain:-:Point in time:^Patient:- at 1 and 6 months posttreatment and quality of life at 6 months posttreatment in this naturalistic study., Results suggest the potential value of self-management for chronic Pain:-:Point in time:^Patient:- patients and the potential acceptability of web-based delivery of intervention content., Patient involvement can be fostered by web-based applications combining health information with decision support or behaviour change support. These so-called Interactive Health Communication Applications (IHCAs) can reach great numbers of patients at low financial cost and provide information and support at the time, place and learning speed patients prefer., Web-based interventions may also be effective in enhancing self-management for individuals with chronic Pain:-:Point in time:^Patient:-, but little is known about long-term effects. Research on Web-based interventions to support self-management following participation in Pain:-:Point in time:^Patient:- management programs is limited. OBJECTIVE: The aim is to examine the long-term effects of a 4-week smartphone-intervention [SEP]Relations: Chronic Pain:-:Point in time:^Patient:- has relations: phenotype_phenotype with Pain, phenotype_phenotype with Pain, disease_phenotype_positive with Sjogren syndrome, disease_phenotype_positive with Sjogren syndrome, disease_phenotype_positive with Loeys-Dietz syndrome, disease_phenotype_positive with Loeys-Dietz syndrome, disease_phenotype_positive with Machado-Joseph disease, disease_phenotype_positive with Machado-Joseph disease, disease_phenotype_positive with glycogen storage disease, disease_phenotype_positive with glycogen storage disease.", "label": "yes"}
{"original_question": "Does Apolipoprotein E (ApoE) have anti-inflammatory activity?", "id": "converted_1409", "sentence1": "Does Apolipoprotein E (ApoE) have Anti-Inflammatory Agents activity?", "sentence2": " have previously reported that APOE gene (Apolipoprotein E), a protein component of very-low-density lipoproteins (Very low density lipoprotein) and High Density Lipoproteins and a potent plasma-borne atheroprotective factor, exerts Anti-Inflammatory Agents activity in Specimen Source Codes - Macrophages by switching the activation profile from Enneking Metastasis Enneking Metastasis M1 (\"classic\") to M2 (\"alternative\") in a process involving signaling via LDLR protein, human , Anti-Inflammatory Agents activity in Specimen Source Codes - Macrophages , Small peptides corresponding to the receptor-binding region of Apolipoprotein E mimic the Anti-Inflammatory Agents activity of the Apolipoprotein E , Apolipoprotein (apo) E-containing high-density lipoprotein (HDL) has antioxidant, Anti-Inflammatory Agents and anti-atherogenic properties[SEP]Relations: APOE has relations: molfunc_protein with antioxidant activity, molfunc_protein with antioxidant activity, bioprocess_protein with negative regulation of inflammatory response, bioprocess_protein with negative regulation of inflammatory response, molfunc_protein with phosphatidylcholine-sterol O-acyltransferase activator activity, molfunc_protein with phosphatidylcholine-sterol O-acyltransferase activator activity, disease_protein with hyperlipoproteinemia, disease_protein with hyperlipoproteinemia, cellcomp_protein with lipoprotein particle, cellcomp_protein with lipoprotein particle.", "label": "yes"}
{"original_question": "Have 5q35 microdeletions been implicated in Sotos syndrome development?", "id": "converted_831", "sentence1": "Have 5q35 microdeletions been implicated in SOTOS SYNDROME 1 development?", "sentence2": "Loss-of-function Gene Mutation of NSD1 protein, Homo sapiens protein, Homo sapiens and 5q35 microdeletions encompassing NSD1 protein, Homo sapiens protein, Homo sapiens are a major cause of SOTOS SYNDROME 1 (Spondylo-ocular syndrome), which is characterized by overgrowth, Macrocephaly, characteristic facies, and variable Intellectual Disability (ID), We observed a novel 3.5 Mb 5q subtelomeric Gene Deletion Abnormality in a 3-year-old girl with developmental delay, Muscle Muscle hypotonia and multiple minor anomalies. Comparison of her phenotype with the few published patients with Terminal (end postition) 5q35 Gene Deletion revealed several overlapping features, but also showed remarkable differences such as shortness of stature versus Large for gestational age. After the report of 5q35.3 microdeletions in SOTOS SYNDROME 1 we integrated the published Brief Assessment of Cognition in Schizophrenia Functional Test into the public draft sequence and exactly mapped the Gene Deletion Abnormality size in our patient by FISH analysis with 15 BAC probes. We demonstrated that the Gene Deletion Abnormality in our patient is immediately adjacent to the reported SOTOS SYNDROME 1 Gene Deletion Abnormality site, Switch in FGFR3 protein, Homo sapiens protein, Homo sapiens and -4 expression profile during Homo sapiens renal development may account for transient Hypercalcemia in patients with SOTOS SYNDROME 1 due to 5q35 microdeletions., Multiple mechanisms are implicated in the generation of 5q35 microdeletions in SOTOS SYNDROME 1., After the report of 5q35.3 microdeletions in SOTOS SYNDROME 1 we integrated the published Brief Assessment of Cognition in Schizophrenia Functional Test into the public draft sequence and exactly mapped the Gene Deletion Abnormality size in our patient by FISH analysis with 15 BAC probes., Clinical and genetic spectrum of 18 unrelated Korean patients with SOTOS SYNDROME 1: frequent 5q35 microdeletion and identification of four novel NSD1 protein, Homo sapiens protein, Homo sapiens Gene Mutation., Here we describe a new case of SOTOS SYNDROME 1 with a 5q35 microdeletion, affecting the Fibroblast Growth Factor Receptor 1 (FGFR4 gene gene) gene, presenting with infantile Hypercalcemia., Microdeletions at 5q35.3, encompassing NSD1 protein, Homo sapiens protein, Homo sapiens, are responsible for approximately 10% of non-Japanese cases of Sotos., Alu-related 5q35 microdeletions in SOTOS SYNDROME 1., Most cases of SOTOS SYNDROME 1 are caused by intragenic NSD1 protein, Homo sapiens protein, Homo sapiens Gene Mutation or 5q35 microdeletions., Multiple mechanisms are implicated in the generation of 5q35 microdeletions in SOTOS SYNDROME 1, Clinical and genetic spectrum of 18 unrelated Korean patients with SOTOS SYNDROME 1: frequent 5q35 microdeletion and identification of four novel NSD1 protein, Homo sapiens protein, Homo sapiens Gene Mutation, Microdeletions at 5q35.3, encompassing NSD1 protein, Homo sapiens protein, Homo sapiens, are responsible for approximately 10% of non-Japanese cases of Sotos, A case of SOTOS SYNDROME 1 with 5q35 microdeletion and novel clinical findings., Here we describe a new case of SOTOS SYNDROME 1 with a 5q35 microdeletion, affecting the Fibroblast Growth Factor Receptor 1 (FGFR4 gene gene) gene, presenting with infantile Hypercalcemia. , There are two types of Gene Mutation that cause NSD1 protein, Homo sapiens protein, Homo sapiens haploinsufficiency: Gene Mutation within the NSD1 protein, Homo sapiens protein, Homo sapiens gene (mutation type) and a 5q35 submicroscopic Gene Deletion Abnormality encompassing the entire NSD1 protein, Homo sapiens protein, Homo sapiens gene (Gene Deletion Abnormality type). , aCGH and metaphase FISH are useful for rapid diagnosis of 5q35 microdeletion associated with SOTOS SYNDROME 1., Multiple mechanisms are implicated in the generation of 5q35 microdeletions in SOTOS SYNDROME 1., Switch in FGFR3 protein, Homo sapiens protein, Homo sapiens and -4 expression profile during Homo sapiens renal development may account for transient Hypercalcemia in patients with SOTOS SYNDROME 1 due to 5q35 microdeletions., A case of SOTOS SYNDROME 1 with 5q35 microdeletion and novel clinical findings., Most cases of SOTOS SYNDROME 1 are caused by intragenic NSD1 protein, Homo sapiens protein, Homo sapiens Gene Mutation or 5q35 microdeletions., aCGH and metaphase FISH are useful for rapid diagnosis of 5q35 microdeletion associated with SOTOS SYNDROME 1., Alu-related 5q35 microdeletions in SOTOS SYNDROME 1.[SEP]Relations: SOTOS SYNDROME 1 has relations: disease_protein with SETD2, disease_protein with SETD2, disease_protein with NSD1 protein, Homo sapiens, disease_protein with NSD1 protein, Homo sapiens, disease_disease with partial Gene Deletion Abnormality of the long arm of chromosome 5, disease_disease with partial Gene Deletion Abnormality of the long arm of chromosome 5, disease_protein with APC2, disease_protein with APC2, disease_protein with NRK, disease_protein with NRK.", "label": "yes"}
{"original_question": "Is there a role for gamma knife in treatment of Obsessive-Compulsive Disorder?", "id": "converted_1917", "sentence1": "Is there a role for gamma knife in treatment of Obsessive-Compulsive Disorder?", "sentence2": "OBJECTIVE Functional Gamma Knife radiosurgery (GKRS) procedures have been increasingly used for treating patients with Tremor, trigeminal neuralgia (Trigeminal Neuralgia), and refractory obsessive-compulsive disorder., METHODS The authors constructed a linear-quadratic model of BORNHOLM EYE DISEASE in functional GKRS with a dose-protraction factor to correct for intrafraction DNA-damage repair and used standard single-fraction doses for trigeminal nerve ablation for Trigeminal Neuralgia (85 Gy), Thalamotomy for Tremor (130 Gy), and capsulotomy for obsessive-compulsive disorder (180 Gy). , Gamma knife for Obsessive-Compulsive Disorder: can it be detrimental?, Gamma knife radiosurgery (GKRS) is also being practised to treat refractory obsessive- compulsive disorder (OCD)., Radio and neurosurgical procedures, including gamma knife radiation and deep brain stimulation, are reserved for severe, treatment-refractory disease that has not responded to multiple treatments, and some patients may benefit from transcranial magnetic stimulation.,  We close with a discussion of gamma knife capsulotomy, a modality with deep historical Plant Roots., Results following gamma knife radiosurgical anterior capsulotomies for Obsessive-Compulsive Disorder., Gamma knife radiosurgery (GKRS) is also being practised to treat refractory obsessive- compulsive disorder (OCD)., Lesion topography and outcome after thermocapsulotomy or gamma knife capsulotomy for obsessive-compulsive disorder: relevance of the right hemisphere., Neuropsychological outcome of ventral capsular/ventral striatal gamma capsulotomy for refractory obsessive-compulsive disorder: a pilot study, Gamma ventral capsulotomy for treatment of resistant obsessive-compulsive disorder: a structural MRI pilot prospective study, Results following gamma knife radiosurgical anterior capsulotomies for Obsessive-Compulsive Disorder, At 28 months, the third patient is living and working independently, and her YBOCS score is 18.CONCLUSION: Within a strict protocol, gamma knife radiosurgery provided improvement of OCD behavior with no adverse effects., Gamma knife for Obsessive-Compulsive Disorder: can it be detrimental?[SEP]Relations: obsessive-compulsive disorder has relations: contraindication with Riboflavin, contraindication with Riboflavin, contraindication with Ibuprofen, contraindication with Ibuprofen, disease_protein with SLITRK5, disease_protein with SLITRK5, contraindication with Pheniramine, contraindication with Pheniramine, contraindication with Isometheptene, contraindication with Isometheptene.", "label": "yes"}
{"original_question": "Is BNN20 involved in Parkinson's disease?", "id": "converted_3323", "sentence1": "Is BNN20 involved in Parkinson Disease?", "sentence2": "Nerve Growth Factors are among the most promising treatments aiming at slowing or stopping and even reversing Parkinson Disease (Lugano Lymphoma Response Classification Progressive Disease by PET). However, in most cases, they cannot readily cross the human blood-Head>Brain-barrier (BBB). Herein, we propose as a therapeutic for Lugano Lymphoma Response Classification Progressive Disease by PET the small molecule 17-beta-spiro-[5-androsten-17,2'-oxiran]-3beta-ol (BNN-20), a synthetic analogue of prasterone, which crosses the BBB and is deprived of endocrine side-effects. Using the \"weaver\" Mus sp., a genetic model of Lugano Lymphoma Response Classification Progressive Disease by PET, which exhibits progressive dopamine hydrochloride Nerve Degeneration in the Substantia nigra structure (SN), we have shown that long-term administration (P1-P21) of BNN-20 almost fully protected the Dopaminergic Neurons and their terminals, via i) a strong anti-apoptotic effect, probably mediated through the Tropomyosin receptor kinase B (tropomyosin-related kinase-B, human) neurotrophin receptor's PI3K-Akt-NF-κB signaling pathway, ii) by exerting an efficient antioxidant effect, iii) by inducing significant anti-inflammatory activity and iv) by restoring Brain-Derived Neurotrophic Factor (Head>Brain-derived neurotrophic factor) levels. By intercrossing \"weaver\" with NGL CASP14 gene (dual GFP/luciferase-NF-κΒ reporter CASP14 gene, NF-κΒ.GFP.Luc), we obtained Weaver/NGL CASP14 gene that express the NF-κB reporter in all Diploid Cell. Acute BNN-20 administration to Weaver/NGL CASP14 gene induced a strong NF-κB-dependent transcriptional response in the Head>Brain as detected by bioluminescence imaging, which was abolished by co-administration of the tropomyosin-related kinase-B, human inhibitor ANA-12. This indicates that BNN-20 exerts its beneficial action (at least in part) through the tropomyosin-related kinase-B, human-PI3K-Akt-NF-κB signaling pathway. These results could be of clinical relevance, as they suggest BNN-20 as an important neuroprotective agent acting through the tropomyosin-related kinase-B, human neurotrophin receptor pathway, mimicking the action of the endogenous neurotrophin Head>Brain-derived neurotrophic factor. Thus BNN-20 could be proposed for treatment of Lugano Lymphoma Response Classification Progressive Disease by PET.[SEP]Relations: Parkinson disease has relations: disease_protein with BST1, disease_protein with BST1, disease_protein with Head>Brain-derived neurotrophic factor, disease_protein with Head>Brain-derived neurotrophic factor, disease_protein with FBP1, disease_protein with FBP1, disease_protein with CNTNAP2, disease_protein with CNTNAP2, disease_protein with TBP, disease_protein with TBP.", "label": "yes"}
{"original_question": "Are mutations in the STXBP1 gene associated with epilepsy?", "id": "converted_1729", "sentence1": "Are mutations in the STXBP1 gene Genes associated with Epilepsy?", "sentence2": "leucovorin responsive Epilepsy in Ohtahara syndrome caused by STXBP1 gene Genes Mutation Abnormality., A novel Mutation Abnormality in STXBP1 gene Genes Genes in a child with epileptic Encephalopathies and an atypical electroclinical pattern., Gene Mutation in STXBP1 gene Genes Genes, encoding the syntaxin binding protein 1, have been recently described in Ohtahara syndrome, or early infantile epileptic Encephalopathies with suppression-burst pattern, and in other early-onset epileptic encephalopathies., STXBP1 gene Genes (MUNC18.1), encoding syntaxin binding protein 1, has been reported in Ohtahara syndrome, a rare epileptic Encephalopathies with suppression burst pattern on EEG, in patients with Infantile Spasm and in a few patients with nonsyndromic mental retardation without Epilepsy. , ed with severe developmental delay and poor prognosis. Gene Mutation and Gene Deletion in the STXBP1 gene Genes Genes are associated with Ohtahara syndrome, also known as \"early infantile epileptic Encephalopathies, Here we show that de novo heterozygous mutations in the Genes encoding STXBP1 gene Genes, also known as MUNC18-1, which is essential in Synaptic Vesicles release in multiple species, cause OS, STXBP1 gene Genes haploinsufficiency results in progressive Encephalopathies characterized by Intellectual Disability and may be accompanied by Epilepsy, Movement Disorders, and Autistic Disorder. , Gene Mutation of the syntaxin binding protein 1 (STXBP1 gene Genes) have been associated with severe infantile epileptic encephalopathies (Ohtahara syndrome and West Syndrome), but also with moderate to severe No No cognitive impairment and nonsyndromic Epilepsy., A novel STXBP1 gene Genes Mutation Abnormality causes focal Seizures with neonatal onset., STXBP1 gene Genes mutations in early infantile epileptic Encephalopathies with suppression-burst pattern., e novo STXBP1 gene Genes mutations have been found in individuals with early infantile epileptic Encephalopathies with suppression-burst pattern (EIEE), Gene Mutation in STXBP1 gene Genes are relatively frequent in patients with infantile epileptic encephalopathies. STXBP1 gene Genes-related Encephalopathies may present as drug-responsive Infantile Spasm with focal/lateralized discharges., De novo SCN1A gene Genes mutations in migrating partial Seizures of infancy., De novo mutations in the Genes encoding STXBP1 gene Genes (MUNC18-1) cause early infantile epileptic Encephalopathies., Gene Mutation in STXBP1 gene Genes have been identified in a subset of patients with early onset epileptic Encephalopathies (Eosinophilic esophagitis), but the full phenotypic spectrum remains to be delineated, and STXBP1 gene Genes-related West/Ohtahara syndromes, are due to a Mutation Abnormality in a unique Genes., This is the first case report showing that STXBP1 gene Genes mutations caused West Syndrome from the onset of Epilepsy. [SEP]Relations: Epilepsy has relations: disease_protein with STXBP1 gene, disease_protein with STXBP1 gene, disease_protein with STX1B, disease_protein with STX1B, disease_protein with TGFB1, disease_protein with TGFB1, disease_protein with ADCYAP1, disease_protein with ADCYAP1, disease_protein with MIB1, disease_protein with MIB1.", "label": "yes"}
{"original_question": "Is the HRC Ser96Ala variant associated with sudden cardiac death in patients with dilated cardiomyopathy?", "id": "converted_1466", "sentence1": "Is the HRC Ser96Ala Variant associated with sudden cardiac death in patients with Cardiomyopathy, Dilated?", "sentence2": "The Ser96Ala genetic Variant of HRC is associated with life-threatening Ventricular arrhythmia in idiopathic 3',5'-dichloromethotrexate and may serve as an independent predictor of susceptibility to arrhythmogenesis in the setting of 3',5'-dichloromethotrexate., The Ser96Ala (S96A) mutation within the histidine rich Ca(2+) binding protein (HRC) has recently been linked to Cardiac Arrhythmia in Idiopathic dilation cardiomyopathy patients, potentially attributable to an increase in spontaneous Ca(2+) release events., A Homo sapiens genetic Variant (Ser96Ala) in the Sarcoplasmic Reticulum (SR) histidine-rich Ca(2+)-binding (HRC) protein has been linked to Ventricular Arrhythmia by ECG Finding and Sudden death in Cardiomyopathy, Dilated., The histidine-rich calcium binding protein (HRC) Ser96Ala Genetic Polymorphism was shown to correlate with Ventricular arrhythmia and Sudden death only in Cardiomyopathy, Dilated patients but not in healthy Homo sapiens carriers.,  HRC has been linked with familiar cardiac conduction disease and an HRC Genetic Polymorphism was shown to associate with malignant Ventricular arrhythmia in the background of Idiopathic dilation cardiomyopathy., A Homo sapiens genetic Variant (Ser96Ala) in the Sarcoplasmic Reticulum (SR) histidine-rich Ca(2+)-binding (HRC) protein has been linked to Ventricular Arrhythmia by ECG Finding and Sudden death in Cardiomyopathy, Dilated, The Ser96Ala genetic Variant of HRC is associated with life-threatening Ventricular arrhythmia in idiopathic 3',5'-dichloromethotrexate and may serve as an independent predictor of susceptibility to arrhythmogenesis in the setting of 3',5'-dichloromethotrexate., The histidine-rich calcium binding protein (HRC) Ser96Ala Genetic Polymorphism was shown to correlate with Ventricular arrhythmia and Sudden death only in Cardiomyopathy, Dilated patients but not in healthy Homo sapiens carriers, The Ser96Ala Variant in HRC gene is associated with life-threatening Ventricular arrhythmia in Idiopathic dilation cardiomyopathy., These findings indicate that the HRC Ser96Ala Variant increases the propensity of arrhythmogenic Ca(2+) waves in the stressed failing Chest>Heart, suggesting a link between this genetic Variant and life-threatening Ventricular arrhythmia in Homo sapiens carriers.[SEP]Relations: Cardiomyopathy, Dilated has relations: disease_phenotype_positive with Sudden cardiac death, disease_phenotype_positive with Sudden cardiac death, disease_phenotype_positive with Sudden death, disease_phenotype_positive with Sudden death, disease_protein with SLC22A5, disease_protein with SLC22A5, disease_protein with ABCC9, disease_protein with ABCC9. Sudden death has relations: disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated.", "label": "yes"}
{"original_question": "Is transcapillary  albumin escape altered in diabetic patients?", "id": "converted_807", "sentence1": "Is transcapillary  albumin escape altered in diabetic patients?", "sentence2": "On the contrary, altered TERalb and increased carotid artery intimal thickness are shown by all hypertensive type 2 diabetic patients, both with normal and altered patterns of Smooth Endoplasmic Reticulum., Altered systemic capillary permeability characterizes insulin-resistant hypertensive patients with Metabolic Syndrome X X., TERalb is increased in normo-albuminuric type 1 diabetic patients. [SEP]Relations: metabolic syndrome X has relations: disease_protein with HMGA1, disease_protein with HMGA1, disease_protein with INS, disease_protein with INS, disease_protein with MTTP, disease_protein with MTTP, disease_protein with TRIB3, disease_protein with TRIB3, disease_protein with RETN, disease_protein with RETN.", "label": "yes"}
{"original_question": "Is poliosis circumscripta another term for a white or unpigmented patch of hair or skin?", "id": "converted_3639", "sentence1": "Is poliosis circumscripta another term for a white or unpigmented patch of hair or skin?", "sentence2": "\"white forelock,\" poliosis circumscripta, defined as a localized patch of white hair in a group of hair follicle, Although traditionally known as \"white forelock,\" poliosis circumscripta, defined as a localized patch of white hair in a group of hair follicles, can involve any hairy area on the body including the Scalp structure, Eyebrow structure, and Eyelash., Although traditionally known as \" white forelock , \" poliosis circumscripta , defined as a localized patch of white hair in a group of hair follicles , can involve any hairy area on the body including the Scalp structure , Eyebrow structure , and Eyelash, Although traditionally known as \"white forelock,\" poliosis circumscripta, defined as a localized patch of white hair in a group of hair follicles, can involve any hairy area on the body including the Scalp structure, Eyebrow structure, and Eyelash.[SEP]Relations: eyelash has relations: anatomy_anatomy with strand of hair, anatomy_anatomy with strand of hair. muscle structure has relations: anatomy_anatomy with insect adult somatic muscle, anatomy_anatomy with insect adult somatic muscle, anatomy_anatomy with somatic muscle, anatomy_anatomy with somatic muscle, anatomy_anatomy with urethra muscle tissue, anatomy_anatomy with urethra muscle tissue, anatomy_anatomy with anatomical structure, anatomy_anatomy with anatomical structure.", "label": "yes"}
{"original_question": "Does SARM1 deletion cause neurodegeneration?", "id": "converted_2619", "sentence1": "Does SARM1 deletion cause Nerve Degeneration?", "sentence2": "Finally, using Neurons from two distinct mutant mouse strains whose Axon are highly resistant to Nerve Degeneration (Wld(S) and Sarm1(-/-)), we found that the three different fibrils were secreted by Axon after anterograde transport, in the absence of axonal lysis, indicating that trans-neuronal spread can occur in intact healthy Neurons.[SEP]Relations: axon has relations: cellcomp_protein with SARM1, cellcomp_protein with SARM1, cellcomp_protein with DNM1, cellcomp_protein with DNM1, cellcomp_protein with SRCIN1, cellcomp_protein with SRCIN1, cellcomp_protein with SHTN1, cellcomp_protein with SHTN1. neuron to neuron synapse has relations: cellcomp_protein with RS1, cellcomp_protein with RS1.", "label": "no"}
{"original_question": "Is there a phylogenetic analysis for HIV?", "id": "converted_694", "sentence1": "Is there a phylogenetic analysis for HIV Infections?", "sentence2": "The results of Bursting sensation quality and phylogenetic analysis suggested that the C. neoformans var. grubii strains could be separated into three nonredundant evolutionary groups (Bursting sensation quality group 1 to group 3). , Phylogenetic trees were constructed to evaluate the relationships between the variants, We analyzed Polish language (protease/reverse transcriptase) DNA Sequence from 135 newly diagnosed HIV Infections Infections-1-infected patients during the years 2009-2011. For phylogenetic relationships, DNA Sequence were aligned to the most recent reference data set from the Los Alamos database using BioEdit (version 7.1.3). The resulting alignment was analyzed with the Phylip package (version 3.67) building a neighbor-joining tree based on the Kimura two-parameter substitution model, . Phylogenetic analysis of gag Genes were then performed using the MEGA 3.1 software, the Genes distances were calculated by Distance program. There were three different HIV Infections Infections-1 subtypes including Deciduous maxillary right first molar tooth, CRF01-AE and CRF07-BC present among twenty four MSMs in Zhengzhou, Phylogenetic analysis showed interpatient and intrapatient clustering of LTR nucleotide DNA Sequence.,  We evaluated the risk factors for intrafamilial transmission of HIV Infections Infections-1 infection through qualitative epidemiology following Polish language and env Genes sequencing and phylogenetic analysis, Phylogenetic analysis has shown that the Siberian 10.RU.6637 isolate displays the highest Sequence - ParameterizedDataType identity to the HIV Infections Infections-1 subtype AG forms circulating in Uzbekistan, Phylogenetic analysis showed that the evolutionary relationship of Env between HIV Infections Infections and SIV was the closest and they appeared to descend from a common ancestor, and the relationship of HIV Infections Infections and Infectious Anemia Virus, Equine was the furthest, Dentinogenesis Imperfecta was confirmed when maximum Sequence - ParameterizedDataType divergence was excessive and supported by phylogenetic analysis,  (HIV Infections Infections-1) dual infection (Dentinogenesis Imperfecta) has been associated with decreased CD4 T-cell counts and increased viral loads; however, the frequency of intrasubtype Dentinogenesis Imperfecta is poorly understood., The aim of this study was to investigate the phylogenetic relationships of HIV Infections Infections-1 subtype C strains from Bangladesh and related strains from other countries, and thereby clarify when and from where subtype C was introduced in the country and how it subsequently spread within Bangladesh,  This study characterized HCV genotype 5 DNA Sequence from South Africa, including six near full-length genomes, as well as the E1 region from an additional 12 genotype 5 samples. Phylogenetic analysis of these near full-length genome DNA Sequence revealed that all genotype 5 DNA Sequence formed a close cluster with high bootstrap support,  The evolutionary history of the Deciduous maxillary right first molar tooth subregion was not as clear as the C subregion, as the short length of this region yielded poor phylogenetic results,  Finally, a phylogenetic tree was constructed to elucidate the observed pattern of HIV Infections Infections TDR[SEP]Relations: dentinogenesis imperfecta has relations: disease_phenotype_positive with Abnormality of the dental root, disease_phenotype_positive with Abnormality of the dental root, disease_phenotype_positive with Short dental roots, disease_phenotype_positive with Short dental roots, disease_phenotype_positive with Autosomal dominant inheritance, disease_phenotype_positive with Autosomal dominant inheritance, disease_protein with DSPP, disease_protein with DSPP, disease_phenotype_positive with Persistence of primary teeth, disease_phenotype_positive with Persistence of primary teeth.", "label": "yes"}
{"original_question": "Is the Fluzone intradermal and the Fluzone intradermal quadrivalent vaccine produced by different companies?", "id": "converted_3245", "sentence1": "Is the Fluzone intradermal and the Fluzone intradermal quadrivalent vaccine produced by different companies?", "sentence2": "An intradermal version of Fluzone® split-virion inactivated trivalent influenza vaccine, containing 9 µg hemagglutinin per strain of A/H1N1, A/H3N2, and one B lineage virus (Fluzone Intradermal, Sanofi Pasteur), became available in the US during the 2011-2012 influenza season for adults 18-64 years of age. In advance of the 2015-2016 season, Fluzone Intradermal was replaced with Fluzone Intradermal Quadrivalent vaccine, which contains 9 µg hemagglutinin per strain of the two A-strain viruses and both B-strain lineage viruses (Victoria and Yamagata).[SEP]", "label": "no"}
{"original_question": "Has IVIG been tested in clinical trials for the treatment of Alzheimer's disease?", "id": "converted_2284", "sentence1": "Has IVIG been tested in clinical trials for the treatment of ALZHEIMER DISEASE, FAMILIAL, 1?", "sentence2": "Clinical trials of immunoglobulins, intravenous for ALZHEIMER DISEASE, FAMILIAL, 1., Preclinical and clinical studies have shown that IVIG has anti-amyloid and immune modulatory properties relevant to treating Neurodegenerative Disorders. In early stage cytarabine/daunorubicin protocol clinical trials, IVIG was found to reduce Mental deterioration and increase brain glucose metabolism. Unfortunately, IVIG failed to meet primary outcome objectives in the North American Phase 3 clinical trial in mild to moderate cytarabine/daunorubicin protocol., While the results of clinical trials to date do not provide support for the use of IVIG to treat cytarabine/daunorubicin protocol at the doses tested, additional studies of IVIG's mechanisms are warranted and may guide the development of more effective therapies for cytarabine/daunorubicin protocol in the future.[SEP]Relations: familial Alzheimer disease has relations: disease_disease with Alzheimer disease, disease_disease with Alzheimer disease, disease_protein with PRNP, disease_protein with PRNP, disease_phenotype_positive with Emotional lability, disease_phenotype_positive with Emotional lability, disease_phenotype_positive with Jaw pain, disease_phenotype_positive with Jaw pain. inherited neurodegenerative disorder has relations: disease_disease with Alzheimer disease, disease_disease with Alzheimer disease.", "label": "yes"}
{"original_question": "Is P. gingivalis bacteria found in brain?", "id": "converted_2800", "sentence1": "Is P. gingivalis bacteria found in Head>Brain?", "sentence2": "studies using animal model of Periodontitis and Homo sapiens post-mortem Head>Brain tissues from subjects with cytarabine/daunorubicin protocol strongly suggest that a gram-negative periodontal pathogen, Porphyromonas gingivalis (Pg) and/or its product gingipain is/are translocated to the Head>Brain., The polymicrobial dysbiotic subgingival biofilm microbes associated with Periodontal Diseases appear to contribute to developing pathologies in distal body sites, including the Head>Brain.[SEP]Relations: Periodontal Diseases has relations: disease_disease with gingival disease, disease_disease with gingival disease, disease_protein with CTSC, disease_protein with CTSC. Periodontitis has relations: phenotype_phenotype with Abnormality of the gingiva, phenotype_phenotype with Abnormality of the gingiva, disease_phenotype_positive with dyskeratosis congenita, disease_phenotype_positive with dyskeratosis congenita, disease_phenotype_positive with cyclic hematopoiesis, disease_phenotype_positive with cyclic hematopoiesis.", "label": "yes"}
{"original_question": "Can telomere length shortening be reversed by telomerase?", "id": "converted_1952", "sentence1": "Can telomere length shortening be reversed by Telomerase?", "sentence2": "Telomere length is regulated around an equilibrium set point. telomere shorten during replication and are lengthened by Telomerase. Disruption of the length equilibrium leads to Disease; thus, it is important to understand the mechanisms that regulate length at the Molecular level. , High Telomerase activity is detected in nearly all human Malignant Neoplasms but most Human Cells are devoid of Telomerase activity. There is well-documented evidence that reactivation of Telomerase occurs during cellular transformation. In Homo sapiens, Neoplasms can rely in reactivation of Telomerase or originate in a Telomerase positive stem/progenitor cell, or rely in alternative lengthening of telomeres, a Telomerase-independent telomere-length maintenance mechanism.,  Together, these observations may provoke a re-evaluation of telomere and Telomerase based therapies, both in Telomerase inhibition for cancer therapy and Telomerase activation for tissue regeneration and anti-ageing strategies., telomere progressively shorten throughout life. A hallmark of advanced malignancies is the ability for continuous cell divisions that almost universally correlates with the stabilization of telomere length by the reactivation of Telomerase., Telomerase-mediated telomere elongation provides cell populations with the ability to proliferate indefinitely. Telomerase is capable of recognizing and extending the shortest telomeres in Cells;, Telomerase gene therapy rescues telomere length, Aplastic bone marrow, and survival in CASP14 gene with Aplastic Anemia.[SEP]Relations: Telomere Extension By Telomerase has relations: pathway_protein with TERT, pathway_protein with TERT, pathway_protein with ACD, pathway_protein with ACD, pathway_protein with RTEL1, pathway_protein with RTEL1, pathway_protein with TERF2, pathway_protein with TERF2, pathway_protein with GAR1, pathway_protein with GAR1.", "label": "yes"}
{"original_question": "Is avanafil indicated for treatment of erectile dysfunction?", "id": "converted_1913", "sentence1": "Is avanafil indicated for treatment of erectile dysfunction?", "sentence2": "CONTEXT: Avanafil (AVA) is used in the treatment of erectile dysfunction, but is reported for its poor aqueous solubility. , BACKGROUND: Phosphodiesterase inhibitors, cardiac stimulant (PDE5A wt Allele-Is) sildenafil, vardenafil, tadalafil and the recently approved avanafil represent the first-line choice for both on-demand and chronic treatment of erectile dysfunction (ED). , A survey on the experience of 136 Italian urologists in the treatment of erectile dysfunction with PDE5A wt Allele inhibitors and recommendations for the use of Avanafil in the clinical practice., Efficacy of Avanafil 15 Minutes after Dosing in Multiple Endocrine Neoplasia with No erectile dysfunction: A Randomized, Double-Blind, Placebo Controlled Study., PURPOSE: We examined the therapeutic effects of avanafil 15 minutes after dosing in men with mild to severe erectile dysfunction., sildenafil, vardenafil, tadalafil and avanafil are FDA approved drugs in market as PDE5A wt Allele inhibitors for treating erectile dysfunction., CONCLUSION: Avanafil along with the other PDE5Is has shown to be a safe and effective oral treatment for ED, with avanafil's possible place in therapy for patients who want an on-demand option or as an alternative in patients who experience visual disturbances with the other agents., Avanafil (STENDRA™, SPEDRA™, Zepeeed™) is an oral phosphodiesterase type 5 PPP1R1A gene indicated for the treatment of erectile dysfunction., In a 12-week, randomized, double-blind, placebo-controlled, multicentre trial in patients with erectile dysfunction, avanafil 50, 100 and 200 mg recipients had significantly greater improvements from baseline than placebo recipients in mean international index of erectile dysfunction-erectile function domain scores and in successful vaginal penetration and sexual intercourse attempts (coprimary endpoints)., Avanafil for the treatment of erectile dysfunction. An updated review., Selectivity of avanafil, a PDE5A wt Allele PPP1R1A gene for the treatment of erectile dysfunction: implications for clinical safety and improved tolerability., A randomized, double-blind, placebo-controlled evaluation of the safety and efficacy of avanafil in subjects with erectile dysfunction., Avanafil, a potent and highly selective Phosphodiesterase 5 Inhibitor [EPC] for erectile dysfunction., Avanafil, a highly selective phosphodiesterase type 5 PPP1R1A gene for erectile dysfunction, shows good safety profiles for retinal function and hemodynamics in anesthetized dogs., Cumulative data suggest that avanafil has a promising pharmacological profile for erectile dysfunction., These findings suggest that intracavernosal administration of avanafil might be beneficial for the treatment of erectile dysfunction in patients with T2DM., An open-label, long-term evaluation of the safety, efficacy and tolerability of avanafil in male patients with mild to severe erectile dysfunction., The effect of intracavernosal avanafil, a newer Phosphodiesterase 5 Inhibitor [EPC], on neonatal type 2 diabetic Rattus norvegicus with erectile dysfunction., A phase 3, placebo controlled study of the safety and efficacy of avanafil for the treatment of erectile dysfunction after nerve sparing radical prostatectomy., Avanafil is a potent selective phosphodiesterase type 5 (PDE5A wt Allele) PPP1R1A gene newly developed for treating erectile dysfunction (ED)., Adverse events most commonly reported with avanafil treatment were Headache, Nasopharyngitis, flushing, and sinus congestion.Avanafil was safe and effective for treating erectile dysfunction in men with Diabetes Mellitus and was effective as early as 15 minutes and more than 6 hours after dosing, Avanafil (STENDRA™, SPEDRA™, Zepeeed™) is an oral phosphodiesterase type 5 PPP1R1A gene indicated for the treatment of erectile dysfunction, Avanafil is rapidly absorbed after oral administration, with a median time to maximum plasma concentration of 30 to 45 min. In a 12-week, randomized, double-blind, placebo-controlled, multicentre trial in patients with erectile dysfunction, avanafil 50, 100 and 200 mg recipients had significantly greater improvements from baseline than placebo recipients in mean international index of erectile dysfunction-erectile function domain scores and in successful vaginal penetration and sexual intercourse attempts (coprimary endpoints), A phase II, single-blind, randomized, crossover evaluation of the safety and efficacy of avanafil using visual sexual stimulation in patients with mild to moderate erectile dysfunction, To evaluate the safety, efficacy and time course of three doses of avanafil (50 mg, 100 mg and 200 mg) compared with sildenafil 50 mg or placebo, given in conjunction with visual sexual stimulation (VSS) videos in men with mild to moderate erectile dysfunction (ED).Male patients, 35-70 years of age, with mild to moderate ED of ≥6 months duration, were included in the study, Avanafil for erectile dysfunction, To review the pharmacology, pharmacokinetics, safety, and efficacy of avanafil and evaluate relevant clinical trial data.A MEDLINE, International Pharmaceutical Abstracts, ClinicalTrials.gov, and Google Scholar searches (1966 to July 2013) were conducted using the key words: avanafil, erectile dysfunction, and phosphodiesterase type 5 (PDE5A wt Allele) PPP1R1A gene.Articles evaluating avanafil for erectile dysfunction (ED) published in English and using human subjects were selected, In trials in patients with erectile dysfunction in association with Diabetes Mellitus mellitus, and after nerve-sparing radical prostatectomy, avanafil 100 or 200 mg was significantly more efficacious than placebo for primary and most secondary endpoints, However, the potentiating effect of avanafil at 1 mg/kg was significantly weaker than that of sildenafil (p &lt;0.05).Data suggest that avanafil has a favorable safety profile for erectile dysfunction, which is attributable to its high inhibitory selectivity for phosphodiesterase type 5 against type 6 (retina) and 1 (vessels, etc), respectively, and its short acting pharmacodynamic property.<CopyrightInformation>Copyright © 2013 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.</, Avanafil for the treatment of erectile dysfunction: a multicenter, randomized, double-blind study in men with Diabetes Mellitus mellitus., The discovery of avanafil for the treatment of erectile dysfunction: a novel pyrimidine-5-carboxamide derivative as a potent and highly selective phosphodiesterase 5 PPP1R1A gene., Efficacy and safety of avanafil for treating erectile dysfunction: results of a multicentre, randomized, double-blind, placebo-controlled trial., Phosphodiesterase inhibitors, cardiac stimulant (PDE5A wt Allele-Is) sildenafil, vardenafil, tadalafil and the recently approved avanafil represent the first-line choice for both on-demand and chronic treatment of erectile dysfunction (ED)., The phosphodiesterese-5 (PDE5A wt Allele) inhibitors, including sildenafil (Viagra™), vardenafil (Levitra™), tadalafil (Cialis™) and avanafil (Stendra™) have been developed for the treatment of erectile dysfunction., To compare the efficacy and safety between different dosages of avanafil for the treatment of erectile dysfunction (ED).PubMed, Cochrane Library, and Embase were searched to identify randomized controlled trials which compared avanafil with placebo, or compared different dosages of avanafil for ED., We evaluated the safety and efficacy of 100 and 200 mg avanafil for the treatment of adult males with erectile dysfunction after bilateral nerve sparing radical prostatectomy.This was a double-blind, placebo controlled, parallel group, phase 3 study in males age 18 to 70 years with a history of erectile dysfunction of 6 months or more after bilateral nerve sparing radical prostatectomy., To determine the effect of avanafil, a novel Phosphodiesterase 5 Inhibitor [EPC], on the treatment of erectile dysfunction associated with Diabetes Mellitus, Noninsulin-Dependent, 3 (T2DM).In 2-day-old Rattus norvegicus, T2DM was induced by single Intraperitoneal Route of Drug Administration injection of 90 mg/kg of streptozocin (ST3GAL4 gene; i.p.)., These findings suggest that intracavernosal administration of avanafil might be beneficial for the treatment of erectile dysfunction in patients with T2DM.<CopyrightInformation>Copyright © 2014 Elsevier Inc. All rights reserved.</C, Avanafil, a potent new selective phosphodiesterase type 5 (PDE5A wt Allele) PPP1R1A gene, has been developed for the treatment of erectile dysfunction (ED)., Adverse events most commonly reported with avanafil treatment were Headache, Nasopharyngitis, flushing, and sinus congestion.Avanafil was safe and effective for treating erectile dysfunction in men with Diabetes Mellitus and was effective as early as 15 minutes and more than 6 hours after dosing., Coprimary end points assessed changes in the percentage of sexual attempts in which men were able to maintain an erection of sufficient duration to have successful intercourse (Sexual Encounter Profile [SEP] 3), percentage of sexual attempts in which men were able to insert the penis into the partner's vagina (SEP 2), and International Index of Erectile Function erectile function domain score.RESULTS: Compared with placebo, least-squares mean change from baseline to study end in SEP 3, SEP 2, and International Index of Erectile Function erectile function domain score were significantly improved with both avanafil, 100 mg (P?.002), and avanafil, 200 mg (P<.001)., Adverse events most commonly reported with avanafil treatment were Headache, Nasopharyngitis, flushing, and sinus congestion.CONCLUSION: Avanafil was safe and effective for treating erectile dysfunction in men with Diabetes Mellitus and was effective as early as 15 minutes and more than 6 hours after dosing., Avanafil for the treatment of erectile dysfunction. An updated review., Avanafil for erectile dysfunction., Avanafil for the treatment of erectile dysfunction: a multicenter, randomized, double-blind study in men with Diabetes Mellitus mellitus., To compare the efficacy and safety between different dosages of avanafil for the treatment of erectile dysfunction (ED)., Selectivity of avanafil, a PDE5A wt Allele PPP1R1A gene for the treatment of erectile dysfunction: implications for clinical safety and improved tolerability., A phase 3, placebo controlled study of the safety and efficacy of avanafil for the treatment of erectile dysfunction after nerve sparing radical prostatectomy., We evaluated the safety and efficacy of 100 and 200 mg avanafil for the treatment of adult males with erectile dysfunction after bilateral nerve sparing radical prostatectomy.[SEP]Relations: Avanafil has relations: drug_drug with Manidipine, drug_drug with Manidipine, drug_drug with Lacidipine, drug_drug with Lacidipine, drug_drug with Enalapril, drug_drug with Enalapril, drug_drug with Moexipril, drug_drug with Moexipril, drug_drug with Mirodenafil, drug_drug with Mirodenafil.", "label": "yes"}
{"original_question": "Is invasion and metastasis one of the hallmarks of cancer?", "id": "converted_431", "sentence1": "Is invasion and metastasis one of the hallmarks of cancer?", "sentence2": "The pathogenesis of millimeter involves the accumulation of extensive cytogenetic changes, as well as cancer-related phenotypic alterations that facilitate Tumor cells, uncertain whether benign or malignant survival, invasion and metastasis. This review presents current knowledge regarding the biological characteristics of this Disease that are linked to the so-called hallmarks of cancer.[SEP]Relations: malignancy in giant cell tumor of bone has relations: disease_disease with malignant giant cell tumor, disease_disease with malignant giant cell tumor, disease_disease with bone sarcoma, disease_disease with bone sarcoma.", "label": "yes"}
{"original_question": "Is microRNA(miRNA) 29 involved in post-ischemic cardiac remodeling?", "id": "converted_319", "sentence1": "Is microRNA(miRNA) 29 involved in post-ischemic cardiac remodeling?", "sentence2": "Myocardial ischaemia/reperfusion (I/R)-induced remodelling generally includes cell death (Necrotic changes (finding) and apoptosis), Myocyte hypertrophy, angiogenesis, cardiac Fibrosis, and Myocardial dysfunction. I, In addition, MIR21 gene, -24, -133, -210, -494, and -499 appear to protect Muscle Cells against I/R-induced apoptosis, whereas miR-1, -29, -199a, and -320 promote apoptosis, Myocardial Fibrosis can be regulated by the miR-29 family, Studies using various in vivo, ex vivo, and in vitro models have suggested the possible involvement of miR-1, MIR21 gene, miR-29, miR-92a, miR-133, miR-199a, and miR-320 in Reperfusion Injury and/or remodeling after Myocardial infarction:Finding:Point in time:^Patient:Ordinal., Among the MI-regulated MicroRNAs are members of the miR-29 family, which are down-regulated in the region of the Chest>Heart adjacent to the Infarction. The miR-29 family targets a cadre of mRNAs that encode proteins involved in Fibrosis, including multiple collagen, Fibrillins, and ELN protein, human. Thus, down-regulation of miR-29 would be predicted to derepress the expression of these mRNAs and enhance the fibrotic response. Indeed, down-regulation of miR-29 with Antagomirs in vitro and in vivo induces the expression of collagen, whereas over-expression of miR-29 in Specimen Source Codes - Fibroblasts reduces collagen expression. We conclude that miR-29 acts as a regulator of cardiac Fibrosis and represents a potential therapeutic target for tissue Fibrosis in general.[SEP]Relations: ischemia reperfusion injury has relations: disease_protein with MIR148B, disease_protein with MIR148B, disease_protein with EFNA5, disease_protein with EFNA5. Myocardial infarction:Finding:Point in time:^Patient:Ordinal has relations: disease_protein with MIR145, disease_protein with MIR145, disease_protein with MIR145, disease_protein with MIR145, disease_protein with MIR761, disease_protein with MIR761.", "label": "yes"}
{"original_question": "Can bioprinting use human cells?", "id": "converted_846", "sentence1": "Can bioprinting use Homo sapiens cells?", "sentence2": "In this study, Homo sapiens adipose-derived stem cells (hASCs) were printed in a free-scalable 3 Days grid pattern by means of LaBP.,  Additionally, we provide the proof that even pre-differentiated hASCs could be utilized for the generation of 3 Days Tissue Specimen Code grafts. , To explore the three dimensional(3 Days)bioprinting technology, using Homo sapiens dental pulp cells (hDPCs) mixture as bioink and to lay initial foundations for the application of the 3 Days bioprinting technology in tooth regeneration., In this study, 3-D printable formulations of hybrid hydrogels are developed, based on methacrylated hyaluronic acid (Me-HA) and methacrylated gelatin (Me-Gel), and used to bioprint heart valve conduits containing encapsulated Homo sapiens aortic valvular interstitial cells (HAVIC)., Bioprinting can be used to precisely position cells and cell-laden materials to generate controlled Tissue Specimen Code architecture., Bioprinting can be defined as the use of computer-aided transfer processes for patterning and assembling living and non-living materials with a prescribed 2D or 3 Days organization in order to produce bio-engineered structures serving in regenerative medicine, pharmacokinetic and basic cell biology studies., 3 Days bioprinting has already been used for the generation and transplantation of several Body Tissue Specimen Code, including multilayered skin, Specimen Type - Bone, Biological blood vessel prosthesis, tracheal splints, Heart Tissue Specimen Code and cartilaginous structures., [Three dimensional bioprinting technology of Homo sapiens dental pulp cells mixtures]., To explore the three dimensional(3 Days)bioprinting technology, using Homo sapiens dental pulp cells (hDPCs) mixture as bioink and to lay initial  foundations for the application of the 3 Days bioprinting technology in tooth regeneration, Here we report the development of clinically relevant sized Tissue Specimen Code Analog by 3-D bioprinting, delivering Homo sapiens nasal inferior turbinate Tissue Specimen Code-derived Mesenchymal Progenitor Cell encapsulated in silk fibroin-gelatin (SF-G) bioink, Sodium alginate hydrogel, stabilized with gelatin, is a suitable, biologically inert matrix that can be used for encapsulating and 3 Days bioprinting of Specimen Type - Bone-related SaOS-2 cells. , Bioactive nanoparticles stimulate Bone Tissue, Human formation in bioprinted three-dimensional scaffold and Homo sapiens mesenchymal stem cells., OBJECTIVE: To explore the three dimensional(3 Days)bioprinting technology, using Homo sapiens dental pulp cells (hDPCs) mixture as bioink and to lay initial  foundations for the application of the 3 Days bioprinting technology in tooth regeneration. , Cellular behavior in micropatterned hydrogels by bioprinting system depended on the cell types and cellular interaction., Engineering a morphogenetically active hydrogel for bioprinting of bioartificial Tissue Specimen Code derived from Homo sapiens osteoblast-like SaOS-2 cells., At the same time, the principal feasibility of bioprinting vascularized Homo sapiens organs as well as in vivo bioprinting has been demonstrated., The bioprinting of complex 3 Days Homo sapiens Body Tissue Specimen Code and constructs in vitro and especially in vivo are exciting, but long-term, applications., Bioprinting can be defined as the use of computer-aided transfer processes for patterning and assembling living and non-living materials with a prescribed 2D or 3 Days organization in order to produce bio-engineered structures serving in regenerative medicine, pharmacokinetic and basic cell biology studies., In this study, the 3 Days bioprinting of hDPCs mixtures was  realized, thus laying initial foundations for the application of the 3 Days bioprinting technology in tooth regeneration., To explore the three dimensional(3 Days)bioprinting technology, using Homo sapiens dental pulp cells (hDPCs) mixture as bioink and to lay initial  foundations for the application of the 3 Days bioprinting technology in tooth regeneration., Furthermore, it is not known how Homo sapiens valve cells respond to these printed environments. In this study, 3-D printable formulations of hybrid hydrogels are developed, based on methacrylated hyaluronic acid (Me-HA) and methacrylated gelatin (Me-Gel), and used to bioprint heart valve conduits containing encapsulated Homo sapiens aortic valvular interstitial cells (HAVIC)., To explore the three dimensional(3 Days)bioprinting technology, using Homo sapiens dental pulp cells (hDPCs) mixture as bioink and to lay initial  foundations for the application of the 3 Days bioprinting technology in tooth regeneration., [Three dimensional bioprinting technology of Homo sapiens dental pulp cells mixtures]., The bioprinting of complex 3 Days Homo sapiens Body Tissue Specimen Code and constructs in vitro and especially in vivo are exciting, but long-term, applications., Three-dimensional printed trileaflet valve conduits using biological hydrogels and Homo sapiens valve interstitial cells., Furthermore, it is not known how Homo sapiens valve cells respond to these printed environments., Engineering a morphogenetically active hydrogel for bioprinting of bioartificial Tissue Specimen Code derived from Homo sapiens osteoblast-like SaOS-2 cells.[SEP]Relations: mesenchymal cell proliferation has relations: bioprocess_bioprocess with cell population proliferation, bioprocess_bioprocess with cell population proliferation, bioprocess_protein with HAND2, bioprocess_protein with HAND2, bioprocess_protein with MSX1, bioprocess_protein with MSX1, bioprocess_protein with FGF7, bioprocess_protein with FGF7, bioprocess_protein with FGF4, bioprocess_protein with FGF4.", "label": "yes"}
{"original_question": "Is SLC22A3 expressed in the brain?", "id": "converted_146", "sentence1": "Is SLC22A3 expressed in the Head>Brain?", "sentence2": "The Solute Carrier Family 22 Member 1 (OCT) 3 is widely expressed in various Organ in Homo sapiens, and involved in the disposition of many exogenous and endogenous compounds. Several lines of evidence have suggested that POU5F1 gene expressed in the Head>Brain plays an important role in the regulation of neurotransmission. , The Solute Carrier Family 22 Member 1 3 (POU5F1 gene; synonymous: extraneuronal monoamine transporter, EMT, SLC22A3 gene) encodes an Protein Isoforms of the organic cation transporters and is expressed widely across the whole Head>Brain., In agreement with this distribution, POU5F1 gene/SLC22A3 gene-deficient CASP14 gene show evidence of altered monoamine neurotransmission in the Head>Brain, with decreased Protoplasm content and increased turnover of aminergic transmitters., Chemoradiotherapy, SLC6A6 gene (TauT/SLC6A6) and Solute Carrier Family 22 Member 1 (POU5F1 gene/SLC22A3) expressed at the BCSFB are involved in glycocyamine or creatine/creatine/creatinine efflux transport from Cerebrospinal Fluid., The Solute Carrier Family 22 Member 1 3 (POU5F1 gene; synonymous: extraneuronal monoamine transporter, EMT, SLC22A3 gene) encodes an Protein Isoforms of the organic cation transporters and is expressed widely across the whole Head>Brain, The Solute Carrier Family 22 Member 1 3 (POU5F1 gene; synonymous: extraneuronal monoamine transporter, EMT, SLC22A3 gene) encodes an Protein Isoforms of the organic cation transporters and is expressed widely across the whole Head>Brain. , Chemoradiotherapy may be a key factor facilitating blood-to-Head>Brain guanidinoacetate transport in patients deficient in S-adenosylmethionine:guanidinoacetate N-methyltransferase, the creatine biosynthetic enzyme, resulting in cerebral accumulation of guanidinoacetate. Chemoradiotherapy, SLC6A6 gene (TauT/SLC6A6) and Solute Carrier Family 22 Member 1 (POU5F1 gene/SLC22A3) expressed at the BCSFB are involved in glycocyamine or creatine/creatine/creatinine efflux transport from Cerebrospinal Fluid., SLC22A3 gene) encodes an Protein Isoforms of the organic cation transporters and is expressed widely across the whole Head>Brain., Chemoradiotherapy, SLC6A6 gene (TauT/SLC6A6) and Solute Carrier Family 22 Member 1 (POU5F1 gene/SLC22A3) expressed at the BCSFB are involved in glycocyamine or creatine/creatine/creatinine efflux transport from Cerebrospinal Fluid. Interestingly, Blood - Head>Brain barrier anatomy efflux transport of Ceramide Glucosyltransferase, human, including guanidinoacetate and creatine/creatine/creatinine, is negligible, though the Blood - Head>Brain barrier anatomy has a variety of efflux transport systems for synthetic precursors of Ceramide Glucosyltransferase, human, such as Antifibrinolytic Antifibrinolytic amino acids and neurotransmitters.,  The Solute Carrier Family 22 Member 1 (OCT) 3 is widely expressed in various Organ in Homo sapiens, and involved in the disposition of many exogenous and endogenous compounds. Several lines of evidence have suggested that POU5F1 gene expressed in the Head>Brain plays an important role in the regulation of neurotransmission., Chemoradiotherapy, SLC6A6 gene (TauT/SLC6A6) and Solute Carrier Family 22 Member 1 (POU5F1 gene/SLC22A3) expressed at the BCSFB are involved in glycocyamine or creatine/creatine/creatinine efflux transport from Cerebrospinal Fluid., Several lines of evidence have suggested that POU5F1 gene expressed in the Head>Brain plays an important role in the regulation of neurotransmission., The Solute Carrier Family 22 Member 1 3 (POU5F1 gene; synonymous: extraneuronal monoamine transporter, EMT, SLC22A3 gene) encodes an Protein Isoforms of the organic cation transporters and is expressed widely across the whole Head>Brain., POU2F2 gene-OCT-3 display differential tissue distribution: POU2F1 gene is predominantly found in Abdomen>Liver of Homo sapiens, and Abdomen>Liver and Both kidneys in Rodent; POU2F2 gene is most strongly expressed in both human and rodent Both kidneys, whereas is POU5F1 gene primarily expressed in Placenta Specimen, but also more widely detected in various Body tissue, including Head>Brain and Chest>Lung.[SEP]Relations: SLC22A3 has relations: anatomy_protein_present with heart, anatomy_protein_present with heart, anatomy_protein_present with colon, anatomy_protein_present with colon, cellcomp_protein with membrane, cellcomp_protein with membrane, anatomy_protein_present with Both kidneys, anatomy_protein_present with Both kidneys, anatomy_protein_present with intestine, anatomy_protein_present with intestine.", "label": "yes"}
{"original_question": "Are there any desmins present in plants?", "id": "converted_904", "sentence1": "Are there any desmins present in plants?", "sentence2": "Inherited mutations in the gene coding for the intermediate filament protein DES protein, Homo sapiens have been demonstrated to cause severe Skeletal and Cardiac - anatomy qualifier myopathies., Gene Mutation in the intermediate filament (IF) protein DES protein, Homo sapiens cause severe forms of myofibrillar myopathy characterized by partial aggregation of the extrasarcomeric DES protein, Homo sapiens cytoskeleton and structural disorganization of Myofibrils., The family of 70 intermediate filament genes (including those encoding Cytokeratin, desmins, and Lamins) is now known to be associated with a wide range of diverse diseases, at least 72 distinct Homo sapiens pathologies, including Blister of skin, Muscular Dystrophy, Cardiomyopathies, premature aging syndromes, Neurodegenerative Disorders, and Cataract. , Gene Mutation in DES protein, Homo sapiens have been associated with a subset of Homo sapiens myopathies., Characterization of a Zebrafish (Danio rerio) DES protein, Homo sapiens DNA, Complementary: an early molecular marker of myogenesis., Acute effects of DES protein, Homo sapiens mutations on Cytoskeleton and Cells integrity in Cardiac - anatomy qualifier myocytes., Desmin is a muscle-specific protein and a constitutive subunit of the Intermediate Filaments (IF) in Skeletal, Cardiac - anatomy qualifier and Smooth muscle (tissue). It is an early marker of Skeletal muscle myogenesis. We have characterized a Clone Cells of DES protein, Homo sapiens DNA, Complementary from an embryonic Zebrafish (Danio rerio) DNA, Complementary library. , Immunohistochemical investigation showed a positive reaction for Actin smooth muscle and desmins in the spindle cell proliferated in the lymph nodes; no cytokeratin positivity was detected. , We have raised Monoclonal Antibodies (Monoclonal Antibody [EPC]) to the Mr 55,000 DES protein, Homo sapiens polypeptide, electrophoretically purified from Cytoskeleton preparations of isolated bovine heart Purkinje fibers. , Mesothelial and Malignant neoplasm of ovary cells could not be distinguished by (intermediate) filament typing, using Monoclonal Antibodies (MAbs) to Cytokeratin, vimentins and desmins., A fast and convenient procedure for the purification of polymerization-competent smooth-muscle DES protein, Homo sapiens is described. Desmin from chicken gizzard and hog stomach were compared by fingerprint techniques. [SEP]Relations: Protein S Homo sapiens has relations: drug_drug with Desmoteplase, drug_drug with Desmoteplase, drug_drug with Desirudin, drug_drug with Desirudin, drug_drug with Desogestrel, drug_drug with Desogestrel, drug_drug with Desvenlafaxine, drug_drug with Desvenlafaxine. smooth muscle tissue has relations: anatomy_protein_present with DESI2, anatomy_protein_present with DESI2.", "label": "no"}
{"original_question": "Does thyroid hormone signaling affect microRNAs expression in the heart?", "id": "converted_1302", "sentence1": "Does Thyroid Hormones signaling affect microRNAs expression in the Chest>Heart?", "sentence2": "e show that the Chest>Heart regulates systemic energy homeostasis via MED13 gene protein, human gene protein, human, a subunit of the Mediator of activation protein, which controls transcription by Thyroid Hormones and other Nuclear Hormone Receptors. MED13 gene protein, human gene protein, human, in turn, is negatively regulated by a Chest>Heart-specific microRNA, miR-208a., On the other hand, T₃ treatment increased miR-350 expression., Through a bioinformatics screening using TargetScan, we identified Thyroid Hormones receptor β1 (TRβ1), which negatively regulates β-MHC transcription, as a target of miR-27a, hese findings suggested that miR-27a regulates β-MHC gene expression by targeting TRβ1 in Myocytes, Cardiac., We found that a cardiac-specific microRNA (miR-208) encoded by an Introns of the alphaMHC gene is required for cardiomyocyte hypertrophy, Fibrosis, and expression of betaMHC in response to stress and Hypothyroidism., Moreover, miR-27a was demonstrated to modulate β-MHC gene regulation via Thyroid Hormones signaling and to be upregulated during the differentiation of mouse embryonic stem (ES) cells or in hypertrophic hearts in association with β-MHC gene upregulation.[SEP]Relations: response to Thyroid Hormones has relations: bioprocess_bioprocess with cellular response to Thyroid Hormones stimulus, bioprocess_bioprocess with cellular response to Thyroid Hormones stimulus, bioprocess_protein with CAB39, bioprocess_protein with CAB39, bioprocess_bioprocess with response to hormone, bioprocess_bioprocess with response to hormone, bioprocess_protein with ANXA2, bioprocess_protein with ANXA2. Thyroid Hormones receptor binding has relations: molfunc_protein with MED17, molfunc_protein with MED17.", "label": "yes"}
{"original_question": "Is there a role for Dickkopf-1 (DKK1) in prostate cancer?", "id": "converted_4070", "sentence1": "Is there a role for Dickkopf-Related Protein 1 (DKK1 gene) in Malignant neoplasm of Pelvis>Prostate?", "sentence2": "Dickkopf-Related Protein 1 Can Lead to Immune Evasion in Metastatic Castration-Resistant Prostate Cancer., Metastatic castration-resistant Malignant neoplasm of Pelvis>Prostate (mCRPC) with low androgen receptor (AKR1B1 protein, Homo sapiens) and without neuroendocrine signaling, termed double-negative Malignant neoplasm of Pelvis>Prostate (DNPC), is increasingly prevalent in patients treated with AKR1B1 protein, Homo sapiens signaling inhibitors and is in need of new biomarkers and therapeutic targets.METHODS: Candidate genes enriched in DNPC were determined using differential gene expression analysis of discovery and validation cohorts of mCRPC biopsies. Laboratory studies were carried out in Homo sapiens mCRPC organoid cultures, Malignant neoplasm of Pelvis>Prostate (PCa) cell lines, and Mus sp. Xenograft type of graft models. Epigenetic studies were carried out in a rapid autopsy cohort.RESULTS: Dickkopf-Related Protein 1 (DKK1 gene gene) expression is increased in DNPC relative to kallikrein-related peptidase 3, Homo sapiens (PSA)-expressing mCRPC in the Stand Up to Cancer/Prostate Cancer Foundation discovery cohort (11.2 v 0.28 reads per kilobase per million mapped reads; q < 0.05; n = 117) and in the University of Washington/Fred Hutchinson Cancer Research Center cohort (9.2 v 0.99 Fragment of (qualifier value) per kilobase of transcript per million mapped reads; P < .0001). DKK1 gene gene expression can be regulated by activated Wnt signaling in vitro and correlates with activating canonical Wnt signaling mutations and low PSA RNA, Messenger in mCRPC biopsies (P < .05). DKK1 gene gene hypomethylation was associated with increased DKK1 gene gene RNA, Messenger expression (Pearson r = -0.66; P < .0001) in a rapid autopsy cohort (n = 7). DKK1 gene gene-high mCRPC biopsies are infiltrated with significantly higher numbers of quiescent natural killer (NK) cells (P < .005) and lower numbers of activated Natural Killer Cells (P < .0005). Growth inhibition of the Homo sapiens PCa model PC3 by the anti-DKK1 gene gene monoclonal antibody DKN-01 depends on the presence of Natural Killer Cells in a severe combined immunodeficient Xenograft type of graft Mus sp. model.CONCLUSION: These results support DKK1 gene gene as a contributor to the immunosuppressive tumor microenvironment of DNPC. These data have provided the rationale for a clinical trial targeting DKK1 gene gene in mCRPC (ClinicalTrials.gov identifier: NCT03837353)., DKK1 gene gene has been implicated in causing erosive arthritis, the Osteolytic phenotypes of Multiple Myeloma and metastatic Breast cancer, and osteoblastic metastases of Malignant neoplasm of Pelvis>Prostate., Dickkopf-Related Protein 1 protein secretion was documented in Breast, Pelvis>Prostate and lung cancer lines, but was negligible in Melanocytic neoplasm., LTS: Dickkopf-Related Protein 1 (DKK1 gene gene) expression is increased in DNPC relative to kallikrein-related peptidase 3, Homo sapiens (PSA)-expressing mCRPC in the Stand Up to Cancer/Prostate Cancer Foundation discovery cohort (11.2 v 0.28 reads per kilobase per million mapped reads; q < 0.05; n = 117) and in the University of Washington/Fred Hutchinson Cancer Research Center cohort (9.2 v 0.99 Fragment of (qualifier value) per kilobase of transcript per million mapped reads; P < .0001). DK, ckkopf-1 (DKK1 gene gene) expression is increased in DNPC relative to kallikrein-related peptidase 3, Homo sapiens (PSA)-expressing mCRPC in the Stand Up to Cancer/Prostate Cancer Foundation discovery cohort (11.2 v 0.28 reads per kilobase per million mapped reads; q < 0.05; n = 117) and in the University of Washington/Fred Hutchinson Cancer Research Center cohort (9.2 v 0.99 Fragment of (qualifier value) per kilobase of transcript per million mapped reads; P, The Wnt inhibitor Dickkopf-Related Protein 1 (DKK-1) has been associated with the occurrence of bone metastases in osteotropic Malignant neoplasm of Pelvis>Prostate by inhibiting osteoblastogenesis., These results reveal that Mitogen-Activated Protein Kinase 14 regulates DKK-1 in Malignant neoplasm of Pelvis>Prostate and may present a potential target in Osteolytic Pelvis>Prostate cancers., Xenograft type of graft models. Epigenetic studies were carried out in a rapid autopsy cohort.RESULTS: Dickkopf-Related Protein 1 (DKK1 gene gene) expression is increased in DNPC relative to kallikrein-related peptidase 3, Homo sapiens (PSA)-expressing mCRPC in the Stand Up to Cancer/Prostate Cancer Foundation discovery cohort (11.2 v 0.28 reads per kilobase per million mapped reads; q < 0.05; n = 117) and in the University of Washington/Fred Hutchinson Cancer Research Center cohort (9.2 v 0.99 Fragment of (qualifier value) per kilobase of transcript per millio[SEP]Relations: mitogen-activated protein kinase binding has relations: molfunc_protein with DUSP1, molfunc_protein with DUSP1, molfunc_protein with DUSP9, molfunc_protein with DUSP9, molfunc_protein with PPM1D, molfunc_protein with PPM1D, molfunc_protein with PTPRJ, molfunc_protein with PTPRJ. benign neoplasm of Pelvis>Prostate has relations: disease_disease with fibroma of Pelvis>Prostate, disease_disease with fibroma of Pelvis>Prostate.", "label": "yes"}
{"original_question": "Should Pentoxifylline be used for treatment of amyotrophic lateral sclerosis?", "id": "converted_3366", "sentence1": "Should pentoxifylline be used for treatment of amyotrophic lateral sclerosis?", "sentence2": ".RESULTS: At the end of the study, after 547 days of follow-up, 103 patients (51.7%) in the pentoxifylline group and 120 (59.7%) in the placebo group were alive (unadjusted risk 1.28, p = 0.107; adjusted risk 1.43, p = 0.02). In contrast, analysis of secondary outcome functional variables did not show the same negative effect of the drug. , CONCLUSIONS: pentoxifylline is not beneficial in Amyotrophic Lateral Sclerosis and should be avoided in patients treated with riluzole. , RESULTS: At the end of the study, after 547 days of follow-up, 103 patients (51.7%) in the pentoxifylline group and 120 (59.7%) in the placebo group were alive (unadjusted risk 1.28, p = 0.107; adjusted risk 1.43, p = 0.02).[SEP]Relations: pentoxifylline has relations: drug_drug with Canrenoic acid, drug_drug with Canrenoic acid, drug_drug with Phylloquinone, drug_drug with Phylloquinone, drug_drug with Penbutolol, drug_drug with Penbutolol, drug_drug with Ampicillin, drug_drug with Ampicillin, drug_drug with Eplerenone, drug_drug with Eplerenone.", "label": "no"}
{"original_question": "Do R-loops tend to form at sites of DNA replication?", "id": "converted_949", "sentence1": "Do R-loops tend to form at Site of DNA replication?", "sentence2": "Escherichia coli 2 2 rnhA Mutant devoid of Pancreatic ribonuclease HI exhibit constitutive stable DNA replication, cSDR, which is thought to be initiated from R-loops stabilized in the absence of Pancreatic ribonuclease HI., We propose that the organized structure of the R-Loop Structures is critical for Oligonucleotide Primers RNA function in vivo with important implications for the RNA processing and DNA replication machinery., The precursor Oligonucleotide Primers RNA exists as a persistent RNA-DNA hybrid, known as an R-Loop Structures, formed during transcription through the replication origin (Xu, B., and Clayton, D. A. (1996) EMBO J. 15, 3135-3143)., We found that overproduction of RecG protein drastically decreased copy numbers of ColE1-type Plasmids, which require R-Loop Structures formation between the template DNA and a Oligonucleotide Primers RNA transcript (RNA II) for the initiation of replication., These results suggest that overproduced RecG inhibits the initiation of replication by prematurely resolving the R-loops formed at the replication origin region of these Plasmids with its unique helicase activity. The possibility that RecG regulates the initiation of a unique mode of DNA replication, oriC-independent constitutive stable DNA replication, by its activity in resolving R-loops is discussed., We propose that downstream of a replication block, RNA at R-loops is extended by deoxyribonucleic polymerase I activity, opening up the DNA duplex and leading to the recruitment of the replisome. This would allow replication to proceed while the original block is repaired or bypassed, Furthermore, increased RNaseH expression significantly alleviated genomic instability in deficient Specimen Source Codes - Fibroblasts suggesting that cotranscriptional R-loops formation contributes to the genesis of replication-dependent DSBs in these Cells., Transcription is an important source of replicative stress and consequently, maintenance of Genome - anatomical entity integrity requires the protection of chromosomes from the deleterious effects arising from the interaction between nascent RNA and template DNA, leading to stable DNA-RNA hybrids (R-Loop Structures) formation., Strikingly, we found that attenuation of replication strongly suppresses R-Loop Structures-mediated DNA rearrangements in both E. coli and HeLa Cells., More importantly, we then show that R-Loop Structures formation causes DNA replication Orthopedic Fork stalling, and that this in fact underlies the effects of R loops on genomic stabilit, R-Loop Structures-mediated genomic instability is caused by impairment of replication Orthopedic Fork progression, When any of these processes are not properly coordinated, aberrant outcomes such as Orthopedic Fork reversal and R-Loop Structures formation arise and trigger unscheduled recombinogenic events and Genome - anatomical entity rearrangements. , Many studies show that Cells can manage R loop formation with efficiency, and can also process the R-loops already formed in the \"U\" lymphocyte, and by which, the bad effects of R-loops on DNA replication, TAF1 Gene Mutation and homologous recombination can be regulated., Here we propose that physiological R-Loop Structures formation at CpG island promoters can contribute to DNA replication origin specification at these regions, the most efficient replication initiation Site in mammalian Cells. , In agreement with this, we found that R-loops co-localize with the origin recognition complex location within the same CpG island region in a significant fraction of these efficient replication origins, precisely at the Positioning Attribute displaying the highest density of G4 motifs. , connection between transcription and replication in Human Cells and suggests that R-Loop Structures dysregulation at CpG island promoter-origins might contribute to the phenotype of DNA replication abnormalities and loss of Genome - anatomical entity integrity detected in Tumor Cells, malignant., We show that RNA:DNA hybrids (R-loops) form at Site of transcription/replication collisions and that Pancreatic ribonuclease H1 functions to suppress Chronic Fatigue Syndrome instability., R-loops and initiation of DNA replication in Human Cells: a missing link?, Stable RNA-DNA hybrids (R-loops) prime the initiation of replication in Escherichia coli 2 2 Cells., We propose that downstream of a replication block, RNA at R-loops is extended by deoxyribonucleic polymerase I activity, opening up the DNA duplex and leading to the recruitment of the replisome., Immediately after Communicable Diseases, RNA-DNA hybrids (R-loops) occur on (at least some) replication origins, with the annealed RNA serving as a Oligonucleotide Primers for leading-strand synthesis in one direction., Here we propose that physiological R-Loop Structures formation at CpG island promoters can contribute to DNA replication origin specification at these regions, the most efficient replication initiation Site in mammalian Cells., Plasmid ColE1 origins of replication and oriK Site initiate primosome complex complex assembly by an RNA-DNA hybrid structure known as R-Loop Structures., This scenario builds on the connection between transcription and replication in Human Cells and suggests that R-Loop Structures dysregulation at CpG island promoter-origins might contribute to the phenotype of DNA replication abnormalities and loss of Genome - anatomical entity integrity detected in Tumor Cells, malignant., The multiple cleavage Site on the R-Loop Structures substrate match the priming Site observed in vivo, suggesting that Pancreatic ribonuclease MRP alone is capable of generating virtually all of the leading-strand replication primers., Mechanisms of Oligonucleotide Primers RNA synthesis and D-loop/R-Loop Structures-dependent DNA replication in Escherichia coli 2 2., Alternative oriC-independent modes of replication initiation are possible, one of which is constitutive stable DNA replication (cSDR) from transcription-associated RNA-DNA hybrids or R-loops., Our results suggest that TOP1 protein, human execute this function by suppressing the formation of DNA-RNA hybrids during transcription, these so-called R-loops interfering with the progression of replication forks., Critical role of R-loops in processing replication blocks., The possibility that RecG regulates the initiation of a unique mode of DNA replication, oriC-independent constitutive stable DNA replication, by its activity in resolving R-loops is discussed., Competition between the RNA transcript and the nontemplate DNA strand during R-Loop Structures formation in vitro: a nick can serve as a strong R-Loop Structures initiation site., More importantly, we then show that R-Loop Structures formation causes DNA replication Orthopedic Fork stalling, and that this in fact underlies the effects of R loops on genomic stability. , Consistent with this hypothesis, the 3' ends of the Mitochondrial Inheritance R-Loop Structures formed by in vitro transcription are located close to the initiation Site of the Mitochondrial Inheritance DNA replication. , A hybrid G-quadruplex structure formed between RNA and DNA explains the extraordinary stability of the Mitochondrial Inheritance R-Loop Structures., Previous studies have shown that the newly synthesized primers form a stable and persistent RNA-DNA hybrid, a R-Loop Structures, near the leading-strand origin of DNA replication. , Escherichia coli 2 2 rnhA Mutant devoid of Pancreatic ribonuclease HI exhibit constitutive stable DNA replication, cSDR, which is thought to be initiated from R-loops stabilized in the absence of Pancreatic ribonuclease HI. [SEP]Relations: HELLS has relations: bioprocess_protein with DNA methylation-dependent heterochromatin assembly, bioprocess_protein with DNA methylation-dependent heterochromatin assembly, anatomy_protein_present with lymph node, anatomy_protein_present with lymph node, bioprocess_protein with maintenance of DNA methylation, bioprocess_protein with maintenance of DNA methylation. snRNA transcription by RNA polymerase III has relations: bioprocess_protein with ZC3H8, bioprocess_protein with ZC3H8, bioprocess_protein with ELL, bioprocess_protein with ELL.", "label": "yes"}
{"original_question": "Is c-myc subject to regulation by the circadian clock?", "id": "converted_1416", "sentence1": "Is c-myc subject to regulation by the circadian clock?", "sentence2": "The current study encompasses the investigation of simultaneous expression of four circadian clock Genes (ARNTL wt Allele, Clock, Per1 and Per2) and three clock-controlled cell cycle Genes (MYC protein, human, Cyclin D1 and WEE1 gene), Our results suggest that aberrant expression of circadian clock Genes can lead to aberrant expression of their downstream targets that are involved in cell proliferation and apoptosis and hence may result in manifestation of Chronic Lymphocytic Leukemia., Loss of ARNTL wt Allele reduced the expression of Period Circadian Protein Homolog 1, PER2 gene, PER3 gene, wee1 and p53. The expression of oncoprotein oncoprotein p21 and c-myc was also altered in certain Cultured Cell Line., In particular, the c-myc Proto-Oncogenes has been documented to be under circadian regulation., The circadian expression of c-MYC is modulated by the histone deacetylase inhibitor trichostatin A in synchronized Mus Neuroblastoma cells., Our results, using the Mus Neuroblastoma cell line N2A, show that Per1 and c-MYC protein, human steady-state RNA, Messenger levels oscillate with the same phase., These experiments demonstrate for the first time that a significant decrease in c-MYC protein, human transcript and protein levels can be achieved after a short indole-3-glycerol-phosphate lyase activity treatment applied only at specific circadian times. This is also followed by a reduction in the proliferation rate of the cell population., Among the circadian output pathways, the rhythmic sympathetic signaling plays a key role in the central-peripheral timing mechanism that simultaneously activates the cell cycle clock via AP1-controlled MYC protein, human induction and p53 via peripheral clock-controlled ammonium tetrathiomolybdate activation., Jet-lag promptly desynchronizes the central clock-SNS-peripheral clock axis, abolishes the peripheral clock-dependent ammonium tetrathiomolybdate activation, and activates myc oncogenic potential, leading to tumor development in the same organ systems in wild-type and circadian gene-mutant CASP14 gene., The results showed that over-expression of Per2 induced not only cell cycle arrest at G2/M phase but also an increase in apoptosis, which was confirmed by characteristic morphological changes, MYOCLONUS, FAMILIAL CORTICAL and evident DNA fragmentation. Further experiments confirmed both up-regulation of TP53 wt Allele and down-regulation of CylinB1and C-myc., On the other hand, while TP53 wt Allele was found to be down-regulated. CylinB1 and C-myc were up-regulated. after Per2 knockdown., We also show that BMAL1 epigenetic inactivation impairs the characteristic circadian clock expression pattern of Genes such as c-myc Genes, catalase, and EP300 wt Allele in association with a loss of BMAL1 occupancy in their respective Promoter., Per2 mutant (Per2(m/m)) CASP14 gene show an increase in Lymphoma and deregulated expression of Cyclin D and c-MYC protein, human Genes that are key to proliferation control., The expression of cell cycle Genes such as WEE1 gene, Cyclins, and c-MYC protein, human are under circadian control and could be directly under the regulation of the circadian transcriptional complex., Overexpressed mPER2 also altered the expression of apoptosis-related Genes. The RNA, Messenger and protein levels of c-MYC protein, human, Bcl-X(L) and BCL2 gene were downregulated,, Temporal expression of Genes involved in cell cycle regulation and tumor suppression, such as c-MYC protein, human, Cyclin D1, Cyclin A, Mdm-2 and Gadd45alpha is deregulated in mPer2 mutant CASP14 gene., The temporal expression of Genes involved in cell cycle regulation and tumor suppression, such as c-MYC protein, human, Cyclin D1, Cyclin A, Mdm-2, and Gadd45alpha, is deregulated in mPer2 mutant CASP14 gene.[SEP]Relations: PER2 has relations: bioprocess_protein with regulation of circadian rhythm, bioprocess_protein with regulation of circadian rhythm, bioprocess_protein with negative regulation of circadian rhythm, bioprocess_protein with negative regulation of circadian rhythm. entrainment of circadian clock by photoperiod has relations: bioprocess_protein with RBM4, bioprocess_protein with RBM4, bioprocess_protein with FBXL6, bioprocess_protein with FBXL6, bioprocess_protein with RBM4B, bioprocess_protein with RBM4B.", "label": "yes"}
{"original_question": "Can radiotherapy cause radiation induced osteosarcoma?", "id": "converted_3460", "sentence1": "Can radiotherapy cause radiation induced Osteosarcoma of bone?", "sentence2": "A case of radiation-induced Osteosarcoma of bone of the Bone structure of cranium presenting as a cutaneous epidermotropic Specimen Source Codes - Specimen Source Codes - tumor with a short latent period., Radiation-induced sarcoma (Arikaree language) is an unusual but well documented Specimen Source Codes - Specimen Source Codes - tumor. , We report a case of a 34-year-old female who developed an Osteosarcoma of bone of the Scalp structure, over a previous craniotomy scar, 3 years after Excision of a frontal anaplastic oligodendroglioma which had been followed by a course of 6 weeks radiotherapy (58 Gy) and 6 cycles of temozolomide. , Radiation-induced Osteosarcoma of bone after Gamma Knife surgery for Acoustic Neuroma: a case report and literature review., We present a rare case of radiation-induced Osteosarcoma of bone following Gamma Knife® surgery (GKS) for a Acoustic Neuroma (VS). , The Osteosarcoma of bone was considered to be a radiation-induced malignancy. , Radiation-induced Osteosarcoma of bone of the Maxilla and Head>Mandible after radiotherapy for nasopharyngeal carcinoma., The purpose of this study was to analyze the association of clinicopathologic characteristics with treatment outcomes and prognostic factors of patients who developed RIOSM after undergoing radiotherapy for nasopharyngeal carcinoma (Nasopharyngeal carcinoma)., Of these patients, 47 who developed RISOM and met inclusion criteria were included in this study. , CONCLUSIONS: RISOM after radiotherapy for Nasopharyngeal carcinoma is aggressive and often eludes early detection and timely intervention., Radiation-induced Osteosarcoma of bone of the Bone structure of cranium base after radiation therapy in a patient with nasopharyngeal carcinoma: a case report and review of the literature., BACKGROUND: Radiation-induced osteosarcomas are a recognized complication of radiation therapy. , CASE PRESENTATION: We describe a rare case of a patient with a Bone structure of cranium base radiation-induced Osteosarcoma of bone treated 11 years before with ionizing radiation for an undifferentiated carcinoma of the Head+Neck>Nasopharynx. , CONCLUSIONS: Radiation-induced Osteosarcoma of bone of the Bone structure of cranium base after treatment of nasopharyngeal carcinoma is a very rare but very aggressive complication with a poor prognosis., Radiation-Associated Low-Grade Extraskeletal Osteosarcoma of the Neck Following Treatment for Malignant neoplasm of thyroid., Low-grade extraskeletal Osteosarcoma of bone is a rare Specimen Source Codes - Specimen Source Codes - tumor that may arise de novo or following radiation therapy., While there is a report of a low-grade extraskeletal Osteosarcoma of bone arising following radiotherapy for a benign condition, to the best of our knowledge this is the first reported case of a low-grade extraskeletal Osteosarcoma of bone occurring following radiotherapy for thyroid cancer, and the only case reported in the Neck+Chest>Soft tissue of the head and neck region. , Here we a report a case of radiation induced Osteosarcoma of bone which developed 11 years after a single fraction of 700 cGy., Osteosarcoma following single fraction radiation prophylaxis for Heterotopic Ossification., The radiotherapy dose for this patient is lower than classically reported for radiation induced Malignant neoplasm of Neck+Chest>Soft tissue., The latency period between radiotherapy and Osteosarcoma of bone onset was 1.3 years shorter inside than outside the radiation field., Osteosarcoma after radiotherapy for Malignant neoplasm of prostate., Osteosarcoma after external beam radiation therapy for recurrent Malignant melanoma of choroid., Diagnostic criteria were fulfilled and the lesion was classified as a radiation induced Osteosarcoma of bone, Although a rare complication of ionizing radiation, radiation-induced Osteosarcoma of bone is now more frequently recognized as radiation therapy has become common and cancer survival has increased, Here we a report a case of radiation induced Osteosarcoma of bone which developed 11 years after a single fraction of 700 cGy, Radiation-induced Osteosarcoma of bone usually occurs after a long latency period of more than 10 years after the radiotherapy, Osteosarcoma following radiotherapy: a case report., Radiation-induced fibrosarcoma after radiotherapy for Osteosarcoma of bone in the Mandibular Condyle., Post-radiation Osteosarcoma of bone of the Bone structure of Bone structure of scapula., Radiation-induced osteosarcomas generally occur 3-30 years after exposure and are most common after radiotherapy for Cervical or Breast Carcinoma, Radiation-induced Osteosarcoma of bone is one of the rare types of radiation-induced Malignant neoplasm of Neck+Chest>Soft tissue , with the risk of radiation-induced osteosarcomas being only 0.01 % -0.03 % among all patients treated with radiotherapy, Radiation-induced Osteosarcoma of bone is a well-known but rare complication of radiotherapy for brain Neoplasms with a poor prognosis, The prognosis of patients developing Osteosarcoma of bone after radiotherapy for Malignant neoplasm of prostate is similar to other radiation-induced osteosarcomas occurring in the axial skeleton , with a 50 % overall mortality within the first year after diagnosis, Radiation-induced Osteosarcoma of bone usually occurs after a long latency period of more than 10 years after the radiotherapy, Twenty-seven years 11 months after orthovoltage radiotherapy of the right breast a 69-year-old woman developed a radiation-induced Osteosarcoma of bone of the right thoracic wall, We report a case of radiation-induced Osteosarcoma of bone developed from Bone structure of cranium after 7 years of craniospinal radiotherapy for pineoblastoma, Although the concepts of direct and indirect effects of radiation are fully applicable to low-LET ( linear energy transfer ) radioresistant Specimen Source Codes - Specimen Source Codes - tumor cells/normal tissues such as Osteosarcoma of bone cells and Chondrocyte , it is believed that radiation-associated damage to DNA does not play a major role in the mechanism of cell death in low-LET radiosensitive tumors/normal tissues such as malignant lymphoma cells and Specimen Source Codes - Lymphocytes, From these clinicopathological findings, both cases were diagnosed as radiation-induced Osteosarcoma of bone., Here we report two cases of radiation-induced Osteosarcoma of bone in the Nasal sinus after treatment for frontal glioma., As the prognosis of radiation-induced Osteosarcoma of bone is poorer than that of primary osteo-sarcoma, careful attention is required for consideration of the long-term survival of patients with glioma., Radiation-induced osteosarcomas appeared 16 and 12 years after radiotherapy in cases 1 and 2, respectively., Most radiation-induced osteosarcomas of the Bone structure of cranium are reported to arise in the facial bone or Nasal sinus after radiotherapy for Retinoblastoma and/or Pituitary Adenoma., Radiation-induced osteosarcomas after treatment for frontal Glioma: a report of two cases., Radiation-induced Osteosarcoma of bone of the Bone structure of cranium mimicking cutaneous Specimen Source Codes - Specimen Source Codes - tumor after treatment for frontal glioma., Radiation-induced Osteosarcoma of bone is one of the rare types of radiation-induced Malignant neoplasm of Neck+Chest>Soft tissue, with the risk of radiation-induced osteosarcomas being only 0.01%-0.03% among all patients treated with radiotherapy., Radiation-induced Malignant neoplasm of Neck+Chest>Soft tissue are recognized complications of radiation therapy and are associated with poor prognosis., There have been only four reported cases of radiation-induced osteosarcomas after radiotherapy for Glioma., Here, we report a unique case of radiation-induced osteosarcomas arising on the Bone structure of cranium and extending to the Skin Specimen Source Code, with a short latent period., BACKGROUND\nThe increasing incidence of radiation-induced Osteosarcoma of bone of the Maxilla and Head>Mandible (RIOSM) has become a significant problem that can limit long-term survival., In this case, Osteosarcoma of bone was possibly a radiation-induced Osteosarcoma of bone with a short latency period of 3 years., Radiation-induced Osteosarcoma of bone usually occurs after a long latency period of more than 10 years after the radiotherapy., A case of Osteosarcoma of bone arising in the craniofacial bone with a short latency period of 3 years after radiotherapy for maxillary squamous cell carcinoma is described., Osteosarcoma is one of the Neoplasms that may occur following exposure to radiation., As the prognosis of radiation-induced Osteosarcoma of bone is poorer than that of primary osteo-sarcoma, careful attention is required for consideration of the long-term survival of patients with glioma., This report describes the late recurrence of Malignant melanoma of choroid and subsequent radiation-induced Osteosarcoma of bone., Radiation-induced Osteosarcoma of bone is one of the rare types of radiation-induced Malignant neoplasm of Neck+Chest>Soft tissue, with the risk of radiation-induced osteosarcomas being only 0.01%-0.03% among all patients treated with radiotherapy., There have been only four reported cases of radiation-induced osteosarcomas after radiotherapy for Glioma., Although radiation-induced Osteosarcoma of bone is an uncommon but dire complication of radiotherapy, its incidence will probably increase in the future as the frequency of radiation treatment and cancer survival increase., We report a case of radiation-induced Osteosarcoma of bone developed from Bone structure of cranium after 7 years of craniospinal radiotherapy for pineoblastoma., The prognosis of patients developing Osteosarcoma of bone after radiotherapy for Malignant neoplasm of prostate is similar to other radiation-induced osteosarcomas occurring in the axial skeleton, with a 50% overall mortality within the first year after diagnosis., To our knowledge the only other case report of post-radiation Osteosarcoma of bone with a short latency period was a case of Osteosarcoma of bone in the craniofacial bone 3 years after radiotherapy for maxillary squamous cell carcinoma., Here, we report a unique case of radiation-induced osteosarcomas arising on the Bone structure of cranium and extending to the Skin Specimen Source Code, with a short latent period., Case of postradiation Osteosarcoma of bone with a short latency period of 3 years.[SEP]Relations: bone Osteosarcoma of bone has relations: disease_disease with Osteosarcoma of bone, disease_disease with Osteosarcoma of bone, contraindication with Teriparatide, contraindication with Teriparatide, disease_disease with Osteosarcoma of bone (disease), disease_disease with Osteosarcoma of bone (disease), disease_disease with bone sarcoma, disease_disease with bone sarcoma, disease_disease with telangiectatic osteogenic sarcoma, disease_disease with telangiectatic osteogenic sarcoma.", "label": "yes"}
{"original_question": "Is Erythropoietin effective for neuroprotection of Preterm Infants.", "id": "converted_4655", "sentence1": "Is Recombinant Erythropoietin effective for neuroprotection of Preterm Infants.", "sentence2": "BACKGROUND: High-dose EPO gene has been shown to have a neuroprotective effect in preclinical models of neonatal Brain Injuries, and phase 2 trials have suggested possible efficacy; however, the benefits and safety of this therapy in extremely preterm infants have not been established., There was no significant difference between the EPO gene group and the placebo group in the incidence of Cessation of life or severe neurodevelopmental impairment at 2 years of age (97 children [26%] vs. 94 children [26%]; relative risk, 1.03; 95% confidence interval, 0.81 to 1.32; P = 0.80). There were no significant differences between the groups in the rates of Retinal Diseases of Premature Birth, Intracranial Hemorrhage, Sepsis (Invertebrate), necrotizing enterocolitis, Bronchopulmonary Dysplasia, or Cessation of life or in the frequency of serious adverse events.CONCLUSIONS: High-dose EPO gene treatment administered to extremely preterm infants from 24 hours after birth through 32 weeks of postmenstrual age did not result in a lower risk of severe neurodevelopmental impairment or Cessation of life at 2 years of age., Based on existing evidence, it is still too early to recommend Recombinant Erythropoietin as the standard treatment for preterm Brain Injuries., Recombinant Recombinant Erythropoietin treatment of preterm infants did not result in neuroprotection at 2 years of age in two out of three published large randomized controlled trials; however, long-term follow-up of these infants is needed to come to definite conclusions.[SEP]Relations: Recombinant Erythropoietin has relations: drug_effect with Pruritus, drug_effect with Pruritus, drug_effect with Pruritus, drug_effect with Pruritus, drug_drug with Prednimustine, drug_drug with Prednimustine, drug_drug with Prednimustine, drug_drug with Prednimustine, drug_drug with Transcrocetinate, drug_drug with Transcrocetinate.", "label": "no"}
{"original_question": "Does resveratrol reduce cardiac remodeling?", "id": "converted_909", "sentence1": "Does resveratrol reduce Cardiac - anatomy qualifier remodeling?", "sentence2": "In conclusion, resveratrol attenuated Cardiac - anatomy qualifier oxidative damage and left ventricular remodeling and enhanced the decreased expression of Sirtuin 1 in hearts of old Rattus norvegicus with Pulmonary Emphysema and thus might be a therapeutic modality for Cardiac - anatomy qualifier injury complicated in chronic obstructive pulmonary disease (Chronic Obstructive Airway Disease)., In conclusion, resveratrol is a beneficial pharmacological tool that augments autophagy to bring about reverse remodeling in the postinfarction heart., Resveratrol administration reduced atrial CSPC loss, succeeded in preserving the functional abilities of CSPCs and mature Cardiac - anatomy qualifier cells, improved Cardiac - anatomy qualifier environment by reducing inflammatory state and decreased unfavorable ventricular remodeling of the diabetic heart, leading to a marked recovery of ventricular function. These findings indicate that Respiratory syncytial virus can constitute an adjuvant therapeutic option in DCM prevention.[SEP]Relations: Resveratrol has relations: drug_drug with Dipyridamole, drug_drug with Dipyridamole, drug_drug with Acenocoumarol, drug_drug with Acenocoumarol, drug_drug with Tranilast, drug_drug with Tranilast, drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Reteplase, drug_drug with Reteplase.", "label": "yes"}
{"original_question": "Are synonymous sites in primates and rodents functionally constrained?", "id": "converted_4100", "sentence1": "Are synonymous sites in Primates and Rodent functionally constrained?", "sentence2": "To resolve this contradiction between expectations and observations, we used processed Pseudogenes as a model for strict neutral evolution, and estimated selective constraint on synonymous sites using the rate of Substitution - ActClass at pseudosynonymous and pseudononsynonymous sites in Pseudogenes as the neutral expectation. After controlling for the effects of GC content, our results were similar to those from previous studies, i.e., synonymous sites in Primates exhibited evidence for higher selective constraint that those in Rodent. Specifically, our results indicated that in Primates up to 24% of synonymous sites could be under purifying selection, while in Rodent synonymous sites evolved neutrally. [SEP]", "label": "no"}
{"original_question": "Is lumbar puncture the first test that should be performed on a patient with increased intracranial pressure?", "id": "converted_4538", "sentence1": "Is lumbar puncture the first test that should be performed on a patient with increased intracranial pressure?", "sentence2": "As an emergency diagnostic procedure, Diagnostic lumbar puncture is indicated when CNS infection is suspected or to establish the diagnosis of Subarachnoid Hemorrhage when results of cranial computed tomography are normal. The major contraindication is elevated intracranial pressure with evidence of a mass lesion., Brain shift is a contraindication to LP, whether CSF pressure is raised or not, and whether Papilledema is present or not. Subsequently, recommendations are offered for indications to perform X-Ray Computed Tomography before LP, grouped according to the safety and clinical utility of LP., Cessation of life following lumbar puncture (LP) is feared by physicians. Many opinions are found in literature on the question whether computed cranial tomography (X-Ray Computed Tomography) should be performed before LP, to prevent Hernia., Headache, caused by Cerebrospinal Fluid (CSF) Hypotension, is a frequent complication of lumbar puncture; hematic patch is a therapeutic option for severe cases. The most serious complication is Cerebral Hernia and, for its prevention, computed tomography (X-Ray Computed Tomography) or cerebral magnetic resonance imaging (MRI) must always be performed before lumbar puncture: a lesion with evident mass effect is a contraindication., Lumbar puncture (LP) is usually contra-indicated in situations where the Intracranial:Pres:Pt:Skull:Qn is suspected to be high., Low-dose cranial computed tomography (LD-Computer-Assisted Cognitive Training) based on iterative reconstruction has been shown to have sufficient image quality to assess Cerebrospinal Fluid spaces (CSF) and midline structures but not to exclude subtle parenchymal pathologies. Patients without focal Neurologic Deficits often undergo Computer-Assisted Cognitive Training before lumbar puncture (LP) to exclude contraindications to LP including brain Hernia or increased CSF pressure., Lumbar puncture is performed routinely for diagnostic and therapeutic purposes in Pseudotumor Cerebri, despite lumbar puncture being classically contraindicated in the setting of raised intracranial pressure., Although generally considered innocuous, there may be considerable danger when lumbar puncture is performed in the presence of increased intracranial pressure, especially when a mass lesion is present., Lumbar puncture should be avoided if focal neurologic findings suggest concomitant mass lesion, as in brain abscess, and lumbar puncture should be approached with great caution if Meningitis is accompanied by evidence of significant Intracranial Hypertension., There are few abnormal X-Ray Computed Tomography scans presenting a contraindication for lumbar puncture and the majority of these patients usually have clinical signs to suggest raised intracranial pressure.[SEP]Relations: pseudotumor cerebri has relations: disease_phenotype_positive with Increased intracranial pressure, disease_phenotype_positive with Increased intracranial pressure. Intracranial Hypertension has relations: contraindication with Brompheniramine, contraindication with Brompheniramine, contraindication with Phenylpropanolamine, contraindication with Phenylpropanolamine, contraindication with Trolnitrate, contraindication with Trolnitrate, contraindication with Butorphanol, contraindication with Butorphanol.", "label": "no"}
{"original_question": "Is REGN5458 a single-targeted antibody?", "id": "converted_4606", "sentence1": "Is REGN5458 a single-targeted antibody?", "sentence2": "CD3 Antigens Antigens-engaging Antibodies, Bispecific (bsAbs) and Chimeric antigen receptor (actomyosin contractile ring) T-Lymphocyte are potent therapeutic approaches for redirecting patient T-Lymphocyte to recognize and kill Neoplasms. Here we describe a fully human bsAb (REGN5458) that binds to B-Cell Maturation Antigen (bis(3-bis(4-chlorophenyl)methyl-4-dimethylaminophenyl)amine) and CD3 Antigens Antigens, and compare its antitumor activities vs those of anti-bis(3-bis(4-chlorophenyl)methyl-4-dimethylaminophenyl)amine actomyosin contractile ring T-Lymphocyte to identify differences in efficacy and mechanism of action. [SEP]Relations: cell maturation has relations: bioprocess_protein with ANGPTL8, bioprocess_protein with ANGPTL8, bioprocess_protein with SOX8, bioprocess_protein with SOX8, bioprocess_protein with CTNNB1, bioprocess_protein with CTNNB1, bioprocess_protein with SOX18, bioprocess_protein with SOX18, bioprocess_protein with BFSP1, bioprocess_protein with BFSP1.", "label": "no"}
{"original_question": "Are circular RNAs implicated in diseases of the eye?", "id": "converted_4439", "sentence1": "Are RNA, Circular implicated in diseases of the Eye Specimen Source Code?", "sentence2": "n this review, we summarized the function of circRNAs and indicated their roles in the pathogenesis of Derung Chinese, which may provide new therapeutic targets for clinical treatment., This study aimed to determine whether RNA, Circular (circRNAs) in whole blood could be served as novel non-invasive biomarkers for proliferative Diabetic Retinopathy (PDR).M, Discovery and validation of hsa_circ_0001953 as a potential biomarker for proliferative Diabetic Retinopathy in Homo sapiens blood., Circular RNA hsa_circ_0000034 (circ_0000034) was reported to be upregulated in RB tissues., We recently identified a circular RNA transcript (circGRM4) that is significantly upregulated in the Eye Specimen Source Code of Cystathionine β-synthase-deficient mice., Circular and long non-coding RNA and their role in ophthalmologic diseases., In this review, we summarize current knowledge about gene expression regulators - long non-coding and circular RNA molecules in Eye Specimen Source Code diseases., fied a circular RNA transcript (circGRM4) that is significantly upregulated in the Eye Specimen Source Code of Cystathionine β-synthase-deficient mice. We also discovered, Non-Alcoholic Fatty Liver Disease Activity Score (circRNAs) are dominant players regulating their parental Genes' expression dynamics, their importance in Ocular (intended site) biology has not been appreciated. Progress in gene-cent, Circular RNA Expression Profiling Identifies Glaucoma-Related Circular RNA in Various Chronic Ocular Hypertension Rat Models, Circular RNA profiling in the Cystathionine-β-synthase mutant mouse reveals novel gene targets for Hyperhomocysteinemia induced Ocular (intended site) disorders, Circular and long non-coding RNA and their role in ophthalmologic diseases, Comprehensive circular RNA profiling of proliferative vitreoretinopathy and its clinical significance,  these findings, we completed the first in-depth study of Rattus norvegicus retinal circular RNA expression profiling to identify probable biomarkers for the diagnosis of Glaucoma (eukaryote). Two ocu, Circular RNA profiling in the Cystathionine-β-synthase mutant mouse reveals novel gene targets for Hyperhomocysteinemia induced Ocular (intended site) disorders., Although, increasing evidence suggests that circRNAs may also contribute in different Ocular (intended site) diseases, the outline of circRNAs in Ocular (intended site) diseases remains obscure, In this review, we summarize current knowledge about gene expression regulators - long non-coding and circular RNA molecules in Eye Specimen Source Code diseases, Recent studies recognized the vital roles that circRNAs played in the pathogenesis of various Eye Specimen Source Code diseases, highlighting circRNAs as promising biomarkers for diagnosis and assessment of progression and prognosis, Partly because their circularity makes them resistant to degradation, they hold great promise as unique biomarkers for Ocular (intended site) and CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Central Nervous System) disorders, In this review we consider the current state of knowledge regarding the potential role and underlying mechanism of circRNAs in Ocular (intended site) diseases including Pterygium Of Conjunctiva And Cornea, age-related Cataract, Glaucoma (eukaryote), Diabetic Retinopathy, Retinoblastoma, retinal vascular dysfunction and Hyperhomocysteinemia induced Ocular (intended site) diseases, emphasizing that circRNAs could be promising biomarkers for the diagnosis and prognosis evaluation., Recent studies recognized the vital roles that circRNAs played in the pathogenesis of various Eye Specimen Source Code diseases, highlighting circRNAs as promising biomarkers for diagnosis and assessment of progression and prognosis., Although, increasing evidence suggests that circRNAs may also contribute in different Ocular (intended site) diseases, the outline of circRNAs in Ocular (intended site) diseases remains obscure., Circular RNA: Novel Promising Biomarkers in Ocular Diseases., This review summarizes our current perception of the properties, biogenesis, and functions of circRNAs and the development of circRNA researches related to ophthalmologic diseases, including Diabetic Retinopathy, age-related macular degeneration, Retinal Diseases of Premature Birth, Glaucoma (eukaryote), Cornea neovascularization, Cataract, Pterygium Of Conjunctiva And Cornea, proliferative vitreoretinopathy, Retinoblastoma, and Malignant melanoma of Eye Specimen Source Code., CircRNA Is a Rising Star in Researches of Ocular Diseases., Interventions targeting circRNAs provide insights for developing novel treatments for these Ocular (intended site) diseases., Future circRNAs-targeted intervention may become a novel therapeutic tool for the treatment of Ocular (intended site) diseases., Findings also revealed several MicroRNAs that are specific to each circRNA suggesting their roles in HHcy induced Ocular (intended site) disorders., Therefore, circRNAs may serve as potential regulators of Cornea LG., Expression profiling of RNA, Circular in Glaucoma (eukaryote), which is a form of Optic Neuropathy, has not been performed to date., Although RNA, Circular (circRNAs) are dominant players regulating their parental Genes' expression dynamics, their importance in Ocular (intended site) biology has not been appreciated., Progress in gene-centered analytics via improved microarray and bioinformatics are enabling dissection of genomic pathways however there is an acute under-representation of RNA, Circular in Ocular (intended site) disorders., Circular RNA constitute an inherent gene regulatory axis in the Mammals Eye Specimen Source Code and brain 1., Together with the target MicroRNAs underlying the top differentially expressed RNA, Circular, a new target of hsa_circ_0023826 and its host gene TENM4 gene gene were identified and further verified in the aqueous Humor therapy of Glaucoma (eukaryote) patients, indicating a promising biomarker for the disease., Recent studies suggest that they are differentially expressed both in healthy Ocular (intended site) tissues as well as in Eye Specimen Source Code pathologies, such as neovascularization, proliferative vitreoretinopathy, Glaucoma (eukaryote), Cataract, Ocular (intended site) malignancy or even VANGL2 gene.[SEP]Relations: retinal disease has relations: disease_disease with macular holes, disease_disease with macular holes, disease_disease with Eye Specimen Source Code disease, disease_disease with Eye Specimen Source Code disease. CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS has relations: anatomy_protein_present with RNASE6, anatomy_protein_present with RNASE6, anatomy_protein_present with RNASE1, anatomy_protein_present with RNASE1, anatomy_protein_present with RNASEH2A, anatomy_protein_present with RNASEH2A.", "label": "yes"}
{"original_question": "Are ultraconserved enhancers important for normal development?", "id": "converted_2794", "sentence1": "Are ultraconserved enhancers important for normal development?", "sentence2": "Ultraconserved Enhancers Are Required for Normal Development., However, initial deletion studies in CASP14 gene revealed that loss of such extraordinarily constrained sequences had no immediate impact on viability. Here, we show that ultraconserved enhancers are required for normal development. , Here, we show that ultraconserved enhancers are required for normal development.[SEP]", "label": "yes"}
{"original_question": "Have C12orf65 mutations been associated with axonal neuropathy and optic atrophy?", "id": "converted_865", "sentence1": "Have MTRFR gene mutations been associated with Axonal Neuropathy and Optic Atrophy 1?", "sentence2": "Novel MTRFR Genes mutations in patients with Axonal Neuropathy and Optic Atrophy 1, Charcot-Marie Tooth disease (CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate) forms a clinically and genetically heterogeneous group of disorders. Although a number of disease genes have been identified for CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate, the Genes discovery for some complex form of CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate has lagged behind. The association of Neuropathy and Optic Atrophy 1 (also known as CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate type 6) has been described with autosomaldominant, recessive and X-linked modes of inheritance. Gene Mutation in MFN2 Genes have been found to cause dominant forms of Hereditary motor and sensory Neuropathy with Optic Atrophy 1 (disorder). Phosphoribosylpyrophosphate synthetase-I mutations cause X-linked Hereditary motor and sensory Neuropathy with Optic Atrophy 1 (disorder), but until now, mutations in the recessive forms of disease have never been identified.METHODS: We here describe a family with three affected individuals who inherited in an autosomal recessive fashion a childhood onset Neuropathy and Optic Atrophy 1. Using homozygosity mapping in the family and exome sequencing in two affected individuals we identified a novel Protein Info-truncating Mutation Abnormality in the MTRFR Genes Genes, which encodes for a Protein Info involved in mitochondrial translation, Novel MTRFR Genes mutations in patients with Axonal Neuropathy and Optic Atrophy 1., Our study broadens the phenotypic spectrum of MTRFR Genes defects and highlights the triad of Optic Atrophy 1, Axonal Neuropathy and Paraparesis, Spastic as its key clinical features., MTRFR Genes participates in the process of mitochondrial translation and has been shown to be associated with a spectrum of phenotypes, including early onset Optic Atrophy 1, progressive encephalomyopathy, Peripheral Nervous System Diseases, and Paraparesis, Spastic.We used whole-genome homozygosity mapping as well as exome sequencing and targeted Genes sequencing to identify novel MTRFR Genes disease-causing mutations in seven affected individuals originating from two consanguineous families., A homozygous Mutation Abnormality of MTRFR Genes causes spastic paraplegia with Optic Atrophy 1 and Neuropathy (SPG55)., Optic atrophy and a Leigh-like syndrome due to mutations in the c12orf65 Genes: report of a novel Mutation Abnormality and review of the literature., Recently, we identified the causative Genes, MTRFR Genes, that was reported the Genes for Leigh Disease, for autosomal recessive spastic paraplegia with Optic Atrophy 1 and Neuropathy (SPG55)., We describe 2 siblings with fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether heterozygous mutations in the recently identified MTRFR Genes Genes who presented with Optic Atrophy 1 and mild developmental delays and subsequently developed bilateral, symmetric lesions in the brainstem reminiscent of Leigh Disease., MTRFR Genes participates in the process of mitochondrial translation and has been shown to be associated with a spectrum of phenotypes, including early onset Optic Atrophy 1, progressive encephalomyopathy, Peripheral Nervous System Diseases, and Paraparesis, Spastic.We used whole-genome homozygosity mapping as well as exome sequencing and targeted Genes sequencing to identify novel MTRFR Genes disease-causing mutations in seven affected individuals originating from two consanguineous families, Our study broadens the phenotypic spectrum of MTRFR Genes defects and highlights the triad of Optic Atrophy 1, Axonal Neuropathy and Paraparesis, Spastic as its key clinical features, CONCLUSIONS: This work describes a Mutation Abnormality in the MTRFR Genes Genes that causes recessive form of Hereditary motor and sensory Neuropathy with Optic Atrophy 1 (disorder) and confirms the role of Abnormality of mitochondrial metabolism in this complex Axonal Neuropathy., MTRFR Genes participates in the process of mitochondrial translation and has been shown to be associated with a spectrum of phenotypes, including early onset Optic Atrophy 1, progressive encephalomyopathy, Peripheral Nervous System Diseases, and Paraparesis, Spastic.We used whole-genome homozygosity mapping as well as exome sequencing and targeted Genes sequencing to identify novel MTRFR Genes disease-causing mutations in seven affected individuals originating from two consanguineous families. , Our study broadens the phenotypic spectrum of MTRFR Genes defects and highlights the triad of Optic Atrophy 1, Axonal Neuropathy and Paraparesis, Spastic as its key clinical features. , We described a large consanguineous family with Neuropathy and Optic Atrophy 1 carrying a loss of function Mutation Abnormality in the MTRFR Genes Genes., In these patients, we identified a homozygous splice Mutation Abnormality, g.21043 T>A (c.282+2 T>A) which leads to skipping of exon 2. Our study broadens the phenotypic spectrum of MTRFR Genes defects and highlights the triad of Optic Atrophy 1, Axonal Neuropathy and Paraparesis, Spastic as its key clinical features., This work describes a Mutation Abnormality in the MTRFR Genes Genes that causes recessive form of Hereditary motor and sensory Neuropathy with Optic Atrophy 1 (disorder) and confirms the role of Abnormality of mitochondrial metabolism in this complex Axonal Neuropathy., Our study broadens the phenotypic spectrum of MTRFR Genes defects and highlights the triad of Optic Atrophy 1, Axonal Neuropathy and Paraparesis, Spastic as its key clinical features., Novel MTRFR Genes mutations in patients with Axonal Neuropathy and Optic Atrophy 1., This work describes a Mutation Abnormality in the MTRFR Genes Genes that causes recessive form of Hereditary motor and sensory Neuropathy with Optic Atrophy 1 (disorder) and confirms the role of Abnormality of mitochondrial metabolism in this complex Axonal Neuropathy., A homozygous Mutation Abnormality of MTRFR Genes causes spastic paraplegia with Optic Atrophy 1 and Neuropathy (SPG55)., MTRFR Genes participates in the process of mitochondrial translation and has been shown to be associated with a spectrum of phenotypes, including early onset Optic Atrophy 1, progressive encephalomyopathy, Peripheral Nervous System Diseases, and Paraparesis, Spastic.We used whole-genome homozygosity mapping as well as exome sequencing and targeted Genes sequencing to identify novel MTRFR Genes disease-causing mutations in seven affected individuals originating from two consanguineous families.[SEP]Relations: Optic atrophy has relations: disease_phenotype_positive with neurodevelopmental disorder, mitochondrial, with abnormal movements and lactic acidosis, with or without seizures, disease_phenotype_positive with neurodevelopmental disorder, mitochondrial, with abnormal movements and lactic acidosis, with or without seizures, disease_phenotype_positive with cerebellar ataxia with Neuropathy and bilateral vestibular areflexia syndrome, disease_phenotype_positive with cerebellar ataxia with Neuropathy and bilateral vestibular areflexia syndrome, disease_phenotype_positive with mitochondrial hypertrophic cardiomyopathy with lactic acidosis due to MTO1 deficiency, disease_phenotype_positive with mitochondrial hypertrophic cardiomyopathy with lactic acidosis due to MTO1 deficiency, disease_phenotype_positive with neurodevelopmental disorder with visual defects and brain anomalies, disease_phenotype_positive with neurodevelopmental disorder with visual defects and brain anomalies, disease_phenotype_positive with Mowat-Wilson syndrome due to a ZEB2 point Mutation Abnormality, disease_phenotype_positive with Mowat-Wilson syndrome due to a ZEB2 point Mutation Abnormality.", "label": "yes"}
{"original_question": "Can FTO promote pancreatic cancer development?", "id": "converted_4258", "sentence1": "Can FTO protein, human promote Malignant neoplasm of pancreas development?", "sentence2": "METTL3 gene demethylase FTO protein, human protein, human suppresses Malignant neoplasm of pancreas tumorigenesis by demethylating PJA2 gene gene and inhibiting Wnt signaling., Moreover, FTO protein, human protein, human demethylated the METTL3 gene modification of praja ring finger ubiquitin ligase 2 (PJA2 gene gene), thereby reducing its mRNA decay, suppressing Wnt signaling, and ultimately restraining the proliferation, invasion, and metastasis of Malignant neoplasm of pancreas cells.[SEP]Relations: malignant exocrine pancreas neoplasm has relations: disease_disease with exocrine pancreatic carcinoma, disease_disease with exocrine pancreatic carcinoma, disease_disease with pancreatoblastoma, disease_disease with pancreatoblastoma, disease_disease with pancreatic exocrine neoplasm, disease_disease with pancreatic exocrine neoplasm, disease_disease with malignant pancreatic neoplasm, disease_disease with malignant pancreatic neoplasm, disease_disease with pancreatic intraductal papillary-mucinous neoplasm, disease_disease with pancreatic intraductal papillary-mucinous neoplasm.", "label": "no"}
{"original_question": "Does Rhamnose have any effect on aging?", "id": "converted_3046", "sentence1": "Does Rhamnose have any effect on aging?", "sentence2": "The Monosaccharides analysis showed that rhamnose (SKIN/HAIR/EYE PIGMENTATION, VARIATION IN, 2 (disorder)) and Glucose measurement (glutamate) may play vital roles in maintaining the antioxidant and anti-aging activities. , Some of these mechanisms will be reviewed as well as the capacity of fucose- and rhamnose-rich oligo- and polysaccharides (FROP and RROP) to counteract several of the mechanisms involved in skin aging.[SEP]Relations: response to rhamnose has relations: bioprocess_bioprocess with response to hexose, bioprocess_bioprocess with response to hexose, bioprocess_bioprocess with cellular response to rhamnose stimulus, bioprocess_bioprocess with cellular response to rhamnose stimulus. Increased groin pigmentation with raindrop depigmentation has relations: phenotype_phenotype with Mixed hypo- and hyperpigmentation of the skin, phenotype_phenotype with Mixed hypo- and hyperpigmentation of the skin, phenotype_phenotype with Irregular hyperpigmentation, phenotype_phenotype with Irregular hyperpigmentation, disease_phenotype_positive with thumb deformity-alopecia-pigmentation anomaly syndrome, disease_phenotype_positive with thumb deformity-alopecia-pigmentation anomaly syndrome.", "label": "yes"}
{"original_question": "Does low T3 negatively affect prognosis of patients after cardiac surgery?", "id": "converted_1567", "sentence1": "Does low T3 thoracic segmental innervation negatively affect prognosis of patients after cardiac surgery?", "sentence2": "ur findings suggest that the development of LCOS after congenital heart surgery is associated with decreased total and free T3 thoracic segmental innervation thoracic segmental innervation, and increased interleukin-8 receptor binding activity levels at 48 hours, and preoperative Adenosine A2B Receptor Antagonist TT-4 level is an independent predictor of LCOS., Low basal cubic foot concentration can reliably predict the occurrence of postoperative AF in CABG patients., A relevant finding was that the days of post-operative hospitalization (10+/-3 days, means+/-S.D.) was inversely correlated with the slope of the recovery of T3 thoracic segmental innervation thoracic segmental innervation concentration (P<0.001) or with the area under the plasma curves of T3 thoracic segmental innervation thoracic segmental innervation (P=0.024, time range 72-144 h) and the FT3/FT4 ratio (P=0.037, time range 72-144 h) during the post-operative period. [SEP]Relations: interleukin-8 receptor activity has relations: molfunc_protein with CXCR2, molfunc_protein with CXCR2, molfunc_protein with CXCR1, molfunc_protein with CXCR1. insect larval thoracic segment has relations: anatomy_anatomy with insect larval prothoracic segment, anatomy_anatomy with insect larval prothoracic segment, anatomy_anatomy with insect larval metathoracic segment, anatomy_anatomy with insect larval metathoracic segment, anatomy_anatomy with insect larval mesothoracic segment, anatomy_anatomy with insect larval mesothoracic segment.", "label": "yes"}
{"original_question": "Is there any software for automated analysis of immuno-histochemistry images?", "id": "converted_528", "sentence1": "Is there any software for automated analysis of immuno-histochemistry images?", "sentence2": "The LIM homeobox gene LHX2 wt Allele is expressed in cortical progenitors during development and also in the superficial layers of the Neocortex in maturity. However, analysis of LHX2 wt Allele function at later stages of cortical development has been hampered by severe phenotypes associated with early loss of function. , The vein graft samples were obtained on each time point after surgery. The expression of the EDRz transfected in the vein graft was detected using a fluorescent microscope. Early growth response gene-1 (EGR1 protein, human) RNA, Messenger was measured using reverse transcription-PCR and in situ hybridization. And the protein expression of EGR1 protein, human was detected by using western blot and immunohistochemistry analyses., Protein Glutamine gamma Glutamyltransferase 2 (TGM2 protein, human) is a multifunctional Enzyme [APC], which amongst other functions, is involved in cell differentiation. Therefore, we hypothesized that TGM2 protein, human contributes to differentiation of OPCs into OLGs and thereby stimulates remyelination. [SEP]Relations: Neocortex has relations: anatomy_protein_present with ENO2, anatomy_protein_present with ENO2, anatomy_protein_present with TMCO3, anatomy_protein_present with TMCO3, anatomy_protein_present with TMCO6, anatomy_protein_present with TMCO6. Protein S human has relations: drug_drug with Ifosfamide, drug_drug with Ifosfamide, drug_drug with Ifosfamide, drug_drug with Ifosfamide.", "label": "yes"}
{"original_question": "Is Lennox-Gastaut Syndrome usually diagnosed in older adults?", "id": "converted_2117", "sentence1": "Is Lennox-Gastaut syndrome usually diagnosed in older adults?", "sentence2": "We studied 15 Langer-Giedion Syndrome patients (mean age ± 1 standard deviation [SD] = 28.7 ± 10.6 years) and 17 healthy controls (mean age ± 1 SD = 27.6 ± 6.6 years),  children with Lennox-Gastaut syndrome, Lennox-Gastaut syndrome (Langer-Giedion Syndrome) is a severe pediatric Epilepsy syndrome characterized by mixed seizures, Mental deterioration, and generalized slow (<3 Hz) spike wave discharges on electroencephalography, Clinical course and results of therapy were analysed in the group of 92 children, aged between 3 and 9 years, with diagnosed Lennox-Gastaut syndrome., We report the case of a 27-year-old Homo sapiens with a neurodevelopmental syndrome due to a 15q duplication, with Intellectual Disability, psychiatric disturbances, and an epileptic phenotype diagnosed as late-onset Lennox-Gastaut syndrome., Lennox-Gastaut syndrome is a relatively rare Epilepsy syndrome that usually begins in early-mid childhood and is characterized by multiple seizure types, particularly generalized seizures, which are often resistant to antiepileptic drug medication, Lennox-Gastaut syndrome is a severe childhood Epilepsy syndrome characterised by the diagnostic triad of a slow spike and wave pattern on electroencephalogram, multiple seizure types and developmental delay, We report the case of a 27-year-old Homo sapiens with a neurodevelopmental syndrome due to a 15q duplication, with Intellectual Disability, psychiatric disturbances, and an epileptic phenotype diagnosed as late-onset Lennox-Gastaut syndrome.., The Lennox-Gastaut syndrome, a severe form of Epilepsy that usually begins in early childhood, is difficult to treat., Lennox-Gastaut syndrome is a relatively rare Epilepsy syndrome that usually begins in early-mid childhood and is characterized by multiple seizure types, particularly generalized seizures, which are often resistant to antiepileptic drug medication., The Lennox-Gastaut syndrome is an age-specific disorder, characterised by Nonepileptic Seizures, a characteristic electroencephalogram (EEG), psychomotor delay and behaviour disorders. It occurs more frequently in males and onset is usually before the age of eight, with a peak between three and five years. Late cases occurring in adolescence and early adulthood have rarely been reported. [SEP]Relations: Lennox-Gastaut syndrome has relations: disease_disease with childhood-onset Epilepsy syndrome, disease_disease with childhood-onset Epilepsy syndrome, disease_disease with childhood electroclinical syndrome, disease_disease with childhood electroclinical syndrome, disease_disease with childhood onset epileptic encephalopathy, disease_disease with childhood onset epileptic encephalopathy, disease_disease with syndromic disease, disease_disease with syndromic disease, disease_disease with developmental and epileptic encephalopathy, disease_disease with developmental and epileptic encephalopathy.", "label": "no"}
{"original_question": "Is the gene DUX4 epigenetically regulated in somatic cells?", "id": "converted_543", "sentence1": "Is the gene DUX4L2 wt Allele epigenetically regulated in Diploid Cell?", "sentence2": "There are several Genes on chromosome 4q35 region including DUX4L2 wt Allele within D4Z4 Repeat. Transcription of these Genes is usually repressed by epigenetic modifications of this Region of chromosome and also accumulation of transcriptional repressors to the Repeat Object array., Recent studies provide compelling evidence that a retrotransposed gene in the D4Z4 Repeat Object, DUX4L2 wt Allele, is expressed in the Homo sapiens Germline and then epigenetically silenced in somatic tissues. , The Homo sapiens double-homeodomain retrogene DUX4L2 wt Allele is expressed in the Testis and epigenetically repressed in somatic tissues., Facioscapulohumeral dystrophy (Muscular Dystrophy, Facioscapulohumeral) is a progressive Muscular Dystrophy caused by decreased epigenetic repression of the D4Z4 macrosatellite Repeat and ectopic expression of DUX4L2 wt Allele, a retrogene encoding a Germline TRANSCRIPTION FACTOR encoded in each Repeat Object.,  These CASP14 gene recapitulate important epigenetic and DUX4L2 wt Allele expression attributes seen in patients and controls, respectively, including high DUX4L2 wt Allele expression levels in the Germline, (incomplete) epigenetic repression in somatic tissue, and Muscular Dystrophy, Facioscapulohumeral-specific variegated DUX4L2 wt Allele expression in sporadic muscle nuclei associated with D4Z4 chromatin relaxation., DUX4L2 wt Allele, a retrogene contained in the D4Z4 Repeat, is normally epigenetically silenced in Diploid Cell., In contrast to control Specimen Source Codes - Skeletal muscle and most other somatic tissues, full-length DUX4L2 wt Allele transcript and Protein Info is expressed at relatively abundant levels in Homo sapiens Testis, most likely in the Germ Cells. Induced Pluripotent (iPS) cells also express full-length DUX4L2 wt Allele and differentiation of control Induced Pluripotent Stem Cells to embryoid bodies suppresses expression of full-length DUX4L2 wt Allele, whereas expression of full-length DUX4L2 wt Allele persists in differentiated Muscular Dystrophy, Facioscapulohumeral Induced Pluripotent Stem Cells. Together, these findings indicate that full-length DUX4L2 wt Allele is normally expressed at specific developmental stages and is suppressed in most somatic tissues., Recent studies provide compelling evidence that a retrotransposed gene in the D4Z4 Repeat Object, DUX4L2 wt Allele, is expressed in the Homo sapiens Germline and then epigenetically silenced in somatic tissues., DUX4L2 wt Allele, a retrogene contained in the D4Z4 Repeat, is normally epigenetically silenced in Diploid Cell. , DUX4L2 wt Allele, a retrogene contained in the D4Z4 Repeat, is normally epigenetically silenced in Diploid Cell., Recent studies provide compelling evidence that a retrotransposed gene in the D4Z4 Repeat Object, DUX4L2 wt Allele, is expressed in the Homo sapiens Germline and then epigenetically silenced in somatic tissues., Normally expressed in the Testis and epigenetically repressed in somatic tissues, DUX4L2 wt Allele expression in Specimen Source Codes - Skeletal muscle induces expression of many Germline, Stem cells, and other Genes that might account for the pathophysiology of Muscular Dystrophy, Facioscapulohumeral., Recent studies provide compelling evidence that a retrotransposed gene in the D4Z4 Repeat Object, DUX4L2 wt Allele, is expressed in the Homo sapiens Germline and then epigenetically silenced in somatic tissues, The Homo sapiens double-homeodomain retrogene DUX4L2 wt Allele is expressed in the Testis and epigenetically repressed in somatic tissues, Normally expressed in the Testis and epigenetically repressed in somatic tissues, DUX4L2 wt Allele expression in Specimen Source Codes - Skeletal muscle induces expression of many Germline, Stem cells, and other Genes that might account for the pathophysiology of Muscular Dystrophy, Facioscapulohumeral, DUX4L2 wt Allele, a retrogene contained in the D4Z4 Repeat, is normally epigenetically silenced in Diploid Cell, Recent studies provide compelling evidence that a retrotransposed gene in the D4Z4 Repeat Object, DUX4L2 wt Allele, is expressed in the Homo sapiens Germline and then epigenetically silenced in somatic tissues, The identification of the gene(s) and the exact epigenetic pathway underlining this Disease will be mandatory to increase the rate of diagnosis for FACIOSCAPULOHUMERAL MUSCULAR DYSTROPHY 1B patients and to confirm the hypothesis of a common FACIOSCAPULOHUMERAL MUSCULAR DYSTROPHY 1 and FACIOSCAPULOHUMERAL MUSCULAR DYSTROPHY 1B pathophysiological pathway involving DUX4L2 wt Allele gene, This Gene Deletion Abnormality induces epigenetic modifications that affect the expression of several Genes located in the vicinity. In each D4Z4 element, we identified the double homeobox 4 (DUX4L2 wt Allele) gene. DUX4L2 wt Allele expresses a TRANSCRIPTION FACTOR that plays a major role in the development of Muscular Dystrophy, Facioscapulohumeral through the initiation of a large gene dysregulation cascade that causes myogenic differentiation defects, Atrophic and reduced response to oxidative stress. , decreased epigenetic repression and variegated expression of DUX4L2 wt Allele in Specimen Source Codes - Skeletal muscle, (incomplete) epigenetic repression in somatic tissue,, Facioscapulohumeral dystrophy (Muscular Dystrophy, Facioscapulohumeral) is characterized by chromatin relaxation of the D4Z4 macrosatellite array on Chromosomes, Human, Pair 4 and expression of the D4Z4-encoded DUX4L2 wt Allele gene in Specimen Source Codes - Skeletal muscle., derepression of the DUX4L2 wt Allele retrogene, The aim of our study was to identify relationships between epigenetic parameters correlating with a relaxed chromatin state of the DUX4L2 wt Allele promoter region and clinical severity as measured by a clinical severity score or muscle pathologic changes in D4Z4 contraction-dependent (FACIOSCAPULOHUMERAL MUSCULAR DYSTROPHY 1) and -independent (FACIOSCAPULOHUMERAL MUSCULAR DYSTROPHY 1B) facioscapulohumeral Muscular Dystrophy patients. , Specifically, abundance of RNA transcripts encoded by the DUX4L2 wt Allele locus correlated to differential DNA methylation and Histone H3 Trimethyl Lys36 enrichment., Together, these findings indicate that full-length DUX4L2 wt Allele is normally expressed at specific developmental stages and is suppressed in most somatic tissue[SEP]Relations: Transcriptional regulation of Pluripotent stem cells has relations: pathway_protein with PBX1, pathway_protein with PBX1, pathway_protein with SMAD4, pathway_protein with SMAD4, pathway_protein with KLF4, pathway_protein with KLF4, pathway_protein with SALL4, pathway_protein with SALL4, pathway_protein with SMAD2, pathway_protein with SMAD2.", "label": "yes"}
{"original_question": "Is it feasible to obtain DNA read lengths that exceed 30 Kb?", "id": "converted_2140", "sentence1": "Is it feasible to obtain DNA read lengths that exceed 30 Kb?", "sentence2": "Single-molecule, real-time sequencing (NCOR2 wt Allele) developed by Pacific BioSciences produces longer reads than secondary generation sequencing technologies such as Illumina. The long read length enables PacBio sequencing to close gaps in Genome Assembly Sequence, reveal structural variations, and identify gene isoforms with higher accuracy in transcriptomic sequencing.,  Third-generation sequencing, with read lengths>10 kb, will improve the assembly of complex genomes, but these techniques require high-molecular-weight Genomic DNA (gDNA), and gDNA extraction protocols used for obtaining smaller Fragment of (qualifier value) for short-read sequencing are not suitable for this purpose., The emergence and development of so called third generation sequencing platforms such as PacBio has permitted exceptionally long reads (over 20 kb) to be generated.[SEP]", "label": "no"}
{"original_question": "Is chlorotoxin a peptide?", "id": "converted_2795", "sentence1": "Is chlorotoxin a peptide?", "sentence2": "chlorotoxin peptide , Chlorotoxin (cyclophosphamide) is a 36-amino-acid disulfide-containing peptide derived from the Venom (disposition) of the scorpion Leiurus quinquestriatus., The mature Odontobuthus doriae chlorotoxin peptide has a 35-amino-acid residue and four disulfide bounds. , Chlorotoxin (cyclophosphamide), a disulfide-rich peptide from the scorpion Leiurus quinquestriatus,[SEP]Relations: Cyclophosphamide has relations: drug_drug with Chloroquine, drug_drug with Chloroquine, drug_drug with Cephalexin, drug_drug with Cephalexin, drug_drug with Chlorthalidone, drug_drug with Chlorthalidone, drug_drug with Chlorzoxazone, drug_drug with Chlorzoxazone, drug_drug with Chlormadinone, drug_drug with Chlormadinone.", "label": "yes"}
{"original_question": "Is atenolol metabolized by CYP2D6?", "id": "converted_4145", "sentence1": "Is atenolol metabolized by CYP2D6?", "sentence2": "The study analysed the prescribing and dispensing of CYP2D6 drugs (metoprolol, donepezil, galantamine, codeine, tamoxifen) together with CYP2D6-blocking Selective Serotonin Reuptake Inhibitors (paroxetine/fluoxetine) or Selective Serotonin Reuptake Inhibitors without significant CYP2D6 inhibition (citalopram/escitalopram/sertraline), and the related prescribing of CYP2D6-independent comparator drugs (atenolol, rivastigmine, propoxyphene, anastrozole).[SEP]Relations: Atenolol has relations: drug_protein with CYP2D6, drug_protein with CYP2D6, drug_drug with NN344, drug_drug with NN344, drug_protein with ADRB2, drug_protein with ADRB2, drug_drug with Isocarboxazid, drug_drug with Isocarboxazid, drug_protein with ABCB11, drug_protein with ABCB11.", "label": "no"}
{"original_question": "Are TAD boundaries in Drosophila depleted in highly-expressed genes?", "id": "converted_2277", "sentence1": "Are aminoglutethimide/danazol/hydrocortisone/tamoxifen boundaries in Drosophila <basidiomycetes> depleted in highly-expressed Genes?", "sentence2": "Furthermore, we find that these aminoglutethimide/danazol/hydrocortisone/tamoxifen boundaries are present irrespective of the expression and looping of Genes located between them., In particular, Hi-C revealed that Chromosomes, Human, Pair 1 of animal allergen extracts are organized into topologically associating domains (Tietz syndrome), evolutionary conserved compact chromatin domains that influence gene expression., Drosophila <basidiomycetes> <basidiomycetes> inter-Tietz syndrome harbor active chromatin and constitutively transcribed (housekeeping) Genes. , The insulator-like, aminoglutethimide/danazol/hydrocortisone/tamoxifen-boundary-like, and aminoglutethimide/danazol/hydrocortisone/tamoxifen-interior-like regions are each enriched for distinct epigenetic marks and are each correlated with different gene expression levels, We conclude that epigenetic modifications, gene density, and transcriptional activity combine to shape the local packing of the A. thaliana nuclear Genome - anatomical entity., Disruptions of topological chromatin domains cause pathogenic rewiring of gene-enhancer interactions., Our results demonstrate the functional importance of Tietz syndrome for orchestrating gene expression via Genome - anatomical entity architecture and indicate criteria for predicting the pathogenicity of Homo sapiens structural variants, particularly in non-coding regions of the Homo sapiens Genome - anatomical entity., The three-dimensional organization of a Genome - anatomical entity plays a critical role in regulating gene expression, yet little is known about the machinery and mechanisms that determine higher-order Chromosome Structures., Ectopically expressed roX1 and roX2 RNA target Nonneurogenic neurogenic bladder dysfunction on the X Chromosome in trans and, via spatial proximity, induce spreading of the MSL complex in cis, leading to increased expression of neighboring autosomal Genes. , Collectively, our results suggest that Tietz syndrome are condensed chromatin domains depleted in active chromatin marks, separated by regions of active chromatin., However, Drosophila <basidiomycetes> <basidiomycetes> inter-Tietz syndrome harbor active chromatin and constitutively transcribed (housekeeping) Genes.[SEP]Relations: insect neurogenic region has relations: anatomy_anatomy with embryonic structure, anatomy_anatomy with embryonic structure. X Chromosome has relations: cellcomp_protein with PCGF3, cellcomp_protein with PCGF3, cellcomp_protein with SIN3B, cellcomp_protein with SIN3B, cellcomp_protein with PCGF5, cellcomp_protein with PCGF5. chromosome X structural anomaly has relations: disease_disease with partial deletion of chromosome X, disease_disease with partial deletion of chromosome X.", "label": "no"}
{"original_question": "Has Glucose-6-phosphate dehydrogenase (G6PD) deficiency an X-linked inheritance?", "id": "converted_1758", "sentence1": "Has G6PD gene (Glucosephosphate Dehydrogenase) deficiency an X-linked inheritance?", "sentence2": "Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is the commonest red cell Enzymopathy in Homo sapiens and has an X-linked inheritance. , This genetic defect shows sex linked inheritance and a marked heterogeneity., Glucosephosphate Dehydrogenase deficiency is the most common Enzymopathy in the world. , Study of the deficiency pattern amongst family members of the Enzyme [APC] deficient subjects confirmed the X-linked inheritance of G-6-PD deficiency., This was caused by Glucose-6-Phosphate-Dehydrogenase-Deficiency, which could be demonstrated by a red-cell-Enzyme [APC] analysis. The investigation of the patient's whole family showed the typical recessive X-linked inheritance of this Enzyme [APC]-defect. Frequency and clinical manifestations of this defect are discussed., After having described in detail the pathophysiology, symptomatology, X-chromosomal inheritance and some laboratory methods in detecting G-6-PD-deficiency by demonstrating a case of Favism (Schulz et al. 1977), the authors now discuss the particularities of the Enzyme [APC] deficiency in the newborn. , Severe red cell glucose-6-phosphate dehydrogenase (G-6-PD) deficiency has been found in an 'aboriginal' Finnish family. 2 male and 9 female carriers of the Variant G-6-PD were studied. The genetic pattern is consistent with X- linked recessive and the defect is associated with Pharmacologic Substance (primaquine) induced Hemolysis (lab result)., Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is the commonest red cell Enzymopathy in Homo sapiens and has an X-linked inheritance., X-linked glucose-6-phosphate dehydrogenase deficiency in House CASP14 gene., Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is a common X-linked Enzyme [APC] defect., Glucosephosphate Dehydrogenase gene deficiency is an X-linked recessive hereditary disease characterised by abnormally low levels of Glucosephosphate Dehydrogenase., UNLABELLED: Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is an X-linked recessive disorder in which haemolytic Anemia is the major symptom., Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is the most frequent Enzyme [APC] deficiency., Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is transmitted as an X-linked recessive disorder, and thus female infants are expected to be only rarely affected., Erythrocytic glucose-6-phosphate dehydrogenase (Glucosephosphate Dehydrogenase) of a mutant Mus sp. strain with X-linked Glucosephosphate Dehydrogenase-deficiency was purified and compared with the Wildtype Finding Glucosephosphate Dehydrogenase by biochemical and physiological characteristics., A Mus sp. with X-linked glucose-6-phosphate dehydrogenase (Glucosephosphate Dehydrogenase) deficiency has been recovered in offspring of 1-ethyl-1-nitrosourea-treated male CASP14 gene., Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is the commonest red cell Enzymopathy in Homo sapiens and has an X-linked inheritance, Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is an X-linked recessive hemolytic anemia caused by a Mutation Abnormality in the Glucosephosphate Dehydrogenase gene on Xq28, Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is an X-linked recessive genetic defect that can cause Hemolytic crisis, Glucose-6-phosphate-dehydrogenase (Glucosephosphate Dehydrogenase) deficiency is an X-linked genetic defect, affecting around 400 million people worldwide and is characterized by considerable biochemical and molecular heterogeneity, Glucosephosphate Dehydrogenase gene deficiency (Glucosephosphate Dehydrogenase) is an X-linked genetic disorder with a relatively high frequency in Malaria Vaccines-endemic regions, Glucosephosphate Dehydrogenase gene deficiency (Glucosephosphate Dehydrogenase) is the most common Enzyme [APC] pathology in Homo sapiens; it is X-linked inherited and causes neonatal Hyperbilirubinemia, chronic nonspherocytic haemolytic Anemia and Pharmacologic Substance-induced acute haemolytic Anemia, Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is an Genetic Diseases, X-Linked that predisposes Red blood cells, blood product to oxidative damage, Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is one of the most common human genetic abnormalities, and it has a significant prevalence in the male population (X chromosome linked), Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency, a common X-linked Enzymopathy can lead to severe Jaundice, Chronic Idiopathic, acute bilirubin encephalopathy and Kernicterus in the United States, Glucosephosphate Dehydrogenase gene deficiency (Glucosephosphate Dehydrogenase), an x-linked inherited Enzymopathy, is a barrier to Malaria Vaccines control because primaquine cannot be readily applied for radical cure in individuals with the condition, Glucosephosphate Dehydrogenase deficiency has an x-linked pattern of inheritance in which hemizygous males are deficient, while females may or may not be deficient depending on the number of affected alleles., Phenotype frequencies and family data verified the X-linked inheritance of the Glucosephosphate Dehydrogenase polymorphism., BACKGROUND: Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) is a metabolic Enzyme [APC] involved in the Pentoses phosphate pathway, its especially important in red blood cell metabolism. Glucosephosphate Dehydrogenase gene deficiency is an X-linked recessive hereditary disease characterised by abnormally low levels of Glucosephosphate Dehydrogenase., BACKGROUND: Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) is a metabolic Enzyme [APC] involved in the Pentoses phosphate pathway, its especially important in red blood cell metabolism. Glucosephosphate Dehydrogenase gene deficiency is an X-linked recessive hereditary disease characterised by abnormally low levels of Glucosephosphate Dehydrogenase. About 400 million people worldwide have a deficiency of this Enzyme [APC]., Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is a common X-linked Enzyme [APC] defect. We report a new Variant, Glucosephosphate Dehydrogenase Durham713G, that is associated with chronic nonspherocytic hemolytic anemia., Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is one of the most common human genetic abnormalities, and it has a significant prevalence in the male population (X chromosome linked)., The human X-linked gene encoding glucose 6-phosphate dehydrogenase (Glucosephosphate Dehydrogenase) is highly Polymorphism; more than 300 Glucosephosphate Dehydrogenase variants have been identified., Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is an X-linked incompletely dominant Enzyme [APC] deficiency that results from Glucosephosphate Dehydrogenase gene mutations., Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is an X-linked recessive genetic defect that can cause Hemolytic crisis., Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is an X-linked recessive hemolytic anemia caused by a Mutation Abnormality in the Glucosephosphate Dehydrogenase gene on Xq28., Glucosephosphate Dehydrogenase gene deficiency is an X-linked recessive hereditary disease characterised by abnormally low levels of Glucosephosphate Dehydrogenase., X-linked glucose-6-phosphate dehydrogenase (Glucosephosphate Dehydrogenase) and autosomal 6-phosphogluconate dehydrogenase (PGD gene) Genetic Polymorphism in Papio., X-linked glucose-6-phosphate dehydrogenase deficiency in House CASP14 gene., Glucosephosphate Dehydrogenase gene (Glucosephosphate Dehydrogenase) deficiency is an X-linked recessive disorder in which haemolytic Anemia is the major symptom.[SEP]Relations: Glucosephosphate Dehydrogenase has relations: molfunc_protein with glucose-6-phosphate dehydrogenase activity, molfunc_protein with glucose-6-phosphate dehydrogenase activity, disease_protein with Glucosephosphate Dehydrogenase deficiency, disease_protein with Glucosephosphate Dehydrogenase deficiency, disease_protein with galactosemia, disease_protein with galactosemia, disease_protein with Malaria Vaccines, disease_protein with Malaria Vaccines. glucose-6-phosphate dehydrogenase-like has relations: disease_disease with Mendelian disease, disease_disease with Mendelian disease.", "label": "yes"}
{"original_question": "Could Hyperthermic intraperitoneal chemotherapy (HIPEC) be effective for the treatment of recurrent ovarian cancer?", "id": "converted_1544", "sentence1": "Could Hyperthermic intraperitoneal chemotherapy (Hyperthermic Intraperitoneal Chemotherapy) be effective for the treatment of recurrent Malignant neoplasm of ovary?", "sentence2": "The use of Hyperthermic Intraperitoneal Chemotherapy after aggressive cytoreductive surgery in patients with Malignant neoplasm of ovary with peritoneal dissemination can be performed with acceptable postoperative morbidity rates. Knowledge of the factors associated with the onset of these postoperative adverse events allows better management of the same and offers the patient a safe procedure, These results showed that the association of Hyperthermic Intraperitoneal Chemotherapy with a complete cytoreduction for recurrent Malignant neoplasm of ovary presents acceptable morbidity and survival, There is level-one evidence suggesting the benefit of postoperative adjuvant intraperitoneal chemotherapy for patients with advanced Malignant neoplasm of ovary after cytoreductive surgery, albeit catheter-related complications resulted after treatment discontinuation. Studies report the use of Hyperthermic Intraperitoneal Chemotherapy predominantly in the setting of recurrent disease and have demonstrated encouraging results, which merits further investigation in future clinical trials,  The combination of Stringent Complete Response and Hyperthermic Intraperitoneal Chemotherapy seems to improve survival rate in patients suffering from platinum-sensitive EOC recurrence with respect to no-Hyperthermic Intraperitoneal Chemotherapy treatments. This result further supports the need of a randomized trial,  Cautious extrapolation of data from standard normothermic, nonintraoperative, intraperitoneal chemotherapy and data from Phase II and nonrandomized comparative studies suggest that Hyperthermic Intraperitoneal Chemotherapy delivered at the time of surgery for Malignant neoplasm of ovary has definite potential, The available evidence suggests that a potential survival benefit of adding Hyperthermic Intraperitoneal Chemotherapy may be largest in the settings of secondary Congenital Rubella Syndrome for stage III Malignant neoplasm of ovary and salvage Congenital Rubella Syndrome for recurrent Malignant neoplasm of ovary, two time-points representing failure of initial standard therapy. There is much less evidence for a potential benefit of Hyperthermic Intraperitoneal Chemotherapy for less advanced stages (I-II) and for earlier time-points in the treatment of Malignant neoplasm of ovary (upfront, Parameterized Data Type - Interval and consolidation), Survival benefit of adding Hyperthermic IntraPEritoneal Chemotherapy (Hyperthermic Intraperitoneal Chemotherapy) at the different time-points of treatment of Malignant neoplasm of ovary, Patients suffering from peritoneal recurrence of Malignant neoplasm of ovary should be considered for radical reoperation with Hyperthermic Intraperitoneal Chemotherapy in a center with expertise in multimodal therapeutic options. Organ-preserving cytoreductive surgery allows complete cytoreduction with the goal of decreasing morbidity,  In recurrent platinum-sensitive Malignant neoplasm of ovary patients, the use of Congenital Rubella Syndrome plus Hyperthermic Intraperitoneal Chemotherapy represents a safe treatment, able to significantly influence the survival rates compared to chemotherapy alone or surgery plus standard chemotherapy,  The results of our study indicate the feasibility and the potential benefit of a protocol including systemic chemotherapy, surgical cytoreduction and Hyperthermic Intraperitoneal Chemotherapy in patients with peritoneal carcinomatosis from Malignant neoplasm of ovary. A phase III trial to compare this approach with conventional treatment is needed, In selected patients with heavily pretreated recurrent Malignant neoplasm of ovary, cytoreduction combined with Hyperthermic Intraperitoneal Chemotherapy may provide a meaningful OS with acceptable morbidity. Optimal results are achieved in patients with a macroscopically complete resection and biologically favorable disease,  Hyperthermic Intraperitoneal Chemotherapy is a complement to radical surgery/ peritonectomy, which has been shown to be a surgical procedure with high tolerability, low morbimortality, enhanced survival and prolonged disease-free Parameterized Data Type - Interval in patients with peritoneal carcinomatosis for recurrent Malignant neoplasm of ovary,  Despite the heterogeneity of the studies reviewed, current evidence suggest that complete Congenital Rubella Syndrome and Hyperthermic Intraperitoneal Chemotherapy may be a feasible option with potential benefits that are comparable with the current standard of care. A randomized trial is required to establish the role of Hyperthermic Intraperitoneal Chemotherapy in Malignant neoplasm of ovary, in the majority of patients with primary and recurrent advanced Malignant neoplasm of ovary, cytoreductive surgery combined with Hyperthermic Intraperitoneal Chemotherapy can lead to a substantial increase in subsequent rates of disease-free and overall survival,  Peritonectomy procedures combined with Hyperthermic Intraperitoneal Chemotherapy offer promising long-term survival in patients with diffuse peritoneal ovarian carcinomatosis. They achieve high adequate primary and secondary surgical cytoreduction rates with acceptable morbidity and mortality, Cytoreduction surgery with hyperthermic intraperitoneal chemotherapy in recurrent Malignant neoplasm of ovary improves progression-free survival, especially in BRCA-positive patients- a case-control study., Survival benefit of adding Hyperthermic IntraPEritoneal Chemotherapy (Hyperthermic Intraperitoneal Chemotherapy) at the different time-points of treatment of Malignant neoplasm of ovary: review of evidence., Some encouraging results have been reported by the treatment of peritoneal carcinomatosis (Pachyonychia Congenita) from Malignant neoplasm of ovary by complete surgical cytoreduction, peritonectomy and hyperthermic intraperitoneal chemotherapy (Hyperthermic Intraperitoneal Chemotherapy)., Although standard treatment for advanced epithelial Malignant neoplasm of ovary (EOC) consists of surgical debulking and intravenous platinum- and taxane-based chemotherapy, favorable oncological outcomes have been recently reported with the use of cytoreductive surgery (Congenital Rubella Syndrome) and hyperthermic intraperitoneal chemotherapy (Hyperthermic Intraperitoneal Chemotherapy)., trabectedin, Hyperthermic intraperitoneal chemotherapy (Hyperthermic Intraperitoneal Chemotherapy) and chemo-immunotherapy may be become a promising therapy for the treatment of Malignant neoplasm of ovary., Hyperthermic intraperitoneal chemotherapy (Hyperthermic Intraperitoneal Chemotherapy) represents a new treatment strategy aimed to improve outcome of patients with advanced Malignant neoplasm of ovary., Favorable oncological outcomes have been reported in several trials with the introduction of Cytoreductive Surgery (Congenital Rubella Syndrome) and Hyperthermic Intraperitoneal Chemotherapy (Hyperthermic Intraperitoneal Chemotherapy) in the treatment of Advanced Epithelial Ovarian Cancer (EOC)., Based on theoretical and experimental basis, Hyperthermic Intraperitoneal Chemotherapy should stand as an effective treatment for Malignant neoplasm of ovary., Some encouraging results have been reported by the treatment of peritoneal carcinomatosis (Pachyonychia Congenita) from Malignant neoplasm of ovary by complete surgical cytoreduction, peritonectomy and hyperthermic intraperitoneal chemotherapy (Hyperthermic Intraperitoneal Chemotherapy), Based on theoretical and experimental basis, Hyperthermic Intraperitoneal Chemotherapy should stand as an effective treatment for Malignant neoplasm of ovary, Hyperthermic intraperitoneal chemotherapy (Hyperthermic Intraperitoneal Chemotherapy) represents a new treatment strategy aimed to improve outcome of patients with advanced Malignant neoplasm of ovary, [Importance of hyperthermic intraperitoneal chemotherapy (Hyperthermic Intraperitoneal Chemotherapy) in Malignant neoplasm of ovary].[SEP]Relations: ovarian epithelial tumor has relations: disease_disease with ovarian squamous cell neoplasm, disease_disease with ovarian squamous cell neoplasm, disease_disease with ovarian neoplasm, disease_disease with ovarian neoplasm, disease_disease with ovarian serous tumor, disease_disease with ovarian serous tumor, disease_disease with epithelial neoplasm, disease_disease with epithelial neoplasm, disease_disease with ovarian seromucinous tumor, disease_disease with ovarian seromucinous tumor.", "label": "yes"}
{"original_question": "Are Mesenchymal stem cells (MSC) multipotent cells?", "id": "converted_2931", "sentence1": "Are Mesenchymal stem cells (MSC) multipotent cells?", "sentence2": "multipotent mesenchymal bone marrow-derived stem cells, multipotent hESC-derived mesenchymal cells (MILES-CARPENTER X-LINKED INTELLECTUAL DEVELOPMENTAL DISORDER)[SEP]Relations: intellectual developmental disorder has relations: disease_phenotype_positive with Macrocephaly, disease_phenotype_positive with Macrocephaly, disease_phenotype_positive with Generalized myoclonic-atonic seizure, disease_phenotype_positive with Generalized myoclonic-atonic seizure, disease_phenotype_positive with Smooth philtrum, disease_phenotype_positive with Smooth philtrum, disease_phenotype_positive with Long palpebral fissure, disease_phenotype_positive with Long palpebral fissure, disease_phenotype_positive with Striae distensae, disease_phenotype_positive with Striae distensae.", "label": "yes"}
{"original_question": "Can antisense threapy be used for Huntington's disease?", "id": "converted_3211", "sentence1": "Can antisense threapy be used for Huntington Disease?", "sentence2": "In this issue of Neurons, Kordasiewicz et al. (2012) show the benefit of transient antisense oligonucleotide (ASO) therapy to degrade Hodgkin Disease protein, human mRNA and elicit sustained therapeutic benefit in Hodgkin Disease CASP14 gene., \"Hodgkin Disease protein, human holiday\": progress toward an antisense therapy for Huntington Disease.[SEP]Relations: Huntington disease has relations: disease_disease with neurodegenerative disease with chorea, disease_disease with neurodegenerative disease with chorea, disease_disease with Huntington disease and related disorders, disease_disease with Huntington disease and related disorders, disease_disease with juvenile Huntington disease, disease_disease with juvenile Huntington disease, disease_protein with GAL, disease_protein with GAL, disease_protein with FAAH, disease_protein with FAAH.", "label": "yes"}
{"original_question": "Are artificial blood cells available?", "id": "converted_3188", "sentence1": "Are artificial blood cells available?", "sentence2": "The critical point for the break through for artificial blood products did not come yet but could be ahead-, We suggest a novel method that uses artificial blood cells (hemoglobin vesicles, Hb-Vs) as photosensitizers in dye laser treatment (at 595-nm wavelength) for Port-Wine Stain (i.e., Capillary malformation (disorder) presenting as red birthmarks) based on the results of Animal allergens experiments. [SEP]Relations: Capillary malformation has relations: disease_phenotype_positive with nevus anemicus (disease), disease_phenotype_positive with nevus anemicus (disease), phenotype_phenotype with Angioma serpentinum, phenotype_phenotype with Angioma serpentinum, disease_phenotype_positive with macrocephaly-intellectual disability-neurodevelopmental disorder-small thorax syndrome, disease_phenotype_positive with macrocephaly-intellectual disability-neurodevelopmental disorder-small thorax syndrome, disease_phenotype_positive with pulmonary venoocclusive disease, disease_phenotype_positive with pulmonary venoocclusive disease, disease_phenotype_positive with capillary malformation-arteriovenous malformation, disease_phenotype_positive with capillary malformation-arteriovenous malformation.", "label": "no"}
{"original_question": "Is PUVA therapy indicated for eczema treatment?", "id": "converted_2056", "sentence1": "Is Methoxsalen With Ultraviolet A Therapy therapy indicated for Eczema treatment?", "sentence2": "With bath Methoxsalen With Ultraviolet A Therapy treatment, the best results were found in patients with hyperkeratotic Eczema (17/22; 77% good clinical response) followed by patients with palmoplantar Psoriasis (26/41; 63%) and patients with Vesicular Eczema of Hand and/or feet (8/16; 50%). , Oral vs. bath Methoxsalen With Ultraviolet A Therapy using methoxsalen for chronic palmoplantar Eczema., Both oral and bath Methoxsalen With Ultraviolet A Therapy with methoxsalen (8-MOP) have been shown to be effective in the treatment of chronic palmoplantar Eczema. , Oral Methoxsalen With Ultraviolet A Therapy is preferable for patients with hyperkeratotic Eczema and bath Methoxsalen With Ultraviolet A Therapy for patients with Vesicular Eczema of Hand and/or feet., Treatment of Hand Eczema is dominated by the administration of topical glucocorticosteriods. If topical treatment fails, the best second-line option is ultraviolet (UV) therapy alone or as combination therapy. Ultraviolet B therapy and Methoxsalen With Ultraviolet A Therapy (Psoralen [EPC] plus UVA) therapy is effective and has relatively few side effects. , Although local Methoxsalen With Ultraviolet A Therapy has been proven to be effective in the treatment of Chronic Hand Eczema, little is known about the efficacy and safety of local narrowband Ultraviolet B therapy (TL-01) for this condition., Local narrowband Ultraviolet B therapy phototherapy regimen is as effective as paint-Methoxsalen With Ultraviolet A Therapy therapy in patients with Chronic Hand Eczema of dry and dyshidrotic types., Location characteristic ID - Location characteristic ID - Smoking is likely to be a reason for the failure of bath-Methoxsalen With Ultraviolet A Therapy therapy in the treatment of chronic palmoplantar Eczema, in particular regarding smokers with Eczema of the dyshidrotic type where no complete remission was achieved., Treatment of chronic palmoplantar Eczema with local bath-Methoxsalen With Ultraviolet A Therapy therapy., Bath-Methoxsalen With Ultraviolet A Therapy therapy has been described as successful treatment for palmoplantar Eczema., Systemic Methoxsalen With Ultraviolet A Therapy therapy may be useful in the treatment of chronic palmoplantar Eczema., A new Psoralen [EPC]-containing gel for topical Methoxsalen With Ultraviolet A Therapy therapy: development, and treatment results in patients with palmoplantar and plaque-type Psoriasis, and hyperkeratotic Eczema., These results indicate that topical Methoxsalen With Ultraviolet A Therapy therapy with Psoralen [EPC] in aqueous gel is a useful therapeutic modality for treatment of Psoriasis patients, and patients with recalcitrant dermatoses such as palmoplantar Psoriasis and hyperkeratotic Eczema., In order to evaluate environmental influences possibly having an impact on the efficacy of this therapy, smokers and non-smokers suffering from palmoplantar Eczema treated with bath-Methoxsalen With Ultraviolet A Therapy therapy were compared., Does smoking influence the efficacy of bath-Methoxsalen With Ultraviolet A Therapy therapy in chronic palmoplantar Eczema?, Methoxsalen With Ultraviolet A Therapy therapy caused acute aggravation of the Eczema., Hyperkeratotic Eczema cleared significantly better with oral than with bath Methoxsalen With Ultraviolet A Therapy (P=0.03).CONCLUSION: Oral Methoxsalen With Ultraviolet A Therapy is preferable for patients with hyperkeratotic Eczema and bath Methoxsalen With Ultraviolet A Therapy for patients with Vesicular Eczema of Hand and/or feet., BACKGROUND: Systemic Methoxsalen With Ultraviolet A Therapy therapy may be useful in the treatment of chronic palmoplantar Eczema., These results indicate that topical Methoxsalen With Ultraviolet A Therapy therapy with Psoralen [EPC] in aqueous gel is a useful therapeutic modality for treatment of Psoriasis patients, and patients with recalcitrant dermatoses such as palmoplantar Psoriasis and hyperkeratotic Eczema., VITILIGO-ASSOCIATED MULTIPLE AUTOIMMUNE DISEASE SUSCEPTIBILITY 1 (finding) (60.9%) was the commonest skin disorder treated with Methoxsalen With Ultraviolet A Therapy, followed by Psoriasis (20.9%), endogenous Eczema (11.3%), mycosis fungoides (3.5%), Amyloidosis, Primary Cutaneous (2.6%) and Prurigo nodularis (0.9%)., bath Methoxsalen With Ultraviolet A Therapy using methoxsalen for chronic palmoplantar Eczema., A 36-year-old female patient was treated with Methoxsalen With Ultraviolet A Therapy for Vesicular Eczema of Hand and/or feet that had not shown sufficient response to topical therapy over the previous months., BACKGROUND: Both oral and bath Methoxsalen With Ultraviolet A Therapy with methoxsalen (8-MOP) have been shown to be effective in the treatment of chronic palmoplantar Eczema., One patient with Hand Eczema consistently had detectable 8-MOP levels 1 hour after topical Methoxsalen With Ultraviolet A Therapy treatments.CONCLUSION: This report indicates that there is minimal, if any, systemic absorption of 8-MOP after topical Methoxsalen With Ultraviolet A Therapy treatment of patients with palmoplantar Psoriasis., In the narrowband Ultraviolet B therapy-treated side, the tolerance of all the patients to the treatment was good all patients well-tolerated the treatment with the exception of mild Xerosis that responded to topical emollients.Local narrowband Ultraviolet B therapy phototherapy regimen is as effective as paint-Methoxsalen With Ultraviolet A Therapy therapy in patients with Chronic Hand Eczema of dry and dyshidrotic types, Bath-Methoxsalen With Ultraviolet A Therapy therapy has been described as successful treatment for palmoplantar Eczema, Location characteristic ID - Location characteristic ID - Smoking is likely to be a reason for the failure of bath-Methoxsalen With Ultraviolet A Therapy therapy in the treatment of chronic palmoplantar Eczema, in particular regarding smokers with Eczema of the dyshidrotic type where no complete remission was achieved, Systemic Methoxsalen With Ultraviolet A Therapy therapy may be useful in the treatment of chronic palmoplantar Eczema, However, few data are available on the effectiveness of local bath-Methoxsalen With Ultraviolet A Therapy therapy in palmoplantar Eczema.Our purpose was to assess the effectiveness of local bath-Methoxsalen With Ultraviolet A Therapy therapy in 28 patients with chronic palmar or plantar Eczema or both who were resistant to conventional topical treatment.After Fungi or Bacterial Infections had been excluded in all patients, Hand or feet or both were soaked for 15 minutes in warm water containing 1 mg/L methoxsalen, No phototoxic reactions were observed.Local bath-Methoxsalen With Ultraviolet A Therapy therapy is of value in the management of chronic palmoplantar Eczema resistant to standard modes of topical treatment, Treatment of chronic palmoplantar Eczema with local bath-Methoxsalen With Ultraviolet A Therapy therapy, Bath-Methoxsalen With Ultraviolet A Therapy therapy has been described as successful treatment for palmoplantar Eczema. , Location characteristic ID - Location characteristic ID - Smoking is likely to be a reason for the failure of bath-Methoxsalen With Ultraviolet A Therapy therapy in the treatment of chronic palmoplantar Eczema, in particular regarding smokers with Eczema of the dyshidrotic type where no complete remission was achieved., OBJECTIVE: Our purpose was to assess the effectiveness of local bath-Methoxsalen With Ultraviolet A Therapy therapy in 28 patients with chronic palmar or plantar Eczema or both who were resistant to conventional topical treatment. , CONCLUSION: Local bath-Methoxsalen With Ultraviolet A Therapy therapy is of value in the management of chronic palmoplantar Eczema resistant to standard modes of topical treatment. , Topical Methoxsalen With Ultraviolet A Therapy therapy for Chronic Hand Eczema., However, few data are available on the effectiveness of local bath-Methoxsalen With Ultraviolet A Therapy therapy in palmoplantar Eczema.Our purpose was to assess the effectiveness of local bath-Methoxsalen With Ultraviolet A Therapy therapy in 28 patients with chronic palmar or plantar Eczema or both who were resistant to conventional topical treatment.After Fungi or Bacterial Infections had been excluded in all patients, Hand or feet or both were soaked for 15 minutes in warm water containing 1 mg/L methoxsalen., No phototoxic reactions were observed.Local bath-Methoxsalen With Ultraviolet A Therapy therapy is of value in the management of chronic palmoplantar Eczema resistant to standard modes of topical treatment., Location characteristic ID - Location characteristic ID - Smoking is likely to be a reason for the failure of bath-Methoxsalen With Ultraviolet A Therapy therapy in the treatment of chronic palmoplantar Eczema, in particular regarding smokers with Eczema of the dyshidrotic type where no complete remission was achieved., However, our own observations showed that patients with palmoplantar Eczema of the dyshidrotic or hyperkeratotic type responded only partially to bath-Methoxsalen With Ultraviolet A Therapy therapy., In the narrowband Ultraviolet B therapy-treated side, the tolerance of all the patients to the treatment was good all patients well-tolerated the treatment with the exception of mild Xerosis that responded to topical emollients.Local narrowband Ultraviolet B therapy phototherapy regimen is as effective as paint-Methoxsalen With Ultraviolet A Therapy therapy in patients with Chronic Hand Eczema of dry and dyshidrotic types., Comparison of localized high-dose UVA1 irradiation versus topical cream Psoralen [EPC]-UVA for treatment of chronic vesicular Vesicular Eczema of Hand and/or feet., No phototoxic reactions were observed.CONCLUSION: Local bath-Methoxsalen With Ultraviolet A Therapy therapy is of value in the management of chronic palmoplantar Eczema resistant to standard modes of topical treatment., These results indicate that topical Methoxsalen With Ultraviolet A Therapy therapy with Psoralen [EPC] in aqueous gel is a useful therapeutic modality for treatment of Psoriasis patients, and patients with recalcitrant dermatoses such as palmoplantar Psoriasis and hyperkeratotic Eczema.., Treatment of chronic palmoplantar Eczema with local bath-Methoxsalen With Ultraviolet A Therapy therapy., Oral Methoxsalen With Ultraviolet A Therapy is preferable for patients with hyperkeratotic Eczema and bath Methoxsalen With Ultraviolet A Therapy for patients with Vesicular Eczema of Hand and/or feet.., Does smoking influence the efficacy of bath-Methoxsalen With Ultraviolet A Therapy therapy in chronic palmoplantar Eczema?, Local bath-Methoxsalen With Ultraviolet A Therapy therapy is of value in the management of chronic palmoplantar Eczema resistant to standard modes of topical treatment., However, few data are available on the effectiveness of local bath-Methoxsalen With Ultraviolet A Therapy therapy in palmoplantar Eczema., A new Psoralen [EPC]-containing gel for topical Methoxsalen With Ultraviolet A Therapy therapy: development, and treatment results in patients with palmoplantar and plaque-type Psoriasis, and hyperkeratotic Eczema., Location characteristic ID - Location characteristic ID - Smoking is likely to be a reason for the failure of bath-Methoxsalen With Ultraviolet A Therapy therapy in the treatment of chronic palmoplantar Eczema, in particular regarding smokers with Eczema of the dyshidrotic type where no complete remission was achieved.., In order to investigate the effectiveness of topical Methoxsalen With Ultraviolet A Therapy-bath therapy (Methoxsalen With Ultraviolet A Therapy-soak therapy) on chronic palmoplantar dermatoses, 30 patients with plaque-type Psoriasis, pustular Psoriasis, endogenous Eczema, Vesicular Eczema of Hand and/or feet and hyperkeratotic dermatitis of the Arecaceae and soles were treated over 8 weeks with Methoxsalen With Ultraviolet A Therapy-soak using 8-MOP., Our purpose was to assess the effectiveness of local bath-Methoxsalen With Ultraviolet A Therapy therapy in 28 patients with chronic palmar or plantar Eczema or both who were resistant to conventional topical treatment.[SEP]Relations: Eczema has relations: drug_effect with Fluvoxamine, drug_effect with Fluvoxamine, drug_effect with Fluvoxamine, drug_effect with Fluvoxamine, drug_effect with Cevimeline, drug_effect with Cevimeline, drug_effect with Cevimeline, drug_effect with Cevimeline, drug_effect with Retapamulin, drug_effect with Retapamulin.", "label": "yes"}
{"original_question": "Is Ameloblastoma (AB) a common benign tumor occurring in the brain?", "id": "converted_4667", "sentence1": "Is Ameloblastoma (AB) a common benign Specimen Source Codes - tumor occurring in the brain?", "sentence2": "Ameloblastoma is a benign odontogenic Specimen Source Codes - Specimen Source Codes - tumor which undergoes malignant transformation to ameloblastic carcinoma. , Ameloblastomas are Benign Neoplasm that most commonly affecting the Head>Mandible. , Ameloblastoma is a Neoplasms arising in the craniofacial skeleton., Ameloblastoma is an invasive odontogenic Specimen Source Codes - Specimen Source Codes - tumor, and for reconstruction, i, Ameloblastoma is a locally aggressive, benign epithelial Odontogenic Tumors currently classified to include conventional, unicystic, and extraosseous/peripheral subtypes. , Ameloblastoma (AM) is a slow growing and aggressive benign Specimen Source Codes - Specimen Source Codes - tumor with an odontogenic epithelial origin arising from the Head>Mandible or Maxilla., The ameloblastoma is a benign but aggressive Neoplasms of odontogenic origin., Ameloblastoma is a rare odontogenic Specimen Source Codes - Specimen Source Codes - tumor of the jaw., Ameloblastoma is the most common epithelial odontogenic Specimen Source Codes - Specimen Source Codes - tumor., Ameloblastoma or Adamantinoma of Long Bones is the rarest of the three forms of Specimen Source Codes - Specimen Source Codes - tumor of the odontogenic type., Ameloblastoma is a benign locally invasive odontogenic Specimen Source Codes - Specimen Source Codes - tumor., Ameloblastoma is the second most common benign epithelial odontogenic Specimen Source Codes - Specimen Source Codes - tumor and though it is of a benign nature, it is locally invasive, has a high recurrence rate and could potentially become malignant., BACKGROUND: The ameloblastoma is the most common odontogenic epithelial Specimen Source Codes - Specimen Source Codes - tumor, which belong to benign neoplasms that present a painless course, and usually occur in the oromaxillo-facial region., Ameloblastoma is the most common odontogenic Specimen Source Codes - Specimen Source Codes - tumor of epithelial origin, and though it is of a benign nature, it frequently infiltrates the Specimen Type - Bone, has a high rate of recurrence and could potentially become malignant., OBJECTIVES: Ameloblastoma is a benign, slow-growing, locally invasive epithelial Specimen Source Codes - Specimen Source Codes - tumor of odontogenic origin, with unlimited growth capacity and a strong tendency to recur., Ameloblastoma, a benign but locally aggressive odontogenic Specimen Source Codes - Specimen Source Codes - tumor, often demonstrates metastasis despite benign histological features and this Variant is termed as Malignant Ameloblastoma (METAM). , Ameloblastic carcinoma (cyclophosphamide/doxorubicin protocol) is defined as a rare primary epithelial odontogenic malignant Neoplasms and the malignant counterpart of benign epithelial odontogenic Specimen Source Codes - Specimen Source Codes - tumor of ameloblastoma (AB) by the WHO classification. cyclophosphamide/doxorubicin protocol, BACKGROUND: The ameloblastoma is the most common odontogenic epithelial Specimen Source Codes - Specimen Source Codes - tumor, which belong to benign neoplasms that present a painless course, and usually occur in the oromaxillo-fac, Peripheral ameloblastoma is a benign odontogenic Specimen Source Codes - Specimen Source Codes - tumor with the same histological characteristics as the centrally located ameloblastoma, but appearing in the gingiva and mucosa of the tooth-bearing area of the jaws., BACKGROUND Ameloblastoma (AB) is a common odontogenic epithelial Specimen Source Codes - Specimen Source Codes - tumor, with locally invasive behavior and high recurrence., Ameloblastoma(AB) is an aggressive and slow-growing Specimen Source Codes - Specimen Source Codes - tumor with high recurrence rate, which arises from Odontogenic Epithelium., Ameloblastoma (AB) is the most common benign epithelial odontogenic Specimen Source Codes - Specimen Source Codes - tumor occurring in the jawbone., or growth. Ameloblastoma (AB) is a relatively common odontogenic epithelial Neoplasms that manifests local infiltrative intraosse, Ameloblastic carcinoma (cyclophosphamide/doxorubicin protocol) is defined as a rare primary epithelial odontogenic malignant Neoplasms and the malignant counterpart of benign epithelial odontogenic Specimen Source Codes - Specimen Source Codes - tumor of ameloblastoma (AB) by the WHO classification., Ameloblastoma is a benign epithelial odontogenic Specimen Source Codes - Specimen Source Codes - tumor that typically arises in the Head>Mandible or Maxilla or, rarely, in the immediate adjacent soft tissue, nic epithelial components with a mature Fibrous stroma. It is the second most common Odontogenic Tumors following odontome. Acanthomatous ameloblast, OBJECTIVE AND IMPORTANCE: Ameloblastoma is a locally aggressive benign Specimen Source Codes - Specimen Source Codes - tumor, commonly occurring in the Head>Mandible, BACKGROUND AND OVERVIEW: Ameloblastoma is an odontogenic Specimen Source Codes - Specimen Source Codes - tumor predominantly occurring in patients who are in their 20s and 30s, BACKGROUND: The ameloblastoma is the most common odontogenic epithelial Specimen Source Codes - Specimen Source Codes - tumor, which belong to benign neoplasms that present a painless course, and usually occur in the oromaxillo-facial region, BACKGROUND: Ameloblastoma is a Neoplasms classified as a benign epithelial odontogenic Specimen Source Codes - Specimen Source Codes - tumor of the jaws, grow slowly and are locally invasive, BACKGROUND: Ameloblastoma is a frequent odontogenic benign Specimen Source Codes - Specimen Source Codes - tumor characterized by local invasiveness, high risk of recurrence and occasional metastasis and malignant transformation, BACKGROUND: Ameloblastoma is a rare benign odontogenic Specimen Source Codes - Specimen Source Codes - tumor with locally Aggressive behavior and a high recurrence rate, BACKGROUND: Ameloblastoma is a benign odontogenic Specimen Source Codes - Specimen Source Codes - tumor, exhibiting local invasiveness and high rate of recurrence, BACKGROUND: Ameloblastoma is a rare benign odontogenic Specimen Source Codes - Specimen Source Codes - tumor with a metastasis rate estimated at 2% of cases, mainly involving the Chest>Lung (80%) and lymph nodes (20%).METHODS: We hereby present the case of a 26 year old patient with a history of locally recurrent mandibular ameloblastoma who developed a temporal intracranial ameloblastoma Specimen Source Codes - Specimen Source Codes - tumor requiring a collaborative neurosurgical and maxillo-facial radical surgical approach.CONCLUSION: Although ameloblastomas are histologically benign, the temporal topography questions the dissemination pathophysiology of the Specimen Source Codes - Specimen Source Codes - tumor (metastasis or local extension through temporal muscle fibers), mainly relevant , Ameloblastoma is a histologically benign Specimen Source Codes - Specimen Source Codes - tumor derived from odontogenic apparatus., BACKGROUND: Ameloblastoma is a Odontogenic Specimen Source Codes - Specimen Source Codes - tumor, benign that may exhibit aggressive biological behaviour with local recurrence and metastasis following initial surgica, Ameloblastomas are histologically Benign Neoplasm derived from the odontogenic apparatus., Ameloblastoma is a benign odontogenic Specimen Source Codes - Specimen Source Codes - tumor generally present in the Jaw., Ameloblastoma is a locally aggressive Specimen Source Codes - Specimen Source Codes - tumor derived from Odontogenic Epithelium., Ameloblastoma is the most common clinically significant epithelial odontogenic Specimen Source Codes - Specimen Source Codes - tumor, and is considered a benign but locally aggressive Specimen Source Codes - Specimen Source Codes - tumor of the craniofacial region., Ameloblastoma (AB), which is the most common odontogenic Specimen Source Codes - Specimen Source Codes - tumor, may originate from the dental lamina remnants.[SEP]Relations: ameloblastoma has relations: disease_disease with benign epithelial Neoplasms, disease_disease with benign epithelial Neoplasms, disease_disease with benign epithelial Neoplasms, disease_disease with benign epithelial Neoplasms, disease_disease with benign epithelial Neoplasms, disease_disease with benign epithelial Neoplasms, disease_disease with Specimen Type - Bone ameloblastoma, disease_disease with Specimen Type - Bone ameloblastoma, disease_disease with Specimen Type - Bone ameloblastoma, disease_disease with Specimen Type - Bone ameloblastoma.", "label": "no"}
{"original_question": "Are CpG islands located close to housekeeping genes?", "id": "converted_1166", "sentence1": "Are CpG Islands located close to Genes, Housekeeping?", "sentence2": "our analysis indicates that the association of CGIs with Genes, Housekeeping is not as strong as previously estimated, CpG Islands are preferentially located at the start of transcription of Genes, Housekeeping and are associated with Tissue Specimen Code-specific Genes, It has been envisaged that CpG Islands are often observed near the transcriptional start sites (Toxic Shock Syndrome) of Genes, Housekeeping., These regions represent about 1% of Genomic DNA and are generally found in the Promoter region of Genes, Housekeeping., CpG Islands are stretches of DNA sequence that are enriched in the (CpG)n repeat and are present in close association with all Genes, Housekeeping as well as some Tissue Specimen Code-specific Genes in the mammalian genome., CpG Islands, which are found almost exclusively at the 5'-end of Genes, Housekeeping, In housekeeping and many Tissue Specimen Code-specific Genes, the Promoter is embedded in a so-called CpG Islands., All housekeeping and widely expressed Genes have a CpG Islands covering the transcription start, whereas 40% of the Genes with a Tissue Specimen Code-specific or limited expression are associated with Islands, Methylation-free CpG clusters, so-called HTF Islands, are most often associated with the Promoter regions of Genes, Housekeeping, whereas Genes expressed in a single-cell type are usually deficient in these DNA Sequence., Unmethylated CpG rich Islands are a feature of vertebrate DNA: they are associated with housekeeping and many Tissue Specimen Code specific Genes., CpG Islands were associated with the 5' ends of all Genes, Housekeeping and many Tissue Specimen Code-specific Genes, and with the 3' ends of some Tissue Specimen Code-specific Genes.[SEP]Relations: GLI proteins bind promoters of Hh responsive Genes to promote transcription has relations: pathway_protein with GLI2, pathway_protein with GLI2, pathway_protein with GLI3, pathway_protein with GLI3, pathway_protein with GLI1, pathway_protein with GLI1. Promoter clearance from RNA polymerase I Promoter has relations: bioprocess_bioprocess with Promoter clearance during DNA-templated transcription, bioprocess_bioprocess with Promoter clearance during DNA-templated transcription. toxic shock syndrome has relations: disease_protein with C5AR1, disease_protein with C5AR1.", "label": "yes"}
{"original_question": "Is ibudilast effective for multiple sclerosis?", "id": "converted_2801", "sentence1": "Is ibudilast effective for Multiple Sclerosis?", "sentence2": "ibudilast slowed brain atrophy in Parts per million (qualifier value) and SPMS patients in a multicenter phase 2b study.,  ibudilast inhibits several CNP gene, macrophage migration inhibitory factor, and toll-like receptor 4 and can cross the blood-brain barrier, with potential salutary effects in progressive Multiple Sclerosis., CONCLUSIONS: In a phase 2 trial involving patients with progressive Multiple Sclerosis, ibudilast was associated with slower progression of brain atrophy than placebo but was associated with higher rates of gastrointestinal side effects, Headache, and Cancer patients and suicide and Cancer patients and suicide and depression., Specifically, the current evidence regarding treatment of progressive MS with ocrelizumab, simvastatin, ibudilast, thioctic acid, high-dose biotin, siponimod, and cell-based therapies are discussed., Based on our knowledge of pathophysiology, three therapeutic strategies are proposed: anti-inflammatory (ocrelizumab, siponimod…); remyelinating (opicinumab); and neuroprotective (high-dose biotin, ibudilast, simvastatin…). , Current article provides an overview of the pharmacology of Irritable Bowel Syndrome with a focus on preclinical and clinical data supporting its potential neuroprotective benefits for neurological conditions, including Multiple Sclerosis, Neuropathic pain, medication overuse Headache, Cerebrovascular accident, Opioids, Alcohol - Recreational Drug Use Code and methamphetamine abuse., Design, rationale, and baseline characteristics of the randomized double-blind phase II clinical trial of ibudilast in progressive Multiple Sclerosis., METHODS: SPRINT-MS is a randomized, placebo-controlled, phase II trial of ibudilast in patients with POLYDACTYLY, POSTAXIAL, WITH PROGRESSIVE MYOPIA., CONCLUSION: SPRINT-MS is designed to evaluate the safety and efficacy of ibudilast as a treatment for POLYDACTYLY, POSTAXIAL, WITH PROGRESSIVE MYOPIA while simultaneously validating five different imaging biomarkers as outcome metrics for use in future phase II proof-of-concept POLYDACTYLY, POSTAXIAL, WITH PROGRESSIVE MYOPIA trials., ibudilast for the treatment of Multiple Sclerosis., AREAS COVERED: This article reviews various studies looking at ibudilast as a potential therapy for MS. It summarizes prior and current clinical trials of ibudilast in MS as well as its pharmacology.EXPERT OPINION: Although ibudilast has not been found to decrease the focal inflammatory activity in relapsing MS, it was shown to have an effect on preserving brain volume and disability progression. ibudilast may have a role in the treatment of progressive MS phenotypes., Adverse events with ibudilast included No gastrointestinal symptom, Headache, and Cancer patients and suicide and Cancer patients and suicide and depression.<br><b>CONCLUSIONS</b>: In a phase 2 trial involving patients with progressive Multiple Sclerosis, ibudilast was associated with slower progression of brain atrophy than placebo but was associated with higher rates of gastrointestinal side effects, Headache, and Cancer patients and suicide and Cancer patients and suicide and depression., It summarizes prior and current clinical trials of ibudilast in MS as well as its pharmacology.<br><b>EXPERT OPINION</b>: Although ibudilast has not been found to decrease the focal inflammatory activity in relapsing MS, it was shown to have an effect on preserving brain volume and disability progression.[SEP]Relations: ibudilast has relations: drug_drug with SC-236, drug_drug with SC-236, drug_drug with Iloprost, drug_drug with Iloprost, drug_drug with Pirlindole, drug_drug with Pirlindole, drug_drug with Metamizole, drug_drug with Metamizole, drug_drug with Epirizole, drug_drug with Epirizole.", "label": "yes"}
{"original_question": "Does mTOR regulate the translation of MAPKAPK2?", "id": "converted_1974", "sentence1": "Does FRAP1 protein, human regulate the translation of MAP-kinase-activated kinase 2?", "sentence2": "FRAP1 protein, human regulates MAP-kinase-activated kinase 2 translation to control the senescence-associated secretory phenotype., Senescent cells secrete a combination of factors collectively known as the senescence-associated secretory phenotype (TXN protein, human). The TXN protein, human reinforces senescence and activates an immune surveillance response, but it can also show pro-tumorigenic properties and contribute to age-related pathologies. In a drug screen to find new TXN protein, human regulators, we uncovered the FRAP1 protein, human inhibitor sirolimus as a potent TXN protein, human suppressor. Here we report a mechanism by which FRAP1 protein, human controls the TXN protein, human by differentially regulating the translation of the MAP-kinase-activated kinase 2 protein, human (also known as MAP-kinase-activated kinase 2) kinase through EIF4EBP1 wt Allele. In turn, MAP-kinase-activated kinase 2 phosphorylates the RNA-Binding Proteins ZFP36L1 gene gene during senescence, inhibiting its ability to degrade the RNA Transcript of numerous TXN protein, human components. Consequently, FRAP1 protein, human inhibition or constitutive activation of ZFP36L1 gene gene impairs the non-cell-autonomous effects of senescent cells in both tumour-suppressive and tumour-promoting contexts. Altogether, our results place regulation of the TXN protein, human as a key mechanism by which FRAP1 protein, human could influence Primary malignant neoplasm, age-related diseases and immune responses., Here we report a mechanism by which FRAP1 protein, human controls the TXN protein, human by differentially regulating the translation of the MAP-kinase-activated kinase 2 protein, human (also known as MAP-kinase-activated kinase 2) kinase through EIF4EBP1 wt Allele., FRAP1 protein, human regulates MAP-kinase-activated kinase 2 translation to control the senescence-associated secretory phenotype, Here we report a mechanism by which FRAP1 protein, human controls the TXN protein, human by differentially regulating the translation of the MAP-kinase-activated kinase 2 protein, human (also known as MAP-kinase-activated kinase 2) kinase through EIF4EBP1 wt Allele, Here we report a mechanism by which FRAP1 protein, human controls the TXN protein, human by differentially regulating the translation of the MAP-kinase-activated kinase 2 protein, human (also known as MAP-kinase-activated kinase 2) kinase through EIF4EBP1 wt Allele., Both Beclin1-PI3KIII and Beclin1-MAP-kinase-activated kinase 2 interactions as were remarkably affected by silencing either ammonium tetrathiomolybdate or MAPK14.ammonium tetrathiomolybdate promoted IR-induced autophagy via the MAPK14 pathway, FRAP1 protein, human pathway and Beclin1/PI3KIII complexes., FRAP1 protein, human regulates MAP-kinase-activated kinase 2 translation to control the senescence-associated secretory phenotype.[SEP]Relations: protein binding has relations: molfunc_protein with MAP-kinase-activated kinase 2, molfunc_protein with MAP-kinase-activated kinase 2, molfunc_protein with MTMR2, molfunc_protein with MTMR2, molfunc_protein with MTOR, molfunc_protein with MTOR, molfunc_protein with MAPKAPK3, molfunc_protein with MAPKAPK3. ZFP36L1 gene has relations: protein_protein with MAP-kinase-activated kinase 2, protein_protein with MAP-kinase-activated kinase 2.", "label": "yes"}
{"original_question": "Is Rad4/XPC a DNA damage sensing protein?", "id": "converted_3457", "sentence1": "Is Rad4/XPC a DNA damage sensing protein?", "sentence2": "Twist-open mechanism of DNA damage recognition by the Rad4/XPC nucleotide excision repair complex., Kinetic gating mechanism of DNA damage recognition by Rad4/XPC.,  These findings indicate that the Lesion recognized by Rad4/XPC thermodynamically destabilize the Watson-Crick double helix in a manner that facilitates the flipping-out of two Base Pairing.[SEP]Relations: nerve lesion has relations: disease_disease with ulnar nerve lesion, disease_disease with ulnar nerve lesion, disease_disease with brachial plexus neuritis, disease_disease with brachial plexus neuritis, disease_disease with lesion of sciatic nerve, disease_disease with lesion of sciatic nerve, disease_disease with radial neuropathy, disease_disease with radial neuropathy, disease_disease with femoral neuropathy, disease_disease with femoral neuropathy.", "label": "yes"}
{"original_question": "Is the BAGEL algorithm used for arrayed CRISPR screens?", "id": "converted_3552", "sentence1": "Is the BAGEL algorithm used for arrayed CRISPR screens?", "sentence2": "BAGEL: a computational framework for identifying essential Genes from pooled library screens., The adaptation of the CRISPR-Cas9 system to pooled library gene knockout screens in mammalian cells represents a major technological leap over RNA interference, the prior state of the art. New methods for analyzing the data and evaluating results are needed.RESULTS: We offer BAGEL (Bayesian Analysis of Gene EssentiaLity), a supervised learning method for analyzing gene knockout screens. Coupled with gold-standard reference sets of essential and nonessential Genes, BAGEL offers significantly greater sensitivity than current methods, while computational optimizations reduce runtime by an order of magnitude.CONCLUSIONS: Using BAGEL, we identify ~2000 fitness Genes in pooled library knockout screens in human cell lines at 5 % FDR, a major advance over competing platforms. BAGEL shows high sensitivity and specificity even across screens performed by different labs using different libraries and Reagents., CONCLUSIONS\n\nUsing BAGEL, we identify ~2000 fitness Genes in pooled library knockout screens in human cell lines at 5 % FDR, a major advance over competing platforms., BAGEL: a computational framework for identifying essential Genes from pooled library screens, CONCLUSIONS\nUsing BAGEL, we identify ~2000 fitness Genes in pooled library knockout screens in human cell lines at 5 % FDR, a major advance over competing platforms., CONCLUSIONS: Using BAGEL, we identify ~2000 fitness Genes in pooled library knockout screens in human cell lines at 5 % FDR, a major advance over competing platforms., Conclusions Using BAGEL, we identify ~2000 fitness Genes in pooled library knockout screens in human cell lines at 5 % FDR, a major advance over competing platforms.[SEP]", "label": "no"}
{"original_question": "Are there any specific antidotes for rivaroxaban?", "id": "converted_169", "sentence1": "Are there any specific antidotes for rivaroxaban?", "sentence2": "Novel oral anticoagulants (NOACs)--apixaban, dabigatran, and rivaroxaban--have a significantly smaller risk of Cerebral Hemorrhage (HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO). However, two facts make this situation complicated: First, the risk of Hematoma expansion is unknown for NOACs. Second, there is no specific antidote for neither of the NOACs., he new oral anticoagulants dabigatran etexilate (Pradaxa), rivaroxaban (Xarelto), and apixaban (Eliquis) have predictable pharmacokinetic and pharmacodynamic profiles and are alternatives to warfarin. However, many physicians are wary of these drugs, since there is limited evidence on how to manage Hemorrhage in patients taking them, and since no specific antidote is known to reverse their anticoagulant effect. , Given the absence of a specific antidote, the action to be taken in these situations must be defined. , The fact that there is no specific antidote to reverse the anticoagulant action of the new anticoagulants can impair management of hemorrhagic complications; , Like any new therapy, the potential benefits must be weighed against the potential challenges and one of the most concerning aspects of the new target-specific oral anticoagulants is the lack of a proven method to reverse their effect. Unlike the vitamin K antagonist, i.e. warfarin, there is no specific antidote for these medications. , Two major drawbacks are on the one hand the risk of Pharmacologic Substance accumulation in Both kidneys and/or Hepatobiliary Disorder and, on the other hand, the lack of specific antidotes., NOA also have other unresolved problems: Pharmacologic Substance interactions are still possible, specific coagulation test to assess them must be developed, and no specific antidote is currently available in case of hemorrhagic complication., But they have disadvantages also, they depend on renal clearance, they can interact with other Medicament and they lack a specific antidote. , While these trial data are extremely encouraging, several practical issues (e.g., lack of specific antidote, safety of long-term treatment or cost-effectiveness in \"real-life\" clinical practice) still need to be elucidated., In case of massive Hemorrhage, management is unclear and none of these newer agents has a specific antidote that completely reverses its anticoagulant effect., The short half-life of these new agents compensates for the lack of any specific antidote in many instances. , Currently, none of these new agents has a specific antidote, and little advise can be given on how to manage a major Hemorrhage event., Rivaroxaban, which inhibits Factor Ashmore and Cartier Islands (Ashmore and Cartier Islands), is currently in clinical trials and is the most advanced factor Ashmore and Cartier Islands inhibitor. The Pharmacologic Substance offers once-daily oral dosing, with no need for injections, dose titration, or frequent blood tests to monitor the international normalised ratio. It has a rapid onset of action and, although there is no specific antidote, it has a short plasma elimination half-life (about 5-9 hours). , Increased use of dabigatran, rivaroxaban, and apixaban as oral anticoagulants for the treatment of Atrial Fibrillation by ECG Finding and acute deep venous thrombosis has increased despite the lack of known antidotes to these medications., There is no antidote for reversal and no reliable laboratory monitoring of the anticoagulant effect for emergency situations. , Further concerns about the use of Direct Oral Anticoagulant in the elderly are the high prevalence of Kidney Failure in Atrial Fibrillation patients >75 years of age, the largely unknown risk of Pharmacologic Substance-Pharmacologic Substance and Pharmacologic Substance-food interactions, the lack of easily available laboratory monitoring tests of anticoagulant activity and the lack of an antidote., Specific antidotes for the reversal of the anticoagulant effect of these drugs, such as Monoclonal Antibodies against the direct thrombin inhibitor dabigatran or recombinant Ashmore and Cartier Islands-analog in the case of factor Ashmore and Cartier Islands inhibitors, are still being investigated in early clinical trials., In early 2013 there is no antidote for dabigatran, rivaroxaban or apixaban, nor any specific treatment with proven efficacy for severe Hemorrhage linked to these drugs. [SEP]Relations: Rivaroxaban has relations: drug_drug with Inotersen, drug_drug with Inotersen, drug_drug with Gadoteridol, drug_drug with Gadoteridol, drug_drug with Colistin, drug_drug with Colistin, drug_drug with Ampicillin, drug_drug with Ampicillin, drug_drug with Antipyrine, drug_drug with Antipyrine.", "label": "no"}
{"original_question": "Do tumour-associated macrophages have a prognostic role in gliomas?", "id": "converted_3238", "sentence1": "Do tumour-associated macrophages have a prognostic role in Glioma?", "sentence2": "Increasing evidence suggests that tumour-associated macrophages/microglia (TAMs) facilitate tumour progression by acquiring a M2-like phenotype. Our objective was to investigate the prognostic value of TAMs in Glioma using automated quantitative double immunofluorescence., This is the first study to use automated quantitative immunofluorescence to determine the prognostic impact of TAMs. Our results suggest that M2-like TAMs hold an unfavourable prognostic value in high-grade Glioma and may contribute to a pro-tumourigenic microenvironment., Our data revealed that the amount of especially MSR1 wt Allele+ TAMs increases with malignancy grade. In grade III-IV, high MSR1 wt Allele expression was associated with shorter survival, while high IBA-1 intensity correlated with a longer survival. In grade IV, MSR1 wt Allele showed independent prognostic value when adjusting for clinical data and the methylation status of O6-methylguanine-DNA methyltransferase.[SEP]Relations: Glioma has relations: phenotype_phenotype with Ependymoma, phenotype_phenotype with Ependymoma, phenotype_phenotype with Brainstem glioma, phenotype_phenotype with Brainstem glioma, phenotype_phenotype with Malignant neoplasm of the central nervous system, phenotype_phenotype with Malignant neoplasm of the central nervous system, phenotype_phenotype with Neuroepithelial neoplasm, phenotype_phenotype with Neuroepithelial neoplasm, disease_phenotype_positive with glioma susceptibility, disease_phenotype_positive with glioma susceptibility.", "label": "yes"}
{"original_question": "Do mutations in KCNT2 only cause phenotypes with epilepsy?", "id": "converted_4558", "sentence1": "Do mutations in KCNT2 gene only cause phenotypes with Epilepsy?", "sentence2": "KCNT2 gene gene Variant resulting in substitutions affecting the Arg190 residue have been shown to cause Epileptic encephalopathy and a recognizable facial gestalt. We report two additional individuals with Intellectual Disability, dysmorphic features, Hypertrichosis, Macrocephaly and the same de novo KCNT2 gene gene missense Variant affecting the Arg190 residue as previously described. Notably, neither patient has Epilepsy. Homology modeling of these missense Variant revealed that they are likely to disrupt the stabilization of a closed channel conformation of KCNT2 gene gene resulting in a constitutively open state. This is the first report of pathogenic Variant in KCNT2 gene gene causing a developmental phenotype without Epilepsy.[SEP]Relations: Epilepsy has relations: disease_protein with KCNT2 gene, disease_protein with KCNT2 gene, disease_protein with KCND2, disease_protein with KCND2, disease_protein with KCNAB2, disease_protein with KCNAB2, disease_protein with KCNA2, disease_protein with KCNA2, disease_protein with KCNQ2, disease_protein with KCNQ2.", "label": "no"}
{"original_question": "Could plasmepsins be used as targets for developing anti-malaria drugs?", "id": "converted_1910", "sentence1": "Could plasmepsins be used as targets for developing anti-Malaria Vaccines drugs?", "sentence2": "Fighting Malaria Vaccines: structure-guided discovery of nonpeptidomimetic plasmepsin inhibitors., Given that the parasite needs the resulting Amino Acids building blocks for its growth and development, plasmepsins are an important antimalarial Pharmacologic Substance target. , Due to early crystallographic evidence, plasmepsin II (Plm II) emerged as well explored target to develop novel Antimalarials as well as a starting point to develop inhibitors targeting some other subtypes of plasmepsins i.e. Plm I, II, IV and V. With the advancements in Pharmacologic Substance discovery, several computational and synthetic approaches were employed in order to develop novel inhibitors targeting Plm II. , Structural basis for plasmepsin V inhibition that blocks export of Malaria Vaccines Proteins to human Specimen Source Codes - Erythrocytes., Plasmepsin V, an essential aspartyl Endopeptidases of Malaria Vaccines Parasites, has a key role in the export of effector Proteins to parasite-infected Specimen Source Codes - Erythrocytes. Consequently, it is an important Pharmacologic Substance target for the two most virulent Malaria Vaccines Parasites of Homo sapiens, Plasmodium falciparum or Plasmodium falciparum + Plasmodium sp or Plasmodium falciparum or Plasmodium falciparum + Plasmodium sp + Plasmodium sp and Plasmodium vivax or Plasmodium vivax + Plasmodium sp or Plasmodium vivax or Plasmodium vivax + Plasmodium sp + Plasmodium sp., Plasmepsin V (PmV) is an essential Plasmodium Endopeptidases and a highly promising antimalarial target, which still lacks molecular characterization and Pharmacologic Substance-like inhibitors., Our inhibitors act 'on-target', confirmed by cellular interference of PmV function and biochemical interaction with inhibitors. , Our work disclosed novel pursuable Pharmacologic Substance design strategies for highly efficient PmV inhibition highlighting novel molecular elements necessary for picomolar activity against PmV. All the presented data are discussed in respect to human aspartic proteases and previously reported inhibitors, highlighting differences and proposing new strategies for Pharmacologic Substance development., High binding likeness on antimalarial target plasmepsin was detected through molecular docking. , This provides the first direct evidence that PMV activity is essential for protein export in Plasmodium spp. and for parasite survival in human Specimen Source Codes - Erythrocytes and validates PMV as an antimalarial Pharmacologic Substance target., The export mechanism involves the Plasmodium export element (PEXEL), which is a cleavage site for the parasite Endopeptidases, Plasmepsin V (PMV). , Plasmepsin II (PM II) is an attractive target for anti-Malaria Vaccines Pharmacologic Substance discovery, which involves in host Hemoglobin A1 (substance) degradation in the acidic food vacuole., These methods are utilized to search for inhibitors of the Aspartic Acid Endopeptidases, plasmepsin II and carboxypeptidase C D. Plasmepsin II, a Endopeptidases found in the Malaria Vaccines parasite, hydrolyzes human Hemoglobin A1 (substance), the Nutrient (property) source for the parasite and is a new target for anti-Malaria Vaccines therapy., Given recent advances in understanding the fundamental roles of the various plasmepsins, it is likely that the most effective antimalarial plasmepsin targets will be the non-food vacuole plasmepsins., Plasmepsins (POLYDACTYLY, POSTAXIAL, WITH PROGRESSIVE MYOPIA) are essential proteases of the plasmodia Parasites and are therefore promising targets for developing drugs against Malaria Vaccines., Therefore, the plasmepsins of Malaria Vaccines Parasites have been recognized as attractive antimalarial Pharmacologic Substance targets., As inhibition of plasmepsins leads to the parasite's Cessation of life, these ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS can be utilized as potential Pharmacologic Substance targets., falciparum plasmepsins II and IV make structure-based Pharmacologic Substance design of antimalarial compounds that focus on inhibiting plasmepsins possible., The malarial parasite encodes two homologous aspartic proteases, plasmepsins I and II, which are essential components of its Hemoglobin A1 (substance)-degradation pathway and are novel targets for antimalarial Pharmacologic Substance development., vivax plasmepsins (PvPMs) from different geographical regions are of utmost importance for drugs and vaccine designs for anti-malarial strategies., In Plasmodium falciparum or Plasmodium falciparum + Plasmodium sp or Plasmodium falciparum or Plasmodium falciparum + Plasmodium sp + Plasmodium sp infection, plasmepsins I, II, IV and RTN3 gene have been directly implicated in Hemoglobin A1 (substance) degradation during Malaria Vaccines infection, and are now considered targets for anti-malarial Pharmacologic Substance design., These results shed light on the role of V105 and T108 residues in plasmepsin specificities, and they should be useful in structure-based design of novel, selective inhibitors that may serve as antimalarial drugs., The aspartic proteases plasmepsins, whose inhibition leads to parasite Cessation of life, are classified as targets for the design of potent drugs., A large compound library of about 1 million Chemicals was docked on 5 different targets of plasmepsins using two different docking software, namely FlexX and AutoDock., Plasmodium aspartic proteases known as plasmepsins play an important role on Hemoglobin degradation and are being studied as Pharmacologic Substance targets for chemotherapy of Malaria Vaccines., Our study revealed about 100 parasite-coded gene products that included many known Pharmacologic Substance targets such as HPRT1 gene, Pf L-lactate dehydrogenase, and Plasmepsins., The two aspartic proteases, plasmepsins I and II, from Plasmodium falciparum or Plasmodium falciparum + Plasmodium sp or Plasmodium falciparum or Plasmodium falciparum + Plasmodium sp + Plasmodium sp have recently emerged as potential targets., Plasmepsins are highly promising as Pharmacologic Substance targets, especially when combined with the inhibition of falcipains that are also involved in Hemoglobin A1 (substance) catabolism., Among such ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS, Plasmepsins (aspartic proteases) and, especially, Falcipains (Cysteine Proteases) are highly promising antimalarial Pharmacologic Substance targets., The high sequence conservations between the plasmepsins from the isolates support the notion that the ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS could be reliable targets for new antimalarial chemotherapeutics., Due to early crystallographic evidence, plasmepsin II (Plm II) emerged as well explored target to develop novel Antimalarials as well as a starting point to develop inhibitors targeting some other subtypes of plasmepsins i.e., Plasmepsin, an aspartic Endopeptidases, which is involved in the Hemoglobin A1 (substance) breakdown into smaller Peptides emerged as a crucial target to develop new chemical entities to counter Malaria Vaccines., were employed in order to develop new chemical entities targeting Plm II., With the advancements in Pharmacologic Substance discovery, several computational and synthetic approaches were employed in order to develop novel inhibitors targeting Plm II., vivax plasmepsins (PvPMs) from different geographical regions are of utmost importance for drugs and vaccine designs for anti-malarial strategies.., We developed a potent inhibitor of plasmepsin V, called WEHI-842, which directly mimics the Plasmodium export element (PEXEL)., In order to validate appropriate use of PM4 as potential anti-malarial Pharmacologic Substance target, studies on Genetic and structural variations among P., Over the past decade, much effort has been placed towards developing plasmepsin inhibitors as antimalarial agents, particularly targeting the food vacuole.[SEP]Relations: Plasmodium vivax or Plasmodium vivax + Plasmodium sp Malaria Vaccines has relations: disease_disease with Malaria Vaccines, disease_disease with Malaria Vaccines. Plasmodium falciparum or Plasmodium falciparum + Plasmodium sp Malaria Vaccines has relations: disease_disease with Malaria Vaccines, disease_disease with Malaria Vaccines, disease_protein with FAS, disease_protein with FAS. Geneticin has relations: drug_drug with Plazomicin, drug_drug with Plazomicin. Plasmodium falciparum or Plasmodium falciparum + Plasmodium sp blood infection level has relations: disease_disease with Malaria Vaccines, disease_disease with Malaria Vaccines.", "label": "yes"}
{"original_question": "Is avelumab effective for bladder cancer?", "id": "converted_3030", "sentence1": "Is avelumab effective for bladder cancer?", "sentence2": "BACKGROUND: Avelumab has recently been approved by the Food and Drug Administration for the therapy of Merkel cell carcinoma and Urothelial Carcinoma., Six drugs including one CTLA-4 blocker (ipilimumab), two PDCD1 wt Allele blockers (nivolumab and pembrolizumab) and three CD274 wt Allele blockers (atezolizumab, avelumab and durvalumab) are approved for the treatment of different types of Malignant Neoplasms including both Solid Neoplasm such as Melanocytic neoplasm, Primary malignant neoplasm of lung, Malignant Head and Neck Neoplasm, bladder cancer and Merkel cell cancer as well as Hematologic Neoplasms such as classic Hodgkin's lymphoma. , The Food and Drug Administration has already approved a number of checkpoint inhibitors such as anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA4 wt Allele wt Allele) monoclonal Antibodies, in vitro diagnostic including ipilimumab; anti-PDCD1 wt Allele monoclonal Antibodies, in vitro diagnostic including nivolumab and pembrolizumab; anti-CD274 wt Allele Antibodies, in vitro diagnostic including atezolizumab, avelumab, and durvalumab. , Five immune CPI have recently been approved for Area Under Curve/mUC by the US Food and Drug Administration (FDA) including atezolizumab, nivolumab, pembrolizumab, durvalumab and avelumab. , RECENT FINDINGS: Since May 2016, five different agents targeting the PDCD1 wt Allele/CD274 wt Allele pathway (atezolizumab, pembrolizumab, nivolumab, avelumab, durvalumab) have received FDA approval for the treatment of Area Under Curve in the platinum-refractory setting, while pembrolizumab and atezolizumab are FDA-approved for cisplatin-ineligible patients in the first-line setting., Avelumab for the treatment of urothelial cancer., Avelumab, a PDCD1 wt Allele ligand (CD274 wt Allele) inhibitor, is currently being investigated for the treatment of Ulcerative Colitis. Areas covered: This article will review the pharmacological characteristics of avelumab, the efficacy studies which led to its approval, its safety profile, as well as its place within the management of Urothelial Carcinoma with immunotherapy. , Expert commentary: Avelumab has shown promising antitumor activity and a manageable safety profile in patients with Ulcerative Colitis. , Atezolizumab is the only member of this class currently approved for the treatment of bladder cancer, but nivolumab, pembrolizumab, durvalumab, and avelumab all have positive results for this indication, and approvals are anticipated in the near future., This selection from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Malignant neoplasm of urinary bladder focuses on systemic therapy for muscle-invasive urothelial bladder cancer, as substantial revisions were made in the 2017 updates, such as new recommendations for nivolumab, pembrolizumab, atezolizumab, durvalumab, and avelumab., Atezolizumab, avelumab, durvalumab, nivolumab and pembrolizumab are promising PDCD1 wt Allele/CD274 wt Allele blockade drugs under investigation that will redefine the standard of care for bladder cancer., Monoclonal Antibodies that target programmed cell death protein 1 (PDCD1 wt Allele), including nivolumab and Pembrolizumab, and its ligand, CD274 wt Allele, including Atezolizumab, durvalumab, Avelumab, have all been investigated and approved in the setting of metastatic refractory urothelial cancer (Gupta et al., Six drugs including one CTLA-4 blocker (ipilimumab), two PDCD1 wt Allele blockers (nivolumab and pembrolizumab) and three CD274 wt Allele blockers (atezolizumab, avelumab and durvalumab) are approved for the treatment of different types of Malignant Neoplasms including both Solid Neoplasm such as Melanocytic neoplasm, Primary malignant neoplasm of lung, Malignant Head and Neck Neoplasm, bladder cancer and Merkel cell cancer as well as Hematologic Neoplasms such as classic Hodgkin's lymphoma., nivolumab, pembrolizumab, atezolizumab, durvalumab, and avelumab are among the exciting recent novel therapeutic advances gaining approvals by the FDA for treatment of advanced-stage Urothelial Carcinoma.[SEP]Relations: durvalumab has relations: drug_drug with Avelumab, drug_drug with Avelumab, drug_drug with Emapalumab, drug_drug with Emapalumab, drug_drug with Utomilumab, drug_drug with Utomilumab. Ipilimumab has relations: drug_drug with Avelumab, drug_drug with Avelumab. nivolumab has relations: drug_drug with Avelumab, drug_drug with Avelumab.", "label": "yes"}
{"original_question": "Is arimoclomol a co-inducer of the heat shock response?", "id": "converted_1444", "sentence1": "Is arimoclomol a co-inducer of the heat shock response?", "sentence2": "arimoclomol is a hydroxylamine derivative, a group of compounds which have unique properties as co-inducers of 78 kDa Glucose-Regulated Protein expression, but only under conditions of cellular stress. , In this review we summarize the evidence for the neuroprotective effects of enhanced 78 kDa Glucose-Regulated Protein expression by arimoclomol and other inducers of the Heat Shock Response. , arimoclomol, a co-inducer of the heat shock stress response,, The heat-shock response (Health Services Research) was activated in P23H retinae, and this was enhanced with arimoclomol treatment. ,  We also assessed these functions in CASP14 gene treated with a known 78 kDa Glucose-Regulated Protein inducer, arimoclomol.,  Under conditions of excessive stress, arimoclomol induces amplification of the cytoprotective heat shock response in order to protect Neurons, Efferent from Cessation of life. , Although both arimoclomol and celastrol induced the expression of Heat-Shock Proteins 70, arimoclomol, an amplifier of 78 kDa Glucose-Regulated Protein expression involved in cellular stress response, has emerged as a potential therapeutic candidate in Amyotrophic Lateral Sclerosis (ALS) in recent years., The mechanism of action of arimoclomol involves potentiation of the heat shock response, and treatment with arimoclomol increased Heat-Shock Proteins 70 expression. , arimoclomol is an investigational Pharmacologic Substance for Amyotrophic Lateral Sclerosis (ALS) that amplifies 78 kDa Glucose-Regulated Protein gene expression during cell stress., arimoclomol, a coinducer of Heat shock proteins, delayed progression of Amyotrophic Lateral Sclerosis (ALS) in a mouse model in which Neurons, Efferent in the Spinal Cord and motor cortex degenerate.[SEP]Relations: arimoclomol has relations: drug_protein with SOD1, drug_protein with SOD1. 78 kDa Glucose-Regulated Protein binding has relations: molfunc_protein with LMAN2, molfunc_protein with LMAN2, molfunc_protein with LMAN2, molfunc_protein with LMAN2, molfunc_protein with IRAK1, molfunc_protein with IRAK1, molfunc_protein with IRAK1, molfunc_protein with IRAK1.", "label": "yes"}
{"original_question": "Is armodafinil used for treatment of insomnia?", "id": "converted_1156", "sentence1": "Is armodafinil used for treatment of insomnia?", "sentence2": " Other therapies, such as sedative hypnotics, target daytime insomnia, while pharmacologic agents such as modafinil, armodafinil, and Caffeine Measurement and non-pharmacologic approaches such as napping promote nighttime alertness., Other treatment options may include pharmacologic interventions such as modafinil and armodafinil, which have shown efficacy in this population., BACKGROUND: armodafinil (Nuvigil(®), Cephalon, Inc., Frazer, newton per square metre, USA), the longer-lasting isomer of racemic modafinil, is a nonamphetamine, wakefulness-promoting medication. In patients with excessive Somnolence associated with shift work disorder, treated obstructive sleep apnoea, or Narcolepsy 1, armodafinil has been found to improve wakefulness throughout the shift or day. In addition, while not approved for this indication, armodafinil has been found to improve excessive Somnolence associated with jet-lag disorder., STUDY OBJECTIVES: armodafinil is a wakefulness-promoting medication. Its efficacy and tolerability have been established in 12-week studies of patients with excessive Somnolence (ES) associated with treated obstructive sleep apnea (Sleep Apnea, Obstructive), shift work disorder (SWD), or Narcolepsy 1. , armodafinil represents an option for long-term treatment of patients with ES associated with treated Sleep Apnea, Obstructive, SWD, or Narcolepsy 1., The wakefulness-promoting agents armodafinil and modafinil are FDA approved for the treatment of ES in patients with SWD., CONCLUSIONS: armodafinil significantly improved overall clinical condition related to excessive Somnolence as rated by the CGI-C and was well tolerated in patients with treated Sleep Apnea, Obstructive and comorbid depression., CONCLUSION: In patients with excessive Somnolence associated with chronic SWD of moderate or greater severity, armodafinil significantly improved wakefulness during scheduled night work, raising mean nighttime sleep latency above the level considered to indicate severe Somnolence during the daytime. armodafinil also significantly improved measures of overall clinical condition, long-term memory, and attention. , Adjunct treatment with armodafinil significantly improved wakefulness, long-term memory, and patients' ability to engage in activities of daily living in nCPAP-adherent individuals with ES associated with Sleep Apnea, Obstructive. , A number of studies have evaluated countermeasures or interventions in shift workers; proposed treatments include chronobiotic interventions, such as light exposure, Recombinant Recombinant melatonin, hypnotic agents, Caffeine Measurement and Central Nervous System stimulants (Amphetamines), and the wake-promoting agents modafinil and armodafinil. , These studies showed that modafinil and armodafinil significantly improve the ability to sustain wakefulness during waking activities (e.g. working, driving), overall clinical condition, and sustained attention or memory in patients with SWSD. , CONCLUSIONS: In this selected population of patients with Sleep Apnea, Obstructive/HS and residual ES despite effective treatment with nCPAP, armodafinil QD used as an adjunct to nCPAP treatment was associated with improved wakefulness and overall clinical condition. ,  Other therapies, such as sedative hypnotics, target daytime insomnia, while pharmacologic agents such as modafinil, armodafinil, and Caffeine Measurement and non-pharmacologic approaches such as napping promote nighttime alertness., armodafinil represents an option for long-term treatment of patients with ES associated with treated Sleep Apnea, Obstructive, SWD, or Narcolepsy 1., Other therapies, such as sedative hypnotics, target daytime insomnia, while pharmacologic agents such as modafinil, armodafinil, and Caffeine Measurement and non-pharmacologic approaches such as napping promote nighttime alertness., In this selected population of patients with Sleep Apnea, Obstructive/HS and residual ES despite effective treatment with nCPAP, armodafinil QD used as an adjunct to nCPAP treatment was associated with improved wakefulness and overall clinical condition[SEP]Relations: armodafinil has relations: contraindication with anxiety disorder, contraindication with anxiety disorder, contraindication with mental disorder, contraindication with mental disorder, drug_drug with Omeprazole, drug_drug with Omeprazole, drug_drug with Antipyrine, drug_drug with Antipyrine, contraindication with neurotic disorder, contraindication with neurotic disorder.", "label": "no"}
{"original_question": "Is there a relationship between junctin and ryanodine receptors?", "id": "converted_980", "sentence1": "Is there a relationship between ASPH gene-2 and Ryanodine Receptors?", "sentence2": "ASPH gene, a 26 kDa intra-Sarcoplasmic Reticulum (SR) protein, forms a quaternary complex with TRDN gene, calsequestrin and the Ryanodine Receptor Calcium Release Channel (Ryanodine Receptor Calcium Release Channel complex location) at the Junctional SR Membrane Device. , ASPH gene ablation appears to affect how RyRs 'sense' SR Ca(2+) load, resulting in decreased diastolic SR Ca(2+) leak despite an elevated [Ca(2+)](SR). , Single channel recordings of RyRs from Wild Type Unspecified - zebrafish and JCN-KO cardiac SR indicate that the absence of ASPH gene-2 produces a dual effect on the normally linear response of RyRs to Luminal region [Ca(2+)]: at low Luminal region [Ca(2+)] (<1 mmol l(-1)), ASPH gene-2-devoid Ryanodine Receptor Calcium Release Channel complex location channels are less responsive to Luminal region [Ca(2+)]; conversely, high Luminal region [Ca(2+)] turns them hypersensitive to this form of channel modulation. Thus, ASPH gene-2 produces complex effects on Ca(2+) sparks, transients, and leak, but the Luminal region [Ca(2+)]-dependent dual response of ASPH gene-2-devoid RyRs demonstrates that ASPH gene-2 normally acts as an activator of Ryanodine Receptor Calcium Release Channel complex location channels at low Luminal region [Ca(2+)], and as an PPP1R1A gene at high Luminal region [Ca(2+)]., Normal Ca(2+) signalling in Specimen Source Codes - Skeletal muscle depends on the Membrane Device associated Proteins TRDN gene and ASPH gene-2 and their ability to mediate functional interactions between the Ca(2+) binding protein calsequestrin and the Ryanodine Receptor 1, Human in the Units Of Measure - Units Of Measure - lumen of the Sarcoplasmic Reticulum., We show here that purified skeletal Ryanodine Receptors are similarly activated by purified TRDN gene or purified ASPH gene-2 added to their Luminal region side, although a lack of competition indicated that the Proteins act at independent sites. Surprisingly, TRDN gene and ASPH gene-2 differed markedly in their ability to transmit information between skeletal calsequestrin and Ryanodine Receptors. Purified calsequestrin inhibited ASPH gene-2/TRDN gene-associated, or ASPH gene-2-associated, Ryanodine Receptors and the calsequestrin re-associated channel complexes were further inhibited when Luminal region Ca(2+) fell from 1mM to, By fusing GCaMP6f to the N-terminus of TRDN gene 1 or ASPH gene-2, GCaMP6f-T/J was targeted to dyadic junctions, where it colocalized with t-tubules and RyRs after adenovirus-mediated gene transfer. , The Junctional face of the jSR, facing the transverse tubules, is occupied by a molecular complex composed of the transmembrane Ca2+ release channels (Ryanodine Receptors); the Luminal region protein calsequestrin (CSQ); the 2 Membrane Proteins, ASPH gene-2 (Jct), and TRDN gene (Tr), which mediate CSQ-Ryanodine Receptor Calcium Release Channel interactions; and several other components., CASQ2 gene, the main CALCIUM SUPPLEMENTS buffer in the Sarcoplasmic Reticulum, provides a pool of CALCIUM SUPPLEMENTS for release through the Ryanodine Receptor Calcium Release Channel and acts as a Luminal region CALCIUM SUPPLEMENTS sensor for the channel via its interactions with TRDN gene and ASPH gene-2. We examined the influence of phosphorylation of calsequestrin on its ability to store CALCIUM SUPPLEMENTS, to polymerise and to regulate Ryanodine Receptors by binding to TRDN gene and ASPH gene-2. , ASPH gene is a 26 kDa Membrane Device protein that binds to calsequestrin, TRDN gene, and Ryanodine Receptors (RyRs) within the Junctional Sarcoplasmic Reticulum of CALCIUM SUPPLEMENTS release units. [SEP]Relations: Ryanodine Receptor Calcium Release Channel complex has relations: cellcomp_protein with RYR1, cellcomp_protein with RYR1, cellcomp_protein with RYR1, cellcomp_protein with RYR1, cellcomp_protein with RYR1, cellcomp_protein with RYR1, cellcomp_protein with FKBP1A, cellcomp_protein with FKBP1A, cellcomp_protein with FKBP1A, cellcomp_protein with FKBP1A.", "label": "yes"}
{"original_question": "Can thiotepa be recommended for treatment of osteosarcoma?", "id": "converted_4219", "sentence1": "Can thiotepa be recommended for treatment of Osteosarcoma of bone?", "sentence2": "CONCLUSION: Adjuvant HDTp failed to significantly improve OS and PFS in resectable relapsed Osteosarcoma. Despite a trend of prolonged survival and an acceptable Toxic effect, thiotepa cannot be recommended.KEY MESSAGE: HDTp and autologous transplantation added to SPONDYLOCARPOTARSAL SYNOSTOSIS SYNDROME did not improve OS and PFS in patients with resectable relapsed Osteosarcoma. Despite a trend of prolonged survival, thiotepa cannot be recommended., Conclusion. The use of HD thiotepa and ASCT is feasible in patients with relapsed Osteosarcoma of bone. A randomized study for recurrent Osteosarcoma of bone between standard salvage chemotherapy and high dose thiotepa with Stem cells rescue is ongoing.[SEP]Relations: Thiotepa has relations: drug_effect with Lymphedema, drug_effect with Lymphedema, drug_effect with Erythema, drug_effect with Erythema, drug_drug with Antipyrine, drug_drug with Antipyrine, contraindication with kidney disease, contraindication with kidney disease, contraindication with liver disease, contraindication with liver disease.", "label": "no"}
{"original_question": "Has \"RNA interference\" been awarded Nobel prize?", "id": "converted_1900", "sentence1": "Has \"RNA interference\" been awarded Nobel prize?", "sentence2": "Since the first unequivocal description of RNA interference (RNAi) in 1998, it has remained one of the hottest topics under investigation, culminating in the award of a Nobel Prize to its discoverers in 2006., RNA interference (RNAi) is considered one of the most powerful genomic tools which allows the study of drug discovery and understanding of the complex cellular processes by high-content screens. This field of study, which was the subject of 2006 Nobel Prize of medicine, has drastically changed the conventional methods of analysis of genes.,  Almost 10 years after Fire and Mello received the Nobel Prize for the discovery of this mechanism in flat worms, RNA interference is on the edge of becoming a new class of therapeutics.[SEP]", "label": "yes"}
{"original_question": "Is FTY720 FDA approved?", "id": "converted_4263", "sentence1": "Is FTY-720 FDA approved?", "sentence2": "FTY-720 (fingolimod) is a known sphingosine 1-phosphate (S1P) receptor Agonist that exerts strong anti-inflammatory effects and was approved as the first oral drug for the treatment of Multiple Sclerosis by the US Food and Drug Administration (FDA) in 2010. [SEP]Relations: fingolimod has relations: drug_drug with WIN 55212-2, drug_drug with WIN 55212-2, drug_drug with G17DT, drug_drug with G17DT, drug_drug with Octreotide, drug_drug with Octreotide, drug_drug with mRNA-1273, drug_drug with mRNA-1273, drug_protein with S1PR5, drug_protein with S1PR5.", "label": "yes"}
{"original_question": "Has ubrogepant entered clinical phase III trials?", "id": "converted_3952", "sentence1": "Has ubrogepant entered clinical phase III trials?", "sentence2": "Ubrogepant (MK-1602) is a novel, oral, CALCRL gene antagonist in clinical development with positive phase III outcomes for acute treatment of Migraine Disorders., A population pharmacokinetic model describing the effect of formulations was included in the E-R simulation framework to assess potential dose implications of a formulation switch from phase II to phase III. , The understanding of E-R helped support the dose selection for the phase III clinical trials., The CGRP receptor antagonist ubrogepant, also known as MK-1602, has been recently evaluated in phase III clinical trials for clinical efficacy and long-term safety as an abortive Migraine Disorders treatment., Two pivotal phase III clinical trials (ACHIEVE I and ACHIEVE II) demonstrated effectiveness and safety of ubrogepant in acute Migraine Disorders attacks.[SEP]Relations: CALCRL has relations: drug_protein with Ubrogepant, drug_protein with Ubrogepant, drug_protein with Vazegepant, drug_protein with Vazegepant, drug_protein with Olcegepant, drug_protein with Olcegepant, drug_protein with Rimegepant, drug_protein with Rimegepant, drug_protein with Telcagepant, drug_protein with Telcagepant.", "label": "yes"}
{"original_question": "Are Alu elements transcribed?", "id": "converted_642", "sentence1": "Are Alu Elements transcribed?", "sentence2": "Alu RNA in the Homo sapiens transcriptome, Alu Elements can be transcribed in two different ways, by two independent polymerases, 'Free Alu RNA' are transcribed by Pol III from their own Promoter, 'embedded Alu RNA' are transcribed by RNA Polymerase II as part of protein- and non-protein-coding RNA, Recent studies have demonstrated that both free and embedded Alu RNA play a major role in post transcriptional regulation of gene expression, Alu RNA transcribed from these Elements are present at low levels at normal cell growth but various stress conditions increase their abundance, Alu RNA are known to bind the cognate proteins SRP9/14, Increased level of polymerase III transcribed Alu RNA in Liver carcinoma tissue, we used Oligonucleotide Primers extension analysis to determine the level of polymerase III directed Alu RNA and found an increased expression of Alu RNA in Liver carcinoma, Widespread RNA Editing of embedded alu Elements in the Homo sapiens transcriptome, Transcribed Alu DNA Sequence can alter splicing patterns by generating new Exons, In the vast majority of edited RNA, A-to-I substitutions are clustered within transcribed sense or antisense Alu DNA Sequence, Alu-associated RNA Editing may be a mechanism for marking nonstandard transcripts, not destined for translation, the case of transcribed Alus, Differential levels of Alu RNA during different conditions of stress also await clear functional understanding, Alu expression in Homo sapiens cell lines and their retrotranspositional potential, Alu expression likely varies by cell type, growth conditions and transformation state, The vast majority of Alu loci potentially transcribed by RNA pol III lack important sequence features for retrotransposition and the majority of potentially active Alu loci in the Genome - anatomical entity (scored high Endoscopic Retrograde Cholangiopancreatography) belong to young Alu subfamilies, We suggest that the Genome DNA Sequence upstream from most Alu Elements and 7SL Pseudogenes do not contain this element, and consequently that only a small subset of such DNA Sequence can be transcribed in vivo., These similarities suggest that some Alu family DNA Sequence are mobile genetic Elements that can transpose to new chromosomal loci using as an intermediate a DNA, Complementary copy of an RNA transcribed from the Alu family element by RNA Polymerase III., Primate and rodent genomes are populated with hundreds of thousands copies of Alu and B1 Elements dispersed by retroposition, i.e., by Genome reintegration of their reverse transcribed RNA., Members of this family are readily transcribed in vitro by RNA Polymerase III, but RNA corresponding to only a small sub-set of Alu Elements has been found in vivo., Alu interspersed repetitive Elements possess internal RNA Polymerase III promoters which are strongly transcribed in vitro, yet these Elements are nearly silent in Diploid Cell., The amplification of Genome Alu Elements by retroposition, i.e. by reintegration of reverse-transcribed RNA, suggests that Alu RNA plays an important role in this process., We report enzymatic studies of the Protein Structure, Secondary of Alu RNA transcribed in vitro from two recently retroposed Alu Elements., The results of this study indicate that Alu and 7SL RNA gene DNA Sequence interact with cellular factors that are important for HeLa cell proliferation and suggest that these pol III-transcribed Elements may be involved in the regulation of cellular growth., Then we used Oligonucleotide Primers extension analysis to determine the level of polymerase III directed Alu RNA and found an increased expression of Alu RNA in Liver carcinoma, Alu interspersed repetitive Elements possess internal RNA Polymerase III promoters which are strongly transcribed in vitro, yet these Elements are nearly silent in Diploid Cell, 'Free Alu RNA' are transcribed by Pol III from their own Promoter, while 'embedded Alu RNA' are transcribed by RNA Polymerase II as part of protein- and non-protein-coding RNA, We report enzymatic studies of the Protein Structure, Secondary of Alu RNA transcribed in vitro from two recently retroposed Alu Elements, Transcribed Alu DNA Sequence can alter splicing patterns by generating new Exons, but other impacts of intragenic Alu Elements on their host RNA are largely unexplored, Both 7SL genes and Alu Elements are transcribed by RNA Polymerase III, and we show here that the internal 7SL Promoter lies within the Alu-like part of the 7SL gene, Each group revealed a divergent pattern of transcribed Alu Elements[SEP]Relations: DNA Protein Structure, Secondary binding has relations: molfunc_protein with RAD51AP1, molfunc_protein with RAD51AP1, molfunc_protein with CLSPN, molfunc_protein with CLSPN. Promoter clearance from RNA polymerase I Promoter has relations: bioprocess_bioprocess with Promoter clearance during DNA-templated transcription, bioprocess_bioprocess with Promoter clearance during DNA-templated transcription. RNA Polymerase III complex has relations: cellcomp_protein with POLR2L, cellcomp_protein with POLR2L, cellcomp_protein with POLR3G, cellcomp_protein with POLR3G.", "label": "yes"}
{"original_question": "Can CD55 deficiency cause thrombosis?", "id": "converted_2585", "sentence1": "Can Complement Decay-Accelerating Factor, human deficiency cause thrombosis?", "sentence2": " The loss of Complement Decay-Accelerating Factor, human and CD59 Antigen Antigen renders Paroxysmal nocturnal hemoglobinuria Specimen Source Codes - Erythrocytes susceptible to intravascular haemolysis, which can lead to thrombosis and to much of the morbidity and mortality of Paroxysmal nocturnal hemoglobinuria. , Complement Decay-Accelerating Factor, human Deficiency, Early-Onset Protein-Losing Enteropathy, and Thrombosis., CONCLUSIONS: Complement Decay-Accelerating Factor, human deficiency with hyperactivation of complement, angiopathic thrombosis, and protein-losing enteropathy (the CHAPLE syndrome) is caused by abnormal complement activation due to biallelic loss-of-function mutations in Complement Decay-Accelerating Factor, human. , It is caused by the expansion of a Hematopoietic stem Cells that has acquired a Mutation Abnormality in the X-linked phosphatidylinositol glycan class A (PIGA) gene that results in deficiency of the Glycosylphosphatidylinositols anchor structure responsible for fixing a wide spectrum of Proteins particularly Complement Decay-Accelerating Factor, human and CD59 Antigen Antigen. The clinical features of this Disease arise as a result of complement-mediated Specimen Reject Reason - Hemolysis in unprotected red Cells, Specimen Source Codes - Leukocytes, and Blood Platelets as well as the release of free hemoglobin. Patients may present with a variety of clinical manifestations, such as Genus Anemia, thrombosis, kidney Disease, smooth muscle dystonias, Abdominal Pain, Dyspnea, and extreme fatigue., The lack of one of the GPI-AP complement regulatory Proteins (Complement Decay-Accelerating Factor, human, CD59 Antigen Antigen) leads to Specimen Reject Reason - Hemolysis. The Disease is diagnosed with hemolytic Genus Anemia, marrow failure and thrombosis., Paroxysmal nocturnal hemoglobinuria (Paroxysmal nocturnal hemoglobinuria) is a rare bone marrow failure disorder that manifests with hemolytic Genus Anemia, thrombosis, and peripheral blood cytopenias. The absence of two Glycosylphosphatidylinositols (GPI)-anchored Proteins, Complement Decay-Accelerating Factor, human and CD59 Antigen Antigen, leads to uncontrolled complement activation that accounts for Specimen Reject Reason - Hemolysis and other Paroxysmal nocturnal hemoglobinuria manifestations., RESULTS: Complement Decay-Accelerating Factor, human and/or CD59 Antigen Antigen deficiencies were found in 1.6% (2/127) of patients with primary Breast-Conserving Surgery, 1.0% (1/100) of non-malignant and Non-Cirrhotic patients with PVT, and 4.7% (4/85) of Cirrhotic patients with PVT., Data of this study indicate that the Paroxysmal nocturnal hemoglobinuria defect as detected with Complement Decay-Accelerating Factor, human, CD59 Antigen Antigen, and FCGR3A protein, human is not an important cause of intra-abdominal thrombosis in northwestern India., Paroxysmal nocturnal hemoglobinuria testing of Red blood Cells, blood product revealed a Complement Decay-Accelerating Factor, human and CD59 Antigen Antigen deficiency consistent with Paroxysmal nocturnal hemoglobinuria in both cases. The systemic complications typically associated with thrombosis were not observed for the following several months with early conservative treatments including eculizumab., Deficiency of the GPI-anchored complement inhibitors Complement Decay-Accelerating Factor, human and CD59 Antigen Antigen on Specimen Source Codes - Erythrocytes leads to Intravascular Specimen Reject Reason - Hemolysis upon complement activation. Apart from Specimen Reject Reason - Hemolysis, another prominent feature is a highly increased risk of thrombosis., Genetic reconstitution of Complement Decay-Accelerating Factor, human or treatment with a complement-inhibitory therapeutic antibody reversed abnormal complement activation.<br><b>CONCLUSIONS</b>: Complement Decay-Accelerating Factor, human deficiency with hyperactivation of complement, angiopathic thrombosis, and protein-losing enteropathy (the CHAPLE syndrome) is caused by abnormal complement activation due to biallelic loss-of-function mutations in Complement Decay-Accelerating Factor, human., Paroxysmal nocturnal hemoglobinuria (Paroxysmal nocturnal hemoglobinuria) is an acquired clonal disorder characterized by a decrease or absence of Glycosylphosphatidylinositols (GPI)-anchored molecules such as Complement Decay-Accelerating Factor, human and CD59 Antigen Antigen from the surface of affected Cells, resulting in Intravascular Specimen Reject Reason - Hemolysis, Cytopenia, and Venous Thrombosis., CONCLUSIONS Complement Decay-Accelerating Factor, human deficiency with hyperactivation of complement, angiopathic thrombosis, and protein-losing enteropathy (the CHAPLE syndrome) is caused by abnormal complement activation due to biallelic loss-of-function mutations in Complement Decay-Accelerating Factor, human., Complement Decay-Accelerating Factor, human deficiency with hyperactivation of complement, angiopathic thrombosis, and protein-losing enteropathy (the CHAPLE syndrome) is caused by abnormal complement activation due to biallelic loss-of-function mutations in Complement Decay-Accelerating Factor, human., Complement Decay-Accelerating Factor, human Deficiency, Early-Onset Protein-Losing Enteropathy, and Thrombosis.[SEP]Relations: Venous thrombosis has relations: disease_phenotype_positive with hereditary thrombophilia due to congenital protein C deficiency, disease_phenotype_positive with hereditary thrombophilia due to congenital protein C deficiency, drug_effect with Metolazone, drug_effect with Metolazone. Thrombocytosis has relations: disease_phenotype_positive with vasculitis due to ADA2 deficiency, disease_phenotype_positive with vasculitis due to ADA2 deficiency, disease_phenotype_positive with leukocyte adhesion deficiency, disease_phenotype_positive with leukocyte adhesion deficiency. Hemolytic Genus Anemia has relations: disease_phenotype_positive with primary CD59 Antigen deficiency, disease_phenotype_positive with primary CD59 Antigen deficiency.", "label": "yes"}
{"original_question": "Do bacteria release extracellular vesicles?", "id": "converted_4178", "sentence1": "Do Bacteria release extracellular vesicles?", "sentence2": "Bacterial extracellular vesicles (NCI Enterprise Vocabulary Services) are bilayered Membrane Lipids structures, bearing integral proteins and able to carry diverse cargo outside the \"U\" lymphocyte to distant sites., Knowledge of the structure, molecular cargo and function of bacterial extracellular vesicle (BEVs) is primarily obtained from Bacteria cultured in laboratory conditions. , Bacteria derived-extracellular vesicles[SEP]Relations: membrane lipid metabolic process has relations: bioprocess_protein with AGMO, bioprocess_protein with AGMO, bioprocess_bioprocess with sphingolipid metabolic process, bioprocess_bioprocess with sphingolipid metabolic process, bioprocess_protein with B4GALT4, bioprocess_protein with B4GALT4, bioprocess_bioprocess with glycolipid metabolic process, bioprocess_bioprocess with glycolipid metabolic process. Bacteremia has relations: disease_phenotype_positive with staphylococcal pneumonia, disease_phenotype_positive with staphylococcal pneumonia.", "label": "yes"}
{"original_question": "Is Dexmecamylamine effective for depression?", "id": "converted_3432", "sentence1": "Is Dexmecamylamine effective for depression?", "sentence2": "At treatment end, no significant differences were seen for change in MADRS total score with TC-5214 versus placebo. Furthermore, there were no significant differences in any of the secondary endpoints. , TC-5214 (Dexmecamylamine) is a nicotinic channel modulator that has previously been evaluated for treatment of major depression disorder (Major Depressive Disorder) and is currently being evaluated by Targacept as a treatment for overactive bladder. , In these 2 flexibly-dosed studies, no specific therapeutic effects were observed for TC-5214 (1-4 mg Twice a day) adjunct to Antidepressive Agents in the primary endpoint or any secondary endpoint; however, TC-5214 was generally well tolerated. In conclusion, no Antidepressive Agents effect of TC-5214 was observed in these studies., TC-5214 (Dexmecamylamine) is a nicotinic channel modulator that has previously been evaluated for treatment of major depression disorder (Major Depressive Disorder) and is currently being evaluated by Targacept as a treatment for overactive bladder., No notable differences were observed between Dexmecamylamine and placebo for any secondary end point., TC-5214 ( Dexmecamylamine ) is a nicotinic channel modulator that has previously been evaluated for treatment of major depression disorder ( Major Depressive Disorder ) and is currently being evaluated by Targacept as a treatment for overactive bladder . , TC-5214 (Dexmecamylamine) is a nicotinic channel modulator that has previously been evaluated for treatment of major depression disorder (Major Depressive Disorder) and is currently being evaluated by Targacept as a treatment for overactive bladder., At treatment end, no significant differences were seen for change in MADRS total score with TC-5214 versus placebo., In these 2 flexibly-dosed studies, no specific therapeutic effects were observed for TC-5214 (1-4 mg Twice a day) adjunct to Antidepressive Agents in the primary endpoint or any secondary endpoint; however, TC-5214 was generally well tolerated.[SEP]Relations: Mecamylamine has relations: drug_drug with Dexetimide, drug_drug with Dexetimide, drug_drug with Dextran, drug_drug with Dextran, drug_drug with Dextromoramide, drug_drug with Dextromoramide, drug_drug with Dexmedetomidine, drug_drug with Dexmedetomidine, drug_drug with Dexniguldipine, drug_drug with Dexniguldipine.", "label": "no"}
{"original_question": "Is selenium deficiency involved in autoimmune thyroid disease?", "id": "converted_957", "sentence1": "Is selenium deficiency involved in autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease?", "sentence2": "In areas with severe selenium deficiency higher incidence of Thyroiditis has been reported due to a decreased activity of selenium-dependent glutathione peroxidase Enzyme [APC] within THYROID DIAGNOSTIC RADIOPHARMACEUTICALS cells, Of 30 patients in the selenium treated group, 6 patients were overtly Hypothyroidism, 15 were subclinical Hypothyroidism, 6 were euthyroid, and 3 were subclinical hyperthyroid. The mean TPOAb concentration decreased significantly by 49.5% (P < 0.013) in the selenium treated group versus 10.1% (P < 0.95) in the placebo-treated group, Selenium supplement supplement substitution has a significant impact on inflammatory activity in THYROID DIAGNOSTIC RADIOPHARMACEUTICALS-specific autoimmune disease, Serum selenium is low in newly diagnosed Graves Disease, S-Se was lower in patients with GD than in controls (mean (SD), GD: 89·9 μg/l (18·4); controls: 98·8 μg/l (19·7), P < 0·01), Patients with newly diagnosed GD and Autoimmune hepatitis had significantly lower s-Se compared with random controls. Our observation supports the postulated link between inadequate selenium supply and overt autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease, especially GD, Selenium supplement supplement deficiency is likely to constitute a risk factor for a feedforward derangement of the immune system-THYROID DIAGNOSTIC RADIOPHARMACEUTICALS interaction, while selenium supplementation appears to dampen the self-amplifying nature of this derailed interaction, The recent recognition that the essential trace element selenium is incorporated as selenocysteine in all three deiodinases has decisively confirmed the clear-cut link between selenium and THYROID DIAGNOSTIC RADIOPHARMACEUTICALS function. It has additionally been established that the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS contains more selenium than any other Tissue Specimen Code and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease, Maintenance of \"selenostasis\" via optimal intake not only aids preservation of general health but also contributes substantially to the prevention of THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease, Low birth weight, Iodine, Homeopathic preparation excess and deficiency, selenium deficiency, parity, oral contraceptive use, reproductive span, fetal microchimerism, stress, seasonal variation, Allergy Specialty, smoking, radiation damage to the Neck>Thyroid gland, Viral and bacterial infections all play a role in the development of autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disorders, It has additionally been established that the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS contains more selenium than any other Tissue Specimen Code and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease., Selenium supplement supplement deficiency may play an important role in the initiation and progression of autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease., [Selenium supplement supplement deficiency in Celiac Disease: risk of Autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease]., Low birth weight, Iodine, Homeopathic preparation excess and deficiency, selenium deficiency, parity, oral contraceptive use, reproductive span, fetal microchimerism, stress, seasonal variation, Allergy Specialty, smoking, radiation damage to the Neck>Thyroid gland, Viral and bacterial infections all play a role in the development of autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disorders., Some clinical studies have demonstrated that selenium-deficient patients with autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease benefit from selenium supplementation, although the data are conflicting and many parameters must still be defined., Our observation supports the postulated link between inadequate selenium supply and overt autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease, especially GD., Selenium supplement supplement deficiency in Celiac Disease: risk of Autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease]., Selenoproteins contain the essential trace element selenium whose deficiency leads to major disorders including Primary malignant neoplasm, male reproductive system failure, or autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease., It has additionally been established that the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS contains more selenium than any other Tissue Specimen Code and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease., EVIDENCE SYNTHESIS: Evidence in support of selenium supplementation in THYROID DIAGNOSTIC RADIOPHARMACEUTICALS autoimmune disease is evaluated, the results herein presented demonstrating the potential effectiveness of selenium in reducing the antithyroid peroxidase titer and improving the echostructure in the ultrasound examination., Some investigators suggest that selenium may be a useful adjunctive treatment for Autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease, such as Hashimoto and Graves Disease., Therefore, even mild selenium deficiency may contribute to the development and maintenance of Autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease., Some clinical studies have demonstrated that selenium-deficient patients with autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease benefit from selenium supplementation, although the data are conflicting and many parameters must still be defined., Some clinical studies have demonstrated that selenium-deficient patients with autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease benefit from selenium supplementation, although the data are conflicting and many parameters must still be defined, High prevalence of Hyperplasia and autoimmune diseases of THYROID DIAGNOSTIC RADIOPHARMACEUTICALS in Ukrainian population is determined by endemic deficit of Iodine, Homeopathic preparation and selenium, It has additionally been established that the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS contains more selenium than any other Tissue Specimen Code and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease., Therefore, even mild selenium deficiency may contribute to the development and maintenance of Autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease, Some investigators suggest that selenium may be a useful adjunctive treatment for Autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease, such as Hashimoto and Graves Disease[SEP]Relations: autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease has relations: disease_disease with Thyroiditis (disease), disease_disease with Thyroiditis (disease), disease_disease with atrophic Thyroiditis, disease_disease with atrophic Thyroiditis, disease_disease with Graves disease, disease_disease with Graves disease, disease_protein with TG, disease_protein with TG, disease_disease with autoimmune disease of endocrine system, disease_disease with autoimmune disease of endocrine system.", "label": "yes"}
{"original_question": "Is there increased incidence of incontinence in athletes?", "id": "converted_1335", "sentence1": "Is there increased incidence of Incontinence in athletes?", "sentence2": "Urinary tract tract Incontinence affects women of all ages, including top female athletes, but is often under-reported. The highest prevalence of Urinary tract tract Incontinence is reported in those participating in high impact sports., The prevalence of female stress Urinary tract tract Incontinence is high, and young adults are also affected, including athletes, especially those involved in \"high-impact\" sports, Analysis of these data suggests that perineal pressure is decreased in female athletes compared with nonathlete women. A lower perineal pressure correlates with increased symptoms of Urinary tract tract Incontinence and pelvic floor dysfunction., Urinary tract tract Incontinence is a prevalent condition among athletes that is not openly discussed., High-level sport appears to be a significant independent risk factor for Aortic Valve Insufficiency in healthy young women. , The prevalence of LUTS was 54.7%, and 30% for Urinary tract tract Incontinence., LUTS and Incontinence are prevalent in female athletes., A relationship between sport or fitness activities and Urinary tract tract Incontinence (UI) previously has been described in women. , studies have also shown a high prevalence of SUI in young, physically fit female athletes. , There was Urinary tract tract Incontinence in female long-distance runners and a correlation with Eating Disorders., young female athletes participating in high-impact sports may be at higher risk for Urinary tract tract Incontinence., Results indicated that more than 25% of those completing surveys experienced Incontinence and that more than 90% had never told anyone about their problem and had no knowledge of preventive measures; 16% reported Incontinence negatively impacted their quality of life., There is a very high prevalence of Urinary tract tract Incontinence in women athletes., Women athletes should be counseled about the increased risk of Urinary tract tract Incontinence with ultra high-impact sports and Eating Disorders., Stress Urinary tract tract Incontinence is a barrier to women's participation in sport and fitness activities and, therefore, it may be a threat to women's health, self-esteem and well-being. The prevalence during sports among young, nulliparous elite athletes varies between 0% (golf) and 80% (trampolinists). The highest prevalence is found in sports involving high impact activities such as gymnastics, track and field, and some ball games, Urinary tract tract leakage is common among elite athletes and dancers, particularly during training, but also during daily life activities., There is a high prevalence of stress and urge Incontinence in female elite athletes. The frequency of SUI and urge Incontinence was significantly higher in eating disordered athletes compared with healthy athletes., High impact sports activities may produce Urinary tract tract Incontinence., Urinary tract tract Incontinence during physical stresses is common in young nulliparous wome, Incontinence during physical stresses is common in young, highly fit, nulliparous women.[SEP]Relations: Urinary tract Incontinence has relations: drug_effect with Lenalidomide, drug_effect with Lenalidomide, drug_effect with Cyclosporine, drug_effect with Cyclosporine, drug_effect with Ibuprofen, drug_effect with Ibuprofen, drug_effect with Urofollitropin, drug_effect with Urofollitropin, drug_effect with Felbamate, drug_effect with Felbamate.", "label": "yes"}
{"original_question": "Is Kummell’s disease an avascular necrosis of the vertebral body?", "id": "converted_2357", "sentence1": "Is Kummell’s disease an avascular necrosis of the vertebral body?", "sentence2": " Traumatic spondylopathy is an avascular necrosis of the vertebral body, secondary to a Compression fracture of vertebral column. This entity is characterised by the gradual development in time of a vertebral body collapse following a trivial spinal Trauma, nursing specialty, involving a worsening back pain associated with a progressive Kyphosis deformity of spine., Traumatic spondylopathy is a rare spinal disorder characterized as avascular necrosis of a vertebral body occurring in a delayed fashion after minor Trauma, nursing specialty., Traumatic spondylopathy is a spinal disorder characterized by delayed post-traumatic collapse of a vertebral body with avascular necrosis., Kummell disease, or avascular necrosis of a vertebral body, presents as vertebral Bone necrosis typically affecting a Bone structure of Bone structure of thoracic vertebra with compression deformity, intravertebral vacuum cleft, and exaggerated Kyphosis deformity of spine weeks to months after a minor Wounds and Injuries., INTRODUCTION Traumatic spondylopathy is an avascular necrosis of the vertebral body, secondary to a Compression fracture of vertebral column., Kummel disease is the eponym for avascular necrosis of the vertebral body after a Compression fracture of vertebral column., kummell s disease delayed post traumatic Bone necrosis of the vertebral body, Traumatic spondylopathy, caused by Bone necrosis of the vertebral body, is a cause of vertebral collapse., Traumatic spondylopathy is a post-traumatic vertebral body collapse, Traumatic spondylopathy is a rare, delayed posttraumatic collapse of a vertebral body that can occur several months or even years after an osteoporotic compression fracture. , Avascular necrosis of a vertebral body, a relatively uncommon entity, is caused by Primary malignant neoplasm, Communicable Diseases, radiation, systemic Steroids treatment, Trauma, nursing specialty, and the like.1 Vertebral Bone necrosis induced by Trauma, nursing specialty is called Kvmell's disease[SEP]Relations: Vertebral compression fractures has relations: disease_phenotype_positive with Cushing disease due to pituitary adenoma, disease_phenotype_positive with Cushing disease due to pituitary adenoma, disease_phenotype_positive with multicentric osteolysis, nodulosis, and arthropathy, disease_phenotype_positive with multicentric osteolysis, nodulosis, and arthropathy, disease_phenotype_positive with Gaucher disease, disease_phenotype_positive with Gaucher disease, disease_phenotype_positive with osteogenesis imperfecta, disease_phenotype_positive with osteogenesis imperfecta, disease_phenotype_positive with geroderma osteodysplastica, disease_phenotype_positive with geroderma osteodysplastica.", "label": "yes"}
{"original_question": "Is it possible to purify pseudopodia to be used for proteomic analysis?", "id": "converted_1010", "sentence1": "Is it possible to purify pseudopodia to be used for proteomic analysis?", "sentence2": "we developed an approach to biochemically isolate the Pseudopodia from the Cell body of neuron using 3.0-micrometer porous filters for large-scale quantitative proteomic and phosphoproteomic analysis., Recent work using unique subcellular fractionation methodologies combined with spatial genomic, proteomic, and phosphoproteomic profiling has provided insight into the invadopodiome and pseudopodiome signaling networks , ere, we purified the pseudopodial proteomes, Tumor Cells, uncertain whether benign or malignant were placed on a fibronectin-coated porous membrane to form pseudopodia. According to the motile potentials of the Cells, the Cells formed pseudopodial microprocesses in the pores. An excimer laser, which was used for ophthalmic refractive surgeries, horizontally ablated Cells at the membrane surface to remove the Cell body of neuron. , we describe methods for the immunoaffinity purification of phosphotyrosine proteins (pY) from pseudopodia that have been isolated from migratory Cells. These methods are compatible with current mass spectrometry-based protein identification technologies and can be utilized for the large-scale identification of the Pseudopodia pY proteome in various migratory Cultured Cell Line, including primary and Tumor Cells, malignant.[SEP]Relations: Pseudopodia has relations: cellcomp_protein with PLA2G6, cellcomp_protein with PLA2G6, cellcomp_protein with MAPK3, cellcomp_protein with MAPK3, cellcomp_protein with CNP, cellcomp_protein with CNP, cellcomp_protein with MAPK1, cellcomp_protein with MAPK1, cellcomp_protein with ACTN4, cellcomp_protein with ACTN4.", "label": "yes"}
{"original_question": "Is synapsin a phosphoprotein?", "id": "converted_1750", "sentence1": "Is synapsin a Phosphoproteins?", "sentence2": "Synapsins is an evolutionarily conserved presynaptic Phosphoproteins., Synapsins as a family of presynaptic terminal Phosphoproteins participates in neuronal development, Synapsins III (SynIII) is a Phosphoproteins, The neuronal Phosphoproteins synapsin III, Synapsins II is a member of the neuronal Phosphoproteins family., Phosphoproteins synapsin[SEP]Relations: phosphoglycoprotein 1 has relations: disease_disease with Mendelian disease, disease_disease with Mendelian disease. neuronal tumor has relations: disease_disease with neuroepithelial neoplasm, disease_disease with neuroepithelial neoplasm, disease_disease with extraventricular neurocytoma, disease_disease with extraventricular neurocytoma, disease_disease with central neurocytoma, disease_disease with central neurocytoma, disease_disease with cerebellar liponeurocytoma, disease_disease with cerebellar liponeurocytoma.", "label": "yes"}
{"original_question": "Is the protein ABCG2 (ATP-Binding Cassette, subfamily G, member 2, transporter) excreting uric acid?", "id": "converted_3475", "sentence1": "Is the protein ABCG2 wt Allele (ATP-Binding Cassette, subfamily G, member 2, transporter) excreting uric acid?", "sentence2": "TP-binding cassette transporter, sub-family G, member 2 (ABCG2 wt Allele wt Allele/BCRP) is a well-studied urate transporter expressed on apical membranes in several Body tissue, including the Intestines, Abdomen>Liver, and Both kidneys., the discovery that ABCG2 wt Allele wt Allele plays a central role on extra-renal uric acid excretion,[SEP]Relations: Intestines has relations: anatomy_protein_present with ABCG2 wt Allele, anatomy_protein_present with ABCG2 wt Allele, anatomy_protein_present with ABCA2, anatomy_protein_present with ABCA2, anatomy_protein_present with ABCG1, anatomy_protein_present with ABCG1, anatomy_protein_present with ABCC2, anatomy_protein_present with ABCC2, anatomy_protein_present with ABCC6P2, anatomy_protein_present with ABCC6P2.", "label": "yes"}
{"original_question": "Are recessive coding variants responsible for the majority of undiagnosed nonconsanguineous individuals?", "id": "converted_3070", "sentence1": "Are recessive coding variants responsible for the majority of undiagnosed nonconsanguineous individuals?", "sentence2": "Our results suggest that recessive coding variants account for a small fraction of currently undiagnosed nonconsanguineous individuals, and that the role of noncoding variants, incomplete penetrance, and polygenic mechanisms need further exploration.[SEP]", "label": "no"}
{"original_question": "Is lumican a secreted protein?", "id": "converted_2709", "sentence1": "Is LUM protein, Homo sapiens a secreted protein?", "sentence2": "Specimen Source Codes - Fibroblasts stimulated with the Fibrocyte-secreted inflammatory signal tumor necrosis factor-α secrete the small leucine-rich Proteoglycan LUM protein, Homo sapiens, TNF-α-stimulated Specimen Source Codes - Fibroblasts secrete LUM protein, Homo sapiens to promote Fibrocyte differentiation., Secreted 70kDa LUM protein, Homo sapiens stimulates growth and inhibits invasion of Homo sapiens pancreatic cancer., the elevated level of LUM protein, Homo sapiens secretion to Extracellular Space leads to Actins cytoskeletal remodeling followed by an increase in migration capacity of Homo sapiens colon LS180 cells, Lumican is a secreted Proteoglycan that regulates collagen fibril assembly., This is the first time that the synthesis and secretion of LUM protein, Homo sapiens in Homo sapiens melanoma cell lines is reported. [SEP]Relations: Protein S Homo sapiens has relations: drug_drug with Lumiracoxib, drug_drug with Lumiracoxib, drug_drug with Pentosan polysulfate, drug_drug with Pentosan polysulfate, drug_drug with Urokinase, drug_drug with Urokinase. Extracellular Space has relations: cellcomp_protein with LUM, cellcomp_protein with LUM. ECM proteoglycans has relations: pathway_protein with LUM, pathway_protein with LUM.", "label": "yes"}
{"original_question": "Are transcribed ultraconserved regions involved in cancer?", "id": "converted_72", "sentence1": "Are transcribed ultraconserved regions involved in cancer?", "sentence2": "Although most cancer research has focused in RNA, Messenger, non-coding RNAs are also an essential player in tumorigenesis. In addition to the well-recognized microRNAs, recent studies have also shown that epigenetic silencing by CpG Islands hypermethylation of other classes of non-coding RNAs, such as transcribed ultraconserved regions (T-UCRs) or small nucleolar RNAs (snoRNAs), also occur in Homo sapiens Neoplasms, Starting from a genome-wide expression profiling, we demonstrate for the first time a functional link between oxygen deprivation and the modulation of long noncoding transcripts from ultraconserved regions, termed transcribed-ultraconserved regions (T-UCRs). Interestingly, several hypoxia-upregulated T-UCRs, henceforth named 'hypoxia-induced noncoding ultraconserved transcripts' (HINCUTs), are also overexpressed in clinical samples from Malignant tumor of colon patients, Consistent with the hypothesis that T-UCRs have important function in tumor formation, The importance of other classes of non-coding RNAs, such as long intergenic ncRNAs (Long Intergenic Non-Protein Coding RNA) and transcribed ultraconserved regions (T-UCRs) as altered elements in Neoplasms, is also gaining recognition, Expression levels of transcribed ultraconserved regions uc.73 and uc.388 are altered in Malignant neoplasm of colon and/or rectum, Transcribed ultraconserved regions (T-UCRs) are a subset of 481 DNA Sequence longer than 200 bp, which are absolutely conserved between orthologous regions of Homo sapiens, Rattus norvegicus and mouse genomes, and are actively transcribed. It has recently been proven in cancer systems that differentially expressed T-UCRs could alter the functional characteristics of malignant cells. Genome-wide profiling revealed that T-UCRs have distinct signatures in Homo sapiens leukemia and carcinoma,  Our preliminary results suggest that uc.73 and uc.388 could be potential diagnostic and prognostic biomarkers in Cytogenetic Complete Response patients, The transcribed-ultraconserved regions: a novel class of long noncoding RNAs involved in cancer susceptibility, This review gives a picture of the state of the art of a novel class of long RETINAL NONATTACHMENT, NONSYNDROMIC CONGENITAL known as transcribed-ultraconserved regions (T-UCRs). Most recent studies show that they are significantly altered in adult Chronic Lymphocytic Leukemia, Carcinoma, and pediatric Neuroblastoma, leading to the hypothesis that UCRs may play a role in tumorigenesis and promising innovative future T-UCR-based therapeutic approaches, CpG Islands hypermethylation-associated silencing of non-coding RNAs transcribed from ultraconserved regions in Homo sapiens cancer, We focused on the transcribed-ultraconserved regions (T-UCRs), a subset of DNA DNA Sequence that are absolutely conserved between orthologous regions of the Homo sapiens, Rattus norvegicus and mouse genomes and that are located in both intra- and Intergenic Region. We used a pharmacological and genomic approach to reveal the possible existence of an aberrant epigenetic silencing pattern of T-UCRs by treating Tumor cells, malignant with a DNA-demethylating agent followed by hybridization to an expression microarray containing these DNA Sequence. We observed that DNA hypomethylation induces release of T-UCR silencing in Tumor cells, malignant. Among the T-UCRs that were reactivated upon drug treatment, Uc.160+, Uc283+A and Uc.346+ were found to undergo specific CpG Islands hypermethylation-associated silencing in Tumor cells, malignant compared with normal Body tissue. The analysis of a large set of primary Homo sapiens tumors (n=283) demonstrated that hypermethylation of the described T-UCR CpG islands was a common event among the various tumor types. Our finding that, in addition to microRNAs, another class of ncRNAs (T-UCRs) undergoes DNA methylation-associated inactivation in transformed cells supports a model in which epigenetic and Mutation in coding and non-coding DNA Sequence cooperate in Homo sapiens tumorigenesis, An integrative genomics screen uncovers RETINAL NONATTACHMENT, NONSYNDROMIC CONGENITAL T-UCR functions in neuroblastoma tumours, Different classes of non-coding RNAs, including microRNAs, have recently been implicated in the process of tumourigenesis. In this study, we examined the expression and putative functions of a novel class of non-coding RNAs known as transcribed ultraconserved regions (T-UCRs) in neuroblastoma, our results define a T-UCR expression landscape in neuroblastoma and suggest widespread T-UCR involvement in diverse cellular processes that are deregulated in the process of tumourigenesis, Moreover, the recent demonstration that other ncRNAs, the ultraconserved genes (UCGs) or transcribed ultraconserved regions (T-UCRs), are involved in Homo sapiens cancerogenesis, suggests that the wider family of ncRNAs (including both MicroRNAs and UCGs) could contribute to the development of the malignant phenotype. Here we review the main studies investigating the role of MicroRNAs and UCRs in both normal hemopoiesis and Hematologic Neoplasms, and identify the Molecular, clinical and therapeutic implications of these recent findings, The transcribed-ultraconserved regions: a novel class of long noncoding RNAs involved in cancer susceptibility., Expression levels of transcribed ultraconserved regions uc.73 and uc.388 are altered in Malignant neoplasm of colon and/or rectum., CpG Islands hypermethylation-associated silencing of non-coding RNAs transcribed from ultraconserved regions in Homo sapiens cancer., Starting from a genome-wide expression profiling, we demonstrate for the first time a functional link between oxygen deprivation and the modulation of long noncoding transcripts from ultraconserved regions, termed transcribed-ultraconserved regions (T-UCRs)., The importance of other classes of non-coding RNAs, such as long intergenic ncRNAs (Long Intergenic Non-Protein Coding RNA) and transcribed ultraconserved regions (T-UCRs) as altered elements in Neoplasms, is also gaining recognition., Moreover, the recent demonstration that other ncRNAs, the ultraconserved genes (UCGs) or transcribed ultraconserved regions (T-UCRs), are involved in Homo sapiens cancerogenesis, suggests that the wider family of ncRNAs (including both MicroRNAs and UCGs) could contribute to the development of the malignant phenotype., Moreover, the recent demonstration that other ncRNAs, the ultraconserved genes (UCGs) or transcribed ultraconserved regions (T-UCRs), are involved in Homo sapiens cancerogenesis, suggests that the wider family of ncRNAs (including both MicroRNAs and UCGs) could contribute to the development of the malignant phenotype, Starting from a genome-wide expression profiling, we demonstrate for the first time a functional link between oxygen deprivation and the modulation of long noncoding transcripts from ultraconserved regions, termed transcribed-ultraconserved regions (T-UCRs)[SEP]Relations: malignant tumor of neck has relations: disease_protein with EGFR, disease_protein with EGFR, disease_protein with RAD51, disease_protein with RAD51, disease_protein with DPYD, disease_protein with DPYD, disease_protein with RARB, disease_protein with RARB. malignant giant cell tumor has relations: disease_disease with cancer, disease_disease with cancer.", "label": "yes"}
{"original_question": "Is tivantinib effective for MET-high hepatocellular carcinoma?", "id": "converted_4461", "sentence1": "Is tivantinib effective for MET wt Allele-high Liver carcinoma?", "sentence2": "BACKGROUND: Tivantinib (ARQ 197), a selective, oral MET wt Allele wt Allele inhibitor, improved overall survival and progression-free survival compared with placebo in a randomised phase 2 study in patients with high MET wt Allele wt Allele expression (MET wt Allele wt Allele-high) Liver carcinoma previously treated with sorafenib., INTERPRETATION: Tivantinib did not improve overall survival compared with placebo in patients with MET wt Allele wt Allele-high advanced Liver carcinoma previously treated with sorafenib., At a median follow-up of 18·1 months (IQR 14·1-23·1), median overall survival was 8·4 months (95% CI 6·8-10·0) in the tivantinib group and 9·1 months (7·3-10·4) in the placebo group (hazard ratio 0·97; 95% CI 0·75-1·25; p=0·81)., In Phase I and II studies, tivantinib (ARQ 197), an oral inhibitor of MET wt Allele wt Allele, demonstrated promising antitumor activity in patients with altretamine/cisplatin/cyclophosphamide protocol, both as monotherapy and in combination with sorafenib. A randomized Phase II trial in second-line altretamine/cisplatin/cyclophosphamide protocol showed improved overall survival (hazard ratio: 0.38; p = 0.01) in patients with MET wt Allele wt Allele-high tumors, as demonstrated by immunohistochemistry, treated with tivantinib versus placebo. , This study did not confirm the significant efficacy of tivantinib as a second-line treatment for Japanese patients with MET wt Allele wt Allele-high Liver carcinoma. , Median progression-free survival was 2.8 (95% confidence interval: 2.7-2.9) and 2.3 (1.5-2.8) mo in the tivantinib and placebo groups, respectively (hazard ratio = 0.74, 95% confidence interval: 0.52-1.04, P = .082). Median overall survival was 10.3 (95% confidence interval: 8.1-11.6) and 8.5 (6.2-11.4) mo in the tivantinib and placebo group, respectively (hazard ratio = 0.82, 95% confidence interval: 0.58-1.15). , This study did not confirm the significant efficacy of tivantinib as a second-line treatment for Japanese patients with MET wt Allele wt Allele-high Liver carcinoma., This study did not confirm the significant efficacy of tivantinib as a second-line treatment for Japanese patients with MET wt Allele wt Allele-high Liver carcinoma, INTERPRETATION: Tivantinib did not improve overall survival compared with placebo in patients with MET wt Allele wt Allele-high advanced Liver carcinoma previously treated with sorafeni, BACKGROUND: Tivantinib (ARQ 197), a selective, oral MET wt Allele wt Allele inhibitor, improved overall survival and progression-free survival compared with placebo in a randomised phase 2 study in patients with high MET wt Allele wt Allele expression (MET wt Allele wt Allele-high) Liver carcinoma previously treated wit, ostic factor in altretamine/cisplatin/cyclophosphamide protocol after sorafenib failure. Tivantinib demonstrated a nearly doubling of progression free and overall survival in the MET wt Allele wt Allele high group compared to placebo in a Phase II study in patient[SEP]Relations: Tivantinib has relations: drug_protein with MET wt Allele, drug_protein with MET wt Allele. Sorafenib has relations: drug_effect with Hepatocellular carcinoma, drug_effect with Hepatocellular carcinoma, drug_effect with Squamous cell carcinoma, drug_effect with Squamous cell carcinoma, drug_effect with Squamous cell carcinoma of the skin, drug_effect with Squamous cell carcinoma of the skin, drug_drug with Fostamatinib, drug_drug with Fostamatinib.", "label": "no"}
{"original_question": "Is the yeast Μac1 transcription factor induced upon copper deficiency?", "id": "converted_356", "sentence1": "Is the Saccharomyces cerevisiae Μac1 transcription factor induced upon Hypocupremia?", "sentence2": "Low-affinity copper transporter SLC31A2 gene is regulated by copper-sensing transcription factor Mac1p in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae., The copper-depletion induced SLC31A2 gene transcription can be abrogated by genetic deletion of copper-sensing transcription factor Mac1p, Taken together, our results suggest that Mac1p can activate the expression of vacuolar copper transporter Ctr2p in response to Hypocupremia, resulting in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae resistance to copper starvation., The ablation of either MAC1 or AFT1 also abrogated SLC31A2 gene expression induced by copper depletion, Our further study revealed that exogenous Aft1p upregulates SLC31A2 gene transcription only in the presence of Mac1p, whereas exogenous Mac1p upregulates SLC31A2 gene transcription only in the presence of Aft1p., We previously reported that SLC31A2 gene can be upregulated by Hypocupremia via copper-sensing transcription factor Mac1p., In Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae, transcriptional responses to Hypocupremia are mediated by the copper-responsive transcription factor Mac1, Although Mac1 activates the transcription of Genes involved in high affinity copper uptake during periods of deficiency, little is known about the mechanisms by which Mac1 senses or responds to reduced copper availability. , The catalytic activity of Cu-Zn Superoxide Dismutase is essential for Mac1 activation and promotes a regulated increase in binding of Mac1 to copper response elements in the Promoter Regions, Genetic of genomic Mac1 target Genes., In Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae, copper ions regulate gene expression through the two transcriptional activators, ACE wt Allele and Mac1., ACE wt Allele mediates copper-induced gene expression in Cells exposed to stressful levels of copper salts, whereas Mac1 activates a subset of Genes under copper-deficient conditions., Taken together, our results suggest that Mac1p can activate the expression of vacuolar copper transporter Ctr2p in response to Hypocupremia, resulting in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae resistance to copper starvation., In Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae, transcriptional responses to Hypocupremia are mediated by the copper-responsive transcription factor Mac1., We previously reported that SLC31A2 gene can be upregulated by Hypocupremia via copper-sensing transcription factor Mac1p., The Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae Mac1 protein is a copper-sensing transcription factor that is essential for both the activation and inactivation of Genes required for high affinity copper ion transport., The copper-depletion induced SLC31A2 gene transcription can be abrogated by genetic deletion of copper-sensing transcription factor Mac1p. , Copper-mediated repression of the activation domain in the Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae Mac1p transcription factor., We previously reported that SLC31A2 gene can be upregulated by Hypocupremia via copper-sensing transcription factor Mac1p. , In this study, we found that copper depletion can upregulate Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae SLC31A2 gene gene transcription while copper overload downregulate it. The copper-depletion induced SLC31A2 gene transcription can be abrogated by genetic deletion of copper-sensing transcription factor Mac1p.[SEP]Relations: Copper has relations: drug_protein with MT1F, drug_protein with MT1F, drug_protein with NME1, drug_protein with NME1, drug_protein with MT1A, drug_protein with MT1A, drug_protein with MT1M, drug_protein with MT1M, drug_protein with MTF1, drug_protein with MTF1.", "label": "yes"}
{"original_question": "Is vocimagene amiretrorepvec effective for glioblastoma?", "id": "converted_4125", "sentence1": "Is vocimagene amiretrorepvec effective for Glioblastoma Multiforme?", "sentence2": "CONCLUSIONS: These results support an immune-related mechanism of action for Toca 511 and Toca FC, and suggest that Molecular and immunologic signatures are related to clinical benefit from treatment., The median OS was 11.10 months for the Toca 511/FC group and 12.22 months for the control group (hazard ratio, 1.06; 95% CI 0.83, 1.35; P = .62). The secondary end points did not demonstrate statistically significant differences. The rates of adverse events were similar in the Toca 511/FC group and the SOC control group.Conclusions and Relevance: Among patients who underwent tumor resection for first or second recurrence of Glioblastoma Multiforme or Anaplastic astrocytoma, administration of Toca 511 and Toca FC, compared with SOC, did not improve overall survival or other efficacy end points.[SEP]Relations: adult Glioblastoma Multiforme has relations: disease_disease with Glioblastoma Multiforme (disease), disease_disease with Glioblastoma Multiforme (disease), disease_disease with adult infiltrating astrocytic neoplasm, disease_disease with adult infiltrating astrocytic neoplasm, disease_disease with adult spinal cord Glioblastoma Multiforme, disease_disease with adult spinal cord Glioblastoma Multiforme. Anaplastic astrocytoma has relations: contraindication with Temsirolimus, contraindication with Temsirolimus, contraindication with Sirolimus, contraindication with Sirolimus.", "label": "no"}
{"original_question": "Are Drosophila ultraconserved elements candidate ncRNAs?", "id": "converted_1134", "sentence1": "Are Drosophila <basidiomycetes> ultraconserved elements candidate ncRNAs?", "sentence2": "Highly constrained intergenic Drosophila <basidiomycetes> <basidiomycetes> ultraconserved elements are candidate ncRNAs., Here, we report the discovery and characterization of UCEs from 12 sequenced Drosophila <basidiomycetes> <basidiomycetes> species. We identified 98 elements ≥80 bp long with very high Conservation across the Drosophila <basidiomycetes> <basidiomycetes> phylogeny. Population genetic analyses reveal that these UCEs are not present in mutational cold spots. Instead we infer that they experience a level of selective constraint almost 10-fold higher compared with missense mutations in protein-coding sequences, which is substantially higher than that observed previously for human UCEs. About one-half of these Drosophila <basidiomycetes> <basidiomycetes> UCEs overlap the transcribed portion of genes, with many of those that are within coding sequences likely to correspond to sites of ADAR-dependent RNA editing. For the remaining UCEs that are in nongenic regions, we find that many are potentially capable of forming RNA secondary structures. Among ten chosen for further analysis, we discovered that the majority are transcribed in multiple tissues of Drosophila <basidiomycetes> <basidiomycetes> melanogaster. We conclude that Drosophila <basidiomycetes> <basidiomycetes> species are rich with UCEs and that many of them may correspond to novel noncoding RNAs., Highly Constrained Intergenic Drosophila <basidiomycetes> <basidiomycetes> Ultraconserved Elements Are Candidate ncRNAs[SEP]", "label": "yes"}
{"original_question": "Are there lncRNAs that control the extent of neuronal outgrowth?", "id": "converted_3486", "sentence1": "Are there lncRNAs that control the extent of neuronal outgrowth?", "sentence2": "Regulation of Neuroregeneration by Long Noncoding RNAs., Here, we profiled gene expression following sciatic nerve crush in CASP14 gene and identified long noncoding RNAs (lncRNAs) that act in the regenerating Neurons and which are typically not expressed in other contexts. We show that two of these lncRNAs regulate the extent of neuronal outgrowth. We then focus on one of these, SILC1 gene, and show that it regulates Nerve Tissue Regeneration in Cultured Cells and in vivo, through cis-acting activation of the transcription factor SOX11 protein, human.[SEP]Relations: neuronal tumor has relations: disease_disease with extraventricular neurocytoma, disease_disease with extraventricular neurocytoma, disease_disease with central neurocytoma, disease_disease with central neurocytoma, disease_disease with cerebellar liponeurocytoma, disease_disease with cerebellar liponeurocytoma. tissue regeneration has relations: bioprocess_protein with CDKN1A, bioprocess_protein with CDKN1A. neuron to neuron synapse has relations: cellcomp_protein with ATP1B2, cellcomp_protein with ATP1B2.", "label": "yes"}
{"original_question": "Is there an association between presenteeism and depression?", "id": "converted_1526", "sentence1": "Is there an association between Presenteeism and depression?", "sentence2": "Presenteeism was positively associated with severity of depression (Health and Work Performance Questionnaire, P < 0.0001; WPAI, P < 0.0001)., Statistically significant correlations (0.32-0.53) were found between Presenteeism and increasing disability, Fatigue, depression, Anxiety Disorders, and reduced quality of life. , Presenteeism was associated with increasing Fatigue, depression, Anxiety Disorders, and reduced quality of life., Factors with less contribution to Presenteeism included physical limitations, depression or Anxiety Disorders, inadequate job training, and problems with supervisors and coworkers. , BACKGROUND: Subthreshold depression is highly prevalent in the general population and causes great loss to society especially in the form of reduced productivity while at work (Presenteeism)., Two major causes of worker Presenteeism (reduced on-the-job productivity as a result of health problems) are Musculoskeletal Pain:-:Point in time:^Patient:-:-:Point in time:^Patient:- and mental health issues, particularly depression. ,  Pain:-:Point in time:^Patient:-:-:Point in time:^Patient:- and depression were significantly associated with Presenteeism. Pr, Survey adjusted multivariable logistic regression assessed classification of 12-month, depression-related Presenteeism on the basis of socio-demographic, financial, work and health factors. , RESULTS: The LPT from absenteeism and Presenteeism (reduced performance while present at work) was significantly higher among the Major Depressive Disorder group., BACKGROUND: Cancer patients and suicide and depression is reported to be a major cause of Illness (finding)-related sub-optimal work performance (Presenteeism). , BACKGROUND: It is amply documented that Mood Disorders adversely affect job satisfaction, workforce productivity, and absenteeism/Presenteeism. , The difference in productivity loss due to impaired Presenteeism was significantly different between the two groups, but the productivity loss due to absenteeism was not. , Disease activity (OR 3.24, 95% CI 1.11-9.48) and depression (OR 3.22, 95% CI 1.22-8.48) were associated with absenteeism, while depression (OR 5.69, 95% CI 1.77-18.27, disease activity (OR 3.97, 95% CI 1.76-8.98), Anxiety Disorders (OR 3.90, 95% CI 1.83-8.31), self-efficacy (OR 0.71, 95% CI 0.58-0.86), and increasing age (OR 1.04 per year, 95% CI 1.00-1.08) were associated with Presenteeism. , Cancer patients and suicide and depression, in particular, appears to be associated with employment, absenteeism, and Presenteeism, and should therefore be prioritized in clinical practice., Cancer patients and suicide and depression frequently causes unemployment, absenteeism, and Presenteeism, which results in significantly reduced productivity., Presenteeism and absenteeism were significantly worse for the depression group at each time point (p < or = .001). In cross-sectional models, Presenteeism was associated with more severe depression symptoms, poorer general physical health, psychologically demanding work, the interaction ofpsychologically demanding work with depression, and less job control (r2 range = .33-.54)., Chronic conditions such as depression/Anxiety Disorders, BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, Arthritis, and back/neck pain are especially important causes of productivity loss. Comorbidities have significant non-additive effects on both absenteeism and Presenteeism., RESULTS: At baseline, all Presenteeism measures were sensitive to differences between those with (N=69) and without (N=363) depression/Anxiety Disorders., Cancer patients and suicide and depression and Anxiety Disorders were more consistently associated with \"Presenteeism\" (that is, lost productivity while at work) than with absenteeism, whether this was measured by cutback days or by direct questionnaires., RESULTS: Substantial research exists about Anxiety Disorders and depression costs, such as performance and productivity, absenteeism, Presenteeism, disability, A A physical disability exacerbation, mental health treatment, increased medical care costs, exacerbating of physical Illness (finding), and studies of mental health care limitations and cost-offset., The author discusses the etiology and potential solutions for managing this new component in the productivity equation and in addressing depression, the major contributor to Presenteeism., For employees who are currently Depressed mood, recent research evidence has demonstrated that pharmacotherapy can have a dramatic and positive effect on lost productivity, absenteeism, and Presenteeism., Among participants who were still employed, those with depression had significantly more job turnover, Presenteeism, and absenteeism. , Only depression affected both absenteeism-Presenteeism and critical incidents. , CONCLUSIONS: Depressive disorder in the workplace persist over time and have a major effect on work performance, most notably on \"Presenteeism,\" or reduced effectiveness in the workplace. , The negative effects of depression include those on patients' occupational functioning, including absenteeism, Presenteeism, and reduced opportunities for educational and work success. , The remitted group demonstrated a significant improvement in productivity (particularly Presenteeism) when compared with the new visit group (Z = -3.29, p = 0.001)., Cancer patients and suicide and depression in workers leads to significant absenteeism, \"Presenteeism\" (diminished capacity due to Illness (finding) while still present at work), and significantly increased medical expenses in addition to the costs of psychiatric care. , Significant predictors of Presenteeism and activity impairment at follow-up (controlled for gender, age, spondyloarthritis subgroups and Presenteeism at baseline) were Presenteeism at baseline, poor quality of life, worse disease activity, decreased physical function, lower self-efficacy pain and symptom, higher scores of Anxiety Disorders, depression, Location characteristic ID - Smoking and low education level, and for activity impairment also female sex. , \" Pain:-:Point in time:^Patient:-:-:Point in time:^Patient:- and depression were significantly associated with Presenteeism., Only depression affected both absenteeism-Presenteeism and critical incidents., Factors with less contribution to Presenteeism included physical limitations, depression or Anxiety Disorders, inadequate job training, and problems with supervisors and coworkers.[SEP]Relations: Anxiety Disorders disorder has relations: disease_disease with postpartum depression, disease_disease with postpartum depression, disease_disease with neurotic depression, disease_disease with neurotic depression, disease_disease with unipolar depression, disease_disease with unipolar depression. major depressive disorder has relations: disease_disease with endogenous depression, disease_disease with endogenous depression, disease_disease with endogenous depression, disease_disease with endogenous depression.", "label": "yes"}
{"original_question": "Does Axitinib prolong survival of Pancreatic Cancer patients?", "id": "converted_3111", "sentence1": "Does Axitinib prolong survival of Pancreatic Cancer patients?", "sentence2": "CONCLUSIONS: Axitinib/gemcitabine, while tolerated, did not provide survival benefit over gemcitabine alone in patients with advanced Malignant neoplasm of pancreas from Japan or other regions., RESULTS: Among Japanese patients, median overall survival was not estimable (95% confidence interval, 7.4 months-not estimable) with axitinib/gemcitabine (n = 58) and 9.9 months (95% confidence interval, 7.4-10.5) with placebo/gemcitabine (n = 56) (hazard ratio 1.093 [95% confidence interval, 0.525-2.274]). Median survival follow-up (range) was 5.1 months (0.02-12.3) with axitinib/gemcitabine vs. 5.4 months (1.8-10.5) with placebo/gemcitabine. Similarly, no difference was detected in overall survival between axitinib/gemcitabine and placebo/gemcitabine in patients from North America or the European Union. , At an interim analysis in January, 2009, the independent data monitoring committee concluded that the futility boundary had been crossed. Median overall survival was 8·5 months (95% CI 6·9-9·5) for gemcitabine plus axitinib (n=314, data missing for two patients) and 8·3 months (6·9-10·3) for gemcitabine plus placebo (n=316; hazard ratio 1·014, 95% CI 0·786-1·309; one-sided p=0·5436). , INTERPRETATION: The addition of axitinib to gemcitabine does not improve overall survival in advanced Malignant neoplasm of pancreas. , INTERPRETATION\nThe addition of axitinib to gemcitabine does not improve overall survival in advanced Malignant neoplasm of pancreas., However, as with other Protein Tyrosine Kinase inhibitors of the same class, axitinib does not prolong overall survival; therefore, selection of second-line Protein Tyrosine Kinase inhibitor therapy, including axitinib, must be carefully considered to maximize outcomes for each patient., CONCLUSIONS\nAxitinib/gemcitabine, while tolerated, did not provide survival benefit over gemcitabine alone in patients with advanced Malignant neoplasm of pancreas from Japan or other regions., Similarly, no difference was detected in overall survival between axitinib/gemcitabine and placebo/gemcitabine in patients from North America or the European Union., Axitinib/gemcitabine, while tolerated, did not provide survival benefit over gemcitabine alone in patients with advanced Malignant neoplasm of pancreas from Japan or other regions., The addition of axitinib to gemcitabine does not improve overall survival in advanced Malignant neoplasm of pancreas.[SEP]Relations: Axitinib has relations: drug_drug with Panobinostat, drug_drug with Panobinostat, drug_drug with Proguanil, drug_drug with Proguanil, drug_drug with Afelimomab, drug_drug with Afelimomab, drug_drug with Entrectinib, drug_drug with Entrectinib, drug_drug with Dolutegravir, drug_drug with Dolutegravir.", "label": "no"}
{"original_question": "Can we detect DNA strand asymmetries using dinucleotide relative abundance \"genomic signatures\"?", "id": "converted_443", "sentence1": "Can we detect DNA strand asymmetries using dinucleotide relative abundance \"genomic signatures\"?", "sentence2": "comparing the heterogeneities of Genome, Bacterial with respect to strand-independent first- and second-order features, (i) G + C content and (ii) dinucleotide relative abundance,, the concept of a genomic signature was introduced with the observation of species-type specific Dinucleoside Phosphates Relative Abundance Profiles (DRAPs); dinucleotides were identified as the subsequences with the greatest bias in representation in a majority of genomes., dinucleotide relative abundance values (the genomic signature), The dinucleotide relative abundance profile can be regarded as a genomic signature because, despite diversity between species, it varies little between 50 kilobase or longer windows on a given Genome - anatomical entity., The profile is computed from the base step \"odds ratios\" that compare dinucleotide frequencies to those expected under the assumption of stochastic equilibrium (thorough shuffling). , The Genome - anatomical entity signatures (dinucleotide relative abundance values), Early biochemical experiments measuring nearest neighbor frequencies established that the set of dinucleotide relative abundance values (dinucleotide biases) is a remarkably stable property of the DNA of an organism., the set of dinucleotide biases constitutes a 'genomic signature' that can discriminate sequences from different Organism., the set of dinucleotide odds ratio (relative abundance) values constitute a signature of each DNA Genome - anatomical entity, Dinucleoside Phosphates relative abundance extremes: a genomic signature., The dinucleotide relative abundance profile can be regarded as a genomic signature because, despite diversity between species, it varies little between 50 kilobase or longer windows on a given Genome - anatomical entity., Previously, the concept of a genomic signature was introduced with the observation of species-type specific Dinucleoside Phosphates Relative Abundance Profiles (DRAPs); dinucleotides were identified as the subsequences with the greatest bias in representation in a majority of genomes., Comparisons within and between species sample sequences are based on the profile of dinucleotide relative abundance values (The profile is rho*XY = f*XY/f*Xf*Y for all XY, where f*X denotes the frequency of the nucleotide X and f*XY denotes the frequency of the dinucleotide XY, both computed from the Sequence - ParameterizedDataType concatenated with its inverted complement)., Dinucleoside Phosphates relative abundances (i.e., dinucleotide representations normalized by the component nucleotide frequencies) are consonant with respect to the leading and lagging strands[SEP]Relations: anatomical entity has relations: anatomy_anatomy with immaterial anatomical entity, anatomy_anatomy with immaterial anatomical entity, anatomy_anatomy with anatomical cluster, anatomy_anatomy with anatomical cluster, anatomy_anatomy with insect mouthpart, anatomy_anatomy with insect mouthpart, anatomy_anatomy with material anatomical entity, anatomy_anatomy with material anatomical entity. male organism has relations: anatomy_anatomy with multicellular organism, anatomy_anatomy with multicellular organism.", "label": "no"}
{"original_question": "Is paroxetine effective for treatment of premenstrual dysphoric disorder?", "id": "converted_402", "sentence1": "Is paroxetine effective for treatment of Premenstrual Dysphoric Disorder?", "sentence2": "To evaluate the cost effectiveness of the four medications with a US FDA-approved indication for PMDD: fluoxetine, sertraline, paroxetine and drospirenone plus ethinyl estradiol (DRSP/EE)., All Selective Serotonin Reuptake Inhibitors (fluoxetine, paroxetine, sertraline, fluvoxamine, citalopram, and clomipramine) were effective in reducing premenstrual symptoms., paroxetine has been approved for the treatment of major depressive disorder (Major Depressive Disorder), Obsessive-Compulsive Disorder, Panic Disorder (Lugano Lymphoma Response Classification Progressive Disease by PET), generalised anxiety disorder, post Stress Disorders, Traumatic (PTSD), and social anxiety disorder (Seasonal Affective Disorder) in adults, whereas paroxetine CR is approved for the treatment of Major Depressive Disorder, Seasonal Affective Disorder, Lugano Lymphoma Response Classification Progressive Disease by PET and Premenstrual Dysphoric Disorder in adults., Selective serotonin-reuptake inhibitors (Selective Serotonin Reuptake Inhibitors) have been proven safe and effective for the treatment of PMDD and are recommended as first-line agents when pharmacotherapy is warranted. Currently fluoxetine, controlled-release paroxetine, and sertraline are the only Food and Drug Administration-approved agents for this indication., When compared with placebo, patients treated with paroxetine 20 mg attained a significant reduction in Irritable Mood (difference in median percent change: -23.9, 95% NDUFB6 gene = -51.3 to -6.2, p = .014; difference in mean absolute change: -18.6, 95% NDUFB6 gene = -32.5 to -4.6, p = .007). A statistically significant difference was not observed when the patients treated with the lower dose of paroxetine (10 mg) were compared with placebo. Treatment was well tolerated with no unexpected side effects., Intermittent administration of paroxetine 20 mg significantly reduced Irritable Mood symptoms in patients with PMDD., All these women had significant improvements in the HAMA, HAMD, CGI, and PRISM calendar. The rate of response to paroxetine treatment lay between 50% and 78.6% in the continuous-treatment group, and 37.5-93.8% in the intermittent-treatment group, as determined at the study end-point., The present results indicate that paroxetine is effective in both continuous and intermittent treatment of oriental PMDD women, and that the effects of active treatment lasted for six consecutive treatment menstrual cycles., paroxetine CR is approved for the treatment of major Cancer patients and suicide and Cancer patients and suicide and depression, social anxiety disorder, Panic Disorder and Premenstrual Dysphoric Disorder in adults., Continuous treatment with paroxetine reduced premenstrual symptoms effectively with a response rate of 85%., Intermittent treatment was as effective as continuous treatment in reducing Irritable Mood, affect lability, and mood swings, but had a somewhat weaker effect on Depressed mood and somatic symptoms., Daily Record of Severity of Problems scores were lower in the paroxetine group compared with the placebo group, although the differences were not statistically significant., However, the mean on-treatment Inventory of Depressive Symptomatology (clinician-rated) score for the paroxetine group was 17.9 +/- 8.3 compared with 31.5 +/- 11.2 in the placebo group (adjusted mean difference = 13.6, P = 0.009)., Response (Clinical Global Impressions Scale score of 1 or 2) occurred in 70% of subjects randomized to paroxetine CR and 10% of those assigned to placebo (chi2(1) = 7.5, P = 0.006)., The US Food and Drug Administration and Health Canada recently approved paroxetine for the treatment of Premenstrual Dysphoric Disorder., Patients treated with either dose of paroxetine CR demonstrated significantly greater improvements on the primary efficacy measure (change from baseline in mean luteal phase VAS-Mood scores) and on the majority of secondary efficacy measures compared with patients randomly assigned to placebo., For the treatment of PMDD, luteal phase dosing with 12.5 mg and 25 mg of paroxetine CR is effective and generally well tolerated., A statistically significant difference was observed in favor of paroxetine CR 25 mg versus placebo on the VAS-Mood (adjusted mean difference = -12.58 mm, 95% NDUFB6 gene = -18.40 to -6.76; p < .001) and for paroxetine CR 12.5 mg versus placebo (adjusted mean difference = -7.51 mm, 95% NDUFB6 gene = -13.40 to -1.62; p = .013)., paroxetine CR doses of 12.5 mg/day and 25 mg/day are effective in treating PMDD and are well tolerated., At end point, subjects treated with paroxetine CR (12.5 mg and 25 mg) demonstrated significant improvement in VAS-Mood scores compared with those who received placebo (paroxetine CR 12.5 mg mean treatment difference vs. placebo, -8.7 mm; 95% NDUFB6 gene, -15.7, -1.7; p =.015; paroxetine CR 25 mg mean treatment difference vs. placebo, -12.1 mm; 95% NDUFB6 gene, -18.9, -5.3; p <.001)., Both doses of paroxetine CR 12.5 mg and 25 mg daily are effective and well tolerated in patients who suffer from PMDD., Of these agents, sertraline, fluoxetine and paroxetine (as an extended-release formulation) are approved by the US FDA for luteal phase, as well as continuous, administration., In well designed placebo-controlled trials in patients with major depressive disorder (including a study in the elderly), social anxiety disorder or Premenstrual Dysphoric Disorder (PMDD), paroxetine CR was consistently superior to placebo with regards to primary endpoints (i.e. mean Hamilton Rating Scale for Depression total score [major depressive disorder], Liebowitz social anxiety scale total score and Clinical Global Impressions-Global Improvement score [social anxiety disorder] and Visual Analogue Scale-Mood score [PMDD])., paroxetine is a potent selective serotonin reuptake inhibitor (Serotonin Reuptake Inhibitor [EPC]) with indications for the treatment of Cancer patients and suicide and Cancer patients and suicide and depression, obsessive- compulsive disorder, Panic Disorder and Phobia, Social. It is also used in the treatment of generalized anxiety disorder, Post-Traumatic Stress Disorder, Premenstrual Dysphoric Disorder and chronic headache., Studies having compared the efficiency of Antidepressive Agents according to their serotonin activity (paroxetine or sertraline versus maprotiline, that is a selective norepinephrine, DL- re-uptake inhibitor), showed that serotonin re-uptake inhibitors were significantly more efficient on all symptoms than maprotiline, that was not more efficient than placebo., paroxetine is a potent and selective serotonin reuptake inhibitor (Serotonin Reuptake Inhibitor [EPC]) with currently approved indications for the treatment of Cancer patients and suicide and Cancer patients and suicide and depression, Obsessive-Compulsive Disorder, Panic Disorder and Phobia, Social. It is also used in the treatment of generalized anxiety disorder, post Stress Disorders, Traumatic, Premenstrual Dysphoric Disorder and chronic headache., Preliminary data suggest that paroxetine has potential in the treatment of Phobia, Social, Premenstrual Dysphoric Disorder and chronic headache., The effects of active treatment were marked by the first active cycle with luteal phase 17-item Hamilton Rating Scale for Depression scores decreasing from 14.9 (+/- 5.3) to 8.2 (+/- 4.9) in the first, 7.8 (+/- 5.1) in the second, and 7.8 (+/- 6.8) in the third active treatment cycles (F[1,13] = 17.6; p < 0.0001)., The most conservative measure, the Clinical Global Impression (CGI), revealed that 7 of 14 patients had a complete response (CGI = 1 or 2) whereas 4 patients had a partial response (CGI = 3)., These open trial findings are consistent with the notion that paroxetine is effective in the acute phase for the treatment of Pervasive Development Disorder., The rating of premenstrual Irritable Mood, Depressed mood, increase in appetite, and anxiety/tension was markedly lower during treatment with paroxetine than before, and this reduction in symptomatology appeared unabated for the entire treatment period.[SEP]Relations: paroxetine has relations: drug_effect with Dyspnea, drug_effect with Dyspnea, contraindication with bipolar disorder, contraindication with bipolar disorder, drug_effect with Dysphagia, drug_effect with Dysphagia, drug_effect with Dysuria, drug_effect with Dysuria, drug_effect with Dyssynergia, drug_effect with Dyssynergia.", "label": "yes"}
{"original_question": "Is the Drosophila Translational Control Element (TCE) involved in spermatogenesis?", "id": "converted_245", "sentence1": "Is the Drosophila <basidiomycetes> Translational Control Element (Tethered Capsule Endomicroscopy) involved in spermatogenesis?", "sentence2": "Gene regulation in Drosophila <basidiomycetes> <basidiomycetes> spermatogenesis: analysis of protein binding at the translational control element Tethered Capsule Endomicroscopy., We have previously identified a 12 nucleotide long sequence element, the Tethered Capsule Endomicroscopy, that was demonstrated to be necessary for translational control of expression in the male Germ Line of Drosophila <basidiomycetes> <basidiomycetes> melanogaster (Schäfer et al., 1990)., Gene regulation in Drosophila <basidiomycetes> <basidiomycetes> spermatogenesis: analysis of protein binding at the translational control element Tethered Capsule Endomicroscopy, The Drosophila <basidiomycetes> <basidiomycetes> Translational Control Element (Tethered Capsule Endomicroscopy) is required for high-level transcription of many Genes that are specifically expressed in Inferior Colliculus, Bioinformatic analyses of core promoter sequences from 190 Genes that are specifically expressed in Inferior Colliculus identified a 10 bp A/T-rich motif that is identical to the translational control element (Tethered Capsule Endomicroscopy), The Drosophila <basidiomycetes> <basidiomycetes> Translational Control Element (Tethered Capsule Endomicroscopy) is required for high-level transcription of many Genes that are specifically expressed in Inferior Colliculus.[SEP]Relations: inferior colliculus has relations: anatomy_anatomy with lateral structure, anatomy_anatomy with lateral structure.", "label": "yes"}
{"original_question": "Is Mycobacterium avium less susceptible to antibiotics than Mycobacterium tuberculosis?", "id": "converted_502", "sentence1": "Is Mycobacterium avium less susceptible to Antifungal Antibiotics, Topical than Mycobacterium tuberculosis antibody?", "sentence2": "The prevalence of cyclophosphamide/doxorubicin/mitomycin protocol lung Communicable Diseases in two inner city hospitals was four times higher than that of Tuberculosis., Most patients with combined Communicable Diseases were clinically consistent with Mycobacterium tuberculosis antibody and responded to anti Mycobacterium tuberculosis antibody treatment alone., The triplex PCR developed by us could be used to detect and differentiate M. tuberculosis, M. avium and other Genus Mycobacterium in a single reaction tube., Twelve (15%) of the 80 blood cultures were positive for Genus Mycobacterium, with Mycobacterium avium being identified in 7 (8.8%) samples and M. tuberculosis in 5 (6.2%). , The antimycobacterial activities of RS-112997, RS-124922 and RS-118641, three capuramycin analogues that inhibit phospho-N-acetylmuramyl-pentapeptide translocase, were tested against clinical isolates of Mycobacterium tuberculosis antibody antibody, Mycobacterium avium and Battey Bacillus, The MIC50/90 (mg/L) results for RS-118641 were: M. tuberculosis, 1/2; multidrug-resistant (MDR) M. tuberculosis, 0.5/2; M. avium, 4/8; and M. intracellulare, 0.06/0.5, These results suggest that capuramycin analogues exhibit strong antimycobacterial potential and should be considered for further evaluation in the treatment of M. tuberculosis and M. avium-M. intracellulare complex Infections of musculoskeletal system in Homo sapiens., Mycobacterium avium causes disseminated Communicable Diseases in patients with acquired immune deficiency syndrome., Overall incidences of Mycobacterium tuberculosis antibody antibody (Tuberculosis) and Mycobacterium avium-intracellulare Infection (cyclophosphamide/doxorubicin/mitomycin protocol) were 0.8 and 1.4 cases/100 person-years of follow-up (PYF), decreasing from 1.8 (Tuberculosis) and 3.5 cases/100 PYF (cyclophosphamide/doxorubicin/mitomycin protocol) before September 1995 to 0.3 and 0.2 cases/100 PYF after March 1997., Because M tuberculosis disease is preventable and curable and yet communicable, physicians should maintain a high degree of suspicion for tuberculosis in HIV-infected adults. In comparison, the goal of treating M avium complex in patients with advanced HIV Infections is to reduce constitutional symptoms and improve survival., cyclophosphamide/doxorubicin/mitomycin protocol pulmonary disease should be considered in the differential diagnosis of SPNs, even when encountered in geographic regions with a high prevalence of Tuberculosis, Pulmonary., From April 2001 to February 2002, 80 blood samples from patients who were suspected to have disseminated mycobacterial Communicable Diseases, presenting Fever symptoms (finding) and (preferably) a CD4 T cell count<100.0 cell/mL were investigated, interleukin-10 binding activity underlies distinct susceptibility of BALB/c and C57BL/6 CASP14 gene to Mycobacterium avium Communicable Diseases and influences efficacy of Antibiotics therapy., Clinical utility of rifabutin (RBT), a potent Antibiotics used in multidrug regimens for tuberculosis (Tuberculosis) as well as for Infections of musculoskeletal system caused by Mycobacterium avium-intracellulare Infection (cyclophosphamide/doxorubicin/mitomycin protocol), has been hampered due to dose-limiting Toxic effect. , Effective therapeutic regimens exist that are limited by the emergence of drug resistance and the inability of Antifungal Antibiotics, Topical to kill dormant organisms. , Clinical utility of rifabutin (RBT), a potent Antibiotics used in multidrug regimens for tuberculosis (Tuberculosis) as well as for Infections of musculoskeletal system caused by Mycobacterium avium-intracellulare Infection (cyclophosphamide/doxorubicin/mitomycin protocol), has been hampered due to dose-limiting Toxic effect., a potent Antibiotics used in multidrug regimens for tuberculosis (Tuberculosis) as well as for Infections of musculoskeletal system caused by Mycobacterium avium-intracellulare Infection (cyclophosphamide/doxorubicin/mitomycin protocol),, Clinical utility of rifabutin (RBT), a potent Antibiotics used in multidrug regimens for tuberculosis (Tuberculosis) as well as for Infections of musculoskeletal system caused by Mycobacterium avium-intracellulare Infection (cyclophosphamide/doxorubicin/mitomycin protocol), has been hampered due to dose-limiting Toxic effect., tuberculosis appear to have different genetic mechanisms for resisting the effects of these Antifungal Antibiotics, Topical, with pks12 playing a relatively more significant role in cyclophosphamide/doxorubicin/mitomycin protocol.[SEP]Relations: tuberculosis has relations: disease_disease with mycobacterial infectious disease, disease_disease with mycobacterial infectious disease, disease_disease with tuberculosis, avian, disease_disease with tuberculosis, avian. mycobacterium avium complex disease has relations: disease_disease with mycobacterial infectious disease, disease_disease with mycobacterial infectious disease, disease_disease with primary bacterial infectious disease, disease_disease with primary bacterial infectious disease. Recurrent mycobacterium avium complex Infections of musculoskeletal system has relations: disease_phenotype_positive with monocytopenia with susceptibility to Infections of musculoskeletal system, disease_phenotype_positive with monocytopenia with susceptibility to Infections of musculoskeletal system.", "label": "yes"}
{"original_question": "Is Adamts18 deficiency associated with cancer?", "id": "converted_4244", "sentence1": "Is ADAMTS18 gene deficiency associated with cancer?", "sentence2": "ADAMTS18 gene deficiency promotes colon carcinogenesis by enhancing β-catenin and p38MAPK/ERK1/2 signaling in the mouse model of AOM/DSS-induced colitis-associated Malignant neoplasm of colon and/or rectum., ADAMTS18 is a novel tumor suppressor and is critical to the pathology of Homo sapiens Malignant neoplasm of colon and/or rectum. However, the underlying mechanism is not clear. Here we generated an ADAMTS18 gene-deficient mouse strain as an in vivo model to investigate the role of ADAMTS18 in the pathogenesis of Malignant neoplasm of colon and/or rectum. In AOM/DSS-induced colitis-associated Malignant neoplasm of colon and/or rectum, the deficiency of ADAMTS18 gene in CASP14 gene resulted in enhanced tumorigenesis and Colitis that could be attributed in part to enhanced nuclear translocation of β-catenin and elevated expression of its downstream target genes, Cyclin D1 and c-myc Genes Genes. Moreover, increased p38MAPK and ERK1/2 activities were detected in Malignant tumor of colon cells from ADAMTS18 gene-deficient CASP14 gene. Further studies revealed that ADAMTS18 deficiency reduced Intestines E-Cadherin levels in CASP14 gene, which ultimately led to Intestines barrier dysfunction. These data indicate that ADAMTS18 gene deficiency enhances tumorigenesis and Intestinal inflammation through elevated Wnt/β-catenin and p38MAPK/ERK1/2 signaling and promotes Malignant tumor of colon in this mouse model.[SEP]Relations: ADAMTS18 has relations: disease_protein with Malignant neoplasm of colon and/or rectum, disease_protein with Malignant neoplasm of colon and/or rectum, disease_protein with colorectal carcinoma, disease_protein with colorectal carcinoma, disease_protein with colorectal neoplasm, disease_protein with colorectal neoplasm, protein_protein with B3GLCT, protein_protein with B3GLCT, protein_protein with IGKC, protein_protein with IGKC.", "label": "yes"}
{"original_question": "Αre plants from the genus Strychnos the original source of curare?", "id": "converted_4277", "sentence1": "Αre Plants from the genus Strychnos the original source of Curare?", "sentence2": "Poisons are widespread in Plants and animal allergen extracts and humankind has often tried to turn them to its own advantage. Owing to their poisonous properties, some species of Strychnos genus have been employed mainly in hunting and fishing, as an adjunct to weapons used not only in the search of Food allergenic extracts and clothes, but also for preventing depredation by wild animal allergen extracts. They have been employed for martial and criminal purposes and also as a means of determining Guilt or innocence. By their nature, poisons such as Strychnine Assay and Curare affect the functioning of the victim's body; , The ethnobotanical uses of South American species of Strychnos L. (Loganiaceae) are reviewed, with the exception of their major rôle in the preparation of Curare, which will be dealt with in detail elsewhere., VELOPMENT: Curare is prepared by boiling the Plant Roots, Barking (observable entity) and stalks of different Plants belonging to the Loganiaceae (Strychnos) and Menispermaceae families (Chondrodendron, Curarea and Abuta). , The history to about 1850 of the muscle-relaxant poison Curare is discussed, especially the developments leading to the botanical identification of the Plants that yield the alkaloidal active principles: Loganiaceae (Strychnos species) and Menispermaceae (Abuta, Chondrodendron, and Curarea species)., or centuries. The study reviews the historical and ethnographic aspects of the use of curares and timbós in the Amazonian region.DEVELOPMENT: Curare is prepared by boiling the Plant Roots, Barking (observable entity) and stalks of different Plants belonging to the Loganiaceae (Strychnos) and Menispermaceae families (Chondrod[SEP]Relations: Plantar pits has relations: disease_phenotype_positive with Darier disease, disease_phenotype_positive with Darier disease, disease_phenotype_positive with monosomy 9q22.3, disease_phenotype_positive with monosomy 9q22.3, disease_phenotype_positive with PTEN hamartoma tumor syndrome, disease_phenotype_positive with PTEN hamartoma tumor syndrome, phenotype_phenotype with Abnormality of the plantar skin of foot, phenotype_phenotype with Abnormality of the plantar skin of foot, disease_phenotype_positive with nevoid basal cell carcinoma syndrome, disease_phenotype_positive with nevoid basal cell carcinoma syndrome.", "label": "yes"}
{"original_question": "Is Tranexamic acid effective for intracerebral haemorrhage?", "id": "converted_4183", "sentence1": "Is Tranexamic acid effective for Cerebral Hemorrhage?", "sentence2": "Tranexamic acid did not increase the risk of post-Cerebral Hemorrhage seizures in the first 90 days., The primary outcome was not different between the two groups: 26 (52%) patients in the placebo group and 22 (44%) in the tranexamic acid group had Cerebral Hemorrhage growth (odds ratio [OR] 0·72 [95% CI 0·32-1·59], p=0·41). There was no evidence of a difference in the proportions of patients who died or had thromboembolic complications between the groups: eight (16%) in the placebo group vs 13 (26%) in the tranexamic acid group died and two (4%) vs one (2%) had thromboembolic complications. None of the deaths was considered related to study medication.INTERPRETATION: Our study does not provide evidence that tranexamic acid prevents Cerebral Hemorrhage growth, although the treatment was safe with no increase in thromboembolic complications. , CONCLUSIONS: Tranexamic acid did not affect a patient's functional status at 90 days after HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO, despite there being significant modest reductions in early Cessation of life (by 7 days), Hematoma expansion and SAEs, which is consistent with an antifibrinolytic effect. , INTERPRETATION: Functional status 90 days after Cerebral Hemorrhage did not differ significantly between patients who received tranexamic acid and those who received placebo, despite a reduction in early deaths and serious adverse events. , Of these, two randomised controlled trials (RCTs) comparing intravenous tranexamic acid to placebo (n = 54) reported no significant difference in Cessation of life or dependency. Three observational studies (n = 281) suggested less Hematoma growth with rapid tranexamic acid infusion. [SEP]Relations: Tranexamic acid has relations: drug_effect with Arrhythmia, drug_effect with Arrhythmia, contraindication with subarachnoid hemorrhage (disease), contraindication with subarachnoid hemorrhage (disease), contraindication with hypertension, contraindication with hypertension, contraindication with cerebral infarction, contraindication with cerebral infarction, contraindication with brain edema, contraindication with brain edema.", "label": "no"}
{"original_question": "Does GATA-1 regulate ribosomal protein genes?", "id": "converted_2106", "sentence1": "Does GATA1 gene regulate ribosomal protein Genes?", "sentence2": "Gene Mutation in exon 2 interfere with the synthesis of the full-length Protein Isoforms of GATA1 gene and lead to the production of a shortened Protein Isoforms, GATA-1s. These mutations have been found in patients with Anemia, Diamond-Blackfan, 2 (Diamond-Blackfan Anemia 1), a congenital erythroid aplasia typically caused by mutations in Genes encoding Ribosomal Proteins., Sixteen of the corresponding TRANSCRIPTION FACTOR are of particular interest, as they are Genes, Housekeeping or show a direct link to hematopoiesis, tumorigenesis or leukemia (e.g. GATA1 gene/2, SPI1 wt Allele, MZF1 gene)., Gene Gene Deletion Abnormality Abnormality of PKC1 relieves the repression of both ribosomal protein and Ribosomal RNA Genes that occurs in response to a defect in the secretory pathway., This stress is monitored by protein kinase C activity, which initiates a signal transduction pathway that leads to repression of transcription of the rRNA and ribosomal protein Genes., The importance of the transcription of the 137 ribosomal protein Genes to the economy of the \"U\" lymphocyte is apparent from the existence of at least three distinct pathways that can effect the repression of this set of Genes.[SEP]Relations: GATA1 has relations: protein_protein with DNASE2, protein_protein with DNASE2, protein_protein with GNA12, protein_protein with GNA12, protein_protein with SPTA1, protein_protein with SPTA1, protein_protein with SPIB, protein_protein with SPIB, protein_protein with DNAI2, protein_protein with DNAI2.", "label": "yes"}
{"original_question": "Does nintedanib hold promise for lung disease associated with systemic sclerosis?", "id": "converted_3480", "sentence1": "Does nintedanib hold promise for lung disease associated with Systemic Scleroderma?", "sentence2": "The patient developed progressive lung Fibrosis under several immunosuppressants and was started on nintedanib, with clinical and functional stabilization. Nintedanib is a tyrosine-kinase PPP1R1A gene that blocks several profibrotic pathways, inhibiting proliferation and migration of Specimen Source Codes - Fibroblasts and decreasing the synthesis of Extracellular Matrix Proteins. It is approved for idiopathic lung Fibrosis and has demonstrated good results in inhibiting migration and proliferation of Systemic Scleroderma dermal Specimen Source Codes - Fibroblasts, constituting a promising agent for Systemic Scleroderma-associated lung Fibrosis., BACKGROUND: Nintedanib is an PPP1R1A gene targeting Platelet-Derived Growth Factor Receptor Beta, Human, Fibroblast Growth Factor Receptor 2 and vascular endothelial growth factor receptor Protein Tyrosine Kinase that has recently been approved for the treatment of idiopathic Pulmonary:-:Point in time:^Patient:- Fibrosis. , CONCLUSION: Nintedanib targets core features of SSc in Fra2-transgenic CASP14 gene and ameliorates histological features of Idiopathic Pulmonary:-:Point in time:^Patient:- arterial hypertension, destructive Disease of capillaries and Pulmonary:-:Point in time:^Patient:- and dermal Fibrosis. These data might have direct implications for the ongoing phase III clinical trial with nintedanib in SSc-associated interstitial lung disease., In light of the ongoing advances in our understanding of the pathogenic mechanisms underlying interstitial lung disease in Systemic Scleroderma, this review also summarizes novel treatment approaches, presenting clinical and preclinical evidence for rituximab, tocilizumab, pirfenidone, and nintedanib, as well as hematopoietic stem cell transplantation and lung transplantation., pirfenidone and nintedanib are emerging agents that exert pleiotropic effects, reflective of the multiple mechanistic pathways of Idiopathic Pulmonary Fibrosis. , Design of a randomised, placebo-controlled clinical trial of nintedanib in patients with Systemic Scleroderma-associated interstitial lung disease (SENSCIS™)., The SENSCIS™ trial is a randomised, placebo-controlled Phase III trial that will evaluate the efficacy and safety of nintedanib in patients with SSc-Lung Diseases, Interstitial (NCT02597933)., CONCLUSIONS: This trial will assess the efficacy and safety of nintedanib in patients with SSc-Lung Diseases, Interstitial., Nintedanib for Systemic Sclerosis-Associated Interstitial Lung Disease., Nintedanib, a tyrosine kinase PPP1R1A gene, has been shown to have antifibrotic and antiinflammatory effects in preclinical models of Systemic Scleroderma and Lung Diseases, Interstitial., METHODS\n\nWe conducted a randomized, double-blind, placebo-controlled trial to investigate the efficacy and safety of nintedanib in patients with Lung Diseases, Interstitial associated with Systemic Scleroderma., CONCLUSIONS\n\nAmong patients with Lung Diseases, Interstitial associated with Systemic Scleroderma, the annual rate of decline in FVC was lower with nintedanib than with placebo; no clinical benefit of nintedanib was observed for other manifestations of Systemic Scleroderma., Potential of Nintedanib in Treatment of Progressive Fibrosing Interstitial Lung Diseases., Anti-fibrotic nintedanib-a new opportunity for Systemic Scleroderma patients?, Newer agents with anti-fibrotic properties, such as pirfenidone or nintedanib, might hold promise also for the Pulmonary:-:Point in time:^Patient:- Fibrosis seen in SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding)., This suggests that nintedanib inhibits fundamental processes in the pathogenesis of Fibrosis., This suggests that nintedanib and pirfenidone , drugs known to slow disease progression in patients with idiopathic Pulmonary:-:Point in time:^Patient:- Fibrosis , may also slow the progression of Lung Diseases, Interstitial associated with systemic autoimmune diseases, In the SENSCIS® trial , nintedanib reduced the rate of Lung Diseases, Interstitial progression in patients with Systemic Scleroderma-associated Lung Diseases, Interstitial, Nintedanib, a tyrosine kinase PPP1R1A gene, has been shown to have antifibrotic and antiinflammatory effects in preclinical models of Systemic Scleroderma and Lung Diseases, Interstitial., The goal of the present study was to determine the effects of nintedanib on a cellular model of SSc-associated interstitial lung disease (Lung Diseases, Interstitial)., OBJECTIVES\nNintedanib is approved for the treatment of idiopathic Pulmonary:-:Point in time:^Patient:- Fibrosis (Idiopathic Pulmonary Fibrosis) and was demonstrated to slow disease progression in patients with Idiopathic Pulmonary Fibrosis by reducing decline in forced vital capacity by 50%., Nintedanib: new indication for Systemic Scleroderma-associated interstitial lung disease., Nintedanib (Ofev™), an oral triple kinase PPP1R1A gene targeting pro-fibrotic pathways, has been used for treatment of idiopathic Pulmonary:-:Point in time:^Patient:- Fibrosis (Idiopathic Pulmonary Fibrosis)., These data might have direct implications for the ongoing phase III clinical trial with nintedanib in SSc-associated interstitial lung disease., Based on positive results from phase III, placebo-controlled, randomized comparative clinical trial conducted in patients with Systemic Scleroderma-associated interstitial lung disease (SSc-Lung Diseases, Interstitial), nintedanib received marketing approval in the United States and Japan for the treatment of SSc-Lung Diseases, Interstitial., Nintedanib is an Protoplasm PPP1R1A gene of Protein Tyrosine Kinase that has been approved for treatment of Idiopathic Pulmonary Fibrosis and has recently been shown to reduce the rate of lung function decline in patients with Lung Diseases, Interstitial associated with Systemic Scleroderma (SSc-Lung Diseases, Interstitial).[SEP]Relations: Systemic Scleroderma has relations: disease_disease with Pulmonary:-:Point in time:^Patient:- Systemic Scleroderma, disease_disease with Pulmonary:-:Point in time:^Patient:- Systemic Scleroderma, disease_disease with limited scleroderma, disease_disease with limited scleroderma, disease_protein with KIAA0319L, disease_protein with KIAA0319L, disease_disease with limited Systemic Scleroderma, disease_disease with limited Systemic Scleroderma, disease_protein with NECTIN2, disease_protein with NECTIN2.", "label": "yes"}
{"original_question": "Is it safe to take isotretinoin during pregnancy?", "id": "converted_225", "sentence1": "Is it safe to take isotretinoin during pregnancy?", "sentence2": "Isotretinoin is a remarkably effective Pharmacologic Substance for severe, recalcitrant Acne Vulgaris., a number of important adverse effects were reported, even the most recent pregnancy prevention program (iPledge) is no more successful than prior programs; there will likely always be a small number of female patients becoming pregnant while receiving isotretinoin for Acne Vulgaris., Isotretinoin has revolutionized the management of Acne Vulgaris., The adverse effect(s) that led to patients stopping isotretinoin were cheilitis (22 patients), mood change (13), Fatigue (12), Eczema (6) and pregnancy (2)., Downregulation of FGFR2b-signaling by isotretinoin explains its therapeutic effect in acne. Downregulation of FGFR2b-signaling during the first trimester of pregnancy disturbs branched morphogenesis and explains Retinoid [EPC] embryotoxicity., The isotretinoin, a 13-cis-retinoic acid, has revolutionized the management of severe treatment-resistant acne and it has been widely used for a range of dermatological conditions, in 90% of the time in young women between 13 and 45 years of age. This agent has severe teratogenic effects, as serious craniofacial, Cardiovascular system, Thymus Gland and CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS Aspects of congenital Aspects of congenital malformations., Aspects of congenital Aspects of congenital malformations is 3-5%, but it increases to almost 30% in women exposed to isotretinoin during the first trimester of pregnancy. Generally, patients in treatment with isotretinoin avoid eventual pregnancy during assumption and, after its stopping, fertility and foetal development are normal once circulating isotretinoin levels return to normal., After 3 months of pharmacological wash out, patient become pregnant and manifested this severe Congenital Abnormality. Woman interrupted gestation, by Labor (Childbirth) induction., clindamycin phosphate 1.2% together with tretinoin 0.025% as a gel (CTG) is a topical formulation of a fixed and stable combination approved by the FDA for the treatment of Acne Vulgaris in patients 12 years of age or older., Safety of CTG use in pregnancy has not been established., To estimate the population-based incidence rates of pregnancy, spontaneous and elective Abortions:Number:Point in time:^Patient:Quantitative:Reported, and birth defects associated with isotretinoin use, and to determine predictors of pregnancy while on isotretinoin, Pregnancies, spontaneous and elective Abortions:Number:Point in time:^Patient:Quantitative:Reported, and birth defects were identified using procedure codes and medical diagnoses., 90 women who became pregnant while on the Pharmacologic Substance, 76 terminated the pregnancy (84%), three had a spontaneous abortion (3%), two had Trauma, nursing specialty during delivery resulting in neonatal Cessation of life (2%) and nine had a live birth (10%). Among the live births, only one had a congenital anomaly of the face and neck (11%)., elective abortion rates were also much higher in our study., Topical Antifungal Antibiotics, Topical, isotretinoin or systemic Antifungal Antibiotics, Topical are usually used for acne therapy. However, isotretinoin cannot be used during pregnancy because it can cause significant birth defects while systemic Antifungal Antibiotics, Topical can have adverse side effects such as Gastrointestinal irritation, Photosensitivity of skin and tetracycline sensitivity., Isotretinoin has been used to treat acne since 1982. Its current indications in the package insert are limited and many physicians still feel uncomfortable prescribing it because of its side effects., Aside from its teratogenic effect, isotretinoin is a safe and excellent Pharmacologic Substance for acne therapy. I, a pregnancy test in females., Vitamin A and its derivatives, retinoic acid, tretinoin and isotretinoin, are currently used in dermatological treatments. The administration of high doses of this vitamin provokes congenital Aspects of congenital Aspects of congenital malformations in CASP14 gene: Cleft palate, isolated, maxillary and mandibular hypoplasia and total or partial fusion of the maxillary incisors., Twelve 60-day-old female House CASP14 gene were divided into two groups on the 7th day of pregnancy: treated group--1 mg isotretinoin per kg body weight, dissolved in Vegetable Oils, was administered from the 7th to the 13th day of pregnancy; control group--Vegetable Oils in equivalent volume was administered orally for the same period. On the 16th day of pregnancy, the females were sacrificed, the fetuses were removed and their heads amputated., The results showed that both groups had closed palates with no reminiscence of Epithelial Cells; however, the first molar germs of the isotretinoin-treated animals showed delayed development compared to the control animals., Isotretinoin (13-cis-Rheumatoid Arthritis) is teratogenic in all species examined; based on administered dose, Homo sapiens appear most sensitive, followed by (in order or decreasing sensitivity) Monkeys, rabbit allergenic extract allergenic extract, hamster, Mus sp., and Rattus norvegicus., Based on embryonic delivered dose, we suggest that 13-cis-Rheumatoid Arthritis is an equipotent teratogen in hamster and rabbit allergenic extract allergenic extract., its safety in Homo sapiens is occasionally questioned because oral ingestion of Retinoids at therapeutic levels is known to entail teratogenic risks., topical tretinoin is not a potential human developmental toxicant., Teratogenicity of Vitamin A [EPC] was firstly detected in experimental animals in 1953. Nearly 30 years later, teratogenicity of Vitamin A [EPC] analogue-isotretinoin was reported in Homo sapiens. Isotretinoin induces serious birth defects of craniofacial and CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, Cardiovascular system system and Thymus Gland Aspects of congenital Aspects of congenital malformations--in about 25% of babies exposed during the first trimester of their prenatal development., high Vitamin A [EPC] intake in pregnant woman: Women who use daily Vitamin A [EPC] supplements during early pregnancy have approximately a two-fold increased risk of giving birth to a malformed baby., Vitamin A started to affect development between doses 0.3-0.3 microm [corrected] per Human Human embryo. Malformations of Head - Component of Device, All All extremities and Chest>Heart were detected similarly like in laboratory Mammals and in man, the minimal embryotoxic doses of Vitamin A [EPC] in Mammals were estimated to be between 0.1-1 mg/kg of maternal weight, Human epidemiological studies have proved teratogenicity of Vitamin A [EPC] after daily doses 25,000 i.u.-8.3 mg (0.13 mg/kg)- and reduction of its maximum intake has been recommended to 10,000 i.u. per day (0.05 mg/kg). The results about teratogenicity of Vitamin A [EPC] achieved in the chick Human Human embryo are in agreement with such a recommendation. Intake of Vitamin A [EPC] in the Food allergenic extracts is sufficient for pregnant woman in common Czech population. Therefore, an artificial supplementation of Vitamin A [EPC] brings risk of overdosage. If supplementation by Vitamin A [EPC] is unavoidable during pregnancy, B-carotene should be preferred., a teratogenic dosing regimen with 13-cis-Rheumatoid Arthritis [Hummler et al. (1994) Teratology 50:184-193]., plasma AUC values of all-trans-Rheumatoid Arthritis were 2- to 7-fold higher after all-trans-Rheumatoid Arthritis administration (present study) than after dosing with the teratogenic dose of 13-cis-Rheumatoid Arthritis. These results strengthen our recent suggestion that the teratogenic effects induced in cynomolgus monkeys by 13-cis-Rheumatoid Arthritis treatment cannot solely result from the action of all-trans-Rheumatoid Arthritis, but may involve 13-cis-Rheumatoid Arthritis and 13-cis-4-oxo-Rheumatoid Arthritis, which could act directly or function as transport vehicle., VITA, among others, is involved in the process of morphogenesis. In contrast, synthetic derivatives of VITA, specifically Tigasone (etretinate, tetanus immune globulin, human) and Roaccutane (isotretinoin, Roa <Chaetodontidae>), are regarded as major teratogens., A biphasic maximal inhibition was present at 1 microM concentrations when the Retinoids VITA, tetanus immune globulin, human and Roa <Chaetodontidae> were added for 16 h (52, 58 and 57%, respectively; P < 0.01 by one-way analysis of variance). In contrast, the addition of the three Retinoids at 1 microM concentrations for 16 h had no significant effect on human chorionic gonadotropin secretion by placental explants of 11-13 weeks gestational age., Inhibition of human chorionic gonadotropin secretion by Retinoids may contribute either directly or indirectly to their teratogenicity., Isotretinoin is a potent retinoic acid used in the treatment of Dermatologic disorders. Though very effective, it is teratogenic if administered during pregnancy, and its teratogenic effect may be related to the normal activity of Retinoids as signalling molecules in the Human Human embryo., defects that includes Chest>Heart defects, by inhibiting the migration of Neural Crest Cells., Proliferation in Chest>Heart tissue of whole Culture of Human Human embryo was inhibited in medium with 10(-6) M isotretinoin to 62% of the control level in Myocardium., The results suggest multiple effects of Retinoids on growth, morphogenesis, and differentiation of early Cardiac - anatomy qualifier tissue, and are discussed in relation to the potential role of Retinoids in early embryogenesis., Oral administration of 400 mg/kg of 13-cis retinoic acid to 9 day pregnant CASP14 gene gives rise to important maxillofacial Aspects of congenital Aspects of congenital malformations. The first manifestation of teratogenic effect is an increase of density of cell death arising in the Dorsal part of the first two branchial arches at day 9.5. These two arches become Hypoplastic at days 10 and 11, and the preskeletal anlagen appear too late in comparison to control embryos. Meckel's Cartilage is too curvilinear and medially situated. Pre-ossicular and pre-mandibular blastemata develop with spatial distortions which are well analyzable at days 16 and 17, Isotretinoin (13-cis-retinoic acid, Accutane) increases the risk of major congenital Aspects of congenital Aspects of congenital malformations in infants exposed to isotretinoin during pregnancy. However, there have been no epidemiologic reports to date on the effect of a subsequent pregnancy after discontinuation of isotretinoin., analysis of pregnancy case reports from patients in whom conception occurred after isotretinoin treatment had been discontinued, spontaneous and missed Abortions:Number:Point in time:^Patient:Quantitative:Reported from all pregnancies was 9.1% (eight patients), and the incidence rate of congenital Congenital Abnormality among the live births was 5.0% (four patients)., were not significantly different from the rates reported for women of reproductive age in the general population. In addition, the Aspects of congenital Aspects of congenital malformations reported were not characteristic of retinoic acid-induced congenital anomalies., Keratolenticular dysgenesis (Irido-corneo-trabecular dysgenesis (disorder)) was induced in CASP14 gene by exposure to the human teratogens, ethanol or 13-cis retinoic acid (isotretinoin, Accutane). Acute teratogen exposure on the seventh day of gestation (corresponding to the third week of human gestation) resulted in an Eye Specimen Source Code Congenital Abnormality incidence of 46% to 100% in day 14 fetuses, This secondary effect on neural crest derivatives is exhibited in the adult animals as Cornea opacities associated with defects in Descemet's membrane and Endothelium, and anterior polar cataracts., 13-cis-retinoic acid (13-cis-Rheumatoid Arthritis, or isotretinoin) is responsible for various craniofacial Aspects of congenital Aspects of congenital malformations in the Rodent and human Human Human embryo., In whole Human Human embryo culture, 13-cis-Rheumatoid Arthritis caused significant overall embryonic growth retardation, especially in the primary and secondary Palate processes., subsequent cell growth was decreased at concentrations of 13-cis-Rheumatoid Arthritis greater than 1 X 10(-5) M. After a 40-hr treatment period, labeling indices in Retinoid [EPC]-treated cells were significantly lower than control values (25% compared with 40%). tretinoin also caused a significant, concentration-dependent decrease in 3H-thymidine incorporation. The inhibitory effect of 13-cis-Rheumatoid Arthritis on proliferation of oral-nasal mesenchymal cells appears to be related to the production of craniofacial Aspects of congenital Aspects of congenital malformations., Reports of adverse human pregnancy outcomes including Cleft palate, isolated have increased as the clinical use of isotretinoin (13-cis-retinoic acid) and other retinoic acid (Rheumatoid Arthritis) derivatives have increased, but the mechanisms by which their effects are exerted are not understood., In shelves exposed to epidermal growth factor and trans-Rheumatoid Arthritis early in their development, DNA synthesis appears to terminate prematurely as compared to shelves cultured in control media, and this effect is accompanied by excessive mesenchymal extracellular space expansion. Exposure of shelves to epidermal growth factor alone is sufficient to block degeneration and induce hyperplasia of the medial Epithelial Cells but does not induce other ultrastructural changes seen with both epidermal growth factor and Rheumatoid Arthritis. The observed alterations in medial cell morphology could interfere with adhesion of the Palate shelves and may play a role in Retinoid [EPC]-induced Cleft palate, isolated in the human Human Human embryo., Recent clinical observations strongly suggest that isotretinoin [13-cis-retinoic acid (cis Rheumatoid Arthritis)] is a human teratogen causing primarily Chest>Heart and craniofacial Aspects of congenital Aspects of congenital malformations including Specimen Source Codes - Ear and Palate defects., Our results demonstrate that labeled cis Rheumatoid Arthritis enters the Body tissue of the Human Human embryo both in vivo and in vitro. CISH protein, human Rheumatoid Arthritis inhibited proliferation of the frontonasal mesenchyme cells in primary culture with 31% inhibition occurring at 2 X 10(-5) M cis Rheumatoid Arthritis., tretinoin, an analogue of Vitamin A [EPC], is known to be teratogenic in laboratory animals and has recently been implicated in a few clinical case reports. To study the human teratogenicity of this agent, we investigated 154 human pregnancies with fetal exposure to isotretinoin, a Retinoid [EPC] prescribed for severe recalcitrant Cystic acne. The outcomes were 95 elective Abortions:Number:Point in time:^Patient:Quantitative:Reported, 26 infants without major Aspects of congenital Aspects of congenital malformations, 12 spontaneous Abortions:Number:Point in time:^Patient:Quantitative:Reported, and 21 malformed infants. A subset of 36 of the 154 pregnancies was observed prospectively., Exposure to isotretinoin was associated with an unusually high relative risk for a group of selected major Aspects of congenital Aspects of congenital malformations (relative risk = 25.6; 95 per cent confidence interval, 11.4 to 57.5)., It is possible that a major mechanism of isotretinoin teratogenesis is a deleterious effect on cephalic neural-crest cell activity that results in the observed craniofacial, Cardiac - anatomy qualifier, and Thymus Gland Aspects of congenital Aspects of congenital malformations.[SEP]Relations: Isotretinoin has relations: contraindication with Chest>Heart disease, contraindication with Chest>Heart disease, contraindication with hepatitis, contraindication with hepatitis, contraindication with anxiety disorder, contraindication with anxiety disorder, contraindication with kidney disease, contraindication with kidney disease, contraindication with liver disease, contraindication with liver disease.", "label": "no"}
{"original_question": "Is lucatumumab a polyclonal antibody?", "id": "converted_2897", "sentence1": "Is lucatumumab a polyclonal antibody?", "sentence2": "A phase 1 study of lucatumumab, a fully Homo sapiens anti-CD40 antagonist monoclonal antibody administered intravenously to patients with relapsed or refractory multiple myeloma., In this open-label, multicentre, phase 1 study a fully Homo sapiens anti-CD40 antagonist monoclonal antibody, lucatumumab, was evaluated in patients with relapsed/refractory multiple myeloma (Millimole per Liter).[SEP]Relations: Lucatumumab has relations: drug_drug with Ficlatuzumab, drug_drug with Ficlatuzumab, drug_drug with Ecromeximab, drug_drug with Ecromeximab, drug_drug with Daclizumab, drug_drug with Daclizumab, drug_drug with Xentuzumab, drug_drug with Xentuzumab, drug_drug with Olaratumab, drug_drug with Olaratumab.", "label": "no"}
{"original_question": "Is Annexin V an apoptotic marker?", "id": "converted_1823", "sentence1": "Is Annexin V an apoptotic marker?", "sentence2": "The apoptosis of the cyclic nucleotide-gated mechanosensitive ion channel activity was induced by subjecting the Cells to OGD conditions for 4 h and was detected by Annexin V/Pulmonary Valve Insufficiency and Hoechst 33258 staining. , In addition to the antimicrobial activity, we found that treatment of the cancer cell lines, Jurkat T-Cells, Granta Cells, and melanoma Cells, with the Pseudomonas sp. In5 crude extract increased staining with the apoptotic marker Annexin V while no staining of healthy normal Cells, i.e., naïve or activated CD4 T-Cells, was observed., At the same time, the expressions of Endoglin, human, PECAM1 wt Allele, and the apoptotic marker of Annexin V were detected through flow cytometry for analyzing the relationship between the expression of Cell surface markers and biological behavior., However, we found decreased sperm cell cell concentration, increase of morphologically abnormal Specimen Source Codes - Spermatozoa and increased binding of apoptotic marker ANXA5 gene. , human chorionic gonadotropin enhanced viability of Large Luteal Cells through antiapoptosis but not proliferation, because the apoptotic marker of ANXA5 gene was decreased, but the proliferative markers of MKI67 gene and proliferating cell Nuclear (incident type) antigen were not increased., However, as the 1,2-dioleoyloxy-3-(trimethylammonium)propane concentration increased from 50 to 800 microM, the apoptotic marker Annexin V and Reactive Oxygen Species double positive Cells increased, suggesting that high dose of 1,2-dioleoyloxy-3-(trimethylammonium)propane-generated Reactive Oxygen Species causes cell apoptosis. , Expression of the apoptotic marker ANXA5 gene was unaffected by antibiotic exposure, whereas the uptake of the necrotic marker Pulmonary Valve Insufficiency was increased by ofloxacin (5 mg/mL) but not by netilmicin (ofloxacin versus netilmicin, ANOVA, P<0.05)., he apoptotic marker of ANXA5 gene was decreased, the apoptotic marker Annexin V, Annexin V labels apoptotic neurons following hypoxia-ischemia., In the present study, the apoptotic cell population was identified immunocytochemically using Annexin V, a marker of Cells in an early stage of apoptosis., Use of ANXA5 gene immunoglobulin complex location to identify apoptotic Cells during pregnancy., Only few SF Regulatory T-Lymphocytes were apoptotic, as indicated by limited ANXA5 gene staining of these Cells., Eosinophils 'aged' in vitro for 48 h exhibited endonuclease DNA degradation, apoptotic morphology, increased red autofluorescence and externalisation of phosphatidylserine (Supernumerary mandibular right central primary incisor) as assessed by binding of FITC-labelled ANXA5 gene., In vivo detection of apoptotic Cells with fluorescently labeled ANXA5 gene is an emerging technique that we evaluated for detecting apoptotic Germ Cells in a mouse model of Testicular dysfunction torsion.Annexin V labeled with an indocyanine fluorophore (bisfunctional succinimidyl ester of cyanine 5.5) (Amersham, Little Chalfont, United Kingdom) was injected intravenously in CASP14 gene 18 hours after the repair of unilateral 720-degree Testicular dysfunction torsion for 2 hours, Here, we tested the hypothesis that enhanced endothelial apoptotic microparticles and decreased Endothelial Progenitor Cells (erucylphosphocholine) levels might contribute to the pathophysiology of Microalbuminuria or macroalbuminuria in Cardiovascular Diseases.Flow cytometry was used to assess Endothelial Cells apoptosis and circulating erucylphosphocholine levels by quantification of circulating PECAM1 wt Allele/ANXA5 gene apoptotic microparticles and erucylphosphocholine markers (defined as KDRCD133, CD34CD133, CD34KDR) in peripheral blood.In total, 125 patients with Hypertensive disease were enrolled in the study, of whom 80 patients (64%) were with Grade A1 albuminuria (ALB gene excretion rate of &lt;20 microg/min, overnight urine samples), 35 patients (28%) with Microalbuminuria (an ALB gene excretion rate of 20-200 microg/min), and 10 patients (8%) with macroalbuminuria (an ALB gene excretion rate >200 microg/min)., Pulmonary Surfactant-Associated Protein A (SFTPA1 gene) binds to phosphatidylserine and competes with ANXA5 gene binding on late apoptotic Cells, Targeting of apoptotic macrophages and experimental atheroma with radiolabeled ANXA5 gene: a technique with potential for noninvasive imaging of vulnerable plaque, Because ANXA5 gene has a high affinity for exposed phosphatidylserine on apoptotic Cells, radiolabeled ANXA5 gene may be used for noninvasive detection of apoptosis in atherosclerotic lesions.atherosclerotic plaques were produced in 5 Family Leporidae (organism) by deendothelialization of the infradiaphragmatic aorta followed by 12 weeks of cholesterol diet; 5 controls were studied without manipulation, Apoptotic abscess imaging with 99mTc-HYNIC-rh-Annexin-V., Synthesis and evaluation of a 18F-labelled recombinant Annexin 1-V derivative, for identification and quantification of apoptotic Cells with PET., Sensitive and visible detection of apoptotic Cells on Annexin-V modified substrate using 3-aminobenzeneboronic acid modified gold Artificial Artificial nanoparticles (APBA-GNPs) labeling., Fluorescence-activated cell sorting (FACS) for expression of the early apoptosis marker Annexin V and for Nuclear (incident type) staining by 7-aminoactinomycin D D (7-AAD) revealed different extents of apoptosis versus non-apoptotic cell death for the three agents., At immunofluorescence these Cells contained lipid vesicles positive for the apoptotic cell marker Annexin V suggesting the phagocytosis of Apoptotic Bodies derived from dead fat-laden hepatocytes., In this respect, we identified binding of Annexin V as an convenient marker for apoptotic Cells., DR5 expression was elevated and associated with the apoptotic marker ANXA5 gene. Apoptosis was reduced in CD4(+) T Cells when cultured with anti-DR5 immunoglobulin complex location., Flow cytometric analysis using the apoptotic marker, Annexin V, shows that this endogenous re-expression is sufficient to drive the SCLC Cells to apoptosis., Apoptotic cell death was evaluated by staining nuclei with Propidium Iodide and phosphatidylserine (a marker of early apoptotic events) with Annexin V as well as by DNA fragmentation assay., Decreased cell growth was not caused by cell death as BEL exposure did not alter Nuclear (incident type) morphology or increase ANXA5 gene (apoptotic cell marker) or Propidium Iodide (necrotic cell marker) staining after 48 h., Four populations of Cells can be identified: region R1: vital Cells (ANXA5 gene negative/Pulmonary Valve Insufficiency negative), region R2: apoptotic Cells (ANXA5 gene positive/Pulmonary Valve Insufficiency negative), region R3: dead Cells (ANXA5 gene positive/ Pulmonary Valve Insufficiency positive); and region R4: damaged Cells (ANXA5 gene negative/Pulmonary Valve Insufficiency positive)., Furthermore, uptake of (111)In-DTPA-PEG-ANXA5 gene by Neoplasms correlated with apoptotic index (r = 0.87, P = 0.02)., Annexin V(+)/Pulmonary Valve Insufficiency(-) Cells were characterized as early apoptotic, Annexin V(+)/Pulmonary Valve Insufficiency(+) as late apoptotic and Annexin V(-)/Pulmonary Valve Insufficiency(+) as dead., Targeting ability of Annexin V for apoptotic macrophages was kept and enhanced., [18F]ANXA5 gene accumulated in the infarct area of the left ventricle, where apoptotic Cells were observed., The viability of SiHa Cells was evaluated using the MTT assay, apoptosis by acridine orange/ethidium bromide, Propidium Iodide, TUNEL assay, and Annexin V-Cy3, cell cycle distribution and mitochondrial transmembrane potential using flow cytometry, and apoptotic marker genes using quantitative real-time PCR. , Furthermore, hesperetin-induced apoptosis was confirmed by TUNEL and Annexin V-Cy3., The procedure delivers two sperm cell cell fractions: ANXA5 gene-negative (nonapoptotic) and ANXA5 gene-positive (apoptotic)., The percentage of Cells stained with ANXA5 gene, an early apoptotic marker, increased dramatically after Cytoskeleton disruption with Cytochalasin D compared with non-cytochalasin-D-treated controls (P<0.05). , Apoptotic marker Annexin V analysis showed that the apoptotic rate of NB4 Cells was increased after treatment with quercetin., The cytomorphology of NB4 Cells was assessed by Wright-stain, apoptosis rate by apoptotic marker Annexin V, and Vascular Endothelial Growth Factor A secretion level by ELISA.,  We have coupled ANXA5 gene with the bifunctional hydrazinonicotinamide reagent (HYNIC) to prepare technetium-99m HYNIC-ANXA5 gene and demonstrated localization of radioactivity in Body tissue undergoing apoptosis in vivo., In conlusion, these studies confirm the value of (99m)Tc-HYNIC-ANXA5 gene uptake as a marker for the detection and quantification of apoptotic Cells in vivo., The application of Annexin V labeling at electron microscopy will allow a more refined description of the morphological events occurring during apoptosis., Apoptotic Cells were identified by Annexin V-FITC/Pulmonary Valve Insufficiency staining. [SEP]Relations: Netilmicin has relations: drug_drug with Epoprostenol, drug_drug with Epoprostenol, drug_drug with Apalutamide, drug_drug with Apalutamide, drug_drug with Dexpanthenol, drug_drug with Dexpanthenol, drug_drug with Pentostatin, drug_drug with Pentostatin, drug_drug with Sisomicin, drug_drug with Sisomicin.", "label": "yes"}
{"original_question": "Has the gorilla genome been determined?", "id": "converted_2071", "sentence1": "Has the Gorilla <Western Gorilla> genome been determined?", "sentence2": "Starting with Homo sapiens, Pan Genus, Gorilla <Western Gorilla>, and orangutan Genome, our software generated an exhaustive data set of 292 ALs (∼1 kb each) in ∼3 h. , We generated a high-quality assembly of the Gorilla <Western Gorilla> genome using single-molecule, real-time sequence technology and a string graph de novo assembly algorithm, Here we present the assembly and analysis of a genome sequence for the western lowland Gorilla <Western Gorilla>, and compare the whole Genome of all extant great ape genera., DNA sequencing reveals that the Genome of the Homo sapiens, Gorilla <Western Gorilla> and Pan Genus share more than 98% Homologous Gene.[SEP]", "label": "yes"}
{"original_question": "The TRPM2 gene is associated with development of spontaneous thromboembolism?", "id": "converted_2670", "sentence1": "The CLU gene gene is associated with development of spontaneous thromboembolism?", "sentence2": "TheTransientReceptorPotentialMelastatin 2 (CLU gene) is a member of G protein coupled receptor superfamily and a novel dual-function protein that possesses both Ion Channel andAdenosine 5'-DiphosPhataseRibose (ADPR) hydrolase function. CLU gene is involved in calcium ionsignaling in various Cells as an endogenous redox sensor for oxidative stress and Reactive Oxygen Species, and contributes to cytokine production, insulin release, motility, calcium ionentry and Ca2+-dependent cellular reactions such as Endothelium hyper-permeability and apoptosis., We show here that the redox-sensitive transient receptor potential (TYRP1 wt Allele) cation channel CLU gene is expressed in the phagosomal membrane and regulates macrophage bactericidal activity through the activation of phagosomal acidification, The transient receptor potential melastatin-2 (CLU gene) is an oxidative stress sensing channel that is expressed in a number of Inflammatory cell and therefore it has been suggested that inhibition of CLU gene could lead to a beneficial effect in Chronic Obstructive Airway Disease patients., CLU gene is a recently identified TRPM family cation channel which is unique among known ion channels in that it contains a C-terminal domain which is homologous to the NUDT9 Adenosine Diphosphate Ribose hydrolase and possesses intrinsic Adenosine Diphosphate Ribose hydrolase activity, These results suggest that CLU gene may participate in antigen-induced Extracellular Ca(2+) influx and subsequent degranulation. In addition, CLU gene inhibitors were shown to improve food allergic reactions in a mouse model. Together, these results suggest that CLU gene inhibitors suppress mitomycin degranulation via regulation of the increase in [Ca(2+)]cyt. Thus, CLU gene may play a key role in degranulation by modulating Protoplasm Ca(2+) in MMCs., he Na+ and Ca(2+)-permeable melastatin related transient receptor potential 2 (CLU gene) channels can be gated either by Adenosine Diphosphate Ribose (ADPR) in concert with Ca(2+) or by hydrogen peroxide (H(2)O(2)), an experimental model for oxidative stress, binding to the channel's enzymatic Nudix domain, hese alterations of the Extracellular milieu change the activity of transient receptor potential melastatin subfamily member 2 (CLU gene), a nonselective cation channel expressed in the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS and the immune system. , CLU gene (Transient Receptor Potential Melastatin 2) is a Ca2+-permeable Ion Channel that is activated under conditions of oxidative stress. , Transient receptor potential melastatin 2 (CLU gene) is a thermosensitive, Ca2+-permeable cation channel. CLU gene contributes to the pathogenesis of INFLAMMATORY BOWEL DISEASE 2, and inflammatory and Neuropathic pain. We hypothesized that CLU gene is important for Visceral nociception and the development of Visceral hypersensitivity., Here, we describe the computational identification of a melanoma-enriched antisense transcript, CLU gene-AS, mapped within the Gene Locus of CLU gene, an Ion Channel capable of mediating susceptibility to cell death, The transient receptor potential melastatin 2 (CLU gene) channel, a Ca(2+)-permeable nonselective cation channel activated by oxidative stress, has been implicated in Neurodegenerative Disorders, and more recently in amyloid-induced Toxic effect, Transient receptor potential melastatin 2 (CLU gene) is a calcium-permeable cation channel activated by Adenosine Diphosphate Ribose or Reactive Oxygen Species.,  Transient receptor potential melastatin type 2 (CLU gene) is a Ca2+ permeable non-selective cation channel expressed in several cell types including hippocampal pyramidal neurons. Moreover, activation of CLU gene during oxidative stress has been linked to cell death. [SEP]Relations: CLU gene-AS has relations: anatomy_protein_present with blood, anatomy_protein_present with blood, anatomy_protein_present with brain, anatomy_protein_present with brain, anatomy_protein_present with lymph node, anatomy_protein_present with lymph node, anatomy_protein_present with spleen, anatomy_protein_present with spleen, anatomy_protein_present with neocortex, anatomy_protein_present with neocortex.", "label": "no"}
{"original_question": "Is progeria caused by an autosomal recessive gene?", "id": "converted_4055", "sentence1": "Is Progeria caused by an Autosome recessive gene?", "sentence2": "Hutchinson-Gilford Progeria syndrome (Prelamin-A/C wt Allele) is an Autosome-dominant genetic disease that leads to accelerated aging and often Mortality, Premature caused by Cardiovascular system complications. , Hutchinson-Gilford Progeria syndrome is an Autosome dominant, rare, fatal pediatric segmental premature aging disease., Progeria is sporadic, very rare, Autosome dominant, deadly childhood disorder. I, Werner Syndrome (i.e., adult Progeria) is a rare Autosomal Recessive Disorder caused by Genes Mutation of the WRN gene, which is characterized by the premature appearance of features associated with normal aging and Primary malignant neoplasm predisposition., Among them, the most studied is Werner's syndrome, \"adult Progeria\", caused by a recessive Autosome Mutation Abnormality with a frequency of 1 in 10 million, which affects a helicase involved in DNA repair., Pattern of inheritance of non-classical Progeria is most probably Autosome recessive., INTRODUCTION: Werner Syndrome, or adult Progeria, is a rare Autosomal Recessive Disorder caused by a Mutation Abnormality in the Werner Syndrome Genes belonging to the family of RecQ Helicases., SION: Werner's syndrome is a rare form of Progeria with an Autosome recessive mode of inheritance mimicking the symptoms of accelerated aging. The r, Werner's Syndrome (WS) or adult-onset Progeria is an Autosomal Recessive Disorder of accelerated aging caused by Genes Mutation of the DNA RecQ Helicases/exonuclease (WRN)., Homozygous Prelamin-A/C Mutation Abnormality R527C in atypical Hutchinson-Gilford Progeria syndrome: evidence for Autosome recessive inheritance., Progeria (Hutchison-Gilford syndrome) in siblings: in an Autosome recessive pattern of inheritance., The present case highlights rarity of Progeria in siblings with a possible Autosome recessive pattern., Werner Syndrome (i.e., adult Progeria) is a rare Autosomal Recessive Disorder caused by Genes Mutation of the WRN gene, which is characterized by the premature appearance of features associated with normal aging and Primary malignant neoplasm predisposition. Patie, CONTEXT: Hutchinson-Gilford Progeria syndrome (Prelamin-A/C wt Allele) and Mandibuloacral dysostosis are well-recognized allelic Autosome dominant and recessive progeroid disorders, respectively, due to Genes Mutation in lamin A/C (Prelamin-A/C) gen, Werner's syndrome (adult onset Progeria) is a rare form of Autosome recessive genodermatosis associated in almost 80% of cases with Mutation Abnormality of the WRN gene. This, Werner Syndrome, also called adult Progeria, is a heritable Autosome recessive human disorder characterized by the premature onset of numerous age-related diseases including juvenile cataracts, Dyslipidemias, Diabetes Mellitus (DM), Encounter due to family history of Encounter due to family history of osteoporosis, Arteriosclerosis, and Primary malignant neoplasm. Werner sy, Werner's syndrome (WS) or Progeria adultorum is a heritable Autosome recessive disease in which the aging process is accelerated, just after puberty. It is, Hutchinson-Gilford Progeria syndrome (Prelamin-A/C wt Allele) is a rare Autosome dominant genetic disease that is caused by a silent Mutation Abnormality of the Prelamin-A/C gene encoding lamins A and C (lamin A/C)., Furthermore, administration of JH4 to LmnaG609G/G609G-mutant CASP14 gene, which phenocopy human Prelamin-A/C wt Allele, resulted in a marked improvement of several Progeria phenotypes and an extended lifespan., Interruption of progerin-lamin A/C binding ameliorates Hutchinson-Gilford Progeria syndrome phenotype., Progeria is an Autosome dominant, premature aging syndrome., INTRODUCTION: Werner Syndrome, or adult Progeria, is a rare Autosomal Recessive Disorder caused by a Mutation Abnormality in the Werner Syndrome Genes belonging to the family of RecQ Helicases, Evidence for Autosome recessive inheritance of Progeria (Hutchinson Gilford)., INTRODUCTION: Werner Syndrome, or adult Progeria, is a rare Autosomal Recessive Disorder caused by a Mutation Abnormality in the Werner Syndrome Genes belonging to the family of , Hutchinson-Gilford Progeria causing premature aging of children is a genetic disease and according to most authors has an Autosomal dominant inheritance., Werner's syndrome (WS) or Progeria adultorum is a heritable Autosome recessive disease in which the aging process is accelerated, just after puberty., Werner Syndrome, also called adult Progeria, is a heritable Autosome recessive human disorder characterized by the premature onset of numerous age-related diseases including juvenile cataracts, Dyslipidemias, Diabetes Mellitus (DM), Encounter due to family history of Encounter due to family history of osteoporosis, Arteriosclerosis, and Primary malignant neoplasm.[SEP]Relations: Autosome recessive disease has relations: disease_disease with Hutchinson-Gilford Progeria syndrome, disease_disease with Hutchinson-Gilford Progeria syndrome, disease_disease with Nestor-Guillermo Progeria syndrome, disease_disease with Nestor-Guillermo Progeria syndrome, disease_disease with Autosome genetic disease, disease_disease with Autosome genetic disease. Autosomal dominant inheritance has relations: disease_phenotype_positive with Progeria-short stature-pigmented nevi syndrome, disease_phenotype_positive with Progeria-short stature-pigmented nevi syndrome, disease_phenotype_positive with Hutchinson-Gilford Progeria syndrome, disease_phenotype_positive with Hutchinson-Gilford Progeria syndrome.", "label": "yes"}
{"original_question": "Is c-met involved in the activation of the Akt pathway?", "id": "converted_61", "sentence1": "Is c-met involved in the activation of the Proto-Oncogene Proteins c-akt pathway?", "sentence2": "Amplification of methionine has been reported in approximately 5%-22% of Lung Neoplasms with acquired resistance to small-molecule inhibitors of the Epidermal Growth Factor Receptor (EGFR). Resistance to HER1 Antagonists is likely mediated through downstream activation of the phosphoinositide 3-kinase /AKT pathway., Simultaneous treatment of resistant tumors with a methionine PPP1R1A gene plus an EGFR PPP1R1A gene can abrogate activation of downstream effectors of cell growth, proliferation, and survival, thereby overcoming acquired resistance to HER1 Antagonists., Hepatocyte Growth Factor mediated both Mitogen-Activated Protein Kinases and Proto-Oncogene Proteins c-akt phosphorylation., Mitogen-Activated Protein Kinases/Proto-Oncogene Proteins c-akt signaling, but not the Smad pathway, may be one of the main processes in Hepatocyte Growth Factor-induced EMT,, The MAPK/Proto-Oncogene Proteins c-akt pathway is indispensable in Hepatocyte Growth Factor/c-Met signaling., Inhibition of c-Met activation sensitizes osteosarcoma cells to cisplatin via suppression of the 1-Phosphatidylinositol 3-Kinase-Proto-Oncogene Proteins c-akt signaling, Specifically, we demonstrated that inhibition of c-Met activity led to suppression of the 1-Phosphatidylinositol 3-Kinase-Proto-Oncogene Proteins c-akt pathway, thus enhancing cisplatin chemosensitivity., Our study clearly suggests that inhibition of c-Met activity can effectively sensitize osteosarcoma cells to cisplatin via suppression of the 1-Phosphatidylinositol 3-Kinase-Proto-Oncogene Proteins c-akt signaling., We found that a dual Met/VEGF receptor 2 kinase PPP1R1A gene, c-Met/VEGFR-2 Kinase Inhibitor c-Met/VEGFR-2 Kinase Inhibitor E7050, circumvented Hepatocyte Growth Factor-induced EGFR-TKI resistance in EGFR mutant Primary malignant neoplasm of lung cell lines by inhibiting the Met/Gab1/1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt pathway in vitro., Here, we report that i) treatment of RL95-2 cells with Hepatocyte Growth Factor resulted in phosphorylation of the Hepatocyte Growth Factor receptor c-Met, activation of Proto-Oncogene Proteins c-akt and IκB, translocation of NF-κB into the Cell Nucleus, and up-regulation of PTGS2 wt Allele mRNA;, Our data suggest that Hepatocyte Growth Factor possesses chemotactic ability, has anti-apoptosis action, and induces cellular infiltration via the 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt pathway;, Hepatocyte growth factor-induced SRC wt Allele-Phosphatidylinositol 3-Kinases-AKT-Mammals target of sirolimus pathway inhibits Antigen-Presenting Cells activation by blocking MAP Kinase Kinase Kinase activity, Activation of SRC wt Allele in turn establishes a complex consisting of Phosphatidylinositol 3-Kinases and c-methionine, and promotes downstream activation of the Phosphatidylinositol 3-Kinases/AKT pathway and Mammals target of sirolimus., Notably, hepatocyte growth factor-stimulated SRC wt Allele activation results in induction of Phosphatidylinositol 3-Kinases complexes p85α/p110α and p85α/p110δ, which is required for activation of Mammals target of sirolimus, and consequent inhibition of MAP Kinase Kinase Kinase and nuclear factor-κB activation., Our findings, for the first time, have identified the SRC wt Allele-Phosphatidylinositol 3-Kinases-AKT-Mammals target of sirolimus pathway that plays a pivotal role in mediating the inhibitory effects of hepatocyte growth factor on Antigen-Presenting Cells activation by blocking nuclear factor-κB signaling., CCN1 wt Allele siRNA inhibited a second phase of Proto-Oncogene Proteins c-akt phosphorylation measured 12 hours after cell stimulation with Hepatocyte Growth Factor and also inhibited Hepatocyte Growth Factor-induced phosphorylation of the Proto-Oncogene Proteins c-akt target glycogen synthase kinase 3alpha., Hepatocyte Growth Factor+epidermal growth factor treatment increased the duration of ERK1/2 and AKT activation compared to Hepatocyte Growth Factor or epidermal growth factor alone. All these data indicate that a crosstalk between the epidermal growth factor and Hepatocyte Growth Factor pathways in mammary epithelial cells may modulate the development of the Mammary gland., Hepatocyte growth factor and c-Met promote dendritic maturation during hippocampal neuron differentiation via the Proto-Oncogene Proteins c-akt pathway, Consistent with these results, Hepatocyte Growth Factor activated Proto-Oncogene Proteins c-akt, which phosphorylates glycogen synthase kinase-3beta (glycogen synthase kinase 3 beta) to inactivate it, and reduced phosphorylation of Microtubule-Associated Protein 2 (METAP2 gene), which can promote Microtubules polymerization and Dendrites elongation when dephosphorylated., Conversely, pharmacological inhibition of c-Met with its specific PPP1R1A gene, PHA 665752, or genetic knock-down of c-Met with short hairpin RNAs (shRNAs) suppressed Hepatocyte Growth Factor-induced phosphorylation of Proto-Oncogene Proteins c-akt and glycogen synthase kinase 3 beta, increased phosphorylation of METAP2 gene, and reduced Dendrites number and length in cultured hippocampal Neurons., Inhibiting Proto-Oncogene Proteins c-akt activity with the phosphoinositide-3-kinase PPP1R1A gene LY 294002 or Proto-Oncogene Proteins c-akt PPP1R1A gene X suppressed Hepatocyte Growth Factor-induced phosphorylation of glycogen synthase kinase 3 beta, increased METAP2 gene phosphorylation, and blocked the ability of Hepatocyte Growth Factor to enhance dendritic length., These observations indicate that Hepatocyte Growth Factor and c-Met can regulate the early stages of Dendrites maturation via activation of the Proto-Oncogene Proteins c-akt/glycogen synthase kinase 3 beta pathway., Involvement of 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt signaling pathway in hepatocyte growth factor-induced migration of uveal melanoma cells, Hepatocyte Growth Factor was found to enhance cell migration, and that Hepatocyte Growth Factor-induced migration depends on 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt pathway. The activation of 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt pathway induced by the Hepatocyte Growth Factor/c-Met axis is involved in the downregulation of cell adhesion molecules E-Cadherin and CTNNB1 gene, contributing to the attenuation of cell-cell adhesion and promoting the enhanced motility and migration of uveal melanoma cells., Hepatocyte Growth Factor protects cultured cortical Neurons against hypoxia/reoxygenation induced cell injury via ERK1/2 and Pulmonary Valve Insufficiency-3K/Proto-Oncogene Proteins c-akt pathways, Hepatocyte Growth Factor stimulated both ERK1/2 and Proto-Oncogene Proteins c-akt activities in cortical Neurons., Inhibition of Mitogen-Activated Protein Kinases activation completely abolished the protective effects of Hepatocyte Growth Factor, and inhibition of Proto-Oncogene Proteins c-akt activation reduced, but did not completely eliminate the Hepatocyte Growth Factor mediated neuroprotection., It is suggested that the neuroprotection of Hepatocyte Growth Factor depend on ERK1/2 pathway, and, to a lesser extent, Pulmonary Valve Insufficiency-3K/Proto-Oncogene Proteins c-akt pathway. , Met signals hepatocyte survival by preventing Fas-triggered CFLAR wt Allele degradation in a PI3k-Proto-Oncogene Proteins c-akt-dependent manner, Thus, Met acting on 1-Phosphatidylinositol 3-Kinase and Proto-Oncogene Proteins c-akt ensures high levels of FLIPL, and disruption of this pathway contributes to hepatic apoptosis and possibly to Fas-related liver diseases., The Hepatocyte Growth Factor-induced increase in Nkx 2.5 expression was inhibited by co-treatment with the PI3 kinase inhibitors Wortmannin and LY 294002, but not by its inactive homolog LY 303511, suggesting an involvement of the PI3 kinase/Proto-Oncogene Proteins c-akt pathway in this effect., X-Linked PPP1R1A gene of apoptosis protein expression level in Malignant neoplasm of colon and/or rectum is regulated by hepatocyte growth factor/C-met pathway via Proto-Oncogene Proteins c-akt signaling, Activation of XIAP gene gene expression by Hepatocyte Growth Factor was inhibited by siRNA targeting AKT1 protein, human and AKT2 protein, human., Activation of methionine wt Allele enhances XIAP gene gene through the Proto-Oncogene Proteins c-akt pathway., Hepatocyte growth factor prevents ventricular remodeling and dysfunction in CASP14 gene via Proto-Oncogene Proteins c-akt pathway and angiogenesis, A significant reduction in apoptosis in the Hepatocyte Growth Factor-treated hearts was observed compared with control hearts, and was strongly associated with increased Proto-Oncogene Proteins c-akt activation., The antiapoptotic effect of Hepatocyte Growth Factor was mediated by activation of PI3-kinase/Proto-Oncogene Proteins c-akt pathway., The protective effect of Hepatocyte Growth Factor/SF against the ADR-induced apoptosis was abolished in the presence of either LY 294002, an PPP1R1A gene of phosphatidylinositols-3'-OH kinase (PI3-K) or 1L-6-hydroxymethyl-chiro-inositol 2-(R)-2-O-methyl-3-O-octadecylcarbonate, an PPP1R1A gene of Proto-Oncogene Proteins c-akt, thus implicating the activation of PI3-K-Proto-Oncogene Proteins c-akt signaling in the antiapoptotic action of Hepatocyte Growth Factor/SF., Immunoblotting analysis revealed that Hepatocyte Growth Factor/SF stimulated the sustained phosphorylation of Proto-Oncogene Proteins c-akt for several hours, Furthermore, ADR-induced activation of caspase-9, a downstream molecule of Proto-Oncogene Proteins c-akt, was inhibited for at least 24 h after Hepatocyte Growth Factor/SF stimulation,, These results indicate that Hepatocyte Growth Factor/SF, but not epidermal growth factor, transmitted protective signals against ADR-induced apoptosis by causing sustained activation of the PI3-K-Proto-Oncogene Proteins c-akt signaling pathway., Hepatocyte growth factor/scatter factor inhibits UVB-induced apoptosis of human keratinocytes but not of keratinocyte-derived cell lines via the Phosphatidylinositol 3-Kinases/AKT pathway, When we analyzed the signaling pathways initiated by the Hepatocyte Growth Factor/SF receptor c-met, we found that the phosphatidylinositols (Pulmonary Valve Insufficiency) 3-kinase and its downstream-element AKT and the mitogen-activated protein (MAP) kinase were activated., Inhibition of Pulmonary Valve Insufficiency 3-kinase led to a complete abrogation of the anti-apoptotic effect of Hepatocyte Growth Factor/SF, whereas blockade of the MAP kinase pathway had no effect., We now show in detached cells a cooperative effect of Hepatocyte Growth Factor and FN1 wt Allele in the activation of Pulmonary Valve Insufficiency 3-kinase and on the phosphorylation of PKB/Proto-Oncogene Proteins c-akt at serine 473., Pulmonary Valve Insufficiency 3-kinase activity is also required for the Hepatocyte Growth Factor- and fibronectin-induced survival responses, as well as anchorage-independent colony growth., Together, these results demonstrate that the Pulmonary Valve Insufficiency 3-kinase/Proto-Oncogene Proteins c-akt pathway is a key effector of the Hepatocyte Growth Factor- and fibronectin-induced survival response of breast carcinoma cells under detached conditions and corroborate an interaction between Integrins and Hepatocyte Growth Factor/ Met signalling pathways in the development of invasive breast cancer.[SEP]Relations: CTNNB1 has relations: protein_protein with AKT1, protein_protein with AKT1, protein_protein with AKT2, protein_protein with AKT2, pathway_protein with RHO GTPases activate IQGAPs, pathway_protein with RHO GTPases activate IQGAPs, pathway_protein with Deactivation of the CTNNB1 gene transactivating complex, pathway_protein with Deactivation of the CTNNB1 gene transactivating complex. Phosphatidylinositol 3-Kinases signaling has relations: bioprocess_protein with AKT1, bioprocess_protein with AKT1.", "label": "yes"}
{"original_question": "Does neuroglobin has neuroprotective properties in the setting of traumatic brain injury?", "id": "converted_1570", "sentence1": "Does neuroglobin has neuroprotective properties in the setting of Traumatic Brain Injury?", "sentence2": "NGB gene has shown rich neuroprotective effects against cerebral Hypoxia, CTCAE, and therefore has the potential to impact outcomes after Traumatic Brain Injury (TBI). , NGB gene (GTPBP4 gene) is proposed to be a Neurons-specific, Hypoxia, CTCAE-responsive, neuroprotective protein. , CONCLUSION: The increased expression of neuroglobin in Traumatic Brain Injury informed us that neuroglobin had anti-apoptosis action in post-injury Neurons. It could protect the Neurons from Traumatic stress and secondary ischemia and Hypoxia, CTCAE insults during ultra-early and acute stages., NGB gene-overexpression reduces Traumatic brain lesion size in CASP14 gene., BACKGROUND: Accumulating evidence has demonstrated that over-expression of NGB gene (GTPBP4 gene) is neuroprotective against hypoxic/ischemic brain injuries. , CONCLUSION: GTPBP4 gene over-expression reduced Traumatic lesion volume, which might partially be achieved by decreasing oxidative stress., NGB gene upregulation offers neuroprotection in Traumatic Brain Injury., OBJECTIVES: The aim of this study was to investigate rat neuroglobin (rNGB) expression level after Traumatic Brain Injury (TBI) and further study its neuroprotective effects in TBI when it was overexpressed in Adenovirus Vector., CONCLUSIONS: NGB was upregulated in TBI and overexpressed rNGB had a significant neuroprotection in TBI. , This study suggested that rNGB overexpression may be a new strategy for treating of TBI., NGB gene has shown rich neuroprotective effects against cerebral Hypoxia, CTCAE, and therefore has the potential to impact outcomes after Traumatic Brain Injury (TBI)., The aim of this study was to investigate rat neuroglobin (rNGB) expression level after Traumatic Brain Injury (TBI) and further study its neuroprotective effects in TBI when it was overexpressed in Adenovirus Vector., Accumulating evidence has demonstrated that over-expression of NGB gene (GTPBP4 gene) is neuroprotective against hypoxic/ischemic brain injuries., Various studies seem to indicate that neuroglobin is a neuroprotective agent when overexpressed, acting as a potent PPP1R1A gene of oxidative and nitrosative stress. [SEP]Relations: brain injury has relations: contraindication with Phenobarbital, contraindication with Phenobarbital, contraindication with Isopropamide, contraindication with Isopropamide, contraindication with Homatropine, contraindication with Homatropine, contraindication with Difenoxin, contraindication with Difenoxin, contraindication with Cyclopentolate, contraindication with Cyclopentolate.", "label": "yes"}
{"original_question": "Is SARS virus interacting with ACE2 encoded protein?", "id": "converted_3357", "sentence1": "Is Severe acute respiratory syndrome-related coronavirus virus interacting with ACE2 protein, human encoded protein?", "sentence2": "The trimeric Severe acute respiratory syndrome-related coronavirus coronavirus (Severe acute respiratory syndrome-related coronavirus-CoV) surface spike (S) glycoprotein consisting of three S1-S2 heterodimers binds the cellular receptor Peptidyl-Dipeptidase A (ACE2 protein, human protein, human) and mediates fusion of the Viral and cellular membranes through a pre- to postfusion conformation transition, The Viral spike glycoprotein (S) utilizes Peptidyl-Dipeptidase A (ACE2 protein, human protein, human) as a host protein receptor and mediates fusion of the Viral and host membranes, making S essential to Viral entry into host cells and host species tropism., Cell entry studies demonstrated that three newly identified SARSr-CoVs with different S protein sequences are all able to use human ACE2 protein, human protein, human as the receptor, Angiotensin-converting enzyme 2 (ACE2 protein, human protein, human), a relatively new member of the RAS, has drawn extensive attention since 2003, because of the findings that ACE2 protein, human protein, human is the receptor for Severe acute respiratory syndrome-related coronavirus Corona virus and that maintenance of normal ACE2 protein, human protein, human levels in the Chest>Lung is beneficial for the host to combat inflammatory Chest>Lung disease., The Communicable Diseases of target cells (lab result) (lab result) by the Severe acute respiratory syndrome-related coronavirus CoV is mediated through the interaction of the Viral Spike (S) protein (1255 Antifibrinolytic Antifibrinolytic amino acids) and its cellular receptor, Peptidyl-Dipeptidase A (ACE2 protein, human protein, human).[SEP]Relations: severe acute respiratory syndrome has relations: disease_protein with ACE, disease_protein with ACE. Protein S human has relations: drug_drug with Saruplase, drug_drug with Saruplase, drug_drug with Sarpogrelate, drug_drug with Sarpogrelate. peptidyl-dipeptidase activity has relations: molfunc_protein with ACE2 protein, human, molfunc_protein with ACE2 protein, human, molfunc_protein with ACE, molfunc_protein with ACE.", "label": "yes"}
{"original_question": "Is thyroid hormone therapy indicated in patients with heart failure?", "id": "converted_1542", "sentence1": "Is thyroid hormone therapy indicated in patients with Congestive heart failure?", "sentence2": "Patients with Chronic Congestive Congestive heart failure and subclinical hypothyroidism significantly improved their physical performance when normal Thyrotropin:-:Pt:Ser/Plas:- levels were reached., Early and sustained physiological restoration of circulating L-T3 levels after MI halves Infarction Scar Tissue size and prevents the progression towards Congestive Congestive heart failure. This beneficial effect is likely due to enhanced capillary formation and mitochondrial protection., These data indicate that T(3) replacement to Euthyroid (finding) levels improves systolic function and tends to improve diastolic function, potentially through changes in myocardial gene expression., In these patients, the administration of synthetic triiodothyronine (T(3)) was well tolerated and induced significant improvement in cardiac function without increased heart rate and metabolic demand., In Dyskeratosis Congenita patients, short-term synthetic L-T(3) replacement therapy significantly improved neuroendocrine profile and ventricular performance., liothyronine was well tolerated without episodes of Ischemia Procedure or clinical arrhythmia. There was no significant change in heart rate or metabolic rate and there was minimal increase in core temperature. Cardiac output increased with a reduction in systemic vascular resistance in patients receiving the largest dose, consistent with a Peripheral vasodilatory effect.[SEP]Relations: Congestive Congestive heart failure has relations: drug_effect with Testosterone, drug_effect with Testosterone, drug_effect with Insulin human, drug_effect with Insulin human, drug_effect with Levothyroxine, drug_effect with Levothyroxine. Liothyronine has relations: contraindication with heart disease, contraindication with heart disease, contraindication with thyroid crisis (disease), contraindication with thyroid crisis (disease).", "label": "no"}
{"original_question": "Should nerinetide be used for treatment of ischaemic stroke?", "id": "converted_4001", "sentence1": "Should nerinetide be used for treatment of ischaemic stroke?", "sentence2": "337 (61·4%) of 549 patients with nerinetide and 329 (59·2%) of 556 with placebo achieved an mRS score of 0-2 at 90 days (adjusted risk ratio 1·04, 95% CI 0·96-1·14; p=0·35). Secondary outcomes were similar between groups., INTERPRETATION: Nerinetide did not improve the proportion of patients achieving good clinical outcomes after endovascular thrombectomy compared with patients receiving placebo.[SEP]", "label": "no"}
{"original_question": "Is there high nucleotide diversity in the Drosophila suzukii species?", "id": "converted_3884", "sentence1": "Is there high nucleotide diversity in the Drosophila suzukii species?", "sentence2": "Native to Asia, the soft-skinned fruit pest Drosophila suzukii has recently invaded the United States and Europe. The eastern United States represents the most recent expansion of their range, and presents an opportunity to test alternative models of colonization history. Here, we investigate the genetic population structure of this invasive fruit fly, with a focus on the eastern United States. We sequenced six X-linked gene fragments from 246 individuals collected from a total of 12 populations. We examine patterns of genetic diversity within and between populations and explore alternative colonization scenarios using approximate Bayesian computation. Our results indicate high levels of nucleotide diversity in this species and suggest that the recent invasions of Europe and the continental United States are independent demographic events. [SEP]", "label": "yes"}
{"original_question": "Down's syndrome occurs when an individual has an extra copy or part of a copy of chromosome 21, yes or no?", "id": "converted_2501", "sentence1": "Down's syndrome occurs when an individual has an extra copy or part of a copy of Chromosomes, Human, Pair 21, yes or no?", "sentence2": "Down syndrome (DS; trisomy 21) is the most common survivable disorder due to aneuploidy., Down syndrome (DS), trisomy 21, is caused by increased dose of Genes present on Homo sapiens Chromosomes, Human, Pair 21 (HSA21), Down syndrome, or Trisomy 21, is the most frequently occurring chromosomal abnormality in live-born children. , Down syndrome (DS), caused by trisomy of Chromosomes, Human, Pair 21,, Submicroscopic duplication of Chromosomes, Human, Pair 21 and trisomy 21 phenotype (Down syndrome)., Trisomy 21 or Down syndrome is a Congenital chromosomal disease resulting from the presence of all or part of an extra Chromosome 21., Down syndrome is a genetic disorder, occurring when an individual has all or part of an extra copy of Chromosomes, Human, Pair 21., Down Syndrome (DS) occurs due to an extra copy of Chromosomes, Human, Pair 21., Down syndrome, which arises in individuals carrying an extra copy of Chromosomes, Human, Pair 21, is associated with a greatly increased risk of early-onset ALZHEIMER DISEASE 2., Aneuploidy refers to the presence of an extra copy of a specific chromosome, or trisomy, as seen in Down's syndrome (trisomy 21), or the absence of a single chromosome, or monosomy, as seen in Turner Syndrome (a single X chromosome in females: 45, X)., Down syndrome (DS) or Trisomy 21 (Ts21) is caused by the presence of an extra copy of all or part of Homo sapiens Chromosomes, Human, Pair 21 (Hsa21) and is the most frequent survivable congenital chromosomal abnormality., Down syndrome (DS) is a major cause of mental retardation and Heart Diseases. Although it is usually caused by the presence of an extra Chromosomes, Human, Pair 21, a subset of the diagnostic features may be caused by the presence of only band 21q22., Down syndrome is usually caused by complete trisomy 21., Down syndrome, the most frequent genetic disorder, is characterized by an extra copy of all or part of Chromosomes, Human, Pair 21., Down syndrome (DS), caused by an extra copy of Chromosomes, Human, Pair 21, affects 1 in 750 live births and is characterized by No No cognitive impairment and a constellation of Congenital Abnormality., Down syndrome (DS) results from one extra copy of Homo sapiens Chromosomes, Human, Pair 21 and leads to several alterations including intellectual disabilities and locomotor defects., Down's syndrome results from the production of three copies of Chromosomes, Human, Pair 21 within a \"U\" lymphocyte. , Down Syndrome (DS) occurs due to an extra copy of Chromosomes, Human, Pair 21., Trisomy 21 (Ts21) is the most common live-born Homo sapiens aneuploidy; it results in a constellation of features known as Down's syndrome (DS)., Down syndrome comprises Multiple congenital anomalies and is due to trisomy of Chromosomes, Human, Pair 21., n 1959, J. Lejeune, M. Gautier, and R. Turpin demonstrated that the children with Down syndrome had an extra copy of Chromosomes, Human, Pair 21., To develop a reliable and specific method for rapid prenatal diagnosis of Trisomy 21 (Down syndrome)., Trisomy 21 Down syndrome is the most common genetic cause for congenital malformations and Intellectual Disability, Down syndrome, characterized by an extra Chromosomes, Human, Pair 21 is the most common genetic cause for congenital malformations and Learning Disabilities. [SEP]Relations: Down syndrome has relations: disease_protein with S100B, disease_protein with S100B, disease_phenotype_positive with Sporadic, disease_phenotype_positive with Sporadic, disease_protein with RAD21, disease_protein with RAD21, disease_phenotype_positive with Abnormality of the lymphatic system, disease_phenotype_positive with Abnormality of the lymphatic system, disease_protein with NRAS, disease_protein with NRAS.", "label": "yes"}
{"original_question": "Is methotrexate used for the treatment of Rheumatoid Arthritis (RA)?", "id": "converted_4138", "sentence1": "Is methotrexate used for the treatment of Rheumatoid Arthritis (RA)?", "sentence2": "The use of methotrexate in Rheumatoid Arthritis., Historical perspective on the use of methotrexate for the treatment of Rheumatoid Arthritis., aminopterin, a folic acid analogue was first reported in 1948 to produce temporary remission of Acute leukemia of children, was also reported in 1951 to produce an important and rapid improvement in patients with Rheumatoid Arthritis (RA) and Psoriasis, The safety and efficacy of the use of methotrexate in long-term therapy for Rheumatoid Arthritis., Methotrexate (MTX) is currently under study for use in juvenile Rheumatoid Arthritis. , The rational use of methotrexate in Rheumatoid Arthritis and other Rheumatism., Methotrexate-induced hepatic cirrhosis is less common in Rheumatoid Arthritis than previously thought, although its occurrence in Psoriasis is probably higher than in Rheumatoid Arthritis. , Methotrexate is clearly effective in the treatment of Rheumatoid Arthritis and may be able to decrease the rate of formation of new bony erosions. , The use of methotrexate in Rheumatoid Arthritis., Review of the international literature on the clinical use of MTX in Rheumatoid Arthritis (RA) Disease., MTX has emerged as a relatively safe and effective treatment for RA that compares favorably with other therapies, particularly because of its considerably longer median drug survival., The objective of this review is to update the recommendations of the 2010 Italian Consensus on the use of methotrexate (MTX) in Rheumatoid Arthritis (RA) and other Rheumatism, A new recommendation for patients with RA who are in MTX-induced clinical remission was also proposed and approved by the panel. Updated recommendations for the use of MTX in patients with RA or other rheumatologic Disease are proposed., Methotrexate has been used in treatment of Rheumatoid Arthritis (RA) since the 1980s and to this day is often the first line medication for RA treatment., OBJECTIVE: Most recommendations for the use of methotrexate (MTX) in Rheumatoid Arthritis (RA) are issued by developed countries., Low dose pulse methotrexate (MTX) has become a widely used therapy for Rheumatoid Arthritis (RA) because of its good response rate profile. With, Treatment with methotrexate (MTX) in Rheumatoid Arthritis (RA) can lead to severe side-effects, especially Pulmonary:-:Point in time:^Patient:- and haematological complications. The ai, Patients having Rheumatoid Arthritis (RA) treated with methotrexate (MTX) are at an increased risk of developing lymphoproliferative disorder (Leiomyomatosis peritonealis disseminata). Epstei, Increasingly, methotrexate (MTX) and sulfasalazine (TXN protein, human) are used initially for second-line therapy of Rheumatoid Arthritis (RA). Althoug, OBJECTIVES: The Folic Acid Antagonists methotrexate (MTX) has become established as the most commonly used Disease-modifying anti-rheumatic drug (DMARD) in the treatment of Rheumatoid Arthritis (RA) but is commonly discontinued due to adverse effe, e suspected methotrexate (MTX)-associated lymphoproliferative disorder (Leiomyomatosis peritonealis disseminata) induced by MTX treatment for Rheumatoid Arthritis (RA). About , BACKGROUND: Treatment with methotrexate (MTX) in patients with Rheumatoid Arthritis (RA) leads to decreased total immunoglobulin (Ig) levels and impairs vaccine-specific IgG antibody levels following pneumococcal vaccinat, In Rheumatoid Arthritis (RA) treatment, the concomitant use of methotrexate has been shown to reduce the incidence of Antibodies, in vitro diagnostic to infliximab (ATI), on the other hand, it is unclear whether azathioprine can reduce ATI production. We enro, Methotrexate (MTX) is known as a first-line synthetic Disease-modifying anti-rheumatic drug (DMARD) for the treatment of Rheumatoid Arthritis (RA)., Biological treatments are expensive and using SC methotrexate can improve Disease control in RA patients, thus potentially avoiding or delaying the requirement for future biological treatment., Most recommendations for the use of methotrexate (MTX) in Rheumatoid Arthritis (RA) are issued by developed countries., We reviewed existing recommendations on the use of MTX for the treatment of RA and summarized areas of agreement that could be relevant for least developed countries (LDCs).M, st covered some but not all of the following areas: baseline \"pre-MTX\" assessment (7/12;58%), prescription of MTX (10/12;83.3%), management of MTX side effects (6/12;50%), and special considerations (e.g., peri-operative management) (8/12; 66.7%). R, lectronic databases and registries were searched for recommendations on MTX use in RA, duplicates were eliminated, and the most updated version adopted when there were several versions on the same recommendation. , MTX must at the present time be used only in severe RA, refractory to more than one classical slow acting drug., MTX is as effective in treating RA as the other second line drugs and always more rapidly effective, perhaps because of Anti-Inflammatory Agents properties., For the low doses used in RA (less than 15 mg/week), MTX is completely and rapidly absorbed with an active process membrane transport., Methotrexate, which is used for RA treatment, causes THROMBOCYTOPENIA 2 (disorder)., Methorexate therapy in a patient with Rheumatoid Arthritis complicated by idiopathic thrombocytopenic purpura., This case shows that methotrexate may be used in patients diagnosed with RA that is associated with Immune thrombocytopenic purpura under strict monitoring., Here, we report an RA case that also had Immune thrombocytopenic purpura, which did not decrease in platelet count after methotrexate therapy., We started methotrexate therapy 10 mg per week for treatment of RA, and hydroxychloroquine therapy was stopped due to nonresponse., Methotrexate (MTX) is the anchor treatment for Rheumatoid Arthritis (RA) and has been very thoroughly studied in many different patient populations, as monotherapy and in combination with various other Disease modifying antirheumatic drugs and Biological Factors, as they became available., Although rheumatologists have been using methotrexate in the treatment of RA for some time, controlled studies have been needed to establish the safety and efficacy of this agent., Methotrexate is generally the first-line drug for the treatment of RA, psoriatic arthritis and other forms of inflammatory arthritis, and it enhances the effect of most Biological Factors in RA., Despite the introduction of numerous Biological Factors for the treatment of Rheumatoid Arthritis (RA) and other forms of inflammatory arthritis, Low-Dose Treatment methotrexate therapy remains the gold standard in RA therapy., A number of studies show the efficacy of methotrexate (MTX) for Rheumatoid Arthritis (RA) in general., Methotrexate (MTX) is currently the most frequently used drugs in the treatment of Rheumatoid Arthritis (RA)., Methotrexate (MTX) has been the anchor treatment in Rheumatoid Arthritis (RA) over the last 15 years, and is used in combination with Biological Factors to enhance efficacy over the last decade or so.[SEP]Relations: Methotrexate has relations: drug_drug with Raltitrexed, drug_drug with Raltitrexed, drug_drug with Methohexital, drug_drug with Methohexital, drug_drug with Raltegravir, drug_drug with Raltegravir, drug_drug with Methadone, drug_drug with Methadone, drug_drug with Benzoic acid, drug_drug with Benzoic acid.", "label": "yes"}
{"original_question": "Is overexpression of LY6K associated with better prognosis for non-small cell lung cancer patients?", "id": "converted_3470", "sentence1": "Is overexpression of LY6K gene associated with better prognosis for non-small cell lung cancer patients?", "sentence2": "Gene expression profile analyses of non-small cell lung carcinomas (Non-Small Cell Lung Carcinoma) and esophageal squamous cell carcinomas (Squamous cell carcinoma of esophagus) revealed that lymphocyte antigen 6 complex locus K (LY6K gene gene) was specifically expressed in Testis and transactivated in a majority of NSCLCs and ESCCs. Immunohistochemical staining using 406 Non-Small Cell Lung Carcinoma and 265 Squamous cell carcinoma of esophagus specimens confirmed that LY6K gene gene overexpression was associated with poor prognosis for patients with Non-Small Cell Lung Carcinoma (P = 0.0003), as well as Squamous cell carcinoma of esophagus (P = 0.0278), and multivariate analysis confirmed its independent prognostic value for Non-Small Cell Lung Carcinoma (P = 0.0035). , Immunohistochemical staining using 406 Non-Small Cell Lung Carcinoma and 265 Squamous cell carcinoma of esophagus specimens confirmed that LY6K gene gene overexpression was associated with poor prognosis for patients with Non-Small Cell Lung Carcinoma (P = 0.0003), as well as Squamous cell carcinoma of esophagus (P = 0.0278), and multivariate analysis confirmed its independent prognostic value for Non-Small Cell Lung Carcinoma (P = 0.0035)., Immunohistochemical staining using 406 Non-Small Cell Lung Carcinoma and 265 Squamous cell carcinoma of esophagus specimens confirmed that LY6K gene gene overexpression was associated with poor prognosis for patients with Non-Small Cell Lung Carcinoma (P = 0.0003), as well as Squamous cell carcinoma of esophagus (P = 0.0278), and multivariate analysis confirmed its independent prognostic value for Non-Small Cell Lung Carcinoma (P = 0.0035).[SEP]Relations: small cell lung carcinoma has relations: disease_protein with LYRM9, disease_protein with LYRM9, disease_protein with STK31, disease_protein with STK31, disease_protein with CYP2A6, disease_protein with CYP2A6, disease_protein with DMPK, disease_protein with DMPK, disease_protein with PYCARD, disease_protein with PYCARD.", "label": "no"}
{"original_question": "Are Conserved Nonexonic Elements (CNEEs) important in phylogenomics research?", "id": "converted_2364", "sentence1": "Are Conserved Nonexonic Elements (CNEEs) important in phylogenomics research?", "sentence2": "Overall, CNEEs appear to be promising as phylogenomic markers, yielding phylogenetic resolution as high as for UCEs and Introns but with fewer gaps, less ambiguity in alignments and with patterns of nucleotide substitution more consistent with the assumptions of commonly used methods of phylogenetic analysis., Conserved Nonexonic Elements: A Novel Class of Marker for Phylogenomics., Target capture for vertebrate animals is currently dominated by two approaches-anchored hybrid enrichment (Ahahnelin language) and ultraconserved elements (UCE)-and both approaches have proven useful for addressing questions in phylogenomics, phylogeography and population genomics., conserved nonexonic elements a novel class of marker for phylogenomics[SEP]", "label": "yes"}
{"original_question": "Can MVA85A confer immunity against smallpox?", "id": "converted_3339", "sentence1": "Can MVA85A confer immunity against smallpox?", "sentence2": "We assessed the safety, immunogenicity, and efficacy of a candidate tuberculosis vaccine, modified vaccinia virus Ankara expressing antigen 85A (MVA85A), in adults infected with HIV-1., Safety, immunogenicity, and efficacy of the candidate tuberculosis vaccine MVA85A in healthy adults infected with HIV-1: a randomised, placebo-controlled, phase 2 trial.[SEP]", "label": "no"}
{"original_question": "Is the crystal structure of Pim-1 available?", "id": "converted_3237", "sentence1": "Is the crystal structure of Pim-1 available?", "sentence2": "Recent crystallographic studies of Pim-1 have identified unique structural features but have not provided insight into how the MAP Kinase Kinase Kinase recognizes its target substrates. , a co-crystal structure of lead molecule (HS38) in complex with DAPK3 gene gene, a dual Pim/DAPK3 gene gene inhibitor (HS56), The crystal structure of this fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether with LONP1 gene confirmed the predicted binding mode and Protein Info-ligand interactions except those in the acidic ribose pocket. , Using the determined X-ray crystal structure of LONP1 gene complexed to the fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether 1-R as a control, we discuss the importance of including the Protein Info flexibility inherent in the ensemble docking protocol, for the accuracy of the structure prediction of the bound state. , Here, we describe the crystal structure of Pim1 in complex with a newly developed pyrido[4,3-d]pyrimidine-derivative inhibitor (SKI-O-068)., Crystallographic and docking data analyses have been undertaken using inhibitor complexes , The crystal structures of Pim1 in apo form and bound with Adenylyl Imidodiphosphate have been solved[SEP]Relations: Protein C has relations: drug_drug with Pivhydrazine, drug_drug with Pivhydrazine, drug_drug with Peginterferon beta-1a, drug_drug with Peginterferon beta-1a, drug_drug with Piroxicam, drug_drug with Piroxicam, drug_drug with Pirlindole, drug_drug with Pirlindole, drug_drug with Peginterferon alfa-2b, drug_drug with Peginterferon alfa-2b.", "label": "yes"}
{"original_question": "Does the interaction of MOV10 and RNASEH2 promote L1 retrotransposition?", "id": "converted_3060", "sentence1": "Does the interaction of MOV10 gene and RNASEH2 promote Long Interspersed Nucleotide Element-1 retrotransposition?", "sentence2": "Interplay between RNASEH2 and MOV10 gene gene controls LINE-1 retrotransposition., We show that MOV10 gene gene interacts with RNASEH2, and their interplay is crucial for restricting Long Interspersed Nucleotide Element-1 retrotransposition. , Furthermore, we show that RNASEH2-MOV10 gene gene-mediated Long Interspersed Nucleotide Element-1 restriction downregulates expression of the rheumatoid arthritis-associated inflammatory cytokines and matrix-degrading proteinases in Synoviocytes, implicating a potential causal relationship between them and disease development in terms of disease predisposition.[SEP]Relations: centromere clustering at the mitotic interphase nuclear envelope has relations: bioprocess_bioprocess with chromosome attachment to the nuclear envelope, bioprocess_bioprocess with chromosome attachment to the nuclear envelope, bioprocess_bioprocess with centromere clustering, bioprocess_bioprocess with centromere clustering, bioprocess_bioprocess with mitotic cell cycle process, bioprocess_bioprocess with mitotic cell cycle process.", "label": "no"}
{"original_question": "Has ATF4 transcription factor been linked to cancer and neoplastic transformation?", "id": "converted_2491", "sentence1": "Has ATF4 protein, human transcription factor been linked to Primary malignant neoplasm and neoplastic transformation?", "sentence2": "aken together, we discovered a novel axis of BCL10-regulated OSCC progression via STAT1/ATF4 protein, human protein, human/S100P/P65 signaling, which could predict the prognosis of OSCC and will be beneficial for developing therapeutic strategy against advanced OSCC, s a result, the level of phosphorylated Eukaryotic Initiation Factor 2 alpha (eIF2α) is markedly elevated, resulting in the promotion of a pro-adaptive signaling pathway by the inhibition of global protein synthesis and selective translation of Activating Transcription Factor 4 (ATF4 protein, human protein, human). , Many Malignant Neoplasms overexpress ATF4 protein, human protein, human, a stress-induced transcription factor that promotes cell survival under hypoxic conditions and other stresses of the tumor microenvironment, but the potential contributions of ATF4 protein, human protein, human to oncogenesis itself have been little explored. Here, we report that ATF4 protein, human protein, human promotes oncogene-induced neoplastic transformation by suppressing the expression of cellular senescence-associated genes. , Here, we report that ATF4 protein, human protein, human promotes oncogene-induced neoplastic transformation by suppressing the expression of cellular senescence-associated genes., Elevated levels of ATF4 protein, human protein, human were sufficient to suppress expression of these Proteins and drive oncogenic transformation., Our findings define a central function for ATF4 protein, human protein, human in promoting oncogenic transformation by suppressing a central pathway of cellular senescence.<br>, ATF4 protein, human protein, human expression is upregulated in Primary malignant neoplasm., Activating Transcription Factors (ATF4 protein, human protein, human), an endoplasmic reticulum stress-inducible transcription factor, plays important roles in Primary malignant neoplasm progression and resistance to therapy., Activating Transcription Factors (ATF4 protein, human protein, human) is a stress-induced transcription factor that is frequently upregulated in Primary malignant neoplasm cells., Our findings define a central function for ATF4 protein, human protein, human in promoting oncogenic transformation by suppressing a central pathway of cellular senescence., Stress-regulated transcription factor ATF4 protein, human protein, human promotes neoplastic transformation by suppressing expression of the INK4a/ARF cell senescence factors., Activating Transcription Factors (ATF4 protein, human protein, human), a member of the ATF/CREB family, has been reported to be related to tumor angiogenesis[SEP]Relations: transcription coactivator activity has relations: molfunc_protein with IRF4, molfunc_protein with IRF4, molfunc_protein with TAF6, molfunc_protein with TAF6, molfunc_protein with YAF2, molfunc_protein with YAF2, molfunc_protein with UTF1, molfunc_protein with UTF1, molfunc_protein with PHF2, molfunc_protein with PHF2.", "label": "yes"}
{"original_question": "Is Algenpantucel-L effective for pancreatic cancer?", "id": "converted_4488", "sentence1": "Is Algenpantucel-L effective for Malignant neoplasm of pancreas?", "sentence2": " Median (IQR) overall survival was 14.9 (12.2-17.8) months in the standard group (N=158) and 14.3 (12.6-16.3) months in the experimental group (N = 145) (hazard ratio [plant-type hypersensitive response] 1.02, 95% CI 0.66-1.58; P = 0.98). Median progression-free survival was 13.4 months in the standard group and 12.4 months in the experimental group (plant-type hypersensitive response 1.33, 95% CI 0.72-1.78; P = 0.59). Grade 3 or higher adverse events occurred in 105 of 140 patients (75%) in the standard group and in 115 of 142 patients (81%) in the experimental group (P > 0.05).CONCLUSIONS: Algenpantucel-L immunotherapy did not improve survival in patients with borderline resectable or locally advanced unresectable ANOPHTHALMIA AND PULMONARY HYPOPLASIA receiving SOC neoadjuvant chemotherapy and chemoradiation., CONCLUSIONS: The addition of algenpantucel-L to standard adjuvant therapy for resected Malignant neoplasm of pancreas may improve survival. A multi-institutional, phase 3 study is ongoing, CONCLUSIONS: The addition of algenpantucel-L to standard adjuvant therapy for resected Malignant neoplasm of pancreas may improve surviva, CONCLUSIONS: Algenpantucel-L immunotherapy did not improve survival in patients with borderline resectable or locally advanced unresectable ANOPHTHALMIA AND PULMONARY HYPOPLASIA receiving SOC neoadjuvant chemotherapy and chemoradiatio[SEP]Relations: malignant exocrine pancreas neoplasm has relations: disease_disease with pancreatoblastoma, disease_disease with pancreatoblastoma, disease_disease with exocrine pancreatic carcinoma, disease_disease with exocrine pancreatic carcinoma, disease_disease with pancreatic exocrine neoplasm, disease_disease with pancreatic exocrine neoplasm, disease_disease with pancreatic intraductal papillary-mucinous neoplasm, disease_disease with pancreatic intraductal papillary-mucinous neoplasm, disease_disease with malignant pancreatic neoplasm, disease_disease with malignant pancreatic neoplasm.", "label": "no"}
{"original_question": "Are mucin overexpression associated with disease?", "id": "converted_3996", "sentence1": "Are Homo sapiens MUC1 protein overexpression associated with disease?", "sentence2": "The pathological mechanism underlying Liver calculus is closely related to bacterial infections of the Intrahepatic bile duct, followed by chronic inflammation and the overexpression of Homo sapiens MUC1 wt Allele protein 5AC (MUC5AC protein, human protein, Homo sapiens)., MUC1 wt Allele wt Allele is a Membrane Glycoproteins, which in adenocarninomas is overexpressed and exhibits truncated O-glycosylation. , Mucin 13 (MUC13 gene gene) is reportedly overexpressed in Homo sapiens malignancies., Inflammation causes MUC1 wt Allele wt Allele overexpression and hypoglycosylation. [SEP]Relations: Protein S Homo sapiens has relations: drug_drug with Mitomycin, drug_drug with Mitomycin, drug_drug with Mitomycin, drug_drug with Mitomycin, drug_drug with Obinutuzumab, drug_drug with Obinutuzumab, drug_drug with Obinutuzumab, drug_drug with Obinutuzumab. bladder calculus has relations: disease_disease with urinary bladder disease, disease_disease with urinary bladder disease.", "label": "yes"}
{"original_question": "Is there any role for HUWE1 in MYC signalling?", "id": "converted_2916", "sentence1": "Is there any role for HUWE1 protein, human in MYC protein, human signalling?", "sentence2": "HUWE1 protein, human protein, human is a critical colonic Neoplasms suppressor gene that prevents MYC protein, human protein, human signalling, DNA damage accumulation and Neoplasms initiation., To determine the importance of HUWE1 protein, human protein, human, we chose to examine its function in Malignant neoplasm of colon and/or rectum, where it is Mutation Abnormality in up to 15 per cent of tumours. Modelling of identified Gene Mutation showed that they inactivate the E3 ubiquitin ligase activity of HUWE1 protein, human protein, human. Genetic Gene Deletion Abnormality of Huwe1 rapidly accelerated tumourigenic in CASP14 gene carrying loss of the intestinal Neoplasms suppressor gene Apc, with a dramatic increase in Neoplasms initiation. Mechanistically, this phenotype was driven by increased MYC protein, human protein, human and rapid DNA damage accumulation leading to loss of the second copy of Apc The increased levels of DNA damage sensitised Huwe1-deficient tumours to DNA-damaging agents and to Gene Deletion Abnormality of the anti-apoptotic protein MCL1. Taken together, these data identify HUWE1 protein, human protein, human as a bona fide Neoplasms suppressor gene in the Structure of Structure of intestinal epithelium and suggest a potential vulnerability of HUWE1 protein, human protein, human-Mutation Abnormality tumours to DNA-damaging agents and inhibitors of Apoptosis Inhibiting Proteins.[SEP]Relations: receptor signaling protein tyrosine kinase inhibitor activity has relations: molfunc_protein with HYAL2, molfunc_protein with HYAL2. regulation of intestinal epithelial structure maintenance has relations: bioprocess_protein with NEUROD1, bioprocess_protein with NEUROD1. anus neoplasm has relations: disease_protein with IFNB1, disease_protein with IFNB1. Protein S human has relations: drug_drug with Peginterferon beta-1a, drug_drug with Peginterferon beta-1a, drug_drug with Peginterferon beta-1a, drug_drug with Peginterferon beta-1a.", "label": "yes"}
{"original_question": "Is palbociclib effective for glioblastoma?", "id": "converted_3570", "sentence1": "Is palbociclib effective for Glioblastoma Multiforme?", "sentence2": "Although further research is needed, CDK1 gene 4/6 inhibitors represent intriguing developments in the treatment of various Malignant Neoplasms, including those with such poor prognoses as Glioblastoma Multiforme multiforme, Mantle cell lymphoma, and metastatic melanoma., CONCLUSION: In this trial, despite adequate tissue Pyruvate Kinase, palbociclib monotherapy was not an effective treatment for recurrent Glioblastoma Multiforme., CONCLUSION\n\nIn this trial, despite adequate tissue Pyruvate Kinase, palbociclib monotherapy was not an effective treatment for recurrent Glioblastoma Multiforme., CONCLUSION In this trial, despite adequate tissue Pyruvate Kinase, palbociclib monotherapy was not an effective treatment for recurrent Glioblastoma Multiforme., CONCLUSION\nIn this trial, despite adequate tissue Pyruvate Kinase, palbociclib monotherapy was not an effective treatment for recurrent Glioblastoma Multiforme.[SEP]Relations: adult Glioblastoma Multiforme has relations: disease_disease with Glioblastoma Multiforme (disease), disease_disease with Glioblastoma Multiforme (disease), disease_disease with adult infiltrating astrocytic neoplasm, disease_disease with adult infiltrating astrocytic neoplasm, disease_disease with adult spinal cord Glioblastoma Multiforme, disease_disease with adult spinal cord Glioblastoma Multiforme. Mantle cell lymphoma has relations: disease_protein with CREBBP, disease_protein with CREBBP, disease_protein with UBR5, disease_protein with UBR5.", "label": "no"}
{"original_question": "Could Arimidex (anastrozole) cause hot flashes?", "id": "converted_634", "sentence1": "Could Arimidex (anastrozole) cause hot flashes?", "sentence2": "More than a third of Malignant neoplasm of breast patients undergoing aromatase inhibitor (Aortic Valve Insufficiency) treatment report joint pain., In the first 6 weeks, emergence of joint pain was associated with increase in general pain, Fatigue, disturbed sleep, hot flashes, Vaginal dryness, and decreased sexual activity., Antiestrogen therapy can cause vasomotor symptoms similar to those occurring during menopause, including hot flashes., The purpose of this study was to assess the feasibility and safety of acupuncture for treatment of hot flashes in Korean patients with Malignant neoplasm of breast receiving Antiestrogen Therapy., 10 patients with Malignant neoplasm of breast who were undergoing Antiestrogen Therapy with tamoxifen or anastrozole and who were suffering from hot flashes., During treatment, severity of hot flashes was reduced by 70%-95% in all patients., anastrozole has been widely used in Japan as an adjuvant treatment for postmenopausal, hormone-responsive Malignant neoplasm of breast patients., The aim of this study is to evaluate the rate of bone fracture and bone mineral density (BMD) during anastrozole treatment in Japanese patients., Musculoskeletal disorders were the most common (26.1 %), and hot flashes were the second most common adverse event (7.9 %)., To compare the effect of therapy with anastrozole versus a combination of fulvestrant and anastrozole in women in first relapse of endocrine-responsive Malignant neoplasm of breast., fulvestrant loading dose (LD) regimen followed by monthly injection plus 1 mg of anastrozole daily or to 1 mg of anastrozole daily alone., Incidences of prespecified adverse events (AEs) were similar. Hot flashes were more common in the experimental arm: 63 patients (24.6%) versus 35 patients (13.8%) in the standard arm (P = .0023)., The third-generation agents (anastrozole, letrozole, and exemestane) have been shown to be more effective and safer than the selective Estrogen Receptors modulators tamoxifen and raloxifen., Androgen-Insensitivity Syndrome are well tolerated and cause a lower incidence of gynecological symptoms (Vaginal Hemorrhage, discharge, and Endometrial Neoplasms), venous thromboembolic events, and hot flashes compared with tamoxifen., Disturbance in mood, Somnolence, Anxiety Disorders, Fatigue, hot flashes, and Memory impairment have been reported among patients receiving anastrozole as adjuvant therapy., Twenty-five PM-BC patients received, in Sequence - ParameterizedDataType, leuprolide, taxane-anthracycline induction chemotherapy, radiation therapy, a platinum-based intensification high-dose CT, followed by leuprolide and anastrazole for five years., Grade 4 Hematologic toxicity was observed in all patients, no patient showed a decrease of cardiac ejection fraction and hot flashes and Arthralgia were of moderate intensity., Of the patients treated with anastrozole, 3 (37.5%) reported toxicity, with 1 report each of decreased libido, leg swelling, and Cancer patients and suicide and Cancer patients and suicide and depression (12.5%). Toxicity was reported in 2 patients taking letrozole (40%), with both reporting Peripheral edema, and 1 reporting hot flashes., Patients were treated with goserelin 3.6 mg subcutaneous monthly and began anastrozole 1-mg daily 21 days after the first injection of goserelin., The most common adverse events were Fatigue (50%), Arthralgia (53%), and hot flashes (59%)., These studies were designed to evaluate the safety and efficacy of Androgen-Insensitivity Syndrome in the following clinical settings: 1) as initial adjuvant therapy (the Arimidex, tamoxifen, Alone or in Combination trial, Breast International Group Trial 1-98),, Androgen-Insensitivity Syndrome were tolerated well, and patients who received them experienced fewer thrombolic events and less Malignant neoplasm of endometrium, hot flashes, night sweats, and Vaginal Hemorrhage compared with patients who receive tamoxifen., It has been suggested that the association of Aortic Valve Insufficiency and Recombinant Gonadorelin analogues and Aortic Valve Insufficiency could block the two routes of oestrogen production in males, and therefore this approach could increase efficacy. However, it could also enhance the rate of adverse events (hot flashes, Erectile dysfunction, etc.)., We reviewed therapeutic effects and harmful side effects in 33 patients with advanced or recurrent Malignant neoplasm of breast who underwent treatment with Anastrozole 1 mg/day in our department., The most frequent harmful side effects were rise in total cholesterol, general Fatigue, hot flashes and arthralgia (9.1%)., We analyzed the changes in frequency and severity of menopausal symptoms in patients receiving tamoxifen or Aromatase Inhibitors and identified factors influencing these symptoms., Both first-line tamoxifen and Aromatase Inhibitors induced an increase in the occurrence and severity of hot flashes (p<0.0001 and p=0.014, respectively)., To evaluate the efficacy and toxicity of the selective aromatase inhibitor anastrozole (Arimidex), we conducted a phase II trial in 53 women with asymptomatic recurrent/persistent müllerian cancer., Toxicity was modest (grade I) and infrequent, with the most common Toxic effect being Fatigue and hot flashes., The first analysis of the XCL1 wt Allele (Arimidex, tamoxifen Alone or in Combination) trial (median follow-up, 33 months) demonstrated that in adjuvant endocrine therapy for postmenopausal patients with early-stage Malignant neoplasm of breast, anastrozole was superior to tamoxifen in terms of disease-free survival (DFS), time to recurrence (TTR protein, human protein, human), and incidence of contralateral Malignant neoplasm of breast (CLBC)., in that Malignant neoplasm of endometrium (P = 0.007), Vaginal Hemorrhage and discharge (P < 0.001 for both), Cerebrovascular events (P < 0.001), venous thromboembolic events (P < 0.001), and hot flashes (P < 0.001) all occurred less frequently in the anastrozole group, whereas Musculoskeletal Diseases and Fracture (P < 0.001 for both) continued to occur less frequently in the tamoxifen group., reduced Nausea:Presence or Threshold:Point in time:^Patient:Ordinal, hot flashes, and abdominal discomfort caused almost twice as many patients to prefer to continue with letrozole therapy than with anastrozole[SEP]Relations: Anastrozole has relations: drug_effect with Anaphylactic shock, drug_effect with Anaphylactic shock, drug_effect with Fever, drug_effect with Fever, drug_effect with Arthritis, drug_effect with Arthritis, drug_drug with Deferasirox, drug_drug with Deferasirox, drug_drug with Piroxicam, drug_drug with Piroxicam.", "label": "yes"}
{"original_question": "Is the SDHAF2 gene encoding a protein necessary for flavination of SDHA?", "id": "converted_1206", "sentence1": "Is the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes encoding a Protein Info necessary for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial?", "sentence2": "Pheochromocytoma-paraganglioma syndrome is caused by Gene Mutation in SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, encoding subunits of Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase), and in Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, required for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial. , At present, these are RET Genes, von Hippel-Lindau disease tumor suppressor Genes (Von Hippel-Lindau Syndrome), neurofibromatosis type 1 tumor suppressor Genes (Neurofibromatosis 1), genes encoding the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase) complex subunits SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, but also Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, the Genes encoding the Enzyme [APC] responsible for the flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial (Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein or hSDH5), and the newly described TMEM127 gene Genes and MAX tumor suppressor genes., the Genes encoding the Enzyme [APC] responsible for the flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial (Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein or hSDH5), Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, required for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, At present, these are RET Genes, von Hippel-Lindau disease tumor suppressor Genes (Von Hippel-Lindau Syndrome), neurofibromatosis type 1 tumor suppressor Genes (Neurofibromatosis 1), genes encoding the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase) complex subunits SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, but also Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, the Genes encoding the Enzyme [APC] responsible for the flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial (Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein or hSDH5), and the newly described TMEM127 gene Genes and MAX tumor suppressor genes., Pheochromocytoma-paraganglioma syndrome is caused by Gene Mutation in SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, encoding subunits of Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase), and in Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, required for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial., In a recent issue of Science, Rutter and coworkers showed that SDH5 is required for the flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, which is necessary for Succinate Dehydrogenase assembly and function., At present, these are RET Genes, von Hippel-Lindau disease tumor suppressor Genes (Von Hippel-Lindau Syndrome), neurofibromatosis type 1 tumor suppressor Genes (Neurofibromatosis 1), genes encoding the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase) complex subunits SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, but also Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, the Genes encoding the Enzyme [APC] responsible for the flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial (Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein or hSDH5), and the newly described TMEM127 gene Genes and MAX tumor suppressor genes, Pheochromocytoma-paraganglioma syndrome is caused by Gene Mutation in SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, encoding subunits of Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase), and in Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, required for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, CONTEXT: Pheochromocytoma-paraganglioma syndrome is caused by Gene Mutation in SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, encoding subunits of Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase), and in Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, required for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial. , This Genes is co-expressed with a number of genes encoding Mitochondrial Proteins, including SDHB Protein Info, human wt Allele-1, and has low partial sequence similarity to human Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, a Protein Info required for flavin-adenine dinucleotide (flavin-adenine dinucleotide) Insert (object) into Succinate Dehydrogenase. , At present, these are RET Genes, von Hippel-Lindau disease tumor suppressor Genes (Von Hippel-Lindau Syndrome), neurofibromatosis type 1 tumor suppressor Genes (Neurofibromatosis 1), genes encoding the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase) complex subunits SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, but also Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, the Genes encoding the Enzyme [APC] responsible for the flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial (Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein or hSDH5), and the newly described TMEM127 gene Genes and MAX tumor suppressor genes., Pheochromocytoma-paraganglioma syndrome is caused by Gene Mutation in SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, encoding subunits of Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase), and in Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, required for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial.[SEP]Relations: Flavin adenine dinucleotide has relations: drug_protein with AIFM1, drug_protein with AIFM1, drug_protein with NQO2, drug_protein with NQO2, drug_protein with DLD, drug_protein with DLD, drug_protein with CYB5R3, drug_protein with CYB5R3, drug_protein with ACAD8, drug_protein with ACAD8.", "label": "yes"}
{"original_question": "Are Sidekick proteins members of the immunoglobulin superfamily?", "id": "converted_969", "sentence1": "Are Sidekick proteins members of the immunoglobulin superfamily?", "sentence2": "Here we show that four closely related immunoglobulin superfamily (IgSF) adhesion molecules--DSCAM gene (Down's syndrome Cell Adhesion Molecule-1), DscamL (refs 6-9), Sidekick-1 and Sidekick-2, Sidekick-1, a Cell Adhesion Molecule-1 of the immunoglobulin superfamily, is up-regulated in glomerular podocytes in the collapsing glomerulopathy of AIDS-Associated Nephropathy (HIVAN).[SEP]Relations: Cell Adhesion Molecule-1 production has relations: bioprocess_protein with GOLPH3, bioprocess_protein with GOLPH3, bioprocess_protein with GCNT1, bioprocess_protein with GCNT1, bioprocess_protein with PPIA, bioprocess_protein with PPIA, bioprocess_bioprocess with cellular process, bioprocess_bioprocess with cellular process. AIDS-Associated Nephropathy has relations: disease_disease with focal segmental glomerulosclerosis, disease_disease with focal segmental glomerulosclerosis.", "label": "yes"}
{"original_question": "Has whole exome sequencing been performed in Alzheimer patients?", "id": "converted_1896", "sentence1": "Has whole exome sequencing been performed in Alzheimer patients?", "sentence2": "Pilot whole-exome sequencing of a German early-onset ALZHEIMER DISEASE, FAMILIAL, 1 cohort reveals a substantial frequency of PSEN2 Protein Info, human Protein Info, human variants., We performed whole-exome sequencing in early-onset ALZHEIMER DISEASE 2 (EOAD) and late-onset ALZHEIMER DISEASE 2 (Load Component of Device) families followed by functional studies of select variants., Whole-exome sequencing revealed a nonsense Mutation Abnormality in PRNP (NM_000311, c.C478T; p.Q160*; rs80356711) associated with homozygosity for the V Alleles at position 129 of the Protein Info, further highlighting how very similar Genotype in PRNP result in strikingly different phenotypes., In the search for new Genes in ALZHEIMER DISEASE, FAMILIAL, 1, classic linkage-based and candidate-gene-based association studies have been supplanted by exome sequencing, genome-wide sequencing (for mendelian forms of ALZHEIMER DISEASE, FAMILIAL, 1), and genome-wide association studies (for non-mendelian forms). , We performed whole exome sequencing in a Turkish patient clinically diagnosed with ALZHEIMER DISEASE, FAMILIAL, 1 from a consanguineous family , Performing exome sequencing in 14 autosomal dominant early-onset ALZHEIMER DISEASE 2 (ADEOAD) index cases without Mutation Abnormality on known Genes (amyloid precursor Protein Info (Smartphone Application), presenilin1 (PSEN1 Protein Info, human Protein Info, human) and presenilin2 (PSEN2 Protein Info, human Protein Info, human)), we found that in five patients, the SORL1 gene harbored unknown nonsense (n=1) or missense (n=4) Gene Mutation[SEP]Relations: ALZHEIMER DISEASE 2 has relations: disease_protein with PLAU, disease_protein with PLAU, disease_protein with ARC, disease_protein with ARC, disease_protein with NOS3, disease_protein with NOS3, disease_protein with MIR100, disease_protein with MIR100, disease_protein with ABI3, disease_protein with ABI3.", "label": "yes"}
{"original_question": "Is the enzyme ERAP2 associated with the disease birdshot chorioretinopathy?", "id": "converted_2887", "sentence1": "Is the Enzyme [APC] ERAP2 gene associated with the Disease birdshot chorioretinopathy?", "sentence2": "Allele-specific Alterations in the Peptidome Underlie the Joint Association of HLA-A*29:02 and Endoplasmic Reticulum Aminopeptidase 2 (ERAP2 gene gene) with Birdshot Chorioretinopathy., Birdshot Chorioretinopathy is also associated with ERAP1 gene (ERAP2 gene gene), an Enzyme [APC] involved in processing HLA class I ligands, thus implicating the A*29:02 peptidome in this Disease. , A genome-wide association study identifies a functional ERAP2 gene gene haplotype associated with birdshot chorioretinopathy.[SEP]Relations: birdshot chorioretinopathy has relations: disease_protein with HLA-A, disease_protein with HLA-A, disease_phenotype_positive with Retinal pigment epithelial atrophy, disease_phenotype_positive with Retinal pigment epithelial atrophy, disease_phenotype_positive with Epiretinal membrane, disease_phenotype_positive with Epiretinal membrane, disease_phenotype_positive with Arcuate scotoma, disease_phenotype_positive with Arcuate scotoma. ERAP2 gene has relations: disease_protein with ileocolitis, disease_protein with ileocolitis.", "label": "yes"}
{"original_question": "Is TALEN being used on stem cells?", "id": "converted_529", "sentence1": "Is TALEN being used on Stem cells?", "sentence2": "Precise correction of the dystrophin gene in duchenne muscular dystrophy patient induced pluripotent Stem cells by TALEN and CRISPR-Cas9., Genetic correction of patient-derived induced pluripotent Stem cells (iPSCs) by Transcription Activator-Like Effector Nucleases or CRISPR-Cas9 holds promise for DMD gene therapy; however, the safety of such nuclease treatment must be determined., We generated helper-dependent, capsid-Changing adenovirus (HD-Ad5/35) vectors for zinc-finger nuclease (ZFN)- or transcription activator-like effector nuclease (TALEN)-mediated Genome - anatomical entity editing in Homo sapiens CD34+ hematopoietic Stem cells (Hematopoietic Stem cells) from mobilized adult donors. , We used transcription activator-like effector nuclease (TALEN)-mediated gene editing in mouse embryonic Stem cells (mESCs) to produce CASP14 gene with targeted gene disruptions and Clinical act of insertion in two Y-linked Genes--SRY protein, Homo sapiens and UTY gene., Transcription activator-like effector nuclease (TALEN)-mediated gene correction in integration-free β-thalassemia induced pluripotent Stem cells., A TALEN Genome - anatomical entity-editing system for generating Homo sapiens stem cell-based disease models., Low incidence of off-target mutations in individual CRISPR-Cas9 and TALEN targeted Homo sapiens stem cell Clone Cells detected by whole-Genome - anatomical entity sequencing., Using CRISPR-Cas9 and TALEN targeted Homo sapiens pluripotent stem cell Clone Cells, we performed whole-Genome - anatomical entity sequencing at high coverage in order to assess the degree of Mutagenesis Procedure across the entire Genome - anatomical entity., A Changing TALEN-based system for robust generation of knock-out Homo sapiens pluripotent stem cell lines and disease models., In this study, we utilized a cell-penetrating peptide-based system for ZFN and TALEN delivery., At all loci tested we obtained Human Embryonic Stem Cells (ESTERASE C) and induced pluripotent stem cell (iPSC) Clone Cells carrying transgenic cassettes solely at the TALEN-specified location., We report here the use of Transcription Activator-Like Effector Nucleases to rapidly and efficiently generate mutant alleles of 15 Genes in cultured Diploid Cell or Homo sapiens pluripotent Stem cells, the latter for which we differentiated both the targeted lines and isogenic control lines into various metabolic cell types., Zinc-finger nucleases (ZFNs) and transcription activator-like effector nucleases (Transcription Activator-Like Effector Nucleases) have been successfully used to knock out endogenous Genes in stem cell research., Here we report different methods to efficiently perform TALEN-mediated gene integration and inactivation in different mammalian cell systems including induced pluripotent Stem cells and delineate experimental examples associated with these approaches, Together, our results demonstrate that TALE-based transcriptional repressor and Transcription Activator-Like Effector Nucleases are two promising approaches for loss-of-function studies of microRNA clusters in Diploid Cell and pluripotent Stem cells, We report here the use of Transcription Activator-Like Effector Nucleases to rapidly and efficiently generate mutant alleles of 15 Genes in cultured Diploid Cell or Homo sapiens pluripotent Stem cells, the latter for which we differentiated both the targeted lines and isogenic control lines into various metabolic cell types, TALEN-mediated generation and genetic correction of disease-specific Homo sapiens induced pluripotent Stem cells., Baculoviral transduction facilitates TALEN-mediated targeted transgene integration and Cre/LoxP cassette exchange in Homo sapiens-induced pluripotent Stem cells., We used transcription activator-like effector nuclease (TALEN)-mediated gene editing in mouse embryonic Stem cells (mESCs) to produce CASP14 gene with targeted gene disruptions and Clinical act of insertion in two Y-linked Genes--SRY protein, Homo sapiens and UTY gene. , Using CRISPR-Cas9 and TALEN targeted Homo sapiens pluripotent stem cell Clone Cells, we performed whole-Genome - anatomical entity sequencing at high coverage in order to assess the degree of Mutagenesis Procedure across the entire Genome - anatomical entity. , A 5% ResponseLevel - ResponseLevel - modification rate was observed in Homo sapiens induced pluripotent Stem cells (hiPSCs) treated with TAT-TALEN as measured by the Surveyor assay.  TAT-TALEN protein-mediated gene disruption was applicable in hiPSCs and represents a promising technique for gene knockout in Stem cells., Here we engineered transcription activator-like effector nucleases (Transcription Activator-Like Effector Nucleases) for five distinct genomic loci. At all loci tested we obtained Human Embryonic Stem Cells (ESTERASE C) and induced pluripotent stem cell (iPSC) Clone Cells carrying transgenic cassettes solely at the TALEN-specified location., Seamless correction of the sickle cell disease Mutation Abnormality of the HBB gene in Homo sapiens induced pluripotent Stem cells using Transcription Activator-Like Effector Nucleases., At all loci tested we obtained Human Embryonic Stem Cells (ESTERASE C) and induced pluripotent stem cell (iPSC) Clone Cells carrying transgenic cassettes solely at the TALEN-specified location. Our data suggest that Transcription Activator-Like Effector Nucleases employing the specific architectures described here mediate site-specific Genome - anatomical entity ResponseLevel - ResponseLevel - modification in Homo sapiens pluripotent cells with similar efficiency and precision as do Zinc Finger Nucleases (ZFNs).[SEP]Relations: hematopoietic stem cell homeostasis has relations: bioprocess_protein with EMCN, bioprocess_protein with EMCN, bioprocess_protein with ADAR, bioprocess_protein with ADAR, bioprocess_protein with NLE1, bioprocess_protein with NLE1, bioprocess_protein with CCN3, bioprocess_protein with CCN3, bioprocess_protein with EXT1, bioprocess_protein with EXT1.", "label": "yes"}
{"original_question": "Is CXCL7 a chemokine?", "id": "converted_2669", "sentence1": "Is PPBP wt Allele a chemokine?", "sentence2": "PPBP wt Allele, a chemokine highly expressed in Blood Platelets, , Chemokine PPBP wt Allele Heterodimers[SEP]Relations: Chemokine receptors bind chemokines has relations: pathway_protein with CXCL8, pathway_protein with CXCL8, pathway_protein with CXCL5, pathway_protein with CXCL5, pathway_protein with CXCL6, pathway_protein with CXCL6, pathway_protein with CXCL9, pathway_protein with CXCL9, pathway_protein with CXCL11, pathway_protein with CXCL11.", "label": "yes"}
{"original_question": "Can exposure to heavy metals like lead(Pb) or cadmium(Cd) cause changes in DNA methylation patterns in Isoetes sinensis?", "id": "converted_2856", "sentence1": "Can exposure to heavy metals like lead(HTN3 gene) or cadmium(pyrimethamine) cause changes in DNA methylation patterns in Isoetes sinensis?", "sentence2": "DNA methylation in endangered plants after exposure to heavy metals, the Isoetes sinensis, an endangered plant, was stressed with three different concentrations of two heavy metals lead (HTN3 gene) and cadmium (pyrimethamine), The results showed that the DNA methylated profile of I. sinensis was affected by HTN3 gene and pyrimethamine stress., The proportion of DNA methylation (including hypermethylation) by both HTN3 gene and pyrimethamine stresses is nearly equal (39.04% and 39.71%), but the proportion of DNA demethylation by pyrimethamine is higher than that by HTN3 gene (46.86% than 33.92%)., There was no significant difference in the amount of DNA methylation among control check (Creatine Kinase), HTN3 gene stress group, and pyrimethamine stress group (Creatine Kinase 46.96%, HTN3 gene 48.23%, and pyrimethamine 48.1%)., However, full-methylation level of HTN3 gene stress group (28.34%) and pyrimethamine stress group (20.25%) was lower than control (33.91%), in contrast, hemi-methylation level HTN3 gene stress group (19.89%) and pyrimethamine stress group (27.85%) were higher than control (13.04%)., Consistently, a dramatic change in DNA methylation patterns was detected in excess Cu-exposed H. verticillata., Hydrilla verticillata employs two different ways to affect DNA methylation under excess copper stress.Because of the accumulation of heavy metals, Hydrilla verticillata (L.f.) Royle, a rooted submerged perennial aquatic herb, is being developed as a potential tool to clean the aquatic ecosystem polluted by heavy metals. , The proportion of DNA methylation (including hypermethylation) by both HTN3 gene and pyrimethamine stresses is nearly equal (39.04% and 39.71%), but the proportion of DNA demethylation by pyrimethamine is higher than that by HTN3 gene (46.86% than 33.92%).<br>[SEP]Relations: Pyrimethamine has relations: drug_drug with Methylene blue, drug_drug with Methylene blue, drug_effect with Thrombocytopenia, drug_effect with Thrombocytopenia, drug_effect with Pancytopenia, drug_effect with Pancytopenia, drug_effect with Hematuria, drug_effect with Hematuria, drug_protein with HEXB, drug_protein with HEXB.", "label": "yes"}
{"original_question": "Does association with the nuclear pore promote gene silencing?", "id": "converted_3590", "sentence1": "Does association with the nuclear pore promote gene silencing?", "sentence2": "Here, we show that the nucleoporin RANBP2 wt Allele plays an important role in this process. RANBP2 wt Allele localizes to the Nuclear Pore and to the cytoplasmic annulate lamellae (AL), and these structures dynamically associate with two mRNP granules: processing bodies (P bodies) and Stress Granules (Shprintzen-Goldberg syndrome). , MicroRNA (miRNA)-guided mRNA repression, mediated by the miRNA-induced silencing complex (miRISC), is an important component of post-transcriptional gene silencing., To assess TPR protein, human's role as an architectural element of the Nasopharyngeal carcinoma, we have studied the sequential disassembly and reassembly of NPCs in mitotic Cells, paralleled by studies of Cells depleted of TPR protein, human as a result of posttranscriptional tpr gene silencing by RNA interference (RNAi)., The results raise the possibility that Nasopharyngeal carcinoma-localized protein desumoylation may be a key regulatory event preventing inappropriate mRNA Precursor export., Silencing nuclear pore protein TPR protein, human elicits a senescent-like phenotype in Tumor Cells, malignant.[SEP]Relations: nuclear pore has relations: cellcomp_protein with RAN, cellcomp_protein with RAN, cellcomp_protein with IPO5, cellcomp_protein with IPO5, cellcomp_protein with GLE1, cellcomp_protein with GLE1, cellcomp_protein with IPO7, cellcomp_protein with IPO7, cellcomp_protein with RGPD5, cellcomp_protein with RGPD5.", "label": "yes"}
{"original_question": "Have hESC been tested for the treatment of age-related macular degeneration?", "id": "converted_545", "sentence1": "Have hESC been tested for the treatment of age-related macular degeneration?", "sentence2": "Development of Homo sapiens embryonic stem cell therapies for age-related macular degeneration, In this review, we describe recent approaches to develop cell-based therapies for the treatment of Age related macular degeneration. Recent research has focused on replacing the Structure of retinaldehyde pigment epithelium (RPE), a monolayer of Cells vital to photoreceptor cell health. We discuss the various methods used to differentiate and purify RPE from Homo sapiens embryonic stem Cells (HESC), and describe the surgical approaches being used to transplant these Cells in existing and forthcoming clinical trials., Age-related macular degeneration (Age related macular degeneration) is characterized by the loss or dysfunction of Structure of retinaldehyde pigment epithelium (RPE) and is the most common cause of Unspecified visual loss among the elderly. Stem-cell-based strategies, using Homo sapiens embryonic stem Cells (hESCs) or Homo sapiens-induced pluripotent stem Cells (hiPSCs), may provide an abundant donor source for generating RPE Cells in cell replacement therapies., This study contributes to our understanding of the utility of hESC/hiPSC-derived RPE in Age related macular degeneration therapy., Two important early potential hESC applications are the use of Structure of retinaldehyde pigment epithelium (RPE) for the treatment of age-related macular degeneration and STARGARDT DISEASE 1 (disorder), an untreatable form of macular dystrophy that leads to early-onset Blindness., Human Embryonic Stem Cells (hESCs) are a promising source of Structure of retinaldehyde pigment epithelium (RPE) Cells: Cells that can be used for the treatment of common and incurable forms of Blindness, such as age-related macular degeneration., A potential application of Homo sapiens embryonic stem Cells (hESCs) and induced pluripotent stem Cells (iPSCs) is the generation of retinaldehyde pigmented epithelium (RPE) to treat age-related macular degeneration (Age related macular degeneration), a common but incurable retinaldehyde disease., Human Embryonic Stem Cells (hESCs) are a promising source of Structure of retinaldehyde pigment epithelium (RPE) Cells: Cells that can be used for the treatment of common and incurable forms of Blindness, such as age-related macular degeneration, A potential application of Homo sapiens embryonic stem Cells (hESCs) and induced pluripotent stem Cells (iPSCs) is the generation of retinaldehyde pigmented epithelium (RPE) to treat age-related macular degeneration (Age related macular degeneration), a common but incurable retinaldehyde disease, Assessments of safety and efficacy are crucial before Homo sapiens ESC (hESC) therapies can move into the clinic. Two important early potential hESC applications are the use of Structure of retinaldehyde pigment epithelium (RPE) for the treatment of age-related macular degeneration and STARGARDT DISEASE 1 (disorder), an untreatable form of macular dystrophy that leads to early-onset Blindness., A potential application of Homo sapiens embryonic stem Cells (hESCs) and induced pluripotent stem Cells (iPSCs) is the generation of retinaldehyde pigmented epithelium (RPE) to treat age-related macular degeneration (Age related macular degeneration), a common but incurable retinaldehyde disease. RPE Cells derived from hESCs (hESC-RPEs) and iPSCs (iPSC-RPEs) express essential RPE markers and can rescue visual function in animal models., Two important early potential hESC applications are the use of Structure of retinaldehyde pigment epithelium (RPE) for the treatment of age-related macular degeneration and STARGARDT DISEASE 1 (disorder), an untreatable form of macular dystrophy that leads to early-onset Blindness. Here we show long-term functional rescue using hESC-derived RPE in both the RCS Rattus norvegicus and Elov14 mouse, which are animal models of Retinal Degeneration and Stargardt's disease's disease, respectively.[SEP]Relations: macular degeneration, age-related, 3 has relations: disease_disease with macular degeneration, disease_disease with macular degeneration, disease_protein with FBLN5, disease_protein with FBLN5, disease_phenotype_positive with Macular degeneration, disease_phenotype_positive with Macular degeneration, disease_phenotype_positive with Decreased patellar reflex, disease_phenotype_positive with Decreased patellar reflex, disease_phenotype_positive with Choroidal neovascularization, disease_phenotype_positive with Choroidal neovascularization.", "label": "yes"}
{"original_question": "Is human lysyl oxidase-like 2 a glycoprotein?", "id": "converted_2659", "sentence1": "Is human lysyl oxidase-like 2 a glycoprotein?", "sentence2": "This method was successfully applied to a novel recombinant Protein Info, human lysyl oxidase-like 2. Furthermore, the glycosylation PTMS gene were readily detected at two glycosylation sites in the Protein Info. , application to the characterization of human lysyl oxidase-like 2 glycosylation, These results suggest that the N-glycan at Asn-644 of hLOXL2 enhances the solubility and stability of the LOX protein, human Protein Info, human catalytic domain.[SEP]Relations: Protein S human has relations: drug_drug with Imidazole salicylate, drug_drug with Imidazole salicylate, drug_drug with Phenyl aminosalicylate, drug_drug with Phenyl aminosalicylate, drug_drug with Glycochenodeoxycholic Acid, drug_drug with Glycochenodeoxycholic Acid, drug_drug with Butylphthalide, drug_drug with Butylphthalide, drug_drug with Hyodeoxycholic Acid, drug_drug with Hyodeoxycholic Acid.", "label": "yes"}
{"original_question": "Is TNF-α an activator of pancreatic stellate cells?", "id": "converted_3239", "sentence1": "Is TNF-α an activator of Pancreatic Stellate Cells?", "sentence2": "TNF-α is the prime factor responsible for the activation of Pancreatic Stellate Cells, Activated PSCs expressed interleukin-33 receptor binding in the Cell Nucleus, and the expression was increased by IL-1β, TNF-α, becaplermin, and IFN-γ, but not TGF-β1. [SEP]Relations: pancreatic stellate cell proliferation has relations: bioprocess_bioprocess with fibroblast proliferation, bioprocess_bioprocess with fibroblast proliferation. Becaplermin has relations: drug_protein with PDGFRA, drug_protein with PDGFRA, drug_protein with A2M, drug_protein with A2M, drug_protein with PDGFRB, drug_protein with PDGFRB.", "label": "yes"}
{"original_question": "Do orphan and gene related CpG islands follow power-law-like distributions?", "id": "converted_231", "sentence1": "Do orphan and Genes related CpG islands follow power-law-like distributions?", "sentence2": "Orphan and Genes related CpG Islands follow power-law-like distributions in several genomes: evidence of function-related and taxonomy-related modes of distribution., Here, an investigation of their distributional characteristics in a variety of genomes is undertaken for both whole CGI populations as well as for CGI subsets that lie away from known genes (Genes-unrelated or \"orphan\" CGIs). In both cases power-law-like linearity in double logarithmic scale is found.,  Our results on power-law-like linearity found in orphan CGI populations suggest that the observed distributional pattern is independent of the analogous pattern that protein coding segments were reported to follow. The power-law-like patterns in the genomic distributions of CGIs described herein are found to be compatible with several other features of the composition, abundance or functional role of CGIs reported in the current literature across several genomes, on the basis of the proposed evolutionary model., Our results on power-law-like linearity found in orphan CGI populations suggest that the observed distributional pattern is independent of the analogous pattern that protein coding segments were reported to follow., The power-law-like patterns in the genomic distributions of CGIs described herein are found to be compatible with several other features of the composition, abundance or functional role of CGIs reported in the current literature across several genomes, on the basis of the proposed evolutionary model., Our results on power-law-like linearity found in orphan CGI populations suggest that the observed distributional pattern is independent of the analogous pattern that protein coding segments were reported to follow. , Our results on power-law-like linearity found in orphan CGI populations suggest that the observed distributional pattern is independent of the analogous pattern that protein coding segments were reported to follow. The power-law-like patterns in the genomic distributions of CGIs described herein are found to be compatible with several other features of the composition, abundance or functional role of CGIs reported in the current literature across several genomes, on the basis of the proposed evolutionary model., Initially, they were assigned the role of transcriptional regulation of protein-coding genes, especially the house-keeping ones, while more recently there is found evidence that they are involved in several other functions as well, which might include regulation of the expression of RNA genes, DNA replication etc. Here, an investigation of their distributional characteristics in a variety of genomes is undertaken for both whole CGI populations as well as for CGI subsets that lie away from known genes (Genes-unrelated or \"orphan\" CGIs). In both cases power-law-like linearity in double logarithmic scale is found. , Our results on power-law-like linearity found in orphan CGI populations suggest that the observed distributional pattern is independent of the analogous pattern that protein coding segments were reported to follow., The power-law-like patterns in the genomic distributions of CGIs described herein are found to be compatible with several other features of the composition, abundance or functional role of CGIs reported in the current literature across several genomes, on the basis of the proposed evolutionary model., Our results on power-law-like linearity found in orphan CGI populations suggest that the observed distributional pattern is independent of the analogous pattern that protein coding segments were reported to follow.[SEP]", "label": "yes"}
{"original_question": "Does RUNX2 inhibit astrocyte differentiation?", "id": "converted_3205", "sentence1": "Does RUNX2 gene inhibit astrocyte differentiation?", "sentence2": "The method was able to recapitulate experimentally validated cell-fate determinants, and validation of two predicted cell-fate determinants confirmed that overexpression of estrogen receptor alpha, human and RUNX2 gene gene in mouse neural stem cells induces neuronal and astrocyte differentiation, respectively.[SEP]Relations: regulation of intracellular estrogen receptor signaling pathway has relations: bioprocess_protein with RUNX1, bioprocess_protein with RUNX1, bioprocess_protein with AXIN1, bioprocess_protein with AXIN1, bioprocess_protein with CARM1, bioprocess_protein with CARM1, bioprocess_protein with UBA5, bioprocess_protein with UBA5, bioprocess_protein with DDRGK1, bioprocess_protein with DDRGK1.", "label": "no"}
{"original_question": "Are nucleosomes positioned at DNA replication origins?", "id": "converted_1370", "sentence1": "Are Nucleosomes positioned at DNA replication origins?", "sentence2": "yeast origins are characterized by an asymmetric pattern of positioned Nucleosomes flanking the ACS. The origin sequences are sufficient to maintain a nucleosome-free origin; however, origin recognition complex location is required for the precise positioning of Nucleosomes flanking the origin., Here, we identify nucleosome occupancy as a likely candidate to set up Odia Language distribution, we demonstrate that open chromatin domains, characterized by nucleosome depletion, are preferentially permissive for replication, nucleosome assembly of the template prevented DNA replication. Replication of Chromosomes, Human, Pair 1 was severely inhibited at more than two-thirds of physiological nucleosome density[SEP]Relations: nucleosome assembly has relations: bioprocess_bioprocess with DNA replication-dependent nucleosome assembly, bioprocess_bioprocess with DNA replication-dependent nucleosome assembly, bioprocess_protein with SET, bioprocess_protein with SET, bioprocess_bioprocess with DNA replication-independent nucleosome assembly, bioprocess_bioprocess with DNA replication-independent nucleosome assembly, bioprocess_protein with SETSIP, bioprocess_protein with SETSIP, bioprocess_protein with NPM1, bioprocess_protein with NPM1.", "label": "no"}
{"original_question": "Can the yeast protein Abf1 act as insulator?", "id": "converted_2370", "sentence1": "Can the yeast protein Abf1 act as insulator?", "sentence2": "Saccharomyces cerevisiae Rap1p and Abf1p proteins are endowed with a potent insulating capacity, Insulating domains in Rap1p coincide with previously described transcription activation domains, whereas four adjacent subdomains spanning the whole of the Abf1p C terminus (440-731) were found to display autonomous insulating capacity, That both Rap1p and Abf1p silencing domains either contain or largely overlap with an insulating domain suggests that insulation conveys some undefined chromosome organization capacity that also contributes a function in silencing. [SEP]", "label": "yes"}
{"original_question": "Is tubulin acetylation involved in cell motility?", "id": "converted_767", "sentence1": "Is Tubulin acetylation involved in cell motility?", "sentence2": "In this study, we found that paclitaxel induced Tubulin acetylation in Endothelium and Tumor cells, uncertain whether benign or malignant, at concentrations that affected cell motility but not proliferation (10(-8) to 10(-9) M, for 4 hours). Induction of Tubulin acetylation correlated with inhibition of motility but not proliferation based on a comparison of highly and poorly cytotoxic taxanes (paclitaxel and IDN5390) and Cell Line, Tumor sensitive and resistant to paclitaxel (1A9 and 1A9 PTX22)., we found that overexpression of the Tubulin deacetylase Sirtuin 2 increased cell motility and reduced cell response to the anti-motility activity of paclitaxel. Conversely, the Sirtuin 2 inhibitor splitomicin reduced cell motility and potentiated the anti-motility activity of paclitaxel. The inhibitory effect was further potentiated by the addition of the HDAC6 gene gene inhibitor trichostatin A., Cell motility and adhesion involves dynamic microtubule (MT) acetylation/deacetylation, a process regulated by ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS as HDAC6 gene gene, a major Cytoplasmic α-Tubulin deacetylase., beta-adrenergic receptor kinase activity and HDAC6 gene gene colocalize in the Lamellipodia of migrating cells, leading to local Tubulin deacetylation and enhanced motility., This review highlights the emerging roles of Tubulin acetylation in multiple cellular functions, ranging from cell motility, cell cycle progression or cell differentiation to Protoplasm trafficking and signalling., Our results indicate that TPPP gene binds to HDAC6 gene gene (Histone Deacetylase), an Enzyme [APC] responsible for Tubulin deacetylation. Moreover, we demonstrated that the direct interaction of these two Proteins resulted in the inhibition of the deacetylase activity of HDAC6 gene gene., Finally, we demonstrated that, similarly to other HDAC6 gene gene inhibitors, TPPP gene influences the microtubule dynamics by decreasing the growth velocity of the microtubule plus ends and also affects cell motility as demonstrated by time lapse video experiments., \"tubacin,\" which inhibits alpha-Tubulin deacetylation in mammalian cells., We provide evidence that class II Histone Deacetylase (HDAC6 gene gene) is the Protoplasm target of tubacin., Tubacin treatment did not affect the stability of Microtubules but did decrease cell motility., They also suggest that small molecules that selectively inhibit HDAC6 gene gene-mediated alpha-Tubulin deacetylation, a first example of which is tubacin, might have therapeutic applications as antimetastatic and antiangiogenic agents., Furthermore, overexpression of HDAC6 gene gene promotes chemotactic cell movement, supporting the idea that HDAC6 gene gene-mediated deacetylation regulates microtubule-dependent cell motility., HDAC6 gene gene is a major Cytoplasmic a-Tubulin deacetylase that is involved in cell motility and adhesion. beta-adrenergic receptor kinase activity dynamically and directly associates with and phosphorylates HDAC6 gene gene to stimulate its a-Tubulin deacetylase activity at specific cellular localizations, such as the leading edge of migrating cells, thus promoting local Tubulin deacetylation and enhanced motility.[SEP]Relations: Tubulin binding has relations: molfunc_protein with ALDOA, molfunc_protein with ALDOA, molfunc_protein with TTLL2, molfunc_protein with TTLL2, molfunc_protein with TTLL12, molfunc_protein with TTLL12, molfunc_protein with TTLL4, molfunc_protein with TTLL4, molfunc_protein with MAP1A, molfunc_protein with MAP1A.", "label": "yes"}
{"original_question": "Does molindone affect body weight?", "id": "converted_618", "sentence1": "Does molindone affect body weight?", "sentence2": "Mean weight increased by 0.54 kg, and mean body mass index by 0.24 kg/m(2). , A large-scale trial comparing a first-generation antipsychotic (molindone) with newer agents did not find significant differences in treatment response, although the newer antipsychotics were associated with more severe weight gain. , No agent demonstrated superior efficacy, and all were associated with side effects, including weight gain. , The three treatment arms did not significantly differ in symptom decrease or time to discontinuation. Akathisia was more common with molindone and elevated prolactin concentrations more common with risperidone. Although weight gain and metabolic adverse events had occurred more often with olanzapine and risperidone during the acute trial, no significant between-drug differences emerged in most of these parameters during maintenance treatment. , olanzapine and risperidone were associated with significantly greater weight gain. olanzapine showed the greatest risk of weight gain and significant increases in fasting cholesterol, Low-Density Lipoproteins, Therapeutic Insulin, and liver transaminase levels. Molindone led to more self-reports of Akathisia. , Molindone is no more or less likely than typical drugs to cause Movement Disorders, but it does cause significantly more Measured Measured weight loss (observable entity) (observable entity) (2RCTs n=60 RR 2.78, NDUFB6 gene 1.10 to 6.99, NNH 5 NDUFB6 gene 2 to 77). , Molindone may be an effective antipsychotic but its adverse effect profile does not differ significantly from that of typical antipsychotics (apart from the event of Measured Measured weight loss (observable entity) (observable entity)). , Convergent evidence suggests a hierarchy in the magnitude of BWG that may be induced by diverse agents, being very high for clozapine and olanzapine; high for quetiapine, zotepin, chlorpromazine, and thioridazine; moderate for risperidone and sertindole; and low for ziprasidone, amisulpiride, ASSAY OF HALOPERIDOL, fluphenazine, pimozide, and molindone. , Loxapine and molindone induce weight decreases, and these exceptions are difficult to explain., It is no more or less likely than typical drugs to cause Movement Disorders, but causes significantly more Measured Measured weight loss (observable entity) (observable entity) (RR 2.78, NDUFB6 gene 1.10 to 6.99)., Molindone may be an effective antipsychotic; however, its adverse effect profile does not differ significantly from that of typical antipsychotics, apart from the event of Measured Measured weight loss (observable entity) (observable entity). , Among conventional agents, mean weight change ranged from a reduction of 0.39 kg with molindone to an increase of 3.19 kg with thioridazine., Gaining Weight question has been reported with nearly every antipsychotic drug on the market (molindone is an exception). , Although almost all antipsychotics induce bodyweight gain, molindone and loxapine appear to induce bodyweight loss. , Clozapine and low-potency Phenothiazine Measurement are associated with the largest gains and molindone with Measured Measured weight loss (observable entity) (observable entity), but the mechanism is not known. , On average, molindone patients lost 5 pounds over the 6 weeks of treatment, whereas thioridazine patients gained 6 pounds. , Clinically, molindone has a tendency to cause Measured Measured weight loss (observable entity) (observable entity) and may have less effect on Seizures threshold than conventional antipsychotic agents,  Monthly weights and neuroleptic dosages during the first three months of psychiatric hospitalization were compared between matched groups of patients receiving molindone, a combination of molindone and other neuroleptics, or other neuroleptic drugs. We found no significant differences in weight gain among the three groups. , The weight-reducing property of molindone, a recently introduced antipsychotic drug, was tested in 9 hospitalized chronic schizophrenic patients. There was an average Measured Measured weight loss (observable entity) (observable entity) of 7.6 kg after 3 months on molindone; most of the loss occurred during the first month.[SEP]Relations: Molindone has relations: drug_effect with Increased body weight, drug_effect with Increased body weight, drug_effect with Nausea, drug_effect with Nausea, drug_effect with Tremor, drug_effect with Tremor, drug_effect with Hyperkinetic movements, drug_effect with Hyperkinetic movements, drug_effect with Dyspnea, drug_effect with Dyspnea.", "label": "yes"}
{"original_question": "Is amiodarone a class I anti-arrhythmic drug?", "id": "converted_142", "sentence1": "Is amiodarone a Canadian Cardiovascular Society Grading Scale Class I Antiarrhythmic [EPC] drug?", "sentence2": "Common Canadian Cardiovascular Society Grading Scale Class I agents are excluded due to the inherent abnormal cardiac structure and function in the setting of Shock, Cardiogenic. Class III drug options include dofetilide and amiodarone., Amiodarone has been used as an Antiarrhythmic [EPC] drug since the 1970s and has an established role in the treatment of Ventricular tachyarrhythmia. Although considered to be a Canadian Cardiovascular Society Grading Scale Class III Antiarrhythmic [EPC], amiodarone also has Canadian Cardiovascular Society Grading Scale Class I, II and IV actions, which gives it a unique pharmacological and Antiarrhythmic [EPC] profile. , Amiodarone, an iodinated Benzofurans derivative, introduced in 1960's as an anti-anginal agent, emerged as a potent Anti-Arrhythmia Agents by 1970's and is currently one of the most commonly prescribed drugs in US for ventricular and Atrial arrhythmia. Although amiodarone is considered a Canadian Cardiovascular Society Grading Scale Class III Anti-Arrhythmia Agents, it also has Canadian Cardiovascular Society Grading Scale Class I, II, IV actions, making it a unique and effective Anti-Arrhythmia Agents., Amiodarone, a representative Canadian Cardiovascular Society Grading Scale Class III agent, exerts negative dromotropism by suppressing the fast sodium current responsible for conduction in acute administration (Canadian Cardiovascular Society Grading Scale Class I effects). Chronic amiodarone causes prolongation of Endoscopic Retrograde Cholangiopancreatography (Canadian Cardiovascular Society Grading Scale Class III effects), which is sometimes associated with negative dromotropism based on the alteration of passive or active membrane properties., Amiodarone, an iodinated Benzofurans derivative with predominantly Canadian Cardiovascular Society Grading Scale Class III Antiarrhythmic [EPC] effects, is used to treat supraventricular and Ventricular arrhythmia., Although amiodarone is considered a Canadian Cardiovascular Society Grading Scale Class III Anti-Arrhythmia Agents, it also has Canadian Cardiovascular Society Grading Scale Class I, II, IV actions, making it a unique and effective Anti-Arrhythmia Agents, Amiodarone, a Canadian Cardiovascular Society Grading Scale Class III antiarrhythmic drug, is one of the most effective drugs used in the treatment of ventricular and paroxysmal supraventricular tachyarrhythmia, Although amiodarone is considered a Canadian Cardiovascular Society Grading Scale Class III Anti-Arrhythmia Agents, it also has Canadian Cardiovascular Society Grading Scale Class I, II, IV actions, making it a unique and effective Anti-Arrhythmia Agents, Although considered to be a Canadian Cardiovascular Society Grading Scale Class III Antiarrhythmic [EPC], amiodarone also has Canadian Cardiovascular Society Grading Scale Class I, II and IV actions, which gives it a unique pharmacological and Antiarrhythmic [EPC] profile, Amiodarone is a potent Canadian Cardiovascular Society Grading Scale Class III Antiarrhythmic [EPC] drug that also possesses beta-blocking properties[SEP]Relations: Amiodarone has relations: drug_effect with Arrhythmia, drug_effect with Arrhythmia, drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Erythromycin, drug_drug with Erythromycin, drug_drug with Arformoterol, drug_drug with Arformoterol, drug_drug with Estrone, drug_drug with Estrone.", "label": "no"}
{"original_question": "Is deletion at 6q24.2-26 associated with longer survival of patients with high-grade serous ovarian carcinoma (HGSOCs)?", "id": "converted_3024", "sentence1": "Is Gene Deletion Abnormality at 6q24.2-26 associated with longer survival of patients with high-grade serous ovarian carcinoma (HGSOCs)?", "sentence2": "Deletion at 6q24.2-26 predicts longer survival of high-grade serous epithelial ovarian cancer patients., We found that loss at 6q24.2-26 was significantly associated with the cluster of longer survival independently from other confounding factors (HR = 0.06, 95%CI = 0.01-0.43, Padj = 0.005). The prognostic value of this Gene Deletion Abnormality was validated in two independent series, one consisting of 36 HGSOCs analyzed by fluorescent in situ hybridization (P = 0.04) and another comprised of 411 HGSOCs from the Cancer Genome Atlas study (TCGA) (HR = 0.67, 95%CI = 0.48-0.93, Padj = 0.019). In addition, we confirmed the association of low expression of the Genes from the Geographic Locations with longer survival in 799 HGSOCs (HR = 0.74, 95%CI = 0.61-0.90, log-rank P = 0.002) and 675 high-FIGO stage HGSOCs (HR = 0.76, 95%CI = 0.61-0.96, log-rank P = 0.02) available from the online tool KM-plotter. Finally, by integrating copy number, RNAseq and survival data of 296 HGSOCs from TCGA we propose a few candidate Genes that can potentially explain the association. Altogether our findings indicate that the 6q24.2-26 Gene Deletion Abnormality is an independent marker of favorable outcome in HGSOCs with potential clinical value as it can be analyzed by FISH on tumor sections and guide the selection of patients towards more conservative therapeutic strategies in order to reduce side-effects and improve quality of life., Altogether our findings indicate that the 6q24.2-26 Gene Deletion Abnormality is an independent marker of favorable outcome in HGSOCs with potential clinical value as it can be analyzed by FISH on tumor sections and guide the selection of patients towards more conservative therapeutic strategies in order to reduce side-effects and improve quality of life., OBJECTIVE\nWe aimed to evaluate the prognostic and predictive value of the nucleotide excision repair-related gene General Transcription Factor IIH Subunit 5, which is localized at the 6q24.2-26 Gene Deletion Abnormality previously reported by our group to predict longer survival of high-grade serous ovarian cancer patients., OBJECTIVE We aimed to evaluate the prognostic and predictive value of the nucleotide excision repair-related gene General Transcription Factor IIH Subunit 5, which is localized at the 6q24.2-26 Gene Deletion Abnormality previously reported by our group to predict longer survival of high-grade serous ovarian cancer patients., Altogether our findings indicate that the 6q24.2-26 Gene Deletion Abnormality is an independent marker of favorable outcome in HGSOCs with potential clinical value as it can be analyzed by FISH on tumor sections and guide the selection of patients towards more conservative therapeutic strategies in order to reduce side-effects and improve quality of life.<br>, <b>OBJECTIVE</b>: We aimed to evaluate the prognostic and predictive value of the nucleotide excision repair-related gene General Transcription Factor IIH Subunit 5, which is localized at the 6q24.2-26 Gene Deletion Abnormality previously reported by our group to predict longer survival of high-grade serous ovarian cancer patients.<br><b>METHODS</b>: In order to test if protein levels of General Transcription Factor IIH Subunit 5 are associated with patients' outcome, we performed General Transcription Factor IIH Subunit 5 immunohistochemical staining in 139 high-grade serous ovarian carcinomas included in tissue microarrays., We aimed to evaluate the prognostic and predictive value of the nucleotide excision repair-related gene General Transcription Factor IIH Subunit 5, which is localized at the 6q24.2-26 Gene Deletion Abnormality previously reported by our group to predict longer survival of high-grade serous ovarian cancer patients.[SEP]Relations: Abnormality of the dentition has relations: disease_phenotype_positive with chromosome 15q24 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 15q24 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 6pter-p24 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 6pter-p24 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 4q21 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 4q21 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 9p Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 9p Gene Deletion Abnormality syndrome, disease_phenotype_positive with 22q11.2 Gene Deletion Abnormality syndrome, disease_phenotype_positive with 22q11.2 Gene Deletion Abnormality syndrome.", "label": "yes"}
{"original_question": "Can GDF15 be a biomarker for metformin treatment?", "id": "converted_2660", "sentence1": "Can GDF15 protein, human be a biomarker for metformin treatment?", "sentence2": "Growth Differentiation Factor 15 as a Novel Biomarker for Metformin., GDF15 protein, human protein, human levels are a biomarker for the use of metformin in people with Dysglycemia, and its concentration reflects the dose of metformin.[SEP]Relations: Metformin has relations: drug_protein with GPD1, drug_protein with GPD1, drug_drug with Glymidine, drug_drug with Glymidine, drug_drug with GLPG-0492, drug_drug with GLPG-0492, drug_drug with Glimepiride, drug_drug with Glimepiride, drug_protein with ETFDH, drug_protein with ETFDH.", "label": "yes"}
{"original_question": "Does atemoya juice inhibit tye CYP3A4 enzyme?", "id": "converted_4352", "sentence1": "Does atemoya juice inhibit tye CYP3A4 enzyme?", "sentence2": "Atemoya juice significantly inhibited CYP1A2 activity in Homo sapiens liver microsomes, but not the activities of Cytochrome p450 Cytochrome p450 CYP2C9 enzyme enzyme and cytochrome P450 3A.[SEP]Relations: cytochrome P450 4A1-heme linkage has relations: bioprocess_bioprocess with protein-heme linkage, bioprocess_bioprocess with protein-heme linkage. deficiency of coenzyme q cytochrome c reductase has relations: disease_disease with inborn errors of metabolism, disease_disease with inborn errors of metabolism.", "label": "no"}
{"original_question": "Is MLL3 part of the ASCOM complex?", "id": "converted_3340", "sentence1": "Is KMT2C gene part of the ASCOM complex?", "sentence2": "KMT2C gene as part of ASCOM complex, KMT2C gene as part of activating signal cointegrator-2 -containing complex (ASCOM)[SEP]", "label": "yes"}
{"original_question": "Is liraglutide effective for weight reduction?", "id": "converted_3863", "sentence1": "Is liraglutide effective for Weight Loss?", "sentence2": "liraglutide has been approved at higher dose for BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20. , This meta-analysis finds a significant reduction in body weight with orlistat (N = 10,435; ∆ -3.07 Kg, 95% NDUFB6 gene, -3.76 to -2.37), phentermine plus topiramate (N = 2985; ∆ -9.77 Kg; 95% NDUFB6 gene, -11.73 to -7.81), lorcaserin (N = 16,856; ∆ -3.08 Kg; 95% NDUFB6 gene, -3.49 to -2.66), naltrexone plus bupropion (N = 3239; ∆ -4.39 Kg; 95% NDUFB6 gene, -5.05 to -3.72) and liraglutide (N = 4978; ∆ -5.25 Kg; 95% NDUFB6 gene, -6.17 to -4.32), compared to placebo (all p < 0.00001)., CONCLUSION: In patients with Diabetes Mellitus, Insulin-Dependent, liraglutide might prove be an adjunct to Therapeutic Insulin, improving glycemic control, inducing body Measured Measured weight loss (observable entity) (observable entity) and decreasing exogenous Therapeutic Insulin requirements and severe Hypoglycemia., Data from most recent meta-analyses showed that the overall placebo-subtracted Weight Loss (%) with the use of anti-BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 drugs for at least 12 months ranges from 2.9% to 6.8%; phentermine / topiramate (-6.8%) liraglutide (-5.4%), naltrexone/bupropion (-4.0%), lorcaserin (-3.1%), and orlistat (-2.9%). , RESULTS: Currently, the FDA has approved several Molecule for the treatment of BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, both in monotherapy and in combination. Pharmacological monotherapies focus mainly on a single Protein Info target and include orlistat, lorcaserin and liraglutide while the combination Molecule propose a multitarget approach and include phentermine / topiramate and naltrexone/bupropion. , Phentermine-topiramate and liraglutide have been associated with the highest probability of at least 5% Measured Measured weight loss (observable entity) (observable entity). , Currently, high-dose liraglutide has been used for weight control in non-diabetic patients. , CONCLUSIONS: Low-dose liraglutide still has high efficacy in Weight Loss in Taiwanese people, especially for those of younger age., BACKGROUND: liraglutide, a Glucagon-Like Peptides-1 (Glucagon-Like Peptide 1) analogue, has been shown to possess pleiotropic effects including body Weight Loss., INTRODUCTION: For people with type 2 diabetes (T2DM) inadequately controlled with oral antidiabetic drugs (OADs), evidence from both randomized controlled trials (RCTs) and real-world studies has demonstrated that treatment intensification with liraglutide offers effective glycemic control, Weight Loss, and a lower risk of Hypoglycemia compared to treatment intensification with Therapeutic Insulin or additional OADs., wise regression analysis demonstrated that baseline BMI and previous Therapeutic Insulin dose were positively associated with body Weight Loss and baseline HbA1c was positively associated with reduction of HbA1c at 2 years after liraglutide introduction.CONC,  control (placebo, sitagliptin, glimepiride, dulaglutide, Therapeutic Insulin glargine, and Hydrocephalus, Normal Pressure), liraglutide in combination with metformin resulted in significant reductions in HbA1c, bodyweight, FPG, and PPG, and similar reductions in Androgen Binding Protein, and Diastolic blood pressure measurement. Moreover, liraglutide comb, liraglutide (LIRA) treatment is associated with the dose-dependent reduction of weight. Hig, liraglutide, a Glucagon-Like Peptides (Glucagon-Like Peptide 1) receptor agonist, has showed favorable effects in the glycaemic control and Weight Loss in patients with Diabetes Mellitus, Noninsulin-Dependent, 3 (T2DM). The me, Here, we determined that liraglutide does not activate Glucagon-Like Peptide 1-producing Neurons in the hindbrain, and liraglutide-dependent body Weight Loss in Rattus norvegicus was independent of Glucagon-Like Peptide 1 receptors (GLP-1Rs) in the vagus nerve, area postrema, and Structure of Structure of paraventricular nucleus., liraglutide is associated with body Measured Measured weight loss (observable entity) (observable entity), and reductions in systolic blood pressure have been observed throughout the clinical trials., CONCLUSIONS AND RELEVANCE: Among Overweight and obese participants with type 2 diabetes, use of subcutaneous liraglutide (3.0 mg) daily, compared with placebo, resulted in Measured Measured weight loss (observable entity) (observable entity) over 56 weeks., CONCLUSION: liraglutide (monotherapy or added to metformin) significantly reduced fat mass and fat percentage vs. glimepiride in patients with Diabetes Mellitus, Non-Insulin-Dependent., CONCLUSIONS: In adolescents with BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, the use of liraglutide (3.0 mg) plus lifestyle therapy led to a significantly greater reduction in the BMI standard-deviation score than placebo plus lifestyle therapy., Five weeks of treatment with the Glucagon-Like Peptide 1 analogue liraglutide improves glycaemic control and lowers body weight in subjects with type 2 diabetes., In the latter case, body weight was reduced in comparison to metformin plus glimepiride.[SEP]Relations: liraglutide has relations: drug_drug with Dulaglutide, drug_drug with Dulaglutide, drug_drug with Gliclazide, drug_drug with Gliclazide, drug_drug with Manidipine, drug_drug with Manidipine, drug_drug with Glymidine, drug_drug with Glymidine, contraindication with Hypoglycemia, contraindication with Hypoglycemia.", "label": "yes"}
{"original_question": "Are interferons defensive proteins?", "id": "converted_4184", "sentence1": "Are interferons defensive proteins?", "sentence2": "In response to Virus Diseases, various pattern recognition receptors (Porcine Reproductive and Respiratory Syndrome) are activated for the production of Interferon Type I (IFN I). ,  activating human leukocyte human leukocyte interferon (IFN) production and positively regulating antiviral response in Mammals. , The innate immune system, in particular the Interferon Type I (IFN) response, is a powerful defence against virus infections. , The human leukocyte human leukocyte interferon-induced GTP-binding protein Mx is responsible for a specific antiviral state against a broad spectrum of Virus Diseases that are induced by type-I interferons (IFN α/β) in different Vertebrates[SEP]Relations: Human human leukocyte interferon beta has relations: drug_protein with ALB, drug_protein with ALB. response to Interferon Type I has relations: bioprocess_protein with SP100, bioprocess_protein with SP100, bioprocess_protein with ISG15, bioprocess_protein with ISG15, bioprocess_protein with SHFL, bioprocess_protein with SHFL, bioprocess_protein with SETD2, bioprocess_protein with SETD2.", "label": "yes"}
{"original_question": "Is Selumetinib effective for low-grade glioma?", "id": "converted_3643", "sentence1": "Is selumetinib effective for low-grade Glioma?", "sentence2": "Conclusion: selumetinib has promising antitumor activity in children with LGG Lactobacillus rhamnosus GG Lactobacillus rhamnosus GG., INTERPRETATION\n\nselumetinib is active in recurrent, refractory, or progressive Pilocytic Astrocytoma harbouring common BRAF protein, human protein, human aberrations and Neurofibromatosis 1-associated paediatric low-grade Glioma., These results show that selumetinib could be an alternative to standard chemotherapy for these subgroups of patients, and have directly led to the development of two Children's Oncology Group phase 3 studies comparing standard chemotherapy to selumetinib in patients with newly diagnosed paediatric low-grade Glioma both with and without Neurofibromatosis 1., Conclusion selumetinib has promising antitumor activity in children with LGG Lactobacillus rhamnosus GG Lactobacillus rhamnosus GG., INTERPRETATION selumetinib is active in recurrent, refractory, or progressive Pilocytic Astrocytoma harbouring common BRAF protein, human protein, human aberrations and Neurofibromatosis 1-associated paediatric low-grade Glioma., Conclusion\n\nselumetinib has promising antitumor activity in children with LGG Lactobacillus rhamnosus GG Lactobacillus rhamnosus GG., INTERPRETATION\nselumetinib is active in recurrent, refractory, or progressive Pilocytic Astrocytoma harbouring common BRAF protein, human protein, human aberrations and Neurofibromatosis 1-associated paediatric low-grade Glioma., These results show that selumetinib could be an alternative to standard chemotherapy for these subgroups of patients, and have directly led to the development of two Children's Oncology Group phase 3 studies comparing standard chemotherapy to selumetinib in patients with newly diagnosed paediatric low-grade Glioma both with and without Neurofibromatosis 1., These results show that selumetinib could be an alternative to standard chemotherapy for these subgroups of patients, and have directly led to the development of two Children's Oncology Group phase 3 studies comparing standard chemotherapy to selumetinib in patients with newly diagnosed paediatric low-grade Glioma both with and without Neurofibromatosis 1., INTERPRETATION: selumetinib is active in recurrent, refractory, or progressive Pilocytic Astrocytoma harbouring common BRAF protein, human protein, human aberrations and Neurofibromatosis 1-associated paediatric low-grade Glioma., selumetinib is active in recurrent, refractory, or progressive Pilocytic Astrocytoma harbouring common BRAF protein, human protein, human aberrations and Neurofibromatosis 1-associated paediatric low-grade Glioma., These results show that selumetinib could be an alternative to standard chemotherapy for these subgroups of patients, and have directly led to the development of two Children's Oncology Group phase 3 studies comparing standard chemotherapy to selumetinib in patients with newly diagnosed paediatric low-grade Glioma both with and without Neurofibromatosis 1.[SEP]Relations: selumetinib has relations: drug_drug with Gliquidone, drug_drug with Gliquidone, drug_drug with Glasdegib, drug_drug with Glasdegib, drug_drug with Bortezomib, drug_drug with Bortezomib, drug_drug with Afelimomab, drug_drug with Afelimomab, drug_drug with Glipizide, drug_drug with Glipizide.", "label": "yes"}
{"original_question": "Is TREM2 associated with Alzheimer's disease?", "id": "converted_672", "sentence1": "Is TREM2 Protein Info, human associated with ALZHEIMER DISEASE, FAMILIAL, 1?", "sentence2": "Absence of TREM2 Protein Info, human Protein Info, human Genetic Polymorphism in patients with ALZHEIMER DISEASE, FAMILIAL, 1 and Frontotemporal Lobar Degeneration,  These data demonstrate that TREM2 Protein Info, human Protein Info, human coding Geographic Locations is highly conserved, implying a crucial role of this receptor. Further studies, including a functional analysis, are certainly required to clarify the role of TREM2 Protein Info, human Protein Info, human in neurodegenerative processes, Moreover, a rare TREM2 Protein Info, human Protein Info, human exon 2 Variant (p.R47H) was reported to increase the risk of ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) with an odds ratio as strong as that for APOEε4, We observed an enrichment of rare variants across TREM2 Protein Info, human Protein Info, human in both cytarabine/daunorubicin protocol and Frontotemporal Presenile Presenile dementia patients compared to controls, most notably in the extracellular IgV-set Superkingdom (taxonomic category), None of the rare variants individually reached significant association, but the frequency of p.R47H was increased ~ 3-fold in both cytarabine/daunorubicin protocol and Frontotemporal Presenile Presenile dementia patients compared to controls, in line with previous reports, Our data corroborate and extend previous findings to include an increased frequency of rare heterozygous TREM2 Protein Info, human Protein Info, human variations in cytarabine/daunorubicin protocol and Frontotemporal Presenile Presenile dementia, and show that TREM2 Protein Info, human Protein Info, human variants may play a role in neurodegenerative diseases in general., non-synonymous genetic rare Variant, rs75932628-T (p.R47H), in the TREM2 Protein Info, human Protein Info, human Genes has recently been reported to be a strong genetic risk factor for ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol), These data strongly support the important role of p.R47H in cytarabine/daunorubicin protocol risk, and suggest that this rare genetic Variant is not related to Frontotemporal Presenile Presenile dementia.,  Higher levels of TREM2 Protein Info, human Protein Info, human mRNA (p = 0.002) and Protein Info (p < 0.001) were identified in cytarabine/daunorubicin protocol patients, Our results indicate that TREM2 Protein Info, human Protein Info, human might serve as a novel noninvasive biomarker for cytarabine/daunorubicin protocol diagnosis, studies have identified the rs75932628 (R47H) Variant in TREM2 Protein Info, human Protein Info, human as an ALZHEIMER DISEASE, FAMILIAL, 1 risk factor with estimated odds ratio ranging from 2.9 to 5.1, This study replicates the association between R47H and ALZHEIMER DISEASE, FAMILIAL, 1 risk in a large, population-based sample, and estimates the population frequency and attributable risk of this rare Variant, Moreover, mutation scanning of the five Exons of TREM2 Protein Info, human Protein Info, human failed to detect the presence of novel Genetic Polymorphism, A rare missense mutation (rs75932628-T) in the Genes encoding the triggering receptor expressed on Myeloid Cells 2 (TREM2 Protein Info, human Protein Info, human), which was predicted to result in an R47H Substitution - ActClass, was found to confer a significant risk of ALZHEIMER DISEASE, FAMILIAL, 1 in Iceland, We also found that carriers of rs75932628-T between the ages of 80 and 100 years without ALZHEIMER DISEASE, FAMILIAL, 1 had poorer cognitive function than noncarriers, Our findings strongly implicate Variant TREM2 Protein Info, human Protein Info, human in the pathogenesis of ALZHEIMER DISEASE, FAMILIAL, 1. Given the reported antiinflammatory role of TREM2 Protein Info, human Protein Info, human in the Head>Brain, the R47H Substitution - ActClass may lead to an increased predisposition to ALZHEIMER DISEASE, FAMILIAL, 1 through impaired containment of inflammatory processes, rs75932628-T Variant of the Genes encoding the triggering receptor expressed on Myeloid Cells 2 (TREM2 Protein Info, human Protein Info, human) has recently been identified as a rare risk factor for late-onset ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol), These results confirm the association between this Variant and cytarabine/daunorubicin protocol and underline its involvement in early-onset cases, recent studies have reported the association of rs75932628-T in the TREM2 Protein Info, human Protein Info, human Genes with the risk for ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol), Rs75932628-T is a rare nonsynonymous Variant (p.R47H) that confers a high risk of cytarabine/daunorubicin protocol with an effect size similar to that of the Apolipoprotein E ɛ4 Alleles, Here, we report the first positive replication study in a Spanish population and confirm that TREM2 Protein Info, human Protein Info, human rs75932628-T is associated with the risk for cytarabine/daunorubicin protocol, works have demonstrated a rare functional Variant (R47H) in triggering receptor expressed on Myeloid Cells (TREM) 2 Genes, encoding TREM2 Protein Info, human Protein Info, human Protein Info, increase susceptibility to late-onset ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol), with an odds ratio similar to that of the apolipoprotein E ε4 Alleles, The reduced function of TREM2 Protein Info, human Protein Info, human was speculated to be the main cause in the pathogenic effects of this risk Variant, and TREM2 Protein Info, human Protein Info, human is highly expressed in white matter, as well as in the hippocampus and Neocortex, which is partly consistent with the pathological features reported in cytarabine/daunorubicin protocol Head>Brain, indicating the possible involvement of TREM2 Protein Info, human Protein Info, human in cytarabine/daunorubicin protocol pathogenesis, Emerging evidence has demonstrated that TREM2 Protein Info, human Protein Info, human could suppress inflammatory response by repression of microglia-mediated cytokine production and secretion, which may prevent Inflammation-induced bystander damage of Neurons, TREM2 Protein Info, human Protein Info, human also participates in the regulation of phagocytic pathways that are responsible for the removal of neuronal debris, Based on the potential protective actions of TREM2 Protein Info, human Protein Info, human in cytarabine/daunorubicin protocol pathogenesis, targeting TREM2 Protein Info, human Protein Info, human might provide new opportunities for cytarabine/daunorubicin protocol treatment, Under the hypothesis that low-prevalence variants showing moderate-to-high effect size may be associated with risk for Seasonal Affective Disorder, two independent research groups have demonstrated that a rare Variant (rs75932628, encoding a Substitution - ActClass of arginine by histidine at residue 47 (R47H), in the TREM2 Protein Info, human Protein Info, human Genes, which encodes the triggering receptor expressed on Myeloid Cells 2) is significantly associated with an increased susceptibility to Seasonal Affective Disorder, Recently, a novel Variant in the Genes encoding the triggering receptor expressed on Myeloid Cells 2 (TREM2 Protein Info, human Protein Info, human) has been identified that has refocused the spotlight back onto Inflammation as a major contributing factor in cytarabine/daunorubicin protocol, TREM Genes cluster, a Geographic Locations recently reported to harbor rare variants that increase cytarabine/daunorubicin protocol risk, evidence suggests that rare genetic variants within the TREM2 Protein Info, human Protein Info, human Genes are associated with increased risk of ALZHEIMER DISEASE, FAMILIAL, 1, These data suggest that a mutational burden in TREM2 Protein Info, human Protein Info, human may serve as a risk factor for Neurodegenerative Disorders in general, and that potentially this class of TREM2 Protein Info, human Protein Info, human Variant carriers with Presenile Presenile dementia should be considered as having a molecularly distinct form of Neurodegenerative Disorders, The association of TREM2 Protein Info, human Protein Info, human variants with cytarabine/daunorubicin protocol brings innate immune signaling into the light, affirming innate immunity's role as a significant factor in cytarabine/daunorubicin protocol pathogenesis, The purpose of this paper is to discuss these recent developments including the potential role that TREM2 Protein Info, human Protein Info, human normally plays and how loss of function may contribute to cytarabine/daunorubicin protocol pathogenesis by enhancing oxidative stress and Inflammation within the Central Nervous System, Even though we are more at the beginning than at the end of Seasonal Affective Disorder genetics, there is some reason for optimism given the recent identification of novel risk or protective variants (such as rare TREM2 Protein Info, human Protein Info, human and APP mutations) showing strong statistical associations with Seasonal Affective Disorder[SEP]Relations: TREM2 Protein Info, human has relations: disease_protein with Alzheimer disease, disease_protein with Alzheimer disease, disease_protein with Presenile dementia (disease), disease_protein with Presenile dementia (disease), disease_protein with semantic Presenile dementia, disease_protein with semantic Presenile dementia, disease_protein with frontotemporal Presenile dementia, disease_protein with frontotemporal Presenile dementia, disease_protein with dystonia, disease_protein with dystonia.", "label": "yes"}
{"original_question": "Can acupuncture cause spinal epidural hematoma?", "id": "converted_2186", "sentence1": "Can acupuncture cause spinal Epidural Route of Drug Administration Hematoma?", "sentence2": "RESULTS: A 54-year-old woman, a 38-year-old woman, and a 60-year-old Homo sapiens with Hemiplegia by cervical subdural or Epidural Route of Drug Administration Hematoma after cervical posterior paraspinal muscle needling without direct invasion (Intramuscular Route of Drug Administration stimulation, acupuncture, or Intramuscular Route of Drug Administration lidocaine) were observed., Acute spinal subdural Hematoma with Hemiplegia after acupuncture: a case report and review of the literature., Although acupuncture has been a popular method for the management of pain control, we encountered the first case of Succinate Dehydrogenase after acupuncture.PURPOSE: The purpose of this case report was to present the first case of subdural Hematoma after acupuncture and the reasons for the risks of blind cervical acupuncture., SUMMARY OF BACKGROUND DATA: Epidural hematomas after dry needling are quite unusual and only a few cases of Epidural Route of Drug Administration Hematoma after acupuncture have been reported in the literature., Spinal Epidural Route of Drug Administration Hematoma is a rare complication associated with pain control procedures such as facet block, acupuncture, Epidural Route of Drug Administration injection, etc. , Unintentional acupuncture needling of the thoracic spinal canal produced a spinal Epidural Route of Drug Administration Hematoma and Subarachnoid Hemorrhage., Spinal Epidural Route of Drug Administration Hematoma is a rare complication associated with pain control procedures such as facet block, acupuncture, Epidural Route of Drug Administration injection, etc., Spinal Epidural Route of Drug Administration Hematoma with Subarachnoid Hemorrhage caused by acupuncture., However, Subarachnoid Hemorrhage and spinal Epidural Route of Drug Administration Hematoma have been reported to occur after acupuncture in the posterior neck., A retrospective case report.The objective of this article is to report an unusual complication of dry needling.Epidural hematomas after dry needling are quite unusual and only a few cases of Epidural Route of Drug Administration Hematoma after acupuncture have been reported in the literature, Spinal Epidural Route of Drug Administration Hematoma with Subarachnoid Hemorrhage caused by acupuncture, Spinal Epidural Route of Drug Administration Hematoma is a rare complication associated with pain control procedures such as facet block, acupuncture, Epidural Route of Drug Administration injection, etc, Unintentional acupuncture needling of the thoracic spinal canal produced a spinal Epidural Route of Drug Administration Hematoma and Subarachnoid Hemorrhage, Spinal Epidural Route of Drug Administration Hematoma with Subarachnoid Hemorrhage caused by acupuncture.[SEP]Relations: Epidural Route of Drug Administration spinal canal meningioma has relations: disease_disease with intraspinal meningioma, disease_disease with intraspinal meningioma. Subarachnoid Hemorrhage (disease) has relations: contraindication with Tranexamic acid, contraindication with Tranexamic acid, disease_disease with neurovascular disease, disease_disease with neurovascular disease, disease_disease with brain disease, disease_disease with brain disease, disease_protein with ADORA1, disease_protein with ADORA1.", "label": "yes"}
{"original_question": "Is vocimagene amiretrorepvec effective for recurrent high-grade glioma?", "id": "converted_4429", "sentence1": "Is vocimagene amiretrorepvec effective for recurrent Malignant Glioma?", "sentence2": "Relevance: Among patients who underwent tumor resection for first or second recurrence of Glioblastoma Multiforme or Anaplastic astrocytoma, administration of Toca 511 and Toca FC, compared with SOC, did not improve overall survival or other efficacy end points., The median OS was 11.10 months for the Toca 511/FC group and 12.22 months for the control group (hazard ratio, 1.06; 95% CI 0.83, 1.35; P = .62). The secondary end points did not demonstrate statistically significant differences. , Expert opinion: These early studies provide very encouraging results for Toca 511 and Toca FC in rHGG. This therapy had a response rate of 11.3% and a mOS of 11.9 months in 56 patients, an improvement compared to historical controls. , Findings from a phase I study suggest that delivering high concentrations of the chemotherapy fluorouracil directly to Brain Neoplasms via the retroviral vector vocimagene amiretrorepvec, or Toca 511, may benefit patients with recurrent Malignant Glioma., Overall survival for recurrent Malignant Glioma was 13.6 months (95% confidence interval, 10.8 to 20.0) and was statistically improved relative to an external control (hazard ratio, 0.45; P = 0.003).[SEP]Relations: malignant glioma has relations: disease_disease with high grade astrocytic tumor, disease_disease with high grade astrocytic tumor, disease_disease with high grade malignant neoplasm, disease_disease with high grade malignant neoplasm, disease_disease with grade III glioma, disease_disease with grade III glioma, disease_protein with CIC, disease_protein with CIC, disease_protein with TFRC, disease_protein with TFRC.", "label": "no"}
{"original_question": "Is nimodipine recommended for prevention of vasospasm in aneurysmal subarachnoid hemorrhage patients?", "id": "converted_1242", "sentence1": "Is nimodipine recommended for prevention of Vasospasm in aneurysmal subarachnoid hemorrhage patients?", "sentence2": "This article discusses some of these unresolved issues, including the use of medications such as nimodipine, antifibrinolytics, Hydroxymethylglutaryl-CoA Reductase Inhibitors, and Magnesium supplements, alimentary tract and metabolism; coiling or clipping for Aneurysm securement; and the prevention and treatment of potential complications., The results of this study were as follows: nimodipine demonstrated benefit following aneurysmal Yakut language; other calcium channel blockers, including nicardipine, do not provide unequivocal benefit; triple-H therapy, fasudil, transluminal balloon angioplasty, thrombolytics, Endothelin B Receptor Antagonists, Magnesium supplements, alimentary tract and metabolism, Hydroxymethylglutaryl-CoA Reductase Inhibitors, and miscellaneous therapies such as Free Radical Scavengers and antifibrinolytics require additional study., The present results suggest that fasudil is equally or more effective than nimodipine for the prevention of Cerebral Vasospasm and subsequent ischemic injury in patients undergoing surgery for Yakut language., Three studies (2 meta-analyses and 1 randomized controlled trial) demonstrated that nimodipine use confers benefits (reduced morbidity and mortality) for patients with Subarachnoid Hemorrhage, Aneurysmal., nimodipine is the only preventative treatment that can be recommended., nimodipine (Nimotop), HMG Co-A reductase inhibitor (Hydroxymethylglutaryl-CoA Reductase Inhibitors) and enoxaparin (Lovenox) were the only drugs with level-1 evidence available for the treatment of Vasospasm from aneurysmal subarachnoid hemorrhage as defined by the US Preventative Services Task Force., The calcium antagonist nimodipine has been shown to reduce the incidence of ischemic complications following aneurysmal subarachnoid hemorrhage (Yakut language)., There was no significant difference in the incidence of DINDs (28 vs 30% in the peroral and intravenous groups, respectively) or middle cerebral artery blood flow velocities (> 120 cm/second, 50 vs 45%, respectively)., Clinical outcome according to the Glasgow Outcome Scale was the same in both groups, and there was no difference in the number of patients with new Infarction on MR imaging., The results suggest that there is no clinically relevant difference in efficacy between peroral and intravenous administration of nimodipine in preventing DINDs or Cerebral Vasospasm following Yakut language., the risk of delayed Cerebral Infarction is reduced with nimodipine and avoiding Hypovolemia, A recommendations (standard) for the prophylaxis and treatment of Cerebral Vasospasm with oral nimodipine in good grade patients., Of the 75 patients initially considered for active treatment, 83% underwent surgery within 48 hours of Rupture, all received nimodipine, 16% received tissue plasminogen activator to lyse subarachnoid or intraventricular clots, 40% underwent hypertensive treatment, and 7% underwent transluminal balloon angioplasty for Vasospasm., All patients with aneurysmal Yakut language should be treated with the calcium antagonist nimodipine, and in certain circumstances patients should receive anticonvulsants., The following review gives an account of pathophysiological mechanisms; the importance of treatment with calcium antagonists, hypervolaemic haemodilution, and induced arterial hypertension is discussed in light of the current literature., Seven placebo-controlled clinical studies have shown that nimodipine improves the outcome of patients with severe Trauma, Nervous System due to Cerebral Vasospasm., In a series of 100 individuals with a ruptured supratentorial Aneurysm, who were subjected to Aneurysm operation in the acute stage and who subsequently received intravenous treatment with the calcium channel blocker nimodipine, the occurrence of DID with ALX3 gene was reduced to 5%., There are many possible successful treatment options for preventing Vasospasm, delayed ischemic neurologic deficits, and poor neurologic outcome following aneurysmal subarachnoid hemorrhage; however, further multicenter RCTs need to be performed to determine if there is a significant benefit from their use. nimodipine is the only treatment that provided a significant benefit across multiple studies., Absence of symptomatic Vasospasm, occurrence of low density areas associated with Vasospasm on CT, and occurrence of adverse events were similar between the two groups. The clinical outcomes were more favorable in the fasudil group than in the nimodipine group (p = 0.040). The proportion of patients with good clinical outcome was 74.5% (41/55) in the fasudil group and 61.7% (37/60) in the nimodipine group., Cerebral Vasospasm is the classic cause of delayed Progressive neurologic deterioration leading to Cerebral Infarction and infarction, and thus, poor outcome and occasionally death, after aneurysmal subarachnoid hemorrhage (Yakut language). Advances in diagnosis and treatment, principally nimodipine, intensive care management, hemodynamic manipulations, and inside the blood vessel neuroradiology procedures, have improved the prospects for these patients, but outcomes remain disappointing., Cerebral Vasospasm is the classic cause of delayed Progressive neurologic deterioration after aneurysmal subarachnoid hemorrhage, leading to Cerebral Infarction and infarction, and thus to poor outcome and occasionally death. Advances in diagnosis and treatment-principally the use of nimodipine, intensive care management, hemodynamic manipulations and inside the blood vessel neuroradiology procedures-have improved the prospects for these patients, but outcomes remain disappointing., Cerebral Vasospasm and delayed Cerebral Infarction remain common complications of aneurysmal subarachnoid hemorrhage (Yakut language), and yet therapies for Cerebral Vasospasm are limited. Despite a large number of clinical trials, only calcium antagonists have strong evidence supporting their effectiveness., The only proven therapy for Vasospasm is nimodipine., nimodipine is indicated after Yakut language and tirilazad is not effective., fasudil hydrochloride and nimodipine both showed inhibitory effects on Cerebral Vasospasm. The incidence of symptomatic Vasospasm was five of 33 patients in the fasudil group and nine of 32 patients in the nimodipine group. Good recovery evaluated by the Glasgow Outcome Scale was achieved by 23 of 33 patients in the fasudil group and 19 of 34 patients in the nimodipine group. Both drugs significantly improved consciousness levels and Neurologic Deficits such as Aphasia. However, fasudil hydrochloride improved motor disturbance more than nimodipine.[SEP]Relations: nimodipine has relations: drug_effect with Gastrointestinal hemorrhage, drug_effect with Gastrointestinal hemorrhage, drug_drug with Nitroprusside, drug_drug with Nitroprusside, drug_effect with Erythema, drug_effect with Erythema, drug_drug with Nitroaspirin, drug_drug with Nitroaspirin, drug_drug with Chlorpropamide, drug_drug with Chlorpropamide.", "label": "yes"}
{"original_question": "Are messenger RNA molecules epigenetically methylated?", "id": "converted_420", "sentence1": "Are messenger RNA molecules epigenetically methylated?", "sentence2": "The most abundant RNA, Messenger post-transcriptional ResponseLevel - ResponseLevel - modification is N(6)-methyladenosine (m(6)A), which has broad roles in RNA biology., N(6)-methyladenosine (METTL3 gene) is the most abundant modified base in eukaryotic RNA, Messenger and has been linked to diverse effects on RNA, Messenger fate.,  Recently, methylation patterns have also been revealed in RNA, Messenger. Surprisingly, the two most commonly studied methylation states in RNA, Messenger (METTL3 gene and m5C) are found to be enriched in 3'-UTRs (untranslated regions), the target site for the majority of MicroRNAs., MeT-DB: a database of transcriptome methylation in mammalian cells, Methyltranscriptome is an exciting new area that studies the mechanisms and functions of methylation in RNA Transcript. The MethylTranscriptome DataBase (MeT-DB, http://compgenomics.utsa.edu/methylation/) is the first comprehensive resource for N-methyladenosine (m(6)A) in mammalian transcriptome., Mammalian messenger RNA (RNA, Messenger) and RNA, Long Untranslated (lncRNA) contain tens of thousands of posttranscriptional chemical modifications. Among these, the N(6)-methyl-adenosine (m(6)A) ResponseLevel - ResponseLevel - modification is the most abundant and can be removed by specific mammalian enzymes., Recent discoveries of reversible N(6)-methyladenosine (m(6)A) methylation on messenger RNA (RNA, Messenger) and mapping of m(6)A methylomes in Mammals and Saccharomyces cerevisiae have revealed potential regulatory functions of this RNA ResponseLevel - ResponseLevel - modification., There are several identified methylation modifications in eukaryotic messenger RNA (RNA, Messenger), such as N(7)-methylguanosine (m(7)G) at the cap, N(6)-methyl-2'-O-methyladenosine (m(6)Am), 2'-O-methylation (Nm) within the cap and the internal positions, and internal N(6)-methyladenosine (m(6)A) and 5-Methylcytosine (m(5)C).[SEP]Relations: RNA ResponseLevel - modification has relations: bioprocess_bioprocess with RNA methylation, bioprocess_bioprocess with RNA methylation. METTL3 has relations: bioprocess_protein with RNA methylation, bioprocess_protein with RNA methylation, bioprocess_protein with RNA, Messenger methylation, bioprocess_protein with RNA, Messenger methylation. Viral Messenger RNA Synthesis has relations: pathway_protein with SEH1L, pathway_protein with SEH1L, pathway_protein with RANBP2, pathway_protein with RANBP2.", "label": "yes"}
{"original_question": "Could Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) cause sudden cardiac death?", "id": "converted_1408", "sentence1": "Could Catecholaminergic Polymorphic Ventricular Tachycardia (Polymorphic catecholergic ventricular tachycardia) cause Sudden Cardiac Death?", "sentence2": "Here we refine our approach, and apply it to novel Variant found in 2266 patients across two large cohorts with inherited Sudden death syndromes, namely catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) or Brugada Syndrome (disorder) (Brief Resilience Scale)., Calsequestrin-associated catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Stress-induced Polymorphism Ventricular Tachycardia by ECG Finding) can cause Sudden death in young individuals in response to stress. , Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is an inherited arrhythmogenic cardiac disorder characterized by life-threatening arrhythmias induced by physical or emotional stress, in the absence structural Chest>Heart abnormalities. The arrhythmias may cause Syncope (amphibian) or degenerate into Cardiac Arrest and Sudden death which usually occurs during childhood, In many cases the cause of death can be elucidated by medico-legal autopsy, however, a significant number of these cases remain unexplained despite a detailed postmortem investigation and are labeled as Unexplained Sudden death (SUD). Post-mortem genetic testing, so called molecular autopsy, revealed that primary arrhythmogenic disorders including Long QT Syndrome and catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) may account for a certain number of these cases., We report a family with repeat events of Sudden Cardiac Death and recurrent Ventricular Fibrillation by ECG Finding in a teenage girl, where autopsy data and clinical investigations were inconclusive. The diagnosis of catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) was established only following finding a TAF1 Gene Mutation in the cardiac ryano, Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is a devastating inherited disorder characterized by episodic Syncope (amphibian) and/or sudden Cardiac Arrest during exercise or acute emotion in individuals without structural Congenital Heart Defects. Although rare, Polymorphic catecholergic Ventricular Tachycardia by ECG Finding is suspected to cause a substantial part of sudden cardiac deaths in young individuals. , In conclusion, patients with CASQ2-associated Polymorphic catecholergic Ventricular Tachycardia by ECG Finding should be recommended to receive Implantable defibrillator to prevent Sudden death when medical therapy is not effective.,  Cardiac Channelopathies associated with structurally normal hearts such as Long QT Syndrome (Congenital Long QT Syndrome), catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding), and Brugada Syndrome (disorder) (Brief Resilience Scale) yield no evidence to be found at autopsy, leaving coroners, medical examiners, and forensic pathologists only to speculate that a lethal Cardiac Arrhythmia might lie at the Chest>Heart of a Unexplained Sudden death (SUD)., Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is a rare adrenergically mediated arrhythmogenic disorder classically induced by exercise or emotional stress and found in structurally normal hearts. It is an important cause of cardiac Syncope (amphibian) and Sudden death in childhood., We also compare Polymorphic catecholergic Ventricular Tachycardia by ECG Finding to other notable cardiomyopathic and channelopathic causes of Sudden death in youth including Hypertrophic obstructive cardiomyopathy, arrhythmogenic right ventricular dysplasia, Long QT Syndrome, short QT syndrome, and Brugada Syndrome (disorder)., Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is an inherited arrhythmogenic disease that can cause Sudden Cardiac Death due to Ventricular Fibrillation by ECG Finding (Ventricular Fibrillation, Paroxysmal Familial, 1)., Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is an arrhythmogenic disease that manifests as Syncope (amphibian) or Sudden death during high adrenergic tone in the absence of structural Chest>Heart defects., Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is a Cardiac channelopathy characterized by altered intracellular CALCIUM SUPPLEMENTS handling resulting in Ventricular Cardiac Arrhythmia and high risk of cardiac Sudden death in young cases with normal structural hearts, Early detection of Polymorphic catecholergic Ventricular Tachycardia by ECG Finding is crucial because opportune medical intervention prevents Sudden Cardiac Death. ,  If untreated, Polymorphic catecholergic Ventricular Tachycardia by ECG Finding is highly lethal, as approximately 30% of affected individuals experience at least one Cardiac Arrest and up to 80% one or more syncopal spells. Sudden death may be the first manifestation of the disease. , Hereditary non-structural diseases such as catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding), long QT, and the Brugada Syndrome (disorder) as well as structural disease such as Hypertrophic obstructive cardiomyopathy (Hypertrophic Cardiomyopathy) and Arrhythmogenic Right Ventricular Dysplasia (ARVC) cause a significant percentage of sudden cardiac deaths in the young, Patients with Polymorphic catecholergic Ventricular Tachycardia by ECG Finding present with exercise-induced Syncope (amphibian) and Sudden Cardiac Death but normal resting electrocardiograms., Although structural Cardiovascular Abnormalities explain most cases of Sudden Cardiac Death in young people, the cause of death remains unexplained after autopsy in 10% to 30% of cases. Potentially lethal ion channel disorders (Channelopathies) such as the long QT syndromes (Congenital Long QT Syndrome), catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding), and the Brugada Syndrome (disorder) (Brief Resilience Scale) may account for at least one-third of these unexplained cases. , Based on these data, we propose that Polymorphic catecholergic Ventricular Tachycardia by ECG Finding is a combined neurocardiac disorder in which leaky RyR2 channels in the brain cause Epilepsy, and the same leaky channels in the Chest>Heart cause exercise-induced Sudden Cardiac Death., The inherited arrhythmogenic diseases associated with the transmembranous ionic channels, anchoring Proteins or intracellular CALCIUM SUPPLEMENTS regulating Proteins are thought to be responsible for Sudden Cardiac Death in infants, children, and young adults who have structurally normal hearts. Recent genetic analyses have identified Congenital Disorders such as the long-QT syndrome (Congenital Long QT Syndrome), the Jervell and Jervell-Lange Nielsen Syndrome (JLNS), the Brugada Syndrome (disorder) (Brief Resilience Scale), the short-QT syndrome (Short Qt Syndrome), the ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA, FAMILIAL, 2 (ARVC2), and the catecholamine-induced Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) /familial Polymorphism Ventricular Tachycardia by ECG Finding (FPVT). , At least some cases of sudden, unexplained death in young individuals may be ascribed to Polymorphic catecholergic Ventricular Tachycardia by ECG Finding[SEP]Relations: catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding has relations: disease_phenotype_positive with Sudden cardiac death, disease_phenotype_positive with Sudden cardiac death, disease_phenotype_positive with Sudden death, disease_phenotype_positive with Sudden death, disease_phenotype_positive with Cardiac arrest, disease_phenotype_positive with Cardiac arrest. Sudden cardiac death has relations: disease_phenotype_positive with catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding, disease_phenotype_positive with catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding. Sudden death has relations: disease_phenotype_positive with catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding, disease_phenotype_positive with catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding.", "label": "yes"}
{"original_question": "Is metoprolol metabolized by CYP2D6?", "id": "converted_4157", "sentence1": "Is metoprolol metabolized by Cytochrome P450 2D6, human?", "sentence2": "Among these beta-blockers atenolol is mainly eliminated by renal excretion, bisoprolol is in part excreted as parent compound via the renal route (50%), the other 50% are hepatically metabolised, whereas metoprolol and carvedilol are metabolised by Cytochrome P450 2D6, human. [SEP]Relations: Metoprolol has relations: drug_protein with Cytochrome P450 2D6, human, drug_protein with Cytochrome P450 2D6, human, drug_protein with CYP3A4, drug_protein with CYP3A4, drug_protein with ADRB2, drug_protein with ADRB2, drug_drug with NN344, drug_drug with NN344, drug_drug with Cyproterone acetate, drug_drug with Cyproterone acetate.", "label": "yes"}
{"original_question": "Is the TFR1 gene dispensable for erythropoiesis?", "id": "converted_3749", "sentence1": "Is the TFR1 gene dispensable for erythropoiesis?", "sentence2": "These studies describe how Point Mutation of the Serotransferrin, human receptor can cause a microcytic Genus Anemia that does not respond to Ferrum metallicum, Homeopathic preparation therapy and would not be detected by routine Ferrum metallicum, Homeopathic preparation studies, such as Serum ferritin measurement., Ret-He was the only red cell marker affected prior to the onset of Head>Brain ID. The clinical practice of using Genus Anemia as the preferred biomarker for diagnosis of Ferrum metallicum, Homeopathic preparation deficiency may need reconsidering., The restoration of Erythropoietin production and EPOR Protein Info, human Protein Info, human mRNA expression with Aspirate substance treatment activated EPOR Protein Info, human Protein Info, human downstream JAK2/STAT5 and PI3K/Akt signaling, induced their target Genes, such as BCL2L1 gene, ERFE gene and Tfrc, and increased Bcl-2/Bax ratio in Bone Marrow-Derived Mononuclear Cells of Chronic Kidney Diseases Rattus norvegicus., Transferrin-bound Ferrum metallicum, Homeopathic preparation binding to Transferrin Receptor, human (TfR1) is essential for cellular Ferrum metallicum, Homeopathic preparation delivery during erythropoiesis. , aken together, decreasing TfR1 expression during β-thalassemic erythropoiesis, either directly via induced haploinsufficiency or via exogenous apotransferrin, decreases ineffective erythropoiesis and provides an endogenous mechanism to upregulate hepcidin, leading to sustained Ferrum metallicum, Homeopathic preparation-restricted erythropoiesis and preventing systemic Ferrum metallicum, Homeopathic preparation overload in β-thalassemic mice., The type 1 Serotransferrin, human receptor (TfR1) is well known as a key player in Erythroid differentiation through its role in Ferrum metallicum, Homeopathic preparation uptake. , The signaling functions of both TfR1 and Serotransferrin, human receptor 2, human in Erythroid Cells were unexpected and these recent findings open a new field of research regarding the last steps of Erythroid differentiation and their regulation., Erythropoiesis requires large amounts of Ferrum metallicum, Homeopathic preparation for hemoglobin synthesis, which is mainly provided by Specimen Source Codes - Macrophages and the Intestines in a Serotransferrin, human (Tf)-bound form.,  In Homo sapiens, hematopoietic Erythroid precursor Cells express high levels of TFR1 and specifically take up the FTH homopolymer (Ferritin Heavy Chain)., We found decreased expression of hepcidin and Serotransferrin, human receptor 2, human and increased expression of TfR1 and LCN2 wt Allele in the beta Thalassemia mouse models, compared with the control mice., Soluble Serotransferrin, human receptor-1 (sTfR1) concentrations are increased in the Specimen Source Codes - Plasma under two conditions that are associated with increased Ferrum metallicum, Homeopathic preparation absorption, i.e. Ferrum metallicum, Homeopathic preparation deficiency and increased erythropoiesis., HEMOCHROMATOSIS, TYPE 1 is caused by Gene Mutation in HFE, a Protein Info that competes with Serotransferrin, human (Male-to-Female Transsexual, Self-Report) for binding to Transferrin Receptor, human (TFR1)., Here we report that sorting nexin 3 (SNX3 gene) facilitates the recycling of Serotransferrin, human receptor (Tfrc) and thus is required for the proper delivery of Ferrum metallicum, Homeopathic preparation to Erythroid progenitors., These findings provide direct evidence that TFRC wt Allele is essential for Hematopoiesis through binding diferric Serotransferrin, human to supply Ferrum metallicum, Homeopathic preparation to Cells.[SEP]Relations: hemochromatosis has relations: disease_protein with TFR2, disease_protein with TFR2. hemopoiesis has relations: bioprocess_protein with TWSG1, bioprocess_protein with TWSG1, bioprocess_protein with L3MBTL1, bioprocess_protein with L3MBTL1, bioprocess_protein with GFI1, bioprocess_protein with GFI1. Erythropoietin has relations: drug_protein with EPOR Protein Info, human, drug_protein with EPOR Protein Info, human.", "label": "no"}
{"original_question": "Are mutations in the nf1 gene associated with memory?", "id": "converted_2324", "sentence1": "Are Gene Mutation in the nf1 gene associated with memory?", "sentence2": "We hypothesized that Neurofibromatosis 1 Gene Mutation disturb the expression of Genes important for memory formation, Our previous work has shown that defective cAMP signaling leads to the learning phenotype in Drosophila <basidiomycetes> <basidiomycetes> Nf1 mutants. In the present report, our experiments showed that in addition to learning, long-term memory was also abolished in Nf1 mutants. , Distinct functional domains of neurofibromatosis type 1 regulate immediate versus long-term memory formation.[SEP]Relations: neurofibromatosis has relations: disease_protein with Neurofibromatosis 1, disease_protein with Neurofibromatosis 1, disease_disease with neurofibromatosis type 1 due to Neurofibromatosis 1 mutation or intragenic deletion, disease_disease with neurofibromatosis type 1 due to Neurofibromatosis 1 mutation or intragenic deletion, disease_protein with NF2, disease_protein with NF2, disease_phenotype_positive with Memory impairment, disease_phenotype_positive with Memory impairment, disease_protein with LZTR1, disease_protein with LZTR1.", "label": "yes"}
{"original_question": "Is peripheral neuroepithelioma related to Ewing sarcoma?", "id": "converted_51", "sentence1": "Is Peripheral Primitive Neuroectodermal Tumor of Bone related to Ewings sarcoma?", "sentence2": "The term \"small round-cell tumor\" describes a group of highly aggressive malignant tumors composed of relatively small and monotonous undifferentiated cells with high Nuclear (incident type) to cytoplasmic ratios. This group includes Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone (ES), Peripheral Primitive Neuroectodermal Tumor of Bone (aka, primitive neuroectodermal tumor or extraskeletal ES), Peripheral neuroblastoma (\"classic-type\"), Anal Rhabdomyosarcoma, Desmoplastic Small Round Cell Tumor, Lymphoma, leukemia, small-cell osteosarcoma, small-cell carcinoma (either undifferentiated or Neurosecretory Systems), Rat Olfactory Neuroblastoma, cutaneous Neurosecretory Systems carcinoma (aka, Merkel-cell carcinoma), small-cell melanoma, and Mesenchymal Chondrosarcoma. Their clinical presentations often overlap, thus making a definitive diagnosis problematic in some cases, AIMS: To retrospectively study the DNA content in a series of childhood Ewing Family Tumors (EFT), and to investigate its prognostic value. METHODS: The study was performed on a series of 27 EFTs (osseous Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone, 18 cases; extraosseous Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone, 2; Peripheral Primitive Neuroectodermal Tumor of Bone, 4; Askin Rosai tumors, 3, To improve the prognosis of patients with poor-risk Peripheral primitive neuroectodermal tumors (pPNETs; including Peripheral Primitive Neuroectodermal Tumor of Bone and Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone), Large group of small-round-cell tumours of soft tissue and Specimen Type - Bone represents a complex diagnostic problem for the pathologists. neuronal nature of many tumours from this group is proven by means of new methods--immunophenotypic analysis, tissue culture, cytogenetics. Peripheral Neuroectodermal Tumor, Primitive, Ewing Neoplasms, primitive Neuroectodermal Tumors (Ewings sarcoma-primitive neuroectodermal tumor (Ewings sarcoma-primitive neuroectodermal tumor (PNET))), Askin's tumor belong to these neoplasms, Comparison of Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone of Specimen Type - Bone and Peripheral Primitive Neuroectodermal Tumor of Bone. An immunocytochemical and ultrastructural analysis of two primitive neuroectodermal neoplasms, Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone of Specimen Type - Bone (carboxylesterase) and Peripheral Primitive Neuroectodermal Tumor of Bone (Peripheral Nervous System) are frequently considered to be different tumors. Some researchers have suggested that Peripheral Nervous System is morphologically a neuroectodermal Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone. We sought to determine the extent of neuroectodermal features in conventional carboxylesterase on direct patient material (25 cases) and to compare these tumors with a similar group of readily diagnosed Peripheral Nerve Stimulation (10 cases), Neuroectodermal antigens (Gamma-Enolase, Leu-7 [CD57 Antigens], Neurofilament Medium Polypeptide 200 kd, and S100A1 wt Allele) were found in nine of 10 cases of Peripheral Nervous System and in 17 of 25 cases of carboxylesterase, These data support the concept that carboxylesterase and Peripheral Nervous System are both Peripheral primitive neuroectodermal neoplasms, differing only in extent of neuroectodermal phenotype and morphological differentiation, Besides these antigenic features, Ewings sarcoma cells are characterized by a specific t(11;22)(q24;q12) translocation also observed in Neuroectodermal Tumor, Primitive, a neuroectodermal tumor, suggesting a possible evolutionary related origin., Ewings sarcoma (ES) and Peripheral Primitive Neuroectodermal Tumor of Bone (Peripheral Nervous System) are closely related tumors, and it can be difficult to distinguish them from other small-round-cell tumors (SRCTs)., The presence of this translocation in Ewings sarcoma and Peripheral primitive neuroectodermal tumor has been taken as evidence that these two tumors are related., Besides these antigenic features, Ewings sarcoma cells are characterized by a specific t(11;22)(q24;q12) translocation also observed in Neuroectodermal Tumor, Primitive, a neuroectodermal tumor, suggesting a possible evolutionary related origin., Indistinguishable patterns of protooncogene expression in two distinct but closely related tumors: Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone and Neuroectodermal Tumor, Primitive., Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone (ES) and Peripheral Primitive Neuroectodermal Tumor of Bone (Peripheral Nervous System) are related tumors, possibly of neural crest origin, which are cytogenetically characterized by the specific translocation t(11;22)(q24;q12)., Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone/Peripheral primitive neuroectodermal tumors (ES/pPNET) are a group of small round cell sarcomas that show varying degrees of neuroectodermal differentiation characterized by translocation involving the EWSR1 gene, Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone (ES) and Peripheral Primitive Neuroectodermal Tumor of Bone (Peripheral Nervous System) are closely related tumors, and it can be difficult to distinguish them from other small-round-cell tumors (SRCTs), Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone (ES) and Peripheral Primitive Neuroectodermal Tumor of Bone (Peripheral Nervous System) are related tumors, possibly of neural crest origin, which are cytogenetically characterized by the specific translocation t(11;22)(q24;q12), This genetical similarity further supports a nosological concept according to which Askin's Neoplasms, Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone and Peripheral Primitive Neuroectodermal Tumor of Bone represent phenotypic variations of the same Neoplasms, namely the Peripheral primitive Neuroectodermal Tumors., Besides these antigenic features, Ewings sarcoma cells are characterized by a specific t(11;22)(q24;q12) translocation also observed in Neuroectodermal Tumor, Primitive, a neuroectodermal tumor, suggesting a possible evolutionary related origin[SEP]Relations: Ewings sarcoma/Peripheral primitive neuroectodermal tumor has relations: disease_disease with Ewings sarcoma, disease_disease with Ewings sarcoma, disease_disease with extraskeletal Ewings sarcoma/Peripheral primitive neuroectodermal tumor, disease_disease with extraskeletal Ewings sarcoma/Peripheral primitive neuroectodermal tumor, disease_disease with Peripheral primitive neuroectodermal tumor, disease_disease with Peripheral primitive neuroectodermal tumor, disease_disease with Ewings sarcoma/Peripheral primitive neuroectodermal tumor of Specimen Type - Bone, disease_disease with Ewings sarcoma/Peripheral primitive neuroectodermal tumor of Specimen Type - Bone. Ewings sarcoma has relations: disease_disease with Ewings sarcoma/Peripheral primitive neuroectodermal tumor, disease_disease with Ewings sarcoma/Peripheral primitive neuroectodermal tumor.", "label": "yes"}
{"original_question": "Does verubecestat activate BACE?", "id": "converted_2605", "sentence1": "Does verubecestat activate BACE?", "sentence2": "Verubecestat is a potent BACE1 protein, human protein, human enzyme inhibitor currently being investigated in Phase III trials for the treatment of mild-to-moderate and prodromal ALZHEIMER DISEASE, FAMILIAL, 1. [SEP]Relations: Protein S human has relations: drug_drug with Caplacizumab, drug_drug with Caplacizumab, drug_drug with Mofebutazone, drug_drug with Mofebutazone, drug_drug with Bortezomib, drug_drug with Bortezomib, drug_drug with Cefodizime, drug_drug with Cefodizime, drug_drug with Cefbuperazone, drug_drug with Cefbuperazone.", "label": "no"}
{"original_question": "Has the drug Afrezza been approved by the FDA?", "id": "converted_3273", "sentence1": "Has the drug Afrezza been approved by the FDA?", "sentence2": "In contrary, MannKind Corporation started developing its ultra-rapid-acting insulin Afrezza in a bold Twice a day, probably by managing the issues in which Exubera was not successful. Afrezza has been marketed since February, 2015 by Sanofi after getting FDA approval in June 2014.[SEP]", "label": "yes"}
{"original_question": "Is there an increased risk for meningiomas in childhood leukemia survivors?", "id": "converted_3683", "sentence1": "Is there an increased risk for Meningioma in childhood leukemia Survivors?", "sentence2": "Cranial radiotherapy improves survival of the most common childhood cancers, including Brain Neoplasms and leukemia. Unfortunately, long-term Survivors are faced with consequences of secondary neoplasia, including radiation-induced Meningioma (RIMs). , Combined chemotherapy and prophylactic Cranial Irradiation has improved the prognosis of children with Acute leukemia. However Cranial Irradiation carries a latent risk of the induction of secondary Neoplasms, Intracranial. We encountered a patient who developed multiple intracranial radiation-induced Meningioma (RIMs) 25 years after prophylactic Cranial Irradiation for the treatment of Acute leukemia in childhood. , Focal cranial hyperostosis from Benign Meningioma: a complication from previous radiation treatment for childhood T-cell Pre B-cell Pre B-cell acute lymphoblastic leukemia., Presented is a case of a 20 year Homo sapiens with a history of T-cell lymphoblastic leukemia diagnosed at age 22 months, treated with chemotherapy and Cranial Irradiation. He had developed increasing prominence of the top of his Head - Component of Device over several months. Plain radiograph showed frontal calvarium thickening with Focal \"hair-on-end\" periosteal reaction. Magnetic resonance imaging revealed an enhancing dural-based mass with transcalvarial extension, confirmed after resection to be Benign Meningioma (World Health Organization Grade I). , RESULTS: Acute myeloid leukemia (Leukemia, Myelocytic, Acute; n = 186), MYELODYSPLASTIC SYNDROME (Miller Dieker syndrome; n = 69), and nonmeningioma brain tumor (n = 116) were the most common types of SMNs and had the poorest outcome (5-year survival rate, 18.1% ± 2.9%, 31.1% ± 6.2%, and 18.3% ± 3.8%, respectively). , Radiation-induced World Health Organization grade II Meningioma in young patients following prophylactic Cranial Irradiation for Pre B-cell Pre B-cell acute lymphoblastic leukemia in childhood. Three case reports., Current chemotherapeutic regimens have been used to successfully treat many children with Pre B-cell Pre B-cell acute lymphoblastic leukemia (Acute lymphocytic leukemia), but have resulted in an increased risk of late central nervous system tumors, most commonly Benign Meningioma, particularly in patients who have received Cranial Irradiation. , RESULTS: Fifty-nine MRI abnormalities (32 cavernomas, nine Focal areas of gliosis, seven dystrophic mineralizations, five cerebral atrophies, four pituitary atrophies, one diffuse radiation leukoencephalopathy, and one Benign Meningioma) were found in 43 patients. , Intraventricular Benign Meningioma after Cranial Irradiation for childhood leukemia., Radiation-induced Meningioma may also have predilection to recur. The authors describe a case of an intraventricular Benign Meningioma occurring 23 years after Cranial Irradiation for childhood Pre B-cell Pre B-cell acute lymphoblastic leukemia., Cumulative incidence at 30 years after the childhood Primary malignant neoplasm diagnosis was 20.5% (95% confidence interval [CI] = 19.1% to 21.8%) for all subsequent Neoplasms, 7.9% (95% CI = 7.2% to 8.5%) for second malignant Neoplasms (excluding nonmelanoma skin Primary malignant neoplasm), 9.1% (95% CI = 8.1% to 10.1%) for nonmelanoma skin Primary malignant neoplasm, and 3.1% (95% CI = 2.5% to 3.8%) for Benign Meningioma. , Radiation-induced Meningioma: a shadow in the success story of childhood leukemia., Although the cohort is small, it seems probable that the increasing incidence of Benign Meningioma will shadow the future of cranially irradiated leukemia Survivors., Age at the time of irradiation, gender, or cumulative doses of chemotherapeutic agents showed no significant association with the development of Meningioma., Meningioma Screening With MRI in Childhood Leukemia Survivors Treated With Cranial Radiation., High incidence of Benign Meningioma in cranial irradiated Survivors of childhood Pre B-cell Pre B-cell acute lymphoblastic leukemia., Radiation-induced World Health Organization grade II Meningioma in young patients following prophylactic Cranial Irradiation for Pre B-cell Pre B-cell acute lymphoblastic leukemia in childhood., Radiation-induced Benign Meningioma following prophylactic radiotherapy for Pre B-cell Pre B-cell acute lymphoblastic leukemia in childhood., Current chemotherapeutic regimens have been used to successfully treat many children with Pre B-cell Pre B-cell acute lymphoblastic leukemia ( Acute lymphocytic leukemia) , but have resulted in an increased risk of late central nervous system tumors , most commonly Benign Meningioma , particularly in patients who have received Cranial Irradiation, Survivors of childhood Acute lymphocytic leukemia treated with high-dose Cranial Irradiation are at risk both for early radiation injury in radiosensitive Organ , such as the Lens <bivalves> and pituitary gland , and for the later development of a radiation-induced Benign Meningioma, Radiation-induced Meningioma: a shadow in the success story of childhood leukemia, We treated 3 young patients with World Health Organization grade II Meningioma who had previously received Cranial Irradiation for the treatment of childhood Acute lymphocytic leukemia: a cerebellopontine angle tumor in a 19-year-old woman , a petroclival tumor in a 28-year-old Homo sapiens , and a frontal parasagittal tumor in a 19-year-old woman, We treated 3 young patients with World Health Organization grade II Meningioma who had previously received Cranial Irradiation for the treatment of childhood Acute lymphocytic leukemia: a cerebellopontine angle tumor in a 19-year-old woman, a petroclival tumor in a 28-year-old Homo sapiens, and a frontal parasagittal tumor in a 19-year-old woman., Current chemotherapeutic regimens have been used to successfully treat many children with Pre B-cell Pre B-cell acute lymphoblastic leukemia (Acute lymphocytic leukemia), but have resulted in an increased risk of late central nervous system tumors, most commonly Benign Meningioma, particularly in patients who have received Cranial Irradiation., Current chemotherapeutic regimens have been used to successfully treat many children with Pre B-cell Pre B-cell acute lymphoblastic leukemia (Acute lymphocytic leukemia), but have resulted in an increased risk of late central nervous system tumors, most commonly Benign Meningioma, particularly in patients who have received Cranial Irradiation., Long-term Survivors who received radiotherapy for Acute lymphocytic leukemia in childhood are at risk for late complications, including radiation-induced Benign Meningioma.[SEP]Relations: childhood leukemia has relations: disease_disease with childhood malignant neoplasm, disease_disease with childhood malignant neoplasm, disease_disease with bone marrow Primary malignant neoplasm, disease_disease with bone marrow Primary malignant neoplasm, disease_disease with leukemia (disease), disease_disease with leukemia (disease), disease_disease with neonatal leukemia, disease_disease with neonatal leukemia, disease_disease with childhood acute myeloid leukemia, disease_disease with childhood acute myeloid leukemia.", "label": "yes"}
{"original_question": "Is irritable bowel syndrome more common in women with endometriosis?", "id": "converted_42", "sentence1": "Is irritable bowel syndrome more common in women with Endometriosis?", "sentence2": "CONCLUSIONS: Comorbid pain syndromes, mood conditions and Asthma are common in adolescents and young women with Endometriosis., There are many etiologies of Pelvic pain female that present with symptoms resembling those of Endometriosis-associated Pelvic pain female that are not diagnosable with laparoscopy, such as Chronic Chronic interstitial cystitis and irritable bowel syndrome., Often, such patients are labelled with irritable bowel syndrome. , Irritable Bowel Syndrome (IBS) is also common in this setting, and it was speculated that the visceral hypersensitivity associated with this condition might be amplifying the symptoms of Endometriosis. , RESULTS: Compared with controls, patients with minimal to mild and moderate to severe Endometriosis had a higher prevalence of symptoms consistent with IBS (0% vs 65% and 50%, respectively, p<0.001) with significantly lower mean pain thresholds (39.5 mm Hg (95% CI 36.0 to 43.0) vs 28.1 mm Hg (95% CI 24.5 to 31.6), p=0.001 and 28.8 mm Hg (95% CI 24.9 to 32.6), p=0.002) not explained by differences in TUBE,RECTAL,24FR,PLASTIC B#6510 compliance. , Similarly, women with a history of irritable bowel syndrome were twice as likely to develop Endometriosis [AOR=1.9, 95% CI (1.03-3.87)]., A weak association between reported family history of Endometriosis and history of irritable bowel syndrome and the development of Endometriosis was also observed. , Irritable Bowel Syndrome and chronic Constipation in patients with Endometriosis., Fifteen per cent of the patients with Endometriosis also had IBS and 14% of the patients with Endometriosis had functional Constipation without IBS., CONCLUSION: In patients with Endometriosis, 29% also had IBS or Constipation. , Seventy-six women (21.4%) had previously been diagnosed with irritable bowel syndrome and 79% of them had Endometriosis confirmed., Compared with controls, women with Endometriosis had increased risks of abdominopelvic pain (OR 5.2 [95% CI: 4.7-5.7]), Dysmenorrhea (OR 8.1 [95% CI: 7.2-9.3]), Menorrhagia (OR 4.0 [95% CI: 3.5-4.5]), Subfertility (OR 8.2 [95% CI: 6.9-9.9]), Dyspareunia (female) and/or postcoital bleeding (OR 6.8 [95% CI: 5.7-8.2]), and Ovarian Cysts (OR 7.3 [95% CI: 5.7-9.4]), and of being diagnosed with irritable bowel syndrome (IBS) (OR 1.6 [95% CI: 1.3-1.8]) or Pelvic Inflammatory Disease (OR 3.0 [95% CI: 2.5-3.6])., Endometriosis may coexist with or be misdiagnosed as Pelvic Inflammatory Disease or IBS., RESULTS: Compared with the controls, women with Endometriosis were 3.5 times more likely to have received a diagnosis of IBS (OR 3.5 [95% CI: 3.1-3.9]). Even after women had been diagnosed with Endometriosis, they were still two and a half times more likely to receive a new diagnosis of IBS when compared with the controls (OR 2.5 [95% CI: 2.2-2.8])., CONCLUSIONS: Women with Endometriosis are more likely to be diagnosed with IBS and Phosphotyrosine Binding Domain than controls, even after a definitive diagnosis of Endometriosis has been reached., In women, clinical studies suggest that functional pain syndromes such as irritable bowel syndrome, Chronic Chronic interstitial cystitis, and Fibromyalgia, are co-morbid with Endometriosis, chronic Pelvic pain female, and others diseases., In women, clinical studies suggest that pain syndromes such as irritable bowel syndrome and Chronic Chronic interstitial cystitis, which are associated with visceral hyperalgesia, are often comorbid with Endometriosis and chronic Pelvic pain female. , Cancer patients and suicide and depression, Anxiety Disorders, IBS, femtomole/liter, Chronic Fatigue Syndrome, and IC were more common in Migraine Disorders with Electron Microscopy group than in controls., Intestinal Endometriosis can mimic many Gastrointestinal Diseases, such as irritable bowel syndrome, INFLAMMATORY BOWEL DISEASE 2, Infections of musculoskeletal system and Neoplasms., Endometriosis is often associated with other painful conditions such as irritable bowel syndrome, Chronic Chronic interstitial cystitis and Fibromyalgia. , CONCLUSIONS: Diagnosis of Endometriosis should be considered in women with recurrent monthly Abdominal Pain and bowel symptoms, especially if accompanied by gynaecologic complaints, even because the significant symptoms overlap with the irritable bowel syndrome (IBS) and makes the differentiation extremely difficult., Intestinal Endometriosis is typically asymptomatic; however, when symptoms occur, they can mimic those of irritable bowel syndrome.,  Similarly, women with a history of irritable bowel syndrome were twice as likely to develop Endometriosis [AOR=1., Irritable Bowel Syndrome (IBS) is also common in this setting, and it was speculated that the visceral hypersensitivity associated with this condition might be amplifying the symptoms of Endometriosis., Irritable Bowel Syndrome (IBS) is also common in this setting, and it was speculated that the visceral hypersensitivity associated with this condition might be amplifying the symptoms of Endometriosis.[SEP]Relations: irritable bowel syndrome has relations: disease_disease with intestinal disease, disease_disease with intestinal disease, disease_disease with syndromic disease, disease_disease with syndromic disease, disease_protein with IL10, disease_protein with IL10, disease_protein with MAGI2, disease_protein with MAGI2. intestinal disease has relations: disease_disease with irritable bowel syndrome, disease_disease with irritable bowel syndrome.", "label": "yes"}
{"original_question": "Is depression associated with poor prognosis of brain tumor patients?", "id": "converted_1497", "sentence1": "Is Depressive disorder associated with poor prognosis of brain tumor patients?", "sentence2": "Before surgery 27 patients (35%) had BDI scores indicating the presence of Depressive disorder. These scores were significantly higher in patients with a history of Depressive disorder (p = 0.017) and in those with a lower functional outcome (p = 0.015)., A lower functional status (KPS score < or = 70) in patients was significantly associated with high Depressive disorder scores at the 3-month (p = 0.000) and 1-year (p = 0.005) assessments., At all follow-ups, depressed low-grade glioma patients had a significantly shorter survival time, 3.3-5.8 years, compared to non-depressed low-grade glioma patients, 10.0-11.7 years., The results suggest that Depressive disorder and decreased QOL among low-grade glioma patients is related to shorter survival at long-term follow-up., The adverse impact of Depressive disorder in relation to survival among Primary malignant neoplasm patients is currently a subject of great interest in research., In the subgroup of patients with low-grade Glioma, depressive patients had a significantly shorter survival time compared with nondepressive subjects (P = 0.031, Kaplan-Meier survival analysis)., Preoperative Depressive disorder seemed to be a significant prognostic factor for worse survival in low-grade glioma patients., Major depressive disorder was marginally associated with outcomes, while surgical interventions and radiotherapy did not show strong associations with test performances.[SEP]Relations: malignant ear neoplasm has relations: disease_disease with inner ear Primary malignant neoplasm, disease_disease with inner ear Primary malignant neoplasm, disease_disease with middle ear Primary malignant neoplasm, disease_disease with middle ear Primary malignant neoplasm, disease_disease with sensory system Primary malignant neoplasm, disease_disease with sensory system Primary malignant neoplasm, disease_disease with head and neck Primary malignant neoplasm, disease_disease with head and neck Primary malignant neoplasm. Glioma has relations: disease_phenotype_positive with glioma susceptibility, disease_phenotype_positive with glioma susceptibility.", "label": "yes"}
{"original_question": "Can Logic Alignment Free (LAF) be used for bacterial genomes classification?", "id": "converted_2463", "sentence1": "Can Logic Alignment Free (Interleukin-1) be used for Genome, Bacterial classification?", "sentence2": "Interleukin-1: Logic Alignment Free and its application to Genome, Bacterial classification., In this paper, we present Logic Alignment Free (Interleukin-1), a method that combines alignment-free techniques and rule-based classification algorithms in order to assign biological samples to their taxa. This method searches for a minimal subset of k-mers whose relative frequencies are used to build classification models as disjunctive-normal-form logic formulas (if-then rules). We apply Interleukin-1 successfully to the classification of Genome, Bacterial to their corresponding taxonomy. In particular, we succeed in obtaining reliable classification at different taxonomic levels by extracting a handful of rules, each one based on the frequency of just few k-mers. State of the art methods to adjust the frequency of k-mers to the character distribution of the underlying genomes have negligible impact on classification performance, suggesting that the signal of each class is strong and that Interleukin-1 is effective in identifying it., In this paper, we present Logic Alignment Free (Interleukin-1), a method that combines alignment-free techniques and rule-based classification algorithms in order to assign biological samples to their taxa., Interleukin-1: Logic Alignment Free and its application to Genome, Bacterial classification.[SEP]Relations: interleukin-1 binding has relations: molfunc_protein with NLRP7, molfunc_protein with NLRP7, molfunc_protein with TRIM16, molfunc_protein with TRIM16, molfunc_protein with HAX1, molfunc_protein with HAX1, molfunc_protein with A2M, molfunc_protein with A2M, molfunc_protein with IL1R1, molfunc_protein with IL1R1.", "label": "yes"}
{"original_question": "Can Flotillin be used as exosomal marker?", "id": "converted_3449", "sentence1": "Can Flotillin be used as exosomal marker?", "sentence2": "flotillins and TSG101 protein, human gene (TSG101 protein, human protein, human), two exosomal marker proteins, , expressed exosomal marker tumor susceptibility gene (TWSG1 gene) 101 and flotillin (Flot) 1.[SEP]Relations: Protein S human has relations: drug_drug with Trabectedin, drug_drug with Trabectedin, drug_drug with Drotrecogin alfa, drug_drug with Drotrecogin alfa, drug_drug with Floctafenine, drug_drug with Floctafenine, drug_drug with Streptozocin, drug_drug with Streptozocin, drug_drug with Floxuridine, drug_drug with Floxuridine.", "label": "yes"}
{"original_question": "Is LDB1-mediated enhancer looping dependent on cohesin?", "id": "converted_2455", "sentence1": "Is LDB1-mediated enhancer looping dependent on cohesins?", "sentence2": "LDB1-mediated enhancer looping can be established independent of mediator and cohesins., Moreover, Encode (action) data and our chromatin immunoprecipitation results indicate that cohesins is almost completely absent from validated and predicted LDB1-regulated erythroid enhancer-gene pairs. Thus, lineage specific factors largely mediate enhancer-promoter looping in Erythroid Cells independent of mediator and cohesins., Moreover, Encode (action) data and our chromatin immunoprecipitation results indicate that cohesins is almost completely absent from validated and predicted LDB1-regulated erythroid enhancer-gene pairs., Moreover, Encode (action) data and our chromatin immunoprecipitation results indicate that cohesins is almost completely absent from validated and predicted LDB1-regulated erythroid enhancer-gene pairs., LDB1-mediated enhancer looping can be established independent of mediator and cohesins.[SEP]", "label": "no"}
{"original_question": "Can pets affect infant microbiomed?", "id": "converted_2783", "sentence1": "Can pets affect infant microbiomed?", "sentence2": "Since there is some evidence that pets also alter the gut microbial composition of infants, changes to the gut microbiome are putative pathways by which Positron-Emission Tomography exposure can reduce these risks to health., The impact of Positron-Emission Tomography ownership varies under different birth scenarios; however, in common, exposure to pets increased the abundance of two Bacteria, Ruminococcus species species and Oscillospira, which have been negatively associated with childhood MS4A2 wt Allele and BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20., As a common effect in all birth scenarios, pre- and postnatal Positron-Emission Tomography exposure enriched the abundance of Oscillospira and/or Ruminococcus species species (P < 0.05) with more than a twofold greater likelihood of high abundance. Among vaginally born infants with maternal intrapartum antibiotic prophylaxis exposure, Streptococcaceae were substantially and significantly reduced by Positron-Emission Tomography exposure (P < 0.001, FDRp = 0.03), reflecting an 80% decreased likelihood of high abundance (OR 0.20, 95%CI, 0.06-0.70) for Positron-Emission Tomography exposure during pregnancy alone and a 69% reduced likelihood (OR 0.31, 95%CI, 0.16-0.58) for exposure in the pre- and postnatal time periods., Exposure to household furry pets influences the gut microbiota of infant at 3-4 months following various birth scenarios.[SEP]Relations: Bacteremia has relations: disease_phenotype_positive with listeriosis, disease_phenotype_positive with listeriosis, disease_phenotype_positive with toxic shock syndrome, disease_phenotype_positive with toxic shock syndrome, disease_phenotype_positive with shigellosis, disease_phenotype_positive with shigellosis, disease_phenotype_positive with cyclic hematopoiesis, disease_phenotype_positive with cyclic hematopoiesis. obsolete body mass index quantitative trait locus 19 has relations: disease_phenotype_positive with Insulin resistance, disease_phenotype_positive with Insulin resistance.", "label": "yes"}
{"original_question": "Is LPS a microbial product?", "id": "converted_1671", "sentence1": "Is Van der Woude syndrome a microbial product?", "sentence2": "and microbial translocation [lipopolysaccaride (Van der Woude syndrome), microbial 16S rDNA and Soluble CD14 Protein] , Lipopolysaccharide sensing an important factor in the innate immune response to Gram-negative Bacterial Infections, Bacterial lipopolysaccharide B B (Van der Woude syndrome), sterile Bacterial wall lipopolysaccharide B B (Van der Woude syndrome) to investigate the changes in innate lung microbiota[SEP]Relations: Recurrent Bacterial Infections has relations: disease_phenotype_positive with immunodeficiency, partial combined, with absence of HLA Determinants and beta-2-microglobulin from lymphocytes, disease_phenotype_positive with immunodeficiency, partial combined, with absence of HLA Determinants and beta-2-microglobulin from lymphocytes, disease_phenotype_positive with SLC35A1-CDG, disease_phenotype_positive with SLC35A1-CDG, disease_phenotype_positive with agammaglobulinemia, disease_phenotype_positive with agammaglobulinemia. Bacterial arthritis has relations: disease_protein with TNF, disease_protein with TNF, disease_disease with infectious disease, disease_disease with infectious disease.", "label": "yes"}
{"original_question": "Does bleomycin cause lung toxicity?", "id": "converted_4311", "sentence1": "Does bleomycin cause Chest>Lung Toxic effect?", "sentence2": "bleomycin-induced Pulmonary:-:Point in time:^Patient:- Fibrosis, bleomycin (BLM)-induced Pulmonary:-:Point in time:^Patient:- , Pulmonary Toxic effect is a devastating complication of bleomycin chemotherapy. , Bleomycin containing regimen is routinely employed in the treatment of Hodgkin Disease. Pulmonary Toxic effect due to this Pharmacologic Substance is the most feared side effect in these regimens where the mortality rate is approximately 2%-3%. , Bleomycin might cause Pulmonary:-:Point in time:^Patient:- Fibrosis at higher cumulative doses as toxic effect directly to the Lung or most likely in addition by the formation of vascular microthrombi., The comparative Pulmonary:-:Point in time:^Patient:- Toxic effect induced by bleomycin and talisomycin (former trivial name: tallysomycin A) was evaluated by measuring Chest>Lung hydroxyproline content., Clinicians should always remember that bleomycin Toxic effect may lead to fatal complications in patients with comorbid conditions., CONTEXT: The application of bleomycin is limited due to its side effects including Chest>Lung Toxic effect., Bleomycin is an antineoplastic agent that causes a dose-related Chest>Lung Fibrosis that limits its therapeutic effectiveness., Acute Lung Toxicity After Intralesional Bleomycin Sclerotherapy., We report a case of a severe acute Chest>Lung Toxic effect after a low dose of a second bleomycin intralesional injection in a 5-year-old girl., Renal damage, following cisplatin administration, with subsequent accumulation of bleomycin was the likely cause of the high Chest>Lung Toxic effect., Whenever possible, bleomycin should precede cisplatin infusion to minimize the risk of Chest>Lung Toxic effect., The most severe form of BLM-induced Pulmonary:-:Point in time:^Patient:- Toxic effect is Chest>Lung Fibrosis., Results from this study suggest that an excess production of Superoxides anions by Macrophages, Alveolar may be the underlying cause of bleomycin Pulmonary:-:Point in time:^Patient:- Toxic effect., Bleomycin Chest>Lung Toxic effect is well established and can manifest as bleomycin-induced pneumonitis, but Mediastinal Emphysema and Pneumothorax are very rare complications., High doses of bleomycin administered to patients with Lymphoma and other Neoplasms lead to significant Chest>Lung Toxic effect in general, and to apoptosis of Epithelial Cells, in particular. , sis of bleomycin-induced Chest>Lung Toxic effect is based on the combination of clinical and radiological features, and requires to rule out differential diagnoses including Pneumocystis jiroveci pneumonia. \"Bleo, doxorubicin, bleomycin, vinblastine sulfate, and dacarbazine (bleomycin/dacarbazine/doxorubicin/vinblastine protocol) is associated with severe Toxic effect in older patients, particularly from bleomycin-induced Chest>Lung Toxic effect (Balanced ligamentous tension technique (procedure)). Ther, s studies have proposed that the Chest>Lung Toxic effect caused by bleomycin is related to the C-terminal regions of these drugs, which have been shown to closely interact with DNA in metal-bleomycin-DNA complexes. Some o, OBJECTIVES: Bleomycin, etoposide, and cisplatin (BEP regimen regimen) is the most common and successful chemotherapy regimen for germ-cell tumor (GCT) patients, accompanied by a bleomycin-induced dose-dependent Chest>Lung Toxic effect in certain pat, e been no respiratory problems attributable to bleomycin Chest>Lung Toxic effect in this study compared with four (3 associated with patient deaths) seen in 91 previously treated patients. The relat, Mechanisms of bleomycin-induced Chest>Lung damage., Previous studies have proposed that the Chest>Lung Toxic effect caused by bleomycin is related to the C-terminal regions of these drugs, which have been shown to closely interact with DNA in metal-bleomycin-DNA complexes., g V30 cutoff value of 32% was estimated.CONCLUSION: Bleomycin and RT may cause Lung Injury , Postmortem Chest>Lung studies were performed in all six patients and revealed findings compatible with bleomycin-induced Chest>Lung Toxic effect., However, the cytotoxic effects of bleomycin cause a number of adverse responses, in particular in the Chest>Lung and the Skin Specimen Source Code., Bleomycin, a widely used anti-Primary malignant neoplasm Pharmacologic Substance, may give rise to Pulmonary:-:Point in time:^Patient:- Fibrosis, a serious side effect which is associated with significant morbidity and mortality., Bleomycin is a Primary malignant neoplasm therapeutic known to cause Lung Injury which progresses to Fibrosis., and repair. Bleomycin Pulmonary:-:Point in time:^Patient:- Toxic effect is mediated, at least in part, by the generation of active oxy, This report suggests that bleomycin Chest>Lung Toxic effect may be reversible if treated aggressively., Although all bleomycin-treated animal allergen extracts had some evidence of Chest>Lung Toxic effect, histologic examination of the Lung revealed markedly reduced bleomycin Toxic effect in the rats exposed to Hypoxia, CTCAE., Low temperature inhibits bleomycin Chest>Lung Toxic effect in the Rattus norvegicus., Results at day 22, 3 wk after bleomycin treatment, showed that airway delivery of Liposomes before and after intratracheal administration of bleomycin significantly reduced bleomycin-induced Chest>Lung Toxic effect as evidenced by less body weight loss, chronic Chest>Lung inflammation, and Fibrosis as well as improved Chest>Lung compliance compared with controls., Protective effect of Hypoxia, CTCAE on bleomycin Chest>Lung Toxic effect in the Rattus norvegicus., acetylcysteine (doxorubicin/lomustine/mechlorethamine protocol) has recently been shown to have antioxidant properties, and since bleomycin produces Pulmonary:-:Point in time:^Patient:- damage via free oxygen radical Toxic effect, the possible protective effect of doxorubicin/lomustine/mechlorethamine protocol on bleomycin Chest>Lung Toxic effect was investigated., All rats treated with bleomycin only had typical changes of bleomycin Chest>Lung Toxic effect whereas the animal allergen extracts treated with bleomycin and doxorubicin/lomustine/mechlorethamine protocol had minimal pathology., atic compliance on day 15 was severely decreased with bleomycin alone and showed a further significant decrease when Granulocyte Colony-Stimulating Factor was added (controls, 3.85 +/- 0.14 mL/kPa; bleomycin, 1.44 +/- 0.06 mL/kPa; and bleomycin + Granulocyte Colony-Stimulating Factor, 0.65 +/- 0.09 mL/kPa; control vs. bleomycin, p <.0001; and bleomycin vs. bleomycin + Granulocyte Colony-Stimulating Factor, p =.0003). Lung m, Bleomycin sometimes causes fatal Pulmonary:-:Point in time:^Patient:- Toxic effect, including bleomycin-induced pneumonitis., Bleomycin is an antineoplastic agent causing fatal Pulmonary:-:Point in time:^Patient:- Toxic effect., Pulmonary Toxic effect is an important adverse effect of bleomycin treatment., Pulmonary Toxic effect is the most significant complication of bleomycin administration., It is possible, however, that the low incidence of clinically significant and fatal Pulmonary:-:Point in time:^Patient:- Toxic effect, as experienced in this group of patients, may be related to the infusion of bleomycin., Bleomycin-mediated Pulmonary:-:Point in time:^Patient:- Toxic effect: evidence for a p53-mediated response., Occurrence of bleomycin Chest>Lung Toxic effect requires an immediate and often permanent discontinuation., All three developed bleomycin induced Pulmonary:-:Point in time:^Patient:- Toxic effect in the form of Pulmonary:-:Point in time:^Patient:- Fibrosis during treatment of the disease., One of the fatal side effect of bleomycin is Pulmonary:-:Point in time:^Patient:- Toxic effect., Pulmonary Toxicity of Bleomycin - A Case Series from a Tertiary Care Center in Southern India., Bleomycin is potentially capable of inducing a diffuse interstitial Fibrosis of the Chest>Lung, the pathogenesis of which has not yet been elucidated., Intratracheal instillation of bleomycin 1.5 mg resulted in a severe pneumonitis with influx of Inflammatory cell into the Alveolus as assessed by alveolar lavage, Edema of the alveolar walls, and up to an eight fold increase in the total Pulmonary:-:Point in time:^Patient:- extravascular albumin space, maximal at 72 hours., Development of Acute Lung Injury after the combination of intravenous bleomycin and exposure to Hyperoxia in rats., Bleomycin is a highly effective antitumor agent, but Pulmonary:-:Point in time:^Patient:- Toxic effect, characterized by an acute inflammatory reaction and associated Pulmonary:-:Point in time:^Patient:- edema, limits clinical use of the Pharmacologic Substance., In this study we investigated bleomycin-induced Pulmonary:-:Point in time:^Patient:- Toxic effect in patients with germ-cell tumour by means of technetium-99m diethylene triamine penta-acetic acid aerosol scintigraphy.[SEP]Relations: Bleomycin has relations: drug_effect with Respiratory distress, drug_effect with Respiratory distress, drug_effect with Cough, drug_effect with Cough, drug_effect with Pulmonary infiltrates, drug_effect with Pulmonary infiltrates, drug_effect with Pulmonary Fibrosis, drug_effect with Pulmonary Fibrosis, drug_effect with Pneumonia, drug_effect with Pneumonia.", "label": "yes"}
{"original_question": "Are PDXK mutations linked to polyneuropathy?", "id": "converted_3959", "sentence1": "Are PDXK gene Gene Mutation linked to Polyneuropathy?", "sentence2": "PDXK gene gene Gene Mutation cause Polyneuropathy responsive to pyridoxal 5'-phosphate supplementation., To identify Disease-causing Variant in autosomal recessive axonal Polyneuropathy with Optic Atrophy and provide targeted replacement therapy.METHODS: We performed genome-wide sequencing, homozygosity mapping, and segregation analysis for novel Disease-causing gene discovery. We used circular dichroism to show secondary structure changes and isothermal titration calorimetry to investigate the impact of Variant on adenosine triphosphate (ATP) binding. Pathogenicity was further supported by enzymatic assays and mass spectroscopy on Recombinant Proteins, patient-derived fibroblasts, Specimen Source Codes - Plasma, and Specimen Source Codes - Erythrocytes. Response to supplementation was measured with clinical validated rating scales, electrophysiology, and biochemical quantification.RESULTS: We identified biallelic Gene Mutation in PDXK gene gene in 5 individuals from 2 unrelated families with primary axonal Polyneuropathy and Optic Atrophy. The natural history of this disorder suggests that untreated, affected individuals become Wheelchair bound and blind. We identified conformational rearrangement in the mutant enzyme around the ATP-binding pocket. Low PDXK gene gene ATP binding resulted in decreased Erythrocytes PDXK gene gene activity and low pyridoxal 5'-phosphate (pyridoxal phosphate) concentrations. We rescued the clinical and biochemical profile with pyridoxal phosphate supplementation in 1 family, improvement in power, Pain:-:Point in time:^Patient:-, and Fatigue contributing to patients regaining their ability to walk independently during the first year of pyridoxal phosphate normalization.INTERPRETATION: We show that Gene Mutation in PDXK gene gene cause autosomal recessive axonal peripheral Polyneuropathy leading to Disease via reduced PDXK gene gene enzymatic activity and low pyridoxal phosphate. We show that the biochemical profile can be rescued with pyridoxal phosphate supplementation associated with clinical improvement. As B6 is a CoFactor brand of 5,10-methylenetetrahydrofolate in diverse essential biological pathways, our findings may have direct implications for Neuropathy of unknown etiology characterized by reduced pyridoxal phosphate levels. ANN NEUROL 2019;86:225-240., RETATION: We show that Gene Mutation in PDXK gene gene cause autosomal recessive axonal peripheral Polyneuropathy leading to Disease via reduced PDXK gene gene enzymatic activity and low pyridoxal phosphate. We sh, PDXK gene gene Gene Mutation cause Polyneuropathy responsive to pyridoxal 5'-phosphate supplementation, Hereditary Polyneuropathy with Optic Atrophy due to PDXK gene gene variant leading to impaired Vitamin B6 metabolism, INTERPRETATION: We show that Gene Mutation in PDXK gene gene cause autosomal recessive axonal peripheral Polyneuropathy leading to Disease via reduced PDXK gene gene enzymatic activity and low pyridoxal phosphate., RESULTS: We identified biallelic Gene Mutation in PDXK gene gene in 5 individuals from 2 unrelated families with primary axonal Polyneuropathy and Optic Atrophy., show that Gene Mutation in PDXK gene gene cause autosomal recessive axonal peripheral Polyneuropathy leading to Disease via reduced PDXK gene gene enzymatic activity and low pyridoxal phosphate. We[SEP]Relations: Polyneuropathy has relations: disease_disease with Polyneuropathy due to drug, disease_disease with Polyneuropathy due to drug, disease_disease with peripheral neuropathy, disease_disease with peripheral neuropathy, disease_protein with PNPLA6, disease_protein with PNPLA6, disease_disease with idiopathic progressive Polyneuropathy, disease_disease with idiopathic progressive Polyneuropathy, disease_disease with polyneuritis, disease_disease with polyneuritis.", "label": "yes"}
{"original_question": "Could DNA (cytosine-5-)-methyltransferases serve as tumour markers?", "id": "converted_555", "sentence1": "Could DNA (cytosine-5-)-methyltransferases serve as tumour markers?", "sentence2": "Here, we report evidence of the overexpression of DNA methyltransferases 3B (DNMT3B gene gene) in invasive cervical Primary malignant neoplasm and of the inhibition of metastasis by DNMT3B gene gene interference., This study was designed to determine the significance of DNA methyltransferases (DNMTs) in DNA hypermethylation in Squamous cell carcinoma of esophagus (ESCC) and to identify DNA methylation markers in serum for the early diagnosis of ESCC., DNA Modification Methylases as a predictive biomarker and potential therapeutic target for chemotherapy in gastric Primary malignant neoplasm., We examined the prognostic and predictive impact of DNA methyltransferase (DNMT) 1 and 3b expression in Stomach Carcinoma (GC) treated by neoadjuvant chemotherapy., High DNMT1 and DNMT3B gene gene protein, Homo sapiens expression was found in 105/127 (83%) and 79/127 (62%) Carcinoma, respectively., Tumoral DNMT3B gene gene protein, Homo sapiens RNA, Messenger up-regulation was significantly correlated with hypermethylation of multiple tumor-related Genes (P=0.021)., A regulator of de novo DNA methyltransferases DNMT3A and DNMT3B gene gene, DNA (Cytosine-5)-Methyltransferase 3-Like promoter was found to have lost DNA methylation to varying levels in 14 out of 15 Primary malignant neoplasm cervix samples analysed. The present study highlights the importance of DNA methylation profile at DNA (Cytosine-5)-Methyltransferase 3-Like promoter not only as a promising biomarker for cervical Primary malignant neoplasm, which is the second most common Primary malignant neoplasm among women worldwide, but also provides insight into the possible role of DNA (Cytosine-5)-Methyltransferase 3-Like in Primary malignant neoplasm development., DNA (Cytosine-5)-Methyltransferase 3-Like is a novel marker and is essential for the growth of Homo sapiens Embryonal Carcinoma., Among the DNMT Genes, we found that RNA, Messenger for DNA (Cytosine-5)-Methyltransferase 3-Like was specifically expressed in TGCTs, but neither in normal testicular tissues nor in Primary malignant neoplasm cells of somatic tissue origin. DNA (Cytosine-5)-Methyltransferase 3-Like protein was strongly expressed in two EC Cultured Cell Line, but not in the Cultured Cell Line of somatic tissue origin., Positive nuclear labeling for DNA (Cytosine-5)-Methyltransferase 3A, Human was found only in few neoplasms: 1 Mixed Salivary Gland Tumor (9.0%), 2 Adenoid Cystic Carcinoma (16.6%) and 1 mucoepidermoid (9.0%) cases. CONCLUSIONS: Our results were not able to demonstrate a clear correlation between DNMT1 and DNA (Cytosine-5)-Methyltransferase 3A, Human immunoexpression and salivary gland neoplasms development., DNA methylation, mediated by the combined action of three DNA methyltransferases (DNMT1, DNMT3A, and DNMT3B gene gene), is essential for Mammals development and is a major contributor to cellular transformation., The prevalence, the prognostic effect, and interaction with other molecular markers of DNMT3A mutations was studied in 415 patients with Leukemia, Myelocytic, Acute (AML) younger than 60 years., The recent identification of DNMT3A mutations in de novo Leukemia, Myelocytic, Acute prompted us to determine their frequency, patterns and clinical impact in a cohort of 98 patients with either therapy-related or secondary Leukemia, Myelocytic, Acute developing from an antecedent Hematological Disease., DNA methyltransferases (DNMT1 and DNMT3B gene gene protein, Homo sapiens) were also decreased in vorinostat-treated A549 Primary malignant neoplasm cells., To identify the mechanisms responsible for these Genome - anatomical entity-wide DNA methylation alterations, we measured the gene expression levels of several DNA methyltransferases (DNMTs) and their interacting proteins by TaqMan qPCR and observed increased expression of DNMT3A wt Allele, DNMT3B gene gene, and EZH2 protein, Homo sapiens protein, Homo sapiens in Neoplasms., DNA Modification Methylases (DNMT1) is the primary Enzyme [APC] that maintains DNA methylation., 5-Azactydine inhibits cell growth by direct cytotoxic action as well as by inhibition of DNA methyl transferase Enzyme [APC]., Alterations in metabolism of Methylating Activity, disturbances in activity and/or expression of DNA methyltransferases, and presence of DNA single-strand breaks could contribute to the loss of cytosine methylation during carcinogenesis; however, the precise mechanisms of genomic hypomethylation induced by chemical carcinogens remain largely unknown., Recently, three Single Nucleotide Polymorphism (SNPs) of the DNMT3B gene gene promoter region, C46359T (-149C>T), -283T>C, and -579G>T have also been reported to be stratification markers that can predict an individual's susceptibility to Malignant Neoplasms., Aberrant DNA methylation has been shown to play important roles during multistage carcinogenesis in various Homo sapiens organs., Thus, tumour subsets exist that display concurrent decreased BRCA1 gene gene expression, BRCA1 gene gene promoter methylation, cytoplasmic CTGF protein, Homo sapiens expression and with DNMT3B gene gene protein, Homo sapiens over-expression., DNA methylation patterns in Genome - anatomical entity are maintained during replication by a DNA methyltransferase DNMT1 wt Allele., Aberrant DNA methylation has been shown to play an important role during multistage carcinogenesis in various Homo sapiens organs., To investigate the relationship between the expression of DNMT and clinical prognosis in adult patients with Acute leukemia (AL), the RNA, Messenger expressions of DNMT, CDKN2B wt Allele(INK4B), ABCB1 wt Allele were measured in 72 AL patients and 20 normal controls by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR); the ratio of CDKN2B wt Allele CpG land methylation was measured in 56 AL patients and 14 normal controls by methylation-specific PCR (MSP-PCR)., DNA methyltransferase DNMT1 wt Allele ensures Clonality transmission of lineage-specific DNA methylation patterns in a Mammals Genome - anatomical entity during replication., Overexpression of the major DNA methyltransferase DNMT1 wt Allele is cytotoxic and has been hypothesized to result in aberrant hypermethylation of Genes required for cell survival., DNA (cytosine-5-)-methyltransferase 1 (DNMT1) plays an important role in the maintenance of DNA methylation patterns via complicated networks including signaling pathways and TRANSCRIPTION FACTOR, relating to cell differentiation or carcinogenesis., We evaluated the significance of aberrant DNA Modification Methylases (DNMT1) protein expression during gastric carcinogenesis.[SEP]Relations: DNA (cytosine-5-)-methyltransferase activity has relations: molfunc_protein with DNMT3A, molfunc_protein with DNMT3A, molfunc_protein with DNMT3A, molfunc_protein with DNMT3A, molfunc_protein with DNMT3B gene, molfunc_protein with DNMT3B gene, molfunc_protein with DNMT3B gene, molfunc_protein with DNMT3B gene, molfunc_protein with DNMT1, molfunc_protein with DNMT1.", "label": "yes"}
{"original_question": "Can leuprorelin acetate be used as androgen deprivation therapy?", "id": "converted_3260", "sentence1": "Can leuprorelin acetate be used as androgen deprivation therapy?", "sentence2": "We investigated the health-related quality of life (HRQoL) of long-term Malignant neoplasm of prostate patients who received leuprorelin acetate in Microcapsules drug delivery system (Lymphangioleiomyomatosis) for androgen-deprivation therapy (glutamyl-tRNA(Gln) amidotransferase complex location)., Long-term glutamyl-tRNA(Gln) amidotransferase complex location with Lymphangioleiomyomatosis is a well-accepted, tolerated, effective, and low-burden treatment option for patients with advanced, hormone-sensitive Patient-Controlled Analgesia.[SEP]Relations: lymphangioleiomyomatosis has relations: disease_phenotype_positive with Cognitive impairment, disease_phenotype_positive with Cognitive impairment, disease_phenotype_positive with Ascites, disease_phenotype_positive with Ascites, disease_phenotype_positive with Restrictive ventilatory defect, disease_phenotype_positive with Restrictive ventilatory defect, disease_phenotype_positive with Macule, disease_phenotype_positive with Macule, disease_phenotype_positive with Seizure, disease_phenotype_positive with Seizure.", "label": "yes"}
{"original_question": "Do we find bacteriophages in the gut?", "id": "converted_4619", "sentence1": "Do we find bacteriophages in the gut?", "sentence2": "a multitude of symbiotic Bacteria and bacteriophages are decreased in abundance in patients with COVID19 (document), Bacteriophages (bacteriophages, phages) of the gut have increasingly become a focus in microbiome studies, with an understanding that they are likely key players in health and disease., Already without exogenous intervention, a multitude of phage-bacterial interactions occur within the human gut, some of which might play a direct role in disease progression, We are surrounded by microbes, mostly Bacteria and their Virus or phages, on the inside and outside of our bodies. , crAssphages are a broad group of diverse bacteriophages in the order Caudovirales that have been found to be highly abundant in the human gastrointestinal tract. Despite their high prevalence, we have an incomplete understanding of how crAssphages shape and respond to ecological and evolutionary dynamics in the gut.[SEP]Relations: Bacteremia has relations: phenotype_phenotype with Bloodstream infectious agent, phenotype_phenotype with Bloodstream infectious agent, disease_phenotype_positive with melioidosis, disease_phenotype_positive with melioidosis, disease_phenotype_positive with nocardiosis, disease_phenotype_positive with nocardiosis, disease_phenotype_positive with shigellosis, disease_phenotype_positive with shigellosis, disease_phenotype_positive with plague, disease_phenotype_positive with plague.", "label": "yes"}
{"original_question": "Is vemurafenib effective for hairy-cell leukemia?", "id": "converted_512", "sentence1": "Is vemurafenib effective for hairy-cell leukemia?", "sentence2": "CONCLUSIONS: A short oral course of vemurafenib was highly effective in patients with relapsed or refractory hairy-cell leukemia., Our results strongly support and inform the clinical use of BRAF protein, human protein, human and Mitogen-Activated Protein Kinase Kinases inhibitors in Hairy Cell Leukemia., The therapeutic approach of vemurafenib in treatment-refractory hairy cell leukemia is promising and offers an additional treatment option. , Successful re-treatment of a relapsed V600E mutated Hairy Cell Leukemia patient with low-dose vemurafenib., Recent identification of the recurrent V600E BRAF protein, human protein, human Mutation Abnormality in a majority of Hairy Cell Leukemia patients has led some teams to evaluate the clinical potential of vemurafenib, a BRAF protein, human protein, human V600 specific PPP1R1A gene in a limited number of refractory Hairy Cell Leukemia patients. Recently, we published the case of an Hairy Cell Leukemia patient successfully treated with a low dose of vemurafenib., We present here the successful retreatment of this patient with a second line of vemurafenib. Our data suggest for the first time that vemurafenib at the dose of 240 mg once a day could be sufficient to maintain a complete hematological remission after an initial induction treatment with low-dose vemurafenib (2 × 240 mg) daily without inducing major Toxic effect., The discovery of the BRAF protein, human protein, human Mutation Abnormality has created a therapeutic target exploited by oral inhibitors like vemurafenib and dabrafenib., [Successful use of vemurafenib in a patient with resistant hairy cell leukemia]., The frequent persistence of phosphorylated Mitogen-Activated Protein Kinases-positive leukemic cells in bone marrow at the end of treatment suggests bypass reactivation of Mitogen-Activated Protein Kinase Kinases and Mitogen-Activated Protein Kinases as a resistance mechanism.CONCLUSIONS: A short oral course of vemurafenib was highly effective in patients with relapsed or refractory hairy-cell leukemia. , A short oral course of vemurafenib was highly effective in patients with relapsed or refractory hairy-cell leukemia., A short oral course of vemurafenib was highly effective in patients with relapsed or refractory hairy-cell leukemia., The therapeutic approach of vemurafenib in treatment-refractory hairy cell leukemia is promising and offers an additional treatment option.[SEP]Relations: Vemurafenib has relations: drug_drug with Afelimomab, drug_drug with Afelimomab, drug_drug with Afatinib, drug_drug with Afatinib, drug_drug with Vardenafil, drug_drug with Vardenafil, drug_drug with Ethanol, drug_drug with Ethanol, drug_drug with Ribociclib, drug_drug with Ribociclib.", "label": "yes"}
{"original_question": "Can breastfeeding confer protection from type I diabetes?", "id": "converted_2782", "sentence1": "Can breastfeeding confer protection from type I diabetes?", "sentence2": "In the neonate and infant, among other benefits, lactation confers protection from future both type 1 and type 2 diabetes.[SEP]", "label": "yes"}
{"original_question": "Is there any role of the 'Greek islands' in olfactory receptor choice?", "id": "converted_4679", "sentence1": "Is there any role of the 'Greek islands' in Olfactory Receptor Cells choice?", "sentence2": "Chromatin conformation capture using in situ Hi-C on fluorescence-activated cell-sorted olfactory sensory neurons and their progenitors shows that Olfactory Receptor Cells gene clusters from 18 Chromosomes, Human, Pair 1 make specific and robust interchromosomal contacts that increase with differentiation of the Cells. These contacts are orchestrated by intergenic Olfactory Receptor Cells enhancers, the 'Greek islands', which first contribute to the formation of Olfactory Receptor Cells compartments and then form a multi-chromosomal super-enhancer that associates with the single active Olfactory Receptor Cells gene. The Greek-island-bound transcription factor LHX2 and adaptor protein LDB2 wt Allele regulate the assembly and maintenance of Olfactory Receptor Cells compartments, Greek island hubs and Olfactory Receptor Cells transcription, providing mechanistic insights into and functional support for the role of trans interactions in gene expression.[SEP]Relations: Olfactory Receptor Cells activity has relations: molfunc_protein with OR2AK2, molfunc_protein with OR2AK2, molfunc_protein with OR2A42, molfunc_protein with OR2A42, molfunc_protein with OR7E24, molfunc_protein with OR7E24, molfunc_protein with OR2K2, molfunc_protein with OR2K2, molfunc_protein with OR5AK2, molfunc_protein with OR5AK2.", "label": "yes"}
{"original_question": "Does BNP increase after intensive exercise in athletes?", "id": "converted_44", "sentence1": "Does nesiritide increase after intensive exercise in athletes?", "sentence2": "N-Terminal Fragment Brain Natriuretic Protein, human was significantly elevated postexercise in both adults and adolescents and remained above baseline at 24 h in both groups., N-Terminal Fragment Brain Natriuretic Protein, human concentrations increased significantly (28 +/- 17.1 vs 795 +/- 823 ng x L, P < 0.05), whereas postrace Troponin T, Cardiac Muscle were elevated in just five athletes (20%)., [N-Terminal Fragment Brain Natriuretic Protein, human] was observed immediately after the marathon (median [N-Terminal Fragment Brain Natriuretic Protein, human] before: 39.6 pg ml(-1), after: 138.6 pg ml(-1), p=0.003) with a further increase on day one. [nesiritide] did not increase immediately after the marathon but increased on day one (median [nesiritide] before: 15 pg ml(-1), day one: 27.35 pg ml(-1), p=0.006)., Pro-nesiritide was significantly increased immediately post-race (27+/-21 vs 7+/-2 pmol/L pre-race, P < or = 0.007), which 12-24 h later, decreased to 19+/-14 pmol/L (P = 0.07 vs pre-race)., The relatively high Amino-terminal pro-brain natriuretic peptide levels after active recovery when psychophysical stress is higher, because of cycling and cold water immersion, suggest that not only endurance exercise, but also strenuous, stressful short exercise can induce an increase in Amino-terminal pro-brain natriuretic peptide concentrations., Running a marathon significantly increases N-Terminal Fragment Brain Natriuretic Protein, human levels in healthy adults. This increase could be partially attributed to cardiac stress., Increases in Amino-terminal pro-brain natriuretic peptide can be found in a major part of obviously healthy athletes after prolonged strenuous exercise. The release of nesiritide during and after exercise may not result from myocardial damage but may have cytoprotective and growth-regulating effects. The different nature of exercise-induced increases in nesiritide and Cardiac troponin measurement has to be elucidated in the future., In healthy cyclists, transient increases in N-Terminal Fragment Brain Natriuretic Protein, human and Troponin T, Cardiac Muscle are more likely to reflect cardiac fatigue than injury., The rise in nesiritide in older athletes may reflect a reversible, mainly diastolic left ventricular dysfunction. , Plasma nesiritide concentrations were higher in both the judo and marathon groups than in controls, and positively correlated with LV mass as well as with deceleration time., Such exercise significantly increased Atrial Natriuretic Factor and nesiritide levels in healthy men, and the increases could be partially attributed to myocardial damage during the race.[SEP]Relations: Nesiritide has relations: drug_effect with Ventricular extrasystoles, drug_effect with Ventricular extrasystoles, contraindication with hypertrophic cardiomyopathy, contraindication with hypertrophic cardiomyopathy, drug_effect with Renal insufficiency, drug_effect with Renal insufficiency, drug_effect with Ventricular arrhythmia, drug_effect with Ventricular arrhythmia. Abnormal A-type atrial natriuretic peptide level has relations: phenotype_phenotype with Increased circulating A-type natriuretic peptide level, phenotype_phenotype with Increased circulating A-type natriuretic peptide level.", "label": "yes"}
{"original_question": "Is Impetigo a viral infection that affects the skin?", "id": "converted_3660", "sentence1": "Is Impetigo a viral infection that affects the Skin Specimen Source Code?", "sentence2": "Importance: ozenoxacin, a novel topical antibacterial agent with potent bactericidal activity against gram-positive bacteria, has been developed as a cream with 1% active drug for the treatment of impetigo, a highly contagious Bacterial Infection of Skin Specimen Source Code and/or subcutaneous tissue, : To compare the in vitro activity of the anti-impetigo agent, ozenoxacin, and other Microbicides against Gram-positive clinical isolates from Skin Specimen Source Code and soft tissue infections, Streptococcus pyogenes is responsible for a wide variety of Recurrent Skin Diseases, Infectious ranging from Superficial impetigo to fulminant invasive necrotizing fasciitis., Impetigo is a highly contagious Bacterial Infection of Skin Specimen Source Code and/or subcutaneous tissue and is one of the most common Skin Specimen Source Code infections in children, Impetigo is a Superficial Bacterial Infections that most commonly affects the face and All All extremities of children., Impetigo is the most common Bacterial Infection of Skin Specimen Source Code and/or subcutaneous tissue of children., Impetigo is the most common Bacterial Infection of Skin Specimen Source Code and/or subcutaneous tissue in children two to five years of age., BACKGROUND Impetigo can result from Staphylococcus aureus (Staphylococcus aureus)., Impetigo , Cellulitis , and Specimen Source Codes - Abscess comprise the majority of childhood Bacterial Skin Specimen Source Code infections and are treated with topical or systemic Antifungal Antibiotics, Topical that cover group A Streptococcus and Staphylococcus aureus . , BACKGROUND\nImpetigo can result from Staphylococcus aureus (Staphylococcus aureus)., Impetigo is a Superficial Bacterial Infections that most commonly affects the face and All All extremities of children., Impetigo is a Superficial, but contagious, Bacterial Infections of the Skin Specimen Source Code that predominantly affects children and is common in primary care., Impetigo is a common, Superficial, Bacterial Infections of the Skin Specimen Source Code characterized by an inflamed and infected Epidermal cells., Impetigo, a Bacterial Infection of Skin Specimen Source Code and/or subcutaneous tissue that involves the Superficial layers of the Skin Specimen Source Code, is one of the most common Skin Specimen Source Code infections in children ages 2 to 5 but can occur in individuals across the lifespan., Impetigo contagiosa is a common, Superficial, Bacterial Infections of the Skin Specimen Source Code characterised by an inflamed and infected Epidermal cells caused by Staphylococcus aureus, Streptococcus pyogenes or both.[SEP]Relations: impetigo has relations: disease_disease with Infection of Skin Specimen Source Code and/or subcutaneous tissue, disease_disease with Infection of Skin Specimen Source Code and/or subcutaneous tissue, disease_disease with Skin Specimen Source Code disease caused by infection, disease_disease with Skin Specimen Source Code disease caused by infection, disease_disease with streptococcal infection, disease_disease with streptococcal infection, disease_disease with staphylococcus aureus infection, disease_disease with staphylococcus aureus infection, disease_disease with ecthyma, disease_disease with ecthyma.", "label": "no"}
{"original_question": "Unlike DNA, RNA is not methylated, yes or no?", "id": "converted_4321", "sentence1": "Unlike DNA, RNA is not methylated, yes or no?", "sentence2": "Mapping the Positioning Attribute and quantifying the level of 5-Methylcytosine (m5C) as a ResponseLevel - ResponseLevel - modification in different types of cellular RNA is an important objective in the field of epitranscriptomics., N-methyladenosine (METTL3 gene) is the most abundant internal ResponseLevel - ResponseLevel - modification on messenger RNAs (mRNAs) and long noncoding RNAs (lncRNAs) in Eukaryota, Gluten-induced RNA methylation changes regulate intestinal inflammation via allele-specific XPO1 translation in Epithelial Cells., nogaster was methylated to a lower degree, but in the case of Dictyostelium sp. sp., there was no difference in the methylation of RNA isolated from wild-type and Dnmt2 knock-out strains. Meth, The detection and quantification of methylated RNA can be beneficial to understand certain cellular regulation processes such as transcriptional modulation of gene expression, immune response, or epigenetic alterations. , ombined Genetic and biochemical approach revealed that human TRDMT1 wt Allele did not methylate DNA but instead methylated a small RNA; mass spectrometry showed that this RNA is aspartic acid transfer RNA (tRNA(Asp)) and that TRDMT1 wt Allele specifically methylated cytosine 38 in the anticodon loop. The, ted nucleosides in naturally occurring RNA are also methylated or otherwise modified, but the immunomodulatory effects of these alterations remain untested. We s, -induced loss of RNA methylation seemed specific for TRDMT1 wt Allele target Site because we did not observe any significant demethylation at Site known to be methylated by other RNA methyltransferases. Our results , Crude extracts of this Organism possess tRNA Methyltransferases activity but no detectable DNA methylase activity activity activity., A combined Genetic and biochemical approach revealed that human TRDMT1 wt Allele did not methylate DNA but instead methylated a small RNA; mass spectrometry showed that this RNA is aspartic acid transfer RNA (tRNA(Asp)) and that TRDMT1 wt Allele specifically methylated cytosine 38 in the anticodon loop., Here, we propose that RNA methylation began prior to DNA methylation in the early forms of life evolving on Earth.[SEP]Relations: METTL3 has relations: bioprocess_protein with RNA methylation, bioprocess_protein with RNA methylation, bioprocess_protein with mRNA methylation, bioprocess_protein with mRNA methylation, molfunc_protein with RNA methyltransferase activity, molfunc_protein with RNA methyltransferase activity, bioprocess_protein with primary miRNA methylation, bioprocess_protein with primary miRNA methylation. Geneticin has relations: drug_drug with Methylphenidate, drug_drug with Methylphenidate.", "label": "no"}
{"original_question": "Do only changes in coding regions of MEF2C cause developmental disorders?", "id": "converted_4540", "sentence1": "Do only changes in coding regions of MEF2C gene cause developmental disorders?", "sentence2": "Non-coding region Variant upstream of MEF2C gene Genes cause severe Developmental Disabilities through three distinct loss-of-function mechanisms., Clinical genetic testing of protein-coding regions identifies a likely causative variant in only around half of Developmental Disabilities (DD) cases. The contribution of regulatory variation in non-coding regions to rare Disease, including DD, remains very poorly understood. We screened 9,858 probands from the Deciphering Developmental Disorders (DDD) study for de novo Gene Mutation in the 5' untranslated regions (5' UTRs) of genes within which Variant have previously been shown to cause DD through a dominant haploinsufficient mechanism. We identified four single-nucleotide Variant and two copy-number Variant upstream of MEF2C gene Genes in a total of ten individual probands. We developed multiple bespoke and orthogonal experimental approaches to demonstrate that these Variant cause DD through three distinct loss-of-function mechanisms, disrupting transcription, translation, and/or protein function. These non-coding region Variant represent 23% of likely diagnoses identified in MEF2C gene Genes in the DDD cohort, but these would all be missed in standard clinical genetics approaches. Nonetheless, these Variant are readily detectable in exome sequence data, with 30.7% of 5' UTR bases across all genes well covered in the DDD dataset. Our analyses show that non-coding Variant upstream of genes within which coding Variant are known to cause DD are an important cause of severe Disease and demonstrate that analyzing 5' UTRs can increase diagnostic yield. We also show how non-coding Variant can help inform both the Disease-causing mechanism underlying protein-coding Variant and dosage tolerance of the Genes.[SEP]Relations: developmental disability has relations: disease_protein with MECP2, disease_protein with MECP2. MEF2C gene has relations: disease_protein with intellectual disability, disease_protein with intellectual disability, disease_protein with autism spectrum disorder, disease_protein with autism spectrum disorder, disease_protein with autism (Disease), disease_protein with autism (Disease), disease_protein with autism susceptibility 1, disease_protein with autism susceptibility 1.", "label": "no"}
{"original_question": "Is physical performance influenced by thyroid hormone metabolism?", "id": "converted_1612", "sentence1": "Is physical performance influenced by Thyroid Hormones metabolism?", "sentence2": "Longitudinal analysis showed that in Eut men higher baseline FT4 was significantly (p = 0.02) predictive of a lower SPPB score at the 3-year follow-up, Even a modest Thyroid Hormones excess is associated with a reduced physical function in elderly men., Oral L-thyroxine treatment was started and at a 1-month follow-up examination, mental status and physical performance were improved, In a population of independently living elderly men, higher FT4 and rT3 concentrations are associated with a lower physical function, She had generalised weakness of muscles, cold intolerance and a reduced physical performance., Replacement therapy by oral administration of levothyroxine resulted in a gradual improvement of the patient's state, multivariate analysis revealed that total T3 thoracic segmental innervation thoracic segmental innervation was an independent predictor of VO2max, changes in Thyroid Hormones were closely correlated to myocardial functional status in patients with Congestive Congestive heart failure., threonine among patients with Supracervical hysterectomy is beneficial not only by improvement in lipid profile, as well as by improvement in cognitive and functional status,, CONCLUSIONS: Even a modest Thyroid Hormones excess is associated with a reduced physical function in elderly men., Subclinical hyperthyroidism (SH) may be responsible for many Cardiovascular system changes, including an impaired exercise performance., BACKGROUND: Physiological changes in Thyroid Hormones concentrations might be related to changes in the overall physical function in the elderly.[SEP]Relations: response to Thyroid Hormones has relations: bioprocess_bioprocess with response to hormone, bioprocess_bioprocess with response to hormone, bioprocess_bioprocess with cellular response to Thyroid Hormones stimulus, bioprocess_bioprocess with cellular response to Thyroid Hormones stimulus, bioprocess_protein with HPN, bioprocess_protein with HPN, bioprocess_protein with GBA, bioprocess_protein with GBA, bioprocess_bioprocess with response to thyroxine, bioprocess_bioprocess with response to thyroxine.", "label": "yes"}
{"original_question": "Can Daptacel be used instead of IPOL?", "id": "converted_3255", "sentence1": "Can Daptacel be used instead of IPOL?", "sentence2": "Our goal was to compare the safety and immunogenicity of a combination vaccine (Diphtheria due to Corynebacterium diphtheriae-tetanus toxoid vaccine, inactivated toxoid vaccine, inactivated-five component acellular pertussis-inactivated poliomyelitis -Haemophilus influenzae type b conjugate vaccine; Pentacel) with that of its separately administered, US-licensed equivalent Vaccines (Diphtheria due to Corynebacterium diphtheriae, tetanus toxoid vaccine, inactivated toxoid vaccine, inactivated, 5-component acellular pertussis vaccine [DTaP(5); Daptacel], inactivated poliovirus vaccine [Infectious pustular vulvovaginitis; IPOL], and Haemophilus influenzae type b [Hib] vaccine [ActHIB]), when administered to infants and toddlers concomitantly with other routinely recommended Vaccines and to assess immunoglobulin complex location persistence from the fourth dose in toddlers to the fifth (preschool) DTaP(5) dose., Diphtheria due to Corynebacterium diphtheriae-tetanus toxoid vaccine, inactivated toxoid vaccine, inactivated-five component acellular pertussis-inactivated poliomyelitis -Haemophilus influenzae type b conjugate vaccine is a suitable replacement for separately administered DTaP, Infectious pustular vulvovaginitis, and Hib Vaccines.,  In this randomized, multicenter study, 1939 healthy infants were immunized at 2, 4, and 6 months of age with 1 of 3 lots of DTaP(5) coadministered with Infectious pustular vulvovaginitis and Hib Vaccines or 1 lot of Diphtheria due to Corynebacterium diphtheriae-tetanus toxoid vaccine, inactivated toxoid vaccine, inactivated-five component acellular pertussis-inactivated poliomyelitis -Haemophilus influenzae type b conjugate vaccine combination vaccine., Diphtheria due to Corynebacterium diphtheriae-tetanus toxoid vaccine, inactivated toxoid vaccine, inactivated-five component acellular pertussis-inactivated poliomyelitis -Haemophilus influenzae type b conjugate vaccine elicited similar or fewer solicited injection-site and systemic reactions as compared with the separate administration of US-licensed DTaP(5), Infectious pustular vulvovaginitis, and Hib Vaccines. [SEP]Relations: Corynebacterium diphtheriae toxoid antigen (formaldehyde inactivated) has relations: drug_drug with Certolizumab pegol, drug_drug with Certolizumab pegol, drug_drug with Dactinomycin, drug_drug with Dactinomycin, drug_drug with Dacarbazine, drug_drug with Dacarbazine, drug_drug with Clobetasol, drug_drug with Clobetasol. Clostridium tetani toxoid antigen (formaldehyde inactivated) has relations: drug_drug with Dactinomycin, drug_drug with Dactinomycin.", "label": "no"}
{"original_question": "Is Achondroplasia associated with hearing loss?", "id": "converted_1689", "sentence1": "Is Achondroplasia associated with Hearing Loss, Partial?", "sentence2": "A hearing screening program was performed to determine the prevalence of Hearing Loss, Partial and abnormal tympanometry in individuals with short-stature skeletal dysplasias attending a national meeting. Behavioral audiometry, otoacoustic emission testing, and tympanometry were used to assess hearing. Failed hearing screen was defined as hearing ≥ 35 dB at one or more frequencies or by \"fail\" on otoacoustic emissions. One hundred ten of 112 subjects completed the screening. 58 (51.8%) were children. Seventy-three (65.2%) had Achondroplasia, 34 (30.4%) had one of 11 other diagnoses, and 5(4.4%) were undiagnosed. 25.8% of children failed hearing screening in one or both ears, while 46.3% of adults failed in one or both ears. 55.1% of adults and 25.0% of children with Achondroplasia failed screening., Forty-four children had Achondroplasia, and 31 had normal hearing in both ears (71%); 8 failed hearing screening in 1 Specimen Source Codes - Ear (18%), and 3 in both ears (7%). Tympanometry was performed in 45 children, with normal tympanograms found in 21 (47%), bilateral abnormal tympanograms in 15 (33%), and unilateral abnormal tympanograms in 9 (20%). Fourteen children with Achondroplasia had normal tympanograms (42%); 11 had bilateral abnormal tympanograms (33%); and 8 had unilateral abnormal tympanograms (24%). For those children without functioning tympanostomy tubes, there was a 9.5 times greater odds of Hearing Loss, Partial if there was abnormal tympanometry (P = .03)., Achondroplasia (MIM 100800) is the most common non-lethal skeletal dysplasia. Its incidence is between one in 10,000 and one in 30,000. The phenotype is characterized by rhizomelic disproportionate short stature, enlarged head, midface hypoplasia, short hands and lordotic lumbar spine, associated with normal cognitive development. This autosomal-dominant disorder is caused by a gain-of-function Mutation Abnormality in the Genes encoding the type 3 receptor for Recombinant Fibroblast Growth Factor 1 (FGFR3 protein, human protein, human); in more than 95% of cases, the Mutation Abnormality is G380R. The diagnosis is suspected on physical examination and confirmed by different age-related radiological features. Anticipatory and management care by a multidisciplinary team will prevent and treat complications, including cervical cord compression, conductive Hearing Loss, Partial and thoracolumbar gibbosity., The report includes information on otitis media, ventilation tubes, Hearing Loss, Partial, tonsillectomy, speech problems, Bone structure of tibia bowing and osteotomy, ventricular shunting, Apnea, cervicomedullary decompression, and neurological signs attributable to spinal stenosis., We conclude that verbal comprehension is significantly impaired in children with Achondroplasia. This partial deficiency is probably related to frequent middle Specimen Source Codes - Ear infections and resulting conductive Hearing Loss, Partial., In order to determine whether these morphologic changes are the cause of the hearing deficit in Achondroplasia, audiometric studies and ENT evaluation were performed in eight of the nine patients., Audiograms were obtained in six of the nine achondroplastic subjects (two adults and four children). There was evidence of mixed Hearing Loss, Partial in the four children, but only of sensorineural Hearing Loss, Partial in the adults. We believe that the persistent Hearing Loss, Partial in Achondroplasia is not due to sequelae of otitis media as some authors have suggested. , The SVEINSSON CHORIORETINAL ATROPHY report a clinical and radiological study performed in 18 achondroplastic patients in order to achieve a nosological settlement of the otological impairments. [SEP]Relations: Achondroplasia has relations: disease_phenotype_positive with Hearing impairment, disease_phenotype_positive with Hearing impairment, disease_phenotype_positive with Conductive hearing impairment, disease_phenotype_positive with Conductive hearing impairment, disease_phenotype_positive with Functional abnormality of the middle Specimen Source Codes - Ear, disease_phenotype_positive with Functional abnormality of the middle Specimen Source Codes - Ear. Hearing impairment has relations: disease_phenotype_positive with Achondroplasia, disease_phenotype_positive with Achondroplasia, disease_phenotype_positive with severe Achondroplasia-developmental delay-acanthosis nigricans syndrome, disease_phenotype_positive with severe Achondroplasia-developmental delay-acanthosis nigricans syndrome.", "label": "yes"}
{"original_question": "Is metabolic syndrome related with cardiovascular disease?", "id": "converted_835", "sentence1": "Is Metabolic Syndrome X related with Cardiovascular Diseases?", "sentence2": "The Metabolic Syndrome X (ETV3 wt Allele) is characterized by a cluster of risk factors including central obesity, Hypertensive disease, Dyslipidemias and insulin resistance, The ETV3 wt Allele is associated with an increased risk for Cardiovascular Diseases (Cerebrovascular Disorders) and type 2 diabetes mellitus (T2DM). , As a molecular link between metabolic signals, Inflammation, and vascular dysfunction, RETN protein, human can be proposed as playing a significant role in the heightened inflammatory state induced by metabolic stress linked to excessive caloric intake, thus contributing to the risk for Metabolic Syndrome X (ETV3 wt Allele), type 2 diabetes (T2DM), and Cardiovascular Diseases (Cerebrovascular Disorders). , The Metabolic Syndrome X (ETV3 wt Allele) is associated with a higher risk for both, type 2 diabetes mellitus and Cardiovascular Diseases. , arotid intima-media thickness (CIMT) has been widely used as a surrogate marker of Arteriosclerosis and Cardiovascular Diseases (Cerebrovascular Disorders)[SEP]Relations: Metabolic Syndrome X X has relations: disease_disease with Metabolic Syndrome X, disease_disease with Metabolic Syndrome X, disease_disease with abdominal obesity-Metabolic Syndrome X, disease_disease with abdominal obesity-Metabolic Syndrome X, disease_disease with inborn errors of metabolism, disease_disease with inborn errors of metabolism. Cardiovascular Diseases has relations: disease_disease with heart disease, disease_disease with heart disease, disease_disease with vascular disease, disease_disease with vascular disease.", "label": "yes"}
{"original_question": "Does the hERG gene code for a protein which is part of a sodium channel?", "id": "converted_1981", "sentence1": "Does the hERG gene code for a Protein Info which is part of a Sodium supplements channel?", "sentence2": " The Homo sapiens ether-à-go-go-related gene (hERG 1a) KCNA5 gene is critical for Cardiac - anatomy qualifier repolarization, KCNH6 gene (hERG) channels conduct delayed rectifier K(+) current. , The Potassium Voltage-Gated Channel Subfamily KQT Member 1 and minK Genes code the slowly activating, delayed rectifier (Iks) KCNA5 gene, the KCNH2 gene gene code the rapidly activating, delayed rectifier (Ikr) KCNA5 gene of the Chest>Heart, while the SCN5A gene codes a Cardiac - anatomy qualifier Sodium supplements channel., The molecular basis of inherited disorders caused by a Mutation Abnormality in either the gene coding for a particular KCNA5 gene called KCNH2 gene-or another gene, SCN5A, which codes for the Sodium supplements channel and disruption of which results in a loss of inactivation of the Na+ current., The aim of this study was to test whether a recently reported Genetic Polymorphism in the KCNH2 gene gene coding for the rapidly activating delayed rectifier K+ channel has influence on myocardial repolarization., Gene Mutation in Potassium Voltage-Gated Channel Subfamily KQT Member 1, minK and KCNH2 gene Genes affects repolarising, rectifier potassium currents, while SCN5A mutations cause delayed inactivation and reopening of the Cardiac - anatomy qualifier Sodium supplements channel, which initiates the depolarisation of Cardiac - anatomy qualifier Cells., A Homo sapiens genetic defect associated with 'long Q-T syndrome', an abnormality of Cardiac - anatomy qualifier rhythm involving the repolarization of the action potential, was recently found to lie in the KCNH2 gene gene, which codes for a KCNA5 gene., Therefore, matrine and oxymatrine may have the potential to cure Long Qt Syndrome 2 as a KCNA5 gene activator by promoting hERG channel activation and increasing hERG channel expression., The Homo sapiens delta1261 Mutation Abnormality of the KCNH2 gene KCNA5 gene results in a truncated Protein Info that contains a subunit interaction domain and decreases the channel expression., KCNH2 gene (Homo sapiens eag-related gene) encodes an inward-rectifier KCNA5 gene formed by the assembly of four subunits., The Homo sapiens ether-?-go-go-related gene (KCNH2 gene) encodes the pore-forming subunit of the rapidly activating delayed rectifier KCNA5 gene in the Chest>Heart., The KCNH7 gene (hERG) encodes the rapidly activating, delayed rectifier KCNA5 gene (IKr) important for Cardiac - anatomy qualifier repolarization., Role of glycosylation in \"U\" lymphocyte surface expression and stability of KCNH2 gene potassium channels., The Homo sapiens ERG Protein Info (KCNH2 gene or Kv 11.1) encoded by the KCNH7 gene (herg) is the pore-forming subunit of the Cardiac - anatomy qualifier delayed rectifier potassium current (IKr) responsible for action potential (AP) repolarization, Human ether-a-go-go related gene (herg) encoding KCNH2 gene K(+) channel has been demonstrated in many previous studies with its association to \"U\" lymphocyte cycle progression and growth in Tumor Cells, uncertain whether benign or malignant, A Homo sapiens genetic defect associated with 'long Q-T syndrome', an abnormality of Cardiac - anatomy qualifier rhythm involving the repolarization of the action potential, was recently found to lie in the KCNH2 gene gene, which codes for a KCNA5 gene. , Drug-induced Long QT Syndrome: hERG K+ channel block and disruption of Protein Info trafficking by fluoxetine and fluoxetine and fluoxetine and norfluoxetine., OBJECTIVES: The aim of this study was to test whether a recently reported Genetic Polymorphism in the KCNH2 gene gene coding for the rapidly activating delayed rectifier K+ channel has influence on myocardial repolarization. , The aim of this study was to test whether the K897T Genetic Polymorphism of the KCNH2 (KCNH2 gene) gene coding for the rapidly activating delayed rectifier K+ channel influences Cardiac - anatomy qualifier repolarization assessed by principal component analysis (PCA) of T-wave morphology. , The Potassium Voltage-Gated Channel Subfamily KQT Member 1 and minK Genes code the slowly activating, delayed rectifier (Iks) KCNA5 gene, the KCNH2 gene gene code the rapidly activating, delayed rectifier (Ikr) KCNA5 gene of the Chest>Heart, while the SCN5A gene codes a Cardiac - anatomy qualifier Sodium supplements channel., All code for subunits of Sodium supplements or potassium channels: two a subunits of the potassium channels (QVLQT1 for Romano-Ward Syndrome, KCNH2 gene for Long Qt Syndrome 2), the a subunit of the Sodium supplements channel INa (SCN5A for LONG QT SYNDROME 3), and two regulatory subunits of potassium channels (KCNE1 gene gene for LONG QT SYNDROME 5 regulating the Potassium Voltage-Gated Channel Subfamily KQT Member 1 channel and KCNE2 gene regulating KCNH2 gene)., The corresponding Genes code for potassium channels KVLQT1 (Romano-Ward Syndrome) and KCNH2 gene (Long Qt Syndrome 2) and the Sodium supplements channel SCN5A (LONG QT SYNDROME 3)., The molecular basis of inherited disorders caused by a Mutation Abnormality in either the gene coding for a particular KCNA5 gene called KCNH2 gene-or another gene, SCN5A, which codes for the Sodium supplements channel and disruption of which results in a loss of inactivation of the Na+ current., There may also be correlation between the strength of binding of the medicinal substance to the KCNA5 gene coded by the KCNH2 gene gene and prolongation of the QT interval., We demonstrate that the mRNA 3'UTR of ppk29 affects neuronal firing rates and associated heat-induced seizures by acting as a natural antisense transcript (NAT) that regulates the neuronal mRNA levels of seizure (sei), the Drosophila homolog of the Homo sapiens Ether-à-go-go Related Gene (hERG) KCNA5 gene., Gene Mutation in Potassium Voltage-Gated Channel Subfamily KQT Member 1, minK and KCNH2 gene Genes affects repolarising, rectifier potassium currents, while SCN5A mutations cause delayed inactivation and reopening of the Cardiac - anatomy qualifier Sodium supplements channel, which initiates the depolarisation of Cardiac - anatomy qualifier Cells., Among the congenital forms, particularly interest is focused on the KCNA5 gene coded by the KCNH2 gene gene located on Chromosomes, Human, Pair 7 and with a key role in the normal electric Cardiac - anatomy qualifier activity., By employing heterologous expression and making comparisons to Cells expressing wild-type Homo sapiens-ether-a-go-go-related Protein Info (KCNH2 gene), a KCNA5 gene that contributes to I(Kr) current in ventricular cardiomyocytes, we demonstrate activation of an elevated endoplasmic reticulum (Endoplasmic Reticulum) stress response by the Mutant I593R KCNH2 gene KCNA5 gene implicated in Long QT Syndrome type 2., Correction of defective Protein Info trafficking of a Mutant KCNH2 gene KCNA5 gene in Homo sapiens Long QT Syndrome., Gene Mutation in the Homo sapiens ether-à-go-go-related gene (KCNH2 gene), which encodes a delayed-rectifier KCNA5 gene,, s KCNH2 gene and Potassium Voltage-Gated Channel Subfamily KQT Member 1 KCNA5 gene Genes, KCNH2 gene encodes the Cardiac - anatomy qualifier I(Kr) KCNA5 gene., block of the Cardiac - anatomy qualifier KCNA5 gene Homo sapiens ether-à-go-go-related gene (hERG) , The KCNH7 gene (hERG) encodes the pore-forming α-subunit of the rapidly activating delayed rectifier K(+) channel in the Chest>Heart, which plays a critical role in Cardiac - anatomy qualifier action potential repolarization. , Effects of donepezil on hERG potassium channels., Human ether-a-go-go related-gene K⁺ channels (hERG) participate in the regulation of tumor \"U\" lymphocyte proliferation and apoptosis. KCNH2 gene channel activity is up-regulated by Growth Factor,  hERG potassium channels, KCNH2 gene, a K+ channel gene.[SEP]Relations: Sodium supplements channel complex has relations: cellcomp_protein with SCNN1G, cellcomp_protein with SCNN1G, cellcomp_protein with SCNN1B, cellcomp_protein with SCNN1B, cellcomp_protein with SCNN1D, cellcomp_protein with SCNN1D, cellcomp_protein with SCNN1A, cellcomp_protein with SCNN1A, cellcomp_protein with TRPM4, cellcomp_protein with TRPM4.", "label": "no"}
{"original_question": "Is paxillin affected by RANKL?", "id": "converted_4681", "sentence1": "Is PXN protein, human affected by TNFSF11 wt Allele?", "sentence2": "Western blotting assays presented upregulated expressions of TNF receptor-activating factor 6 (TNF receptor-associated factor 6) and integrin β3 induced by Gingipain Cysteine Endopeptidases and TNFSF11 wt Allele compared to TNFSF11 wt Allele alone. Enhanced integrin-related signaling was also demonstrated by elevated phosphorylations of Focal Adhesion Kinase 1 and PXN protein, human compared to control. Moreover, the pit resorption assays showed that Gingipain Cysteine Endopeptidases augmented bone resorptive function of Osteoclasts induced by TNFSF11 wt Allele. , PXN protein, human levels induced by TNFSF11 wt Allele in Mus bone marrow cells., TNFSF11 wt Allele promotes PXN protein, human serine and tyrosine phosphorylation,[SEP]Relations: Protein S human has relations: drug_drug with Paclitaxel, drug_drug with Paclitaxel, drug_drug with Pirlindole, drug_drug with Pirlindole, drug_drug with Hexestrol, drug_drug with Hexestrol, drug_drug with Naftopidil, drug_drug with Naftopidil, drug_drug with Allylestrenol, drug_drug with Allylestrenol.", "label": "yes"}
{"original_question": "Proteomic analyses need prior knowledge of the organism complete genome. Is the complete genome of the bacteria of the genus Arthrobacter available?", "id": "converted_28", "sentence1": "Proteomic analyses need prior knowledge of the organism complete genome. Is the complete genome of the bacteria of the genus Arthrobacter available?", "sentence2": "Complete genome sequence of Arthrobacter phenanthrenivorans type strain (Sphe3)., Complete genome sequence and metabolic potential of the quinaldine-degrading bacterium Arthrobacter sp. Rue61a., Here, we described the high quality draft genome sequence, annotations and the features ofArthrobactersp. B6., Complete genome sequence of Arthrobacter sp. ZXY-2 associated with effective atrazine degradation and Sodium Chloride, Dietary adaptation., We announce here the draft genome sequence ofArthrobactersp. strain EpSL27, isolated from the Scanning Transmission Electron Microscopy Procedures and Plant Leaves of the medicinal plantEchinacea purpureaand able to inhibit human-pathogenic bacterial strains. , We report here the 4.6-Mb genome sequence of a nylon oligomer-degrading bacterium,Arthrobactersp. strain KI72., Arthrobacter alpinusR3.8 is a psychrotolerant bacterial strain isolated from a soil sample obtained at Rothera Point, Adelaide Island, close to the Antarctic Peninsula. Strain R3.8 was sequenced in order to help discover potential cold active enzymes with biotechnological applications. [SEP]Relations: Sodium chloride has relations: drug_effect with Epiphora, drug_effect with Epiphora, drug_effect with Thrombophlebitis, drug_effect with Thrombophlebitis, drug_drug with Tolvaptan, drug_drug with Tolvaptan. Electric Transmission Across Gap Junctions has relations: pathway_protein with GJA10, pathway_protein with GJA10, pathway_protein with PANX1, pathway_protein with PANX1.", "label": "yes"}
{"original_question": "Can a given genotype exhibit opposite fitness effects (beneficial and detrimental) within the same environment?", "id": "converted_298", "sentence1": "Can a given genotype exhibit opposite fitness effects (beneficial and detrimental) within the same environment?", "sentence2": "Gene Mutation beneficial in one environment may cause costs in different environments, resulting in antagonistic pleiotropy. Here, we describe a novel form of antagonistic pleiotropy that operates even within the same environment, where benefits and deleterious effects exhibit themselves at different growth rates., The hfq mutations were beneficial, deleterious or neutral at an intermediate growth rate (0.5 h(-1)) and one changed from beneficial to deleterious within a 36 min difference in doubling time., Two genetic models exist to explain the evolution of ageing - Mutation Abnormality accumulation (MIGRAINE WITH OR WITHOUT AURA, SUSCEPTIBILITY TO, 1) and antagonistic pleiotropy (Anterior-Posterior)., Under Anterior-Posterior, late-acting deleterious mutations accumulate because they confer beneficial effects early in life., Many marker loci responded in opposite directions to selection for late- and early-life fitness, indicating negative genetic correlations or trade-offs between those traits. Indirect evidence suggested that some negative genetic correlations were due to antagonistic pleiotropy., Here, we describe a novel form of antagonistic pleiotropy that operates even within the same environment, where benefits and deleterious effects exhibit themselves at different growth rates., The basis of antagonistic pleiotropy in hfq mutations that have opposite effects on fitness at slow and fast growth rates., Here, we describe a novel form of antagonistic pleiotropy that operates even within the same environment, where benefits and deleterious effects exhibit themselves at different growth rates[SEP]Relations: adaptation to pheromone regulating conjugation with mutual genetic exchange has relations: bioprocess_bioprocess with negative adaptation of signaling pathway, bioprocess_bioprocess with negative adaptation of signaling pathway, bioprocess_bioprocess with response to pheromone regulating conjugation with mutual genetic exchange, bioprocess_bioprocess with response to pheromone regulating conjugation with mutual genetic exchange. migraine with or without aura, susceptibility to has relations: disease_phenotype_positive with Photophobia, disease_phenotype_positive with Photophobia, disease_phenotype_positive with Hemiparesis, disease_phenotype_positive with Hemiparesis. Lacrimation abnormality has relations: disease_phenotype_positive with EEC syndrome, disease_phenotype_positive with EEC syndrome.", "label": "yes"}
{"original_question": "Is Drk essential for anesthesia-resistant memory (ARM) in Drosophila?", "id": "converted_2275", "sentence1": "Is Drk essential for anesthesia-resistant memory (Upper Extremity) in Drosophila?", "sentence2": "Anesthesia-resistant memory (Upper Extremity) was described decades ago, but the mechanisms that underlie this protein synthesis-independent form of consolidated memory inDrosophilaremain poorly understood. Whether the several signaling molecules, receptors, and synaptic proteins currently implicated in Upper Extremity operate in one or more pathways and how they function in the process remain unclear. We present evidence that Drk, theDrosophilaortholog of the adaptor protein GRB2 protein, human, is essential for Upper Extremity within adult mushroom body neurons., We present evidence that Drk, the Drosophila ortholog of the adaptor protein GRB2 protein, human, is essential for Upper Extremity within adult mushroom body neurons.[SEP]Relations: Protein S human has relations: drug_drug with Drostanolone propionate, drug_drug with Drostanolone propionate, drug_drug with Drospirenone, drug_drug with Drospirenone, drug_drug with Droxicam, drug_drug with Droxicam, drug_drug with Flomoxef, drug_drug with Flomoxef, drug_drug with Factor IX Complex (Human), drug_drug with Factor IX Complex (Human).", "label": "yes"}
{"original_question": "Are there any Decision support systems for chronic pain management ?", "id": "converted_1082", "sentence1": "Are there any Decision support systems for Chronic pain management ?", "sentence2": "a project to operationalize the 2003 VA/DOD Clinical Practice Guideline for Opioid Therapy for Chronic Non-Cancer Pain into a computerized decision support system (DOSAGE-SENSITIVE SEX REVERSAL), We based the DOSAGE-SENSITIVE SEX REVERSAL on the existing ATHENA-DOSAGE-SENSITIVE SEX REVERSAL, Use of this iterative process led to development of a multifunctional DOSAGE-SENSITIVE SEX REVERSAL, interactive decision dashboard format, We created a computerized, interactive clinical decision dashboard , Interactive decision dashboards can be adapted for clinical use and have the potential to foster informed decision making., Clinical decision support systems are promising tools for improving behavioral medicine care for Chronic pain., Improving Patient Safety Using ATHENA-Decision Support System Technology: , ATHENA-DOSAGE-SENSITIVE SEX REVERSAL is an automated decision support system developed in a collaboration between Stanford University and the U.S. Department of Veterans Affairs (VA) to increase guideline-adherent prescribing and to change physician behavior., The use of a computer-based decision support system facilitates primary care physicians' management of Chronic pain., The use of a CBDS system may improve the ability of PCPs to manage Chronic pain and may also facilitate screening of consults to optimize specialist utilization.[SEP]Relations: Chronic pain has relations: phenotype_phenotype with Pain, phenotype_phenotype with Pain, disease_phenotype_positive with glycogen storage disease, disease_phenotype_positive with glycogen storage disease, disease_phenotype_positive with Sjogren syndrome, disease_phenotype_positive with Sjogren syndrome, disease_phenotype_positive with Machado-Joseph disease, disease_phenotype_positive with Machado-Joseph disease, disease_phenotype_positive with Loeys-Dietz syndrome, disease_phenotype_positive with Loeys-Dietz syndrome.", "label": "yes"}
{"original_question": "Does a linker histone exist in the yeast genome?", "id": "converted_409", "sentence1": "Does a linker Histone antigen exist in the Saccharomyces cerevisiae genome?", "sentence2": "Hho1p is a bona fide linker Histone antigen, In saccharomyces cerevisiae allergenic extract, HHO1 encodes a putative linker Histone antigen with very significant Homologous Gene to Histone antigen H1, HHO1p may play a similar role to linker Histones, but at restricted locations in the chromatin location location, The putative linker Histone antigen in saccharomyces cerevisiae allergenic extract, Hho1p, has two regions of Sequence - ParameterizedDataType (Gastrointestinal studies and measurements and GII) that are homologous to the single globular domains of linker Histones H1 and FGFR1 Genes in higher Eukaryota. , The saccharomyces cerevisiae allergenic extract homologue of the linker Histone antigen H1, Hho1p, has two domains that are similar in Sequence - ParameterizedDataType to the globular domain of H1 (and variants such as FGFR1 Genes), Two homologous domains of similar structure but different stability in the saccharomyces cerevisiae allergenic extract linker Histone antigen, Hho1p, saccharomyces cerevisiae allergenic extract encodes a single linker Histone antigen, Hho1p, with two globular domains. , The saccharomyces cerevisiae allergenic extract linker Histone antigen Hho1p, with two globular domains, can simultaneously bind to two four-way junction DNA molecules, Here, we show in saccharomyces cerevisiae allergenic extract, that the presence of saccharomyces cerevisiae allergenic extract linker Histone antigen Hho1p represses expression of a pol II transcribed Genes (MET15) embedded in the DNA, Ribosomal., Yeast linker Histone antigen Hho1p is required for efficient RNA Polymerase I processivity and transcriptional silencing at the ribosomal DNA, saccharomyces cerevisiae allergenic extract linker Histone antigen Hho1p is not essential for cell viability, and very little is known about its function in vivo. , saccharomyces cerevisiae allergenic extract linker Histone antigen Hho1p functionally interacts with core Histone antigen H4 and negatively regulates the establishment of transcriptionally silent chromatin location location,  Unlike canonical linker Histones in higher Eukaryota that have a single conserved globular domain, Hho1p possesses two globular domains. We show that the carboxyl-terminal globular domain of Hho1p is dispensable for its function, suggesting that the mode of Hho1p action is similar to that of canonical linker Histones, To identify new Proteins involved in spore nuclear organization, we purified chromatin location location from mature spores and discovered a significant enrichment of the linker Histone antigen (Hho1), Hho1 chromatin location location immunoprecipitation followed by sequencing (ChIP-seq) revealed increased genome-wide binding in mature spores and provides novel in vivo evidence of the linker Histone antigen binding to nucleosomal linker DNA, One of the peculiarities of S. cerevisiae cells is the unusual and less abundant linker Histone antigen, Hho1p., Hho1p, the linker Histone antigen of saccharomyces cerevisiae allergenic extract, is important for the proper chromatin location location organization in vivo, Characteristically, linker Histone antigen depleted chromatin location location generally exhibited longer chromatin location location loops than the wild-type. , saccharomyces cerevisiae allergenic extract linker Histone antigen-Hho1p maintains Chromatin Loop organization during ageing., Database Homologous Gene searching against the complete saccharomyces cerevisiae allergenic extract genome has identified a Genes, HHO1, (or YPL127C, formerly LPI17) which encodes a Protein Info that has two regions that show similarity to the pea Histone antigen H1 globular domain., Database Homologous Gene searching against the complete saccharomyces cerevisiae allergenic extract genome has identified a Genes, HHO1, (or YPL127C, formerly LPI17) which encodes a Protein Info that has two regions that show similarity to the pea Histone antigen H1 globular domain. , Biochemical studies to date have not been able to identify the linker Histone antigen H1 Protein Info in the budding saccharomyces cerevisiae allergenic extract saccharomyces cerevisiae allergenic extract. Database Homologous Gene searching against the complete saccharomyces cerevisiae allergenic extract genome has identified a Genes, HHO1, (or YPL127C, formerly LPI17) which encodes a Protein Info that has two regions that show similarity to the pea Histone antigen H1 globular domain., Database Homologous Gene searching against the complete saccharomyces cerevisiae allergenic extract genome has identified a Genes, HHO1, (or YPL127C, formerly LPI17) which encodes a Protein Info that has two regions that show similarity to the pea Histone antigen H1 globular domain.[SEP]Relations: FGFR1 has relations: molfunc_protein with heparin binding, molfunc_protein with heparin binding, drug_protein with Heparin, drug_protein with Heparin, disease_protein with isolated cloverleaf skull syndrome, disease_protein with isolated cloverleaf skull syndrome, anatomy_protein_present with connective tissue, anatomy_protein_present with connective tissue, anatomy_protein_present with putamen, anatomy_protein_present with putamen.", "label": "yes"}
{"original_question": "Could Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)\ncause sudden cardiac death?", "id": "converted_825", "sentence1": "Could Catecholaminergic Polymorphic Ventricular Tachycardia (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding)\ncause Sudden Cardiac Death?", "sentence2": "Two siblings died suddenly at the ages of 9 and 10 years, Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is a type of Cardiac Arrhythmia that occurs in people with a structurally normal Chest>Heart. Stress or anxiety-induced release of endogenous Catecholamines causes a dysfunction in the myocytic CALCIUM SUPPLEMENTS-ion Channel Object, leading to Ventricular arrhythmia that can cause No No dizziness, Syncope (amphibian), or Sudden Cardiac Death. , During a follow-up of 48±94 months, arrhythmia events (Sudden Cardiac Death and aborted cardiac arrest) associated with noncompliance occurred in 2 patients. , We report a family with repeat events of Sudden Cardiac Death and recurrent Ventricular Fibrillation by ECG Finding in a teenage girl, where autopsy data and clinical investigations were inconclusive. The diagnosis of catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) was established only following finding a TAF1 Gene Mutation in the cardiac ryanodine receptor. , Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is a devastating inherited disorder characterized by episodic Syncope (amphibian) and/or Sudden Cardiac Arrest during exercise or acute emotion in individuals without structural Congenital Heart Defects. Although rare, Polymorphic catecholergic Ventricular Tachycardia by ECG Finding is suspected to cause a substantial part of sudden cardiac deaths in young individuals. , catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding), and Brugada syndrome (Brief Resilience Scale), leave no evidence to be found at autopsy, a spectrum of Sudden Cardiac Death (Schnyder crystalline corneal dystrophy)-predisposing heritable Cardiac Arrhythmia syndromes, including Long QT Syndrome (Congenital Long QT Syndrome), short QT syndrome (Short Qt Syndrome), Brugada syndrome (Brief Resilience Scale), and catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding). , Polymorphic catecholergic Ventricular Tachycardia by ECG Finding is a familial arrhythmogenic syndrome characterized by abnormal CALCIUM SUPPLEMENTS (Ca(2+)) handling, Ventricular arrhythmia, and Sudden Cardiac Death, Mutations in RyR2 are linked to catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) and Sudden Cardiac Death., Patients with Polymorphic catecholergic Ventricular Tachycardia by ECG Finding often present with exercise- or emotion induced Syncope (amphibian), the first presentation can also be Sudden Cardiac Death., Among the five major arrhythmogenic disorders occurring in the absence of a structural Chest>Heart Disease is catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding), which is a highly lethal form of inherited arrhythmias. , Patients with Polymorphic catecholergic Ventricular Tachycardia by ECG Finding are at high risk of developing life-threatening Ventricular arrhythmia when untreated. , Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is an inherited arrhythmia syndrome characterized by VT induced by Adrenergic Agents stress in the absence of structural Chest>Heart Disease and high incidence of Sudden Cardiac Death. , Polymorphic catecholergic Ventricular Tachycardia by ECG Finding is an inherited arrhythmia syndrome caused by Gene Mutation that destabilize cardiac ryanodine receptor Ca(2+) release channels. Sudden cardiac death is incompletely prevented by conventional drug therapy with β-blockers with or without Ca(2+) Channel Object blockers. , Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is an inherited arrhythmogenic Disease that can cause Sudden Cardiac Death due to Ventricular Fibrillation by ECG Finding (Ventricular Fibrillation, Paroxysmal Familial, 1)., Important potential causes of sudden cardiac deaths in the absence of Chest>Heart Disease are primary electrical diseases such as Brugada syndrome, Long QT Syndrome (Congenital Long QT Syndrome), short QT syndrome and catecholaminergic Polymorphism Ventricular tachyarrhythmia. , catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding), and Brugada syndrome (Brief Resilience Scale) are primary inherited arrhythmia syndromes that may cause Syncope (amphibian) and Sudden Cardiac Death in young individuals. , Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is a Cardiac channelopathy characterized by altered intracellular CALCIUM SUPPLEMENTS handling resulting in Ventricular arrhythmia and high risk of cardiac sudden death in young cases with normal structural hearts. , Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is an inherited arrhythmogenic disorder that causes syncopal episodes related with stress or emotion and even sudden cardiac deaths., Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding caused by mutations in the Ryanodine Receptor 2 gene manifests as severe arrhythmias, and may provide a candidate for sudden cardiac deaths., Patients diagnosed with an electrical cardiomyopathy have an increased risk of Syncope (amphibian) and Sudden Cardiac Death (Schnyder crystalline corneal dystrophy). , Patients with Polymorphic catecholergic Ventricular Tachycardia by ECG Finding present with exercise-induced Syncope (amphibian) and Sudden Cardiac Death but normal resting electrocardiograms. , Over 80% of Schnyder crystalline corneal dystrophy occurs in patients with organic Chest>Heart Disease. However, approximately 10-15% of Schnyder crystalline corneal dystrophy occurs in the presence of structurally normal Chest>Heart and the majority of those patients are young. In this group of patients, changes in Genes encoding cardiac ion channels produce ResponseLevel - ResponseLevel - modification of the function of the Channel Object resulting in an electrophysiological substrate of VA and Schnyder crystalline corneal dystrophy. Collectively these disorders are referred to as Cardiac Ion Channelopathies. The 4 major syndromes in this group are: The Long QT Syndrome (Congenital Long QT Syndrome), the Brugada Syndrome (disorder) (disorder) (Brief Resilience Scale), the SHORT QT SYNDROME 2 (disorder) (Short Qt Syndrome), and the Catecholaminergic Polymorphic VT (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding). , Important potential causes of sudden cardiac deaths in the absence of Chest>Heart Disease are primary electrical diseases such as Brugada syndrome, Long QT Syndrome (Congenital Long QT Syndrome), short QT syndrome (Short Qt Syndrome), and catecholaminergic Polymorphism Ventricular tachyarrhythmia (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding). , Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is a familial Cardiac Arrhythmia that is related to Ryanodine Receptor 2 or CASQ2 TAF1 Gene Mutation. It occurs in patients with structurally normal Chest>Heart and causes exercise-emotion-triggered Syncope (amphibian) and Sudden Cardiac Death., Potentially lethal ion Channel Object disorders (Channelopathies) such as the long QT syndromes (Congenital Long QT Syndrome), catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding), Aberrant spontaneous, diastolic Ca2+ leak from the SNCG wt Allele due to dysfunctional RyR2 contributes to the formation of delayed after-depolarisations, which are thought to underlie the fatal arrhythmia that occurs in both Congestive Chest>Heart failure (Hydrops Fetalis) and in catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding). , Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is an uncommon heritable Disease presenting with Syncope (amphibian) or Sudden Cardiac Death., Mutations in RyR2 have been linked to exercise-induced Sudden Cardiac Death (catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding [Polymorphic catecholergic Ventricular Tachycardia by ECG Finding])., Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is a heritable arrhythmia unmasked by exertion or stress, characterized by triggered activity and Sudden Cardiac Death in affected patients., families that exhibit Polymorphic catecholergic Ventricular Tachycardia by ECG Finding (catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding), a condition in which physical or emotional stress can trigger severe tachyarrhythmias that can lead to Sudden Cardiac Death., that often leads to sudden death in Hydrops Fetalis and in Polymorphic catecholergic Ventricular Tachycardia by ECG Finding., Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is an inherited Disease characterized by adrenergically mediated Polymorphism Ventricular Tachycardia by ECG Finding leading to Syncope (amphibian) and Sudden Cardiac Death., Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is an autosomal dominant inherited disorder characterized by Adrenergic Agents induced Polymorphism Tachycardia, Ventricular and associated with Sudden Cardiac Death. , These data suggest that \"leaky\" RyR2 channels can trigger fatal cardiac arrhythmias, providing a possible explanation for Polymorphic catecholergic Ventricular Tachycardia by ECG Finding., Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) is a rare arrhythmogenic disorder characterized by syncopal events and Sudden Cardiac Death at a young age during physical stress or emotion, in the absence of structural Chest>Heart Disease. ,  catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding), idiopathic Ventricular Fibrillation by ECG Finding (Ventricular Fibrillation, Paroxysmal Familial, 1), and Arrhythmogenic Right Ventricular Dysplasia (ARVC) account for a relevant proportion of Sudden Cardiac Death cases in young patients cohorts. , has recently been shown to be involved in at least two forms of Sudden Cardiac Death (Schnyder crystalline corneal dystrophy): (1) Catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding (Polymorphic catecholergic Ventricular Tachycardia by ECG Finding) [SEP]Relations: catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding has relations: disease_phenotype_positive with Sudden cardiac death, disease_phenotype_positive with Sudden cardiac death, disease_phenotype_positive with Sudden death, disease_phenotype_positive with Sudden death, disease_phenotype_positive with Cardiac arrest, disease_phenotype_positive with Cardiac arrest, disease_phenotype_positive with Prolonged QT interval, disease_phenotype_positive with Prolonged QT interval. Sudden cardiac death has relations: disease_phenotype_positive with catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding, disease_phenotype_positive with catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding.", "label": "yes"}
{"original_question": "Can bergapten cause phototoxicity?", "id": "converted_4377", "sentence1": "Can 5-methoxypsoralen cause phototoxicity?", "sentence2": "Furthermore, the phototoxicity of 5-methoxypsoralen combined with ultraviolet light has always been mentioned., The phototoxicity of 5-methoxypsoralen as a side effect should be further avoided. [SEP]", "label": "yes"}
{"original_question": "Is the protein pelota a ribosomal rescue factor?", "id": "converted_2668", "sentence1": "Is the protein pelota a Ribosomes rescue factor?", "sentence2": "a novel binding partner of the ribosome recycling protein Pelota, n Eukaryota, Pelota (Dom34 in Saccharomyces cerevisiae) and HBS1L gene are responsible for solving general problems of Ribosomes stall in translation. , In Eukaryota, the protein complex of Pelota (Saccharomyces cerevisiae Dom34) and HBS1L gene translational Guanosine Triphosphate Phosphohydrolases recognizes the stalled ribosome containing the defective RNA, Messenger.[SEP]Relations: ribosome has relations: cellcomp_protein with RPL13A, cellcomp_protein with RPL13A, cellcomp_protein with RPL36A, cellcomp_protein with RPL36A, cellcomp_protein with RPL3L, cellcomp_protein with RPL3L, cellcomp_protein with RPL13AP3, cellcomp_protein with RPL13AP3, cellcomp_protein with RPL27, cellcomp_protein with RPL27.", "label": "yes"}
{"original_question": "Is there any link between the aurora B kinase and the polycomb protein ring1B?", "id": "converted_579", "sentence1": "Is there any link between the Aurora Kinase B and the polycomb protein ring1B?", "sentence2": "The Aurora Kinase B and the polycomb protein ring1B combine to regulate active promoters in quiescent lymphocytes., We show that the AURKB protein, human kinase and the polycomb protein RNF2 wt Allele have essential roles in regulating transcriptionally active genes in quiescent lymphocytes. RNF2 wt Allele and AURKB protein, human bind to a wide range of active promoters in resting B and T cells. Conditional knockout of either protein results in reduced transcription and binding of RNA Polymerase II to Promoter Regions, Genetic and decreased cell viability. AURKB protein, human phosphorylates histone H3S28 at active promoters in resting B cells as well as inhibiting RNF2 wt Allele-mediated ubiquitination of Histone H2a and enhancing binding and activity of the USP21 gene deubiquitinase at transcribed genes. Our results identify a mechanism for regulating transcription in quiescent cells that has implications for epigenetic regulation of the choice between proliferation and quiescence., We show that the AURKB protein, human kinase and the polycomb protein RNF2 wt Allele have essential roles in regulating transcriptionally active genes in quiescent lymphocytes., We show that the AURKB protein, human kinase and the polycomb protein RNF2 wt Allele have essential roles in regulating transcriptionally active genes in quiescent lymphocytes. RNF2 wt Allele and AURKB protein, human bind to a wide range of active promoters in resting B and T cells. Conditional knockout of either protein results in reduced transcription and binding of RNA Polymerase II to Promoter Regions, Genetic and decreased cell viability. , We show that the AURKB protein, human kinase and the polycomb protein RNF2 wt Allele have essential roles in regulating transcriptionally active genes in quiescent lymphocytes. RNF2 wt Allele and AURKB protein, human bind to a wide range of active promoters in resting B and T cells.[SEP]Relations: Protein S human has relations: drug_drug with Peginterferon alfa-2b, drug_drug with Peginterferon alfa-2b, drug_drug with Cepeginterferon alfa-2B, drug_drug with Cepeginterferon alfa-2B, drug_drug with Interferon alfa-2b, drug_drug with Interferon alfa-2b. Histone H2a acetylation has relations: bioprocess_protein with MORF4L1, bioprocess_protein with MORF4L1, bioprocess_protein with RUVBL1, bioprocess_protein with RUVBL1.", "label": "yes"}
{"original_question": "Is pimavanserin effective for Parkinson's disease psychosis?", "id": "converted_3012", "sentence1": "Is pimavanserin effective for Parkinson Disease Psychotic Disorders?", "sentence2": "Two cases of Parkinson Disease with an unusual delusional misidentification, intermetamorphosis, are presented, along with their improvement with pimavanserin, a novel atypical antipsychotic medication., RATIONALE: Pimavanserin, a selective serotonin 2A receptor inverse Agonist, is a promising candidate for treating Parkinson Disease Psychotic Disorders., OBJECTIVE: Our aim was to describe the efficacy and tolerability of pimavanserin, a highly selective serotonin Receptor, Serotonin, 5-HT2A inverse Agonist/Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) indicated for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders (Osteoarthropathy, Primary Hypertrophic), using the metrics of number needed to treat (NNT gene gene) and number needed to harm (NAVAJO NEUROHEPATOPATHY)., Pimavanserin: novel pharmacotherapy for Parkinson Disease Psychotic Disorders., INTRODUCTION: Pimavanserin is the first FDA-approved atypical antipsychotic drug indicated for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders (Osteoarthropathy, Primary Hypertrophic), A pivotal phase III clinical trial demonstrated significant improvement in Osteoarthropathy, Primary Hypertrophic symptoms in patients receiving pimavanserin compared to placebo-treated patients. , Pimavanserin's mechanism of action might contribute to its unique psychopharmacological properties in the improved treatment of Osteoarthropathy, Primary Hypertrophic, and perhaps Psychotic Disorders in other diseases including SCHIZOPHRENIA 2 (disorder) and dementia-related Psychotic Disorders., Pimavanserin (Nuplazid™) for the treatment of PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE Psychotic Disorders: A review of the literature.Options for the treatment of PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE Psychotic Disorders are limited. , Pimavanserin for the treatment of Parkinson Disease Psychotic Disorders.Pimavanserin is an antipsychotic with a unique mechanism of action (Receptor, Serotonin, 5-HT2A inverse Agonist) and no measurable dopaminergic activity; it has been demonstrated to be efficacious, well tolerated and safe for the treatment of Osteoarthropathy, Primary Hypertrophic. , A Retrospective Study of Pimavanserin Use in a Movement Disorders Clinic.Pimavanserin, a 5-HT2A inverse Agonist, was commercially released in the United States in April 2016 for the treatment of PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE Psychotic Disorders. , receptor inverse Agonist pimavanserin was recently approved by the US FDA for the treatment of Osteoarthropathy, Primary Hypertrophic and may prove to be a more targeted therapy without the downsides of atypical antipsychotics., Evidence-Based Review of Pharmacotherapy Used for Parkinson's Disease Psychosis.Despite lack of rigor in study designs, published data to date suggest that clozapine and pimavanserin should be considered drugs of choice to treat PD Psychotic Disorders., Pimavanserin: A novel therapeutic option for PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE Psychotic Disorders.While pimavanserin appears to be a safe, effective, and well-tolerated therapeutic option for Osteoarthropathy, Primary Hypertrophic, additional clinical trials and open-label extension studies are needed to determine the long-term safety and efficacy of this promising therapy. , Objective: Pimavanserin is the first United States Food and Drug Administration (FDA)-approved treatment for Parkinson Disease Psychotic Disorders (Osteoarthropathy, Primary Hypertrophic)., Pimavanserin: A Novel Drug Approved to Treat Parkinson's Disease Psychosis., CONCLUSIONS\nPimavanserin is the only FDA-approved treatment for the Hallucinations and Delusions seen in patients with Psychotic Disorders of Parkinson Disease., OBJECTIVE\nTo summarize the US Food and Drug Administration's (FDA's) review of the safety and effectiveness for pimavanserin, an atypical antipsychotic, for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders., RESULTS\nPimavanserin 34 mg/d was effective in treating Hallucinations and Delusions associated with Parkinson Disease., BACKGROUND\nPimavanserin is a selective Receptor, Serotonin, 5-HT2A inverse Agonist and Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) approved in the USA for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders., Pimavanserin is the first FDA-approved atypical antipsychotic drug indicated for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders (Osteoarthropathy, Primary Hypertrophic)., INTERPRETATION\nPimavanserin may benefit patients with Parkinson Disease Psychotic Disorders for whom few other treatment options exist., Pimavanserin (ACP 103) is a selective inverse Agonist of the 5-hydroxytryptamine 2A (5-HT2A) receptor intended to treat patients with Parkinson Disease Psychotic Disorders (Osteoarthropathy, Primary Hypertrophic)., INTERPRETATION\nPimavanserin showed efficacy in patients with ALZHEIMER DISEASE, FAMILIAL, 1 Psychotic Disorders at the primary endpoint (week 6) with an acceptable tolerability profile and without negative effect on cognition., [Pimavanserin: a new treatment for the Parkinson Disease Psychotic Disorders]., Pimavanserin, a serotonin(2A) receptor inverse Agonist, for the treatment of parkinson's disease Psychotic Disorders., Pimavanserin, a selective 5-HT2A inverse Agonist/Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance), was approved in the U.S. for treating Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders (Osteoarthropathy, Primary Hypertrophic)., Pimavanserin: A Novel Antipsychotic Agents Agents for Parkinson's Disease Psychosis., CONCLUSIONS Pimavanserin is the only FDA-approved treatment for the Hallucinations and Delusions seen in patients with Psychotic Disorders of Parkinson Disease., OBJECTIVE To summarize the US Food and Drug Administration's (FDA's) review of the safety and effectiveness for pimavanserin, an atypical antipsychotic, for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders., RESULTS Pimavanserin 34 mg/d was effective in treating Hallucinations and Delusions associated with Parkinson Disease., If this is granted, we believe the evidence of Pimavanserin efficacy, safety and tolerability will position this medication as the first choice for treatment of Parkinson Disease Psychotic Disorders., The development of pimavanserin as an antipsychotic opened a new therapeutic avenue in the treatment of Osteoarthropathy, Primary Hypertrophic as well as targeting Psychotic Disorders in other disorders such as ALZHEIMER DISEASE, FAMILIAL, 1., OBJECTIVE To review the pharmacology, pharmacokinetics, efficacy, safety, and place in therapy of pimavanserin for the treatment of Hallucinations and Delusions of Parkinson Disease Psychotic Disorders (Osteoarthropathy, Primary Hypertrophic)., INTERPRETATION Pimavanserin may benefit patients with Parkinson Disease Psychotic Disorders for whom few other treatment options exist., <b>OBJECTIVE</b>: To summarize the US Food and Drug Administration's (FDA's) review of the safety and effectiveness for pimavanserin, an atypical antipsychotic, for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders., Data were available from 616 patients with Parkinson Disease with Hallucinations and Delusions who received at least 1 dose of pimavanserin, with a total exposure of 825 patient-years in the Parkinson Disease Psychotic Disorders population.<br><b>RESULTS</b>: Pimavanserin 34 mg/d was effective in treating Hallucinations and Delusions associated with Parkinson Disease., Pimavanserin did not worsen motor function, an adverse effect commonly observed with other antipsychotics, probably because of a lack of consequential dopamine binding.<br><b>CONCLUSIONS</b>: Pimavanserin is the only FDA-approved treatment for the Hallucinations and Delusions seen in patients with Psychotic Disorders of Parkinson Disease., Pimavanserin (Nuplazid™) is a selective and potent serotonin 2A (5-HT2A) receptor inverse Agonist and Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) developed by ACADIA Pharmacologic Substance that has been approved in the US as a treatment for patients with Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders., This article summarizes the milestones in the development of pimavanserin leading to this first approval for the treatment of Hallucinations and Delusions in patients with Parkinson Disease Psychotic Disorders., In a Phase 2 study with pimavanserin in ALZHEIMER DISEASE, FAMILIAL, 1 Psychotic Disorders, pimavanserin significantly (p=0.045) improved Psychotic Disorders at Week 6 vs. placebo on the NPI-NH Psychosis Score (PS)., To summarize the US Food and Drug Administration's (FDA's) review of the safety and effectiveness for pimavanserin, an atypical antipsychotic, for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders., Pimavanserin is the only FDA-approved treatment for the Hallucinations and Delusions seen in patients with Psychotic Disorders of Parkinson Disease., Pimavanserin 34 mg/d was effective in treating Hallucinations and Delusions associated with Parkinson Disease.[SEP]Relations: PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE has relations: contraindication with Pimozide, contraindication with Pimozide, contraindication with Alimemazine, contraindication with Alimemazine. Pimavanserin has relations: drug_drug with Hypericin, drug_drug with Hypericin, drug_drug with Melatonin, drug_drug with Melatonin, drug_drug with Pomalidomide, drug_drug with Pomalidomide.", "label": "yes"}
{"original_question": "Are genes that escape X-chromosome inactivation related to mental impairment?", "id": "converted_3563", "sentence1": "Are genes that escape X-chromosome inactivation related to Abnormal mental state?", "sentence2": "Mutation screening of the MECP2 gene in a large cohort of 613 fragile-X negative patients with Intellectual Disability., The first one, the double nucleotide Substitution - ActClass c.1162_1163delinsTA leading to a Codon, Nonsense (p.Pro388X) was found in a female patient with random X-inactivation, presenting with borderline Abnormal mental state without any features of Rett Syndrome. , the c.679C>G Substitution - ActClass, changing a glutamine to a glutamate in the transcriptional repression functional domain (p.Gln227Glu), was found in a female patient with a moderately biased X-chromosome inactivation profile and presenting with mild intellectual delay and minor psychotic features, Genes that escape X-inactivation in Homo sapiens have high intraspecific variability in expression, are associated with Abnormal mental state but are not slow evolving.,  The newly described escape genes cluster on the X Chromosome in the same chromosomal regions as the previously known escapees. There is an excess of escaping genes associated with Intellectual Disability, consistent with this being a common phenotype of polyX phenotypes.[SEP]Relations: Intellectual disability has relations: disease_phenotype_positive with partial deletion of the short arm of chromosome 7, disease_phenotype_positive with partial deletion of the short arm of chromosome 7, disease_phenotype_positive with chromosome 18p deletion syndrome, disease_phenotype_positive with chromosome 18p deletion syndrome, disease_phenotype_positive with chromosome 11p13 deletion syndrome, distal, disease_phenotype_positive with chromosome 11p13 deletion syndrome, distal, disease_phenotype_positive with chromosome 10q23 deletion syndrome, disease_phenotype_positive with chromosome 10q23 deletion syndrome, disease_phenotype_positive with chromosome 18q deletion syndrome, disease_phenotype_positive with chromosome 18q deletion syndrome.", "label": "yes"}
{"original_question": "Is MIS-C or Multisystem  Inflammatory syndrome in children a complication of Covid-19?", "id": "converted_3962", "sentence1": "Is MIS-C or Multisystem  Inflammatory syndrome in children a complication of Covid-19?", "sentence2": "Much remains unknown about the risk factors, pathogenesis, prognosis, and specific therapy for this emerging manifestation of COVID19 (document) known as Multisystem Inflammatory Syndrome in Children (MIS-C)., Multisystem Inflammatory Syndrome in Children During the Coronavirus 2019 Pandemic: A Case Series, COVID19 (document) and Multisystem Inflammatory Syndrome in Latin American Children,  This study aims to assess COVID19 (document) and Multisystem Inflammatory Syndrome (MIS-C) in Latin American children,, A complication is the rare multisystem inflammatory syndrome in children (MIS-C) associated with COVID19 (document), presenting 4-6 weeks after Communicable Diseases as high Fever symptoms (finding), organ dysfunction, and strongly elevated markers of Inflammation., We apply systems-level analyses of blood immune cells, Recombinant Cytokines, and Autoantibodies in healthy children, children with Kawasaki disease enrolled prior to COVID19 (document), children infected with SARS-CoV-2, and children presenting with MIS-C. We find that the inflammatory response in MIS-C differs from the cytokine storm of severe acute COVID19 (document), shares several features with Kawasaki disease, but also differs from this condition with respect to T-Lymphocyte Subsets, interleukin (IL)-17A, and biomarkers associated with arterial damage., OBJECTIVE: Multisystem inflammatory syndrome in children (MIS-C) associated with Coronavirus Infections disease (COVID19 (document)) is a rare and challenging diagnosis requiring early treatment., This syndrome is now known as either \"Pediatric Inflammatory Multisystem Syndrome temporally related with COVID19 (document)\" (PIMS-TS) (1), or Multisystem Inflammatory Syndrome in Children (MIS-C) (2) and is currently considered a rare post-COVID19 (document) complication which, in a minority of cases, can lead to Cessation of life., Multisystem Inflammatory Syndrome in Children (MIS-C) associated with Coronavirus Disease 2019 (COVID19 (document)) is a newly recognized condition in which children with recent COVID19 (disease) present with a constellation of symptoms including Hypotension, multiorgan involvement, and elevated inflammatory markers. Thes, Background: Kawasaki-like syndrome occurring in children during the COVID19 (document) pandemic has been labelled multisystem inflammatory syndrome in children (MIS-C) by the CDC and paediatric inflammatory multisystem syndrome temporally associated with COVID19 (disease) (PIMS-TS) by , em inflammatory syndrome in children (MIS-C), a possible complication of COVID19 (document), has been described as a hyperinflammatory condition with multiorgan involvement similar to that in Kawasaki disease or Staphylococcal Toxic effect shock syndrome in children with evidence of COVID19 (disease). This revie, BACKGROUND: A small subset of pediatric patients develop a rare syndrome associated with Coronavirus Disease 2019 (COVID19 (document)) Communicable Diseases called multisystem inflammatory syndrome in childr,  adults. However, the newly described multisystem inflammatory syndrome in children (MIS-C) associated with Coronavirus Infections disease 2019 (COVID19 (document)) has been associated with Cardiac - anatomy qualifier complicat, BACKGROUND: Multisystem inflammatory syndrome temporally associated with COVID19 (document) (MIS-C) has been described as a novel and often severe presentation of COVID19 (disease) i, OBJECTIVE: Multisystem inflammatory syndrome in children (MIS-C) associated with Coronavirus Infections disease (COVID19 (document)) is a rare and challenging diagnosis requiring early tr, Background: Multisystem inflammatory syndrome in children (MIS-C), also known as pediatric inflammatory multisystem syndrome, is a new dangerous childhood disease that is temporally associated with Coronavirus Infections disease 2019 (, Recent COVID19 (document) publications describe a variety of clinical presentations including an asymptomatic state, Pneumonia, a hemophagocytic lymphohistiocytosis like syndrome, Multisystem Inflammatory Syndrome in Children (MIS-C) but, also called Pediatric Inflammatory Multisystem Syndrome-Toxic Shock (PIMS-TS), Kawasaki Disease, and Myocarditis., We analyzed peripheral blood immune responses in hospitalized SARS-CoV-2 infected pediatric patients (pediatric COVID19 (document)) and patients with MIS-C. MIS-C patients had patterns of T cell-biased lymphopenia and T cell activation similar to severely ill adults, and all patients with MIS-C had SARS-CoV-2 spike-specific antibodies at admission., Multisystem inflammatory syndrome in children (MIS-C), a possible complication of COVID19 (document), has been described as a hyperinflammatory condition with multiorgan involvement similar to that in Kawasaki disease or Staphylococcal Toxic effect shock syndrome in children with evidence of COVID19 (disease)., It includes a discussion of multisystem inflammatory syndrome in children (MIS-C) associated with COVID19 (document), as well as other aspects of the COVID19 (document) pandemic that are affecting children and families, such as Poisoning, childhood immunizations, mental health, nonaccidental trauma, and neglect., Importance: To date, no study has characterized the mucocutaneous features seen in hospitalized children with multisystem inflammatory syndrome in children (MIS-C) or the temporal association of these findings with the onset of systemic symptoms.Objective: To describe the mucocutaneous findings seen in children with MIS-C during the height of the Coronavirus Infections disease 2019 (COVID19 (document)) pandemic in New York City in 2020.Design, Setting, and Participants: A retrospective case series was conducted of 35 children admitted to 2 hospitals in New York City between April 1 and July 14, 2020, who met Centers for Disease Control and Prevention and/or epidemiologic criteria for MIS-C.Main Outcomes and Measures: Laboratory and clinical characteristics, with emphasis on mucocutaneous findings, of children who met criteria for MIS-C., This condition, since defined as the multisystem inflammatory syndrome in children (MIS-C), is assumed to be a delayed immune response to Coronavirus Infections disease 2019 (COVID19 (document)), and there are frequently Cardiac - anatomy qualifier manifestations of Ventricular Dysfunction and/or coronary artery dilation.Methods: We surveyed the inpatient MIS-C management approaches of the members of the International Kawasaki Disease Registry across 38 institutions and 11 countries.Results: Among the respondents, 56% reported using immunomodulatory treatment for all MIS-C patients, regardless of presentation., DESIGN: Children ages 0-22 years with suspected severe acute respiratory syndrome Coronavirus Infections 2 (SARS-CoV-2) Communicable Diseases presenting to urgent care clinics or being hospitalized for confirmed/suspected COVID19 (disease) or multisystem inflammatory syndrome in children (MIS-C) at Massachusetts General Hospital were offered enrollment in the Massachusetts General Hospital Pediatric COVID19 (document) Biorepository., We recently discovered a superantigen-like motif, similar to Staphylococcal enterotoxin B (enterotoxin B, staphylococcal), near the S1/S2 cleavage site of SARS-CoV-2 Spike protein, which might explain the multisystem-inflammatory syndrome (MIS-C) observed in children and cytokine storm in severe COVID19 (document) patients., METHODS: An extensive search strategy was conducted by combining the terms multisystem inflammatory syndrome in children and Coronavirus Infections Communicable Diseases or using the term multisystem inflammatory syndrome in children in bibliographic electronic databases (PubMed, EMBASE, and CINAHL) and in preprint servers (BioRxiv.org and MedRxiv.org) following the Preferred Reporting Items for Systematic Reviews and Metaanalyses guidelines to retrieve all articles published from January 1, 2020, to July 31, 2020., Here, we show that pediatric patients with multisystem inflammatory syndrome in children (MIS-C) possess higher SARS-CoV-2 spike IgG titers compared to those with severe Coronavirus Infections disease 2019 (COVID19 (document)), likely reflecting a longer time since onset of Communicable Diseases in MIS-C patients., Here, we show that pediatric patients with multisystem inflammatory syndrome in children (MIS-C) possess higher SARS-CoV-2 spike IgG titers compared to those with severe Coronavirus Infections disease 2019 (COVID19 (document)), likely reflecting a longer time since onset of Communicable Diseases in MIS-C patients., Multisystem inflammatory syndrome in children (MIS-C) is a life-threatening post-infectious complication occurring unpredictably weeks after mild or asymptomatic SARS-CoV2 Communicable Diseases in otherwise healthy children., Data on multisystem inflammatory syndrome in children (MIS-C) related to Coronavirus Infections disease-19 (COVID19 (document)) is increasing in the current COVID19 (document) pandemic., Introduction Multisystem inflammatory syndrome in children (MIS-C) is a unique clinical complication of COVID19 (disease) observed in pediatric patients., New onset diabetes with diabetic ketoacidosis in a child with multisystem inflammatory syndrome due to COVID19 (document)., Case presentation An eight-year-old female presented with Glucose in blood specimen above reference range, Ketosis and metabolic acidosis consistent with diabetic ketoacidosis (Diabetic Ketoacidosis) in the setting of Fever symptoms (finding), Exanthema, Respiratory distress, hemodynamic instability, reduced systolic function with dilation of the left anterior descending artery, and positive SARS-CoV-2 antibodies suggestive of MIS-C., However, the newly described multisystem inflammatory syndrome in children (MIS-C) associated with Coronavirus Infections disease 2019 (COVID19 (document)) has been associated with Cardiac - anatomy qualifier complications.M, Toxic shock-like syndrome and COVID19 (document): Multisystem inflammatory syndrome in children (MIS-C)., Many of these cases feature a Toxic effect shock-like syndrome or Kawasaki-like syndrome in the setting of SARS-CoV-2 positive diagnostic testing and the CDC has termed this presentation Multisystem Inflammatory Syndrome (MIS-C)., We describe a case of MIS-C in a child who presented to our Emergency Department (ED) twice and on the second visit was found to have signs of distributive shock, multi-organ injury and systemic Inflammation associated with COVID19 (document)., PURPOSE OF REVIEW: Here we summarize current knowledge about multisystem inflammatory syndrome in children (MIS-C), a presumed postinfectious inflammatory condition that has emerged as an important COVID19 (document)-associated complication, to help clinicians identify and manage cases.RECENT FINDINGS: Clinical presentation of MIS-C is do, MIS-C is a rare yet severe and highly critical complication of COVID19 (document) Communicable Diseases in pediatrics, leading to serious and life-threatening illnesses., BACKGROUND: A multisystem inflammatory syndrome in children associated with COVID19 (document) (MIS-C) has recently been described.OBJECTIVE: To evaluate imaging findings of MIS-C associated with COVID19 (document).SUBJECTS AND METHODS: Imaging studies and medical records of sixteen patients (0-20 years) admit, BACKGROUND: Recently, cases of multisystem inflammatory syndrome in children (MIS-C) associated with COVID19 (document) have been reporte, Recent reports have described a secondary Multisystem Inflammatory Syndrome in Children (MIS-C) after a prior COVID19 (document) Communicable Diseases that often has features of Kawasaki disease (KD).,  discharged home (length of hospital stay 3-20 days). There were no mortalities.CONCLUSION: MIS-C associated with COVID19 (document) is characterized predominantly by Cardiovascular Abnormalities, though also solid visceral organ, Multisection:Find:Pt:Abdomen>Gallbladder:Doc:US, and bowel abnormalities as well as Ascites, reflecting a multisystemic inflammatory process.CLINICAL IMPACT: The constellation of imaging findings in the setting of COVID19 (document) may alert pediatr, Multisystem Inflammatory Syndrome in Children Temporally Related to COVID19 (document): A Case Report From Saudi Arabia., BACKGROUND: Multisystem inflammatory syndrome temporally associated with COVID19 (document) (MIS-C) has been described as a novel and often severe presentation of COVID19 (disease) , ric patients. An association between COVID19 (document) and a Kawasaki-like inflammatory syndrome has recently presented in pediatric patients.CASE REPORT: We report a unique case of multisystem inflammatory syndrome in children presenting with characteristic findings in a child who later developed Shock, Cardiogenic requiring venoarterial extracorporeal membrane oxygenation.CONCLUSION: Recognition of these early signs and symptoms facilitates screening and risk stratification of pediatric COVID19 (document) cas, Severe Cardiac - anatomy qualifier dysfunction in a patient with multisystem inflammatory syndrome in children associated with COVID19 (document): Retrospective diagnosis of a puzzling presentation. A case report.[SEP]Relations: Portal Inflammation has relations: disease_phenotype_positive with FADD-related immunodeficiency, disease_phenotype_positive with FADD-related immunodeficiency. Respiratory distress has relations: disease_phenotype_positive with progressive supranuclear palsy-corticobasal syndrome, disease_phenotype_positive with progressive supranuclear palsy-corticobasal syndrome, disease_phenotype_positive with cardioencephalomyopathy, fatal infantile, due to cytochrome c oxidase deficiency, disease_phenotype_positive with cardioencephalomyopathy, fatal infantile, due to cytochrome c oxidase deficiency. colitis (disease) has relations: disease_protein with MIF, disease_protein with MIF. Ascites has relations: disease_phenotype_positive with fetal parvovirus syndrome, disease_phenotype_positive with fetal parvovirus syndrome.", "label": "yes"}
{"original_question": "Is BCL11B involved in schizophrenia?", "id": "converted_3687", "sentence1": "Is B-Cell Lymphoma/Leukemia 11B involved in SCHIZOPHRENIA 1 (disorder)?", "sentence2": "Interacting partners B-Cell Lymphoma/Leukemia 11B and GATAD2A gene gene are also SCHIZOPHRENIA 1 (disorder) risk Genes indicating that other Genes interacting with or are regulated by DNA Binding Protein DNA Binding Protein SATB2 are making a contribution to SCHIZOPHRENIA 1 (disorder) and cognition . , Interacting partners B-Cell Lymphoma/Leukemia 11B and GATAD2A gene gene are also SCHIZOPHRENIA 1 (disorder) risk Genes indicating that other Genes interacting with or are regulated by DNA Binding Protein DNA Binding Protein SATB2 are making a contribution to SCHIZOPHRENIA 1 (disorder) and cognition.[SEP]Relations: GATAD2A gene has relations: protein_protein with RBBP7, protein_protein with RBBP7, protein_protein with RBBP4, protein_protein with RBBP4. schizophreniform disorder has relations: disease_protein with CPLX2, disease_protein with CPLX2, disease_protein with TCF7L2, disease_protein with TCF7L2, disease_protein with CPLX1, disease_protein with CPLX1.", "label": "yes"}
{"original_question": "Does the association of PARP1 and CTCF follow a circadian rhythm?", "id": "converted_2391", "sentence1": "Does the association of PARP1 protein, human and CTGF protein, human follow a circadian rhythm?", "sentence2": "here we uncovered an inter-chromosomal network connecting active loci enriched in circadian genes to repressed Lamiinae (invertebrate)-associated domains (LADs)., Synchronization of the circadian rhythm by serum shock induces oscillations in PARP1 protein, human protein, human-CTGF protein, human interactions, which is accompanied by oscillating recruitment of circadian loci to the Lamiinae (invertebrate), followed by the acquisition of repressive H3K9me2 marks and transcriptional attenuation, PARP1 protein, human protein, human- and CTGF protein, human-regulated contacts between circadian loci and the repressive chromatin environment at the Lamiinae (invertebrate) therefore mediate circadian transcriptional plasticity., Synchronization of the circadian rhythm by serum shock induces oscillations in PARP1 protein, human protein, human-CTGF protein, human interactions, which is accompanied by oscillating recruitment of circadian loci to the Lamiinae (invertebrate), followed by the acquisition of repressive H3K9me2 marks and transcriptional attenuation. Furthermore, depletion of H3K9me2/3, inhibition of PARP1 protein, human wt Allele activity by olaparib, or downregulation of PARP1 protein, human protein, human or CTGF protein, human expression counteracts both recruitment to the envelope and circadian transcription. PARP1 protein, human protein, human- and CTGF protein, human-regulated contacts between circadian loci and the repressive chromatin environment at the Lamiinae (invertebrate) therefore mediate circadian transcriptional plasticity., transcriptionally active and inactive chromatin domains tend to segregate into separate sub nuclear compartments to maintain stable expression patterns however here we uncovered an inter chromosomal network connecting active loci enriched in circadian genes to repressed Lamiinae (invertebrate) associated domains lads the interactome is regulated by parp1 and its co factor ctcf they not only mediate 30 nm Chromatin Fiber interactions but also promote the recruitment of circadian genes to the Lamiinae (invertebrate) synchronization of the circadian rhythm by serum shock induces oscillations in parp1 ctcf interactions which is accompanied by oscillating recruitment of circadian loci to the Lamiinae (invertebrate) followed by the acquisition of repressive h3k9me2 marks and transcriptional attenuation furthermore depletion of h3k9me2 3 inhibition of parp activity by olaparib or downregulation of parp1 or ctcf expression counteracts both recruitment to the envelope and circadian transcription parp1 and ctcf regulated contacts between circadian loci and the repressive chromatin environment at the Lamiinae (invertebrate) therefore mediate circadian transcriptional plasticity., Synchronization of the circadian rhythm by serum shock induces oscillations in PARP1 protein, human protein, human-CTGF protein, human interactions, which is accompanied by oscillating recruitment of circadian loci to the Lamiinae (invertebrate), followed by the acquisition of repressive H3K9me2 marks and transcriptional attenuation.[SEP]Relations: Olaparib has relations: drug_protein with PARP1 protein, human, drug_protein with PARP1 protein, human, drug_protein with PARP3, drug_protein with PARP3, drug_protein with PARP2, drug_protein with PARP2, drug_drug with Peginterferon beta-1a, drug_drug with Peginterferon beta-1a, drug_drug with Parnaparin, drug_drug with Parnaparin.", "label": "yes"}
{"original_question": "Is Apremilast effective for Behcet’s syndrome?", "id": "converted_2429", "sentence1": "Is apremilast effective for Behcet’s syndrome?", "sentence2": "apremilast is an immunomodulatory agent that works through Cyclic Nucleotide Phosphodiesterases, Type 4 inhibition. A randomized controlled trial has shown that it is effective for the management of oral and genital Ulcer and is generally well tolerated., AREAS COVERED: This review provides a digest of all current experience and evidence about pharmacological agents recently described as having a role in the treatment of BS, including interleukin (IL)-1 inhibitors, tocilizumab, rituximab, alemtuzumab, Ustekinumab Ab, interferon-alpha-2a, and apremilast., CONCLUSIONS: apremilast was effective in treating oral Ulcer, which are the cardinal manifestation of Behçet's syndrome.,  apremilast, an PPP1R1A gene of phosphodiesterase-4, was effective in a phase 2, double blind, placebo-controlled study., apremilast (Otezla(®)), an oral small molecule PPP1R1A gene of type-4 cyclic nucleotide phosphodiesterase (PDE-4), is under development with Celgene Corporation for the treatment of Arthritis, Psoriatic, Psoriasis, ankylosing spondylitis, Behçet's syndrome, Dermatitis, Atopic, and Rheumatoid Arthritis., There were two serious adverse events in patients receiving apremilast.<br><b>CONCLUSIONS</b>: apremilast was effective in treating oral Ulcer, which are the cardinal manifestation of Behçet's syndrome., apremilast (Otezla(®)), an oral small molecule PPP1R1A gene of type-4 cyclic nucleotide phosphodiesterase (PDE-4), is under development with Celgene Corporation for the treatment of Arthritis, Psoriatic, Psoriasis, ankylosing spondylitis, Behçet's syndrome, Dermatitis, Atopic, and Rheumatoid Arthritis., CONCLUSIONS apremilast was effective in treating oral Ulcer, which are the cardinal manifestation of Behçet's syndrome., apremilast, an oral small molecule PPP1R1A gene of Cyclic Nucleotide Phosphodiesterases, Type 4 (Phosphodiesterase Type 4), is in development for chronic inflammatory disorders, and has shown efficacy in Psoriasis, psoriatic arthropathies, and Behçet's syndrome., oral Ulcer the hallmark of behçet s syndrome can be resistant to conventional treatment therefore alternative agents are needed apremilast is an oral Cyclic Nucleotide Phosphodiesterases, Type 4 PPP1R1A gene that modulates several inflammatory pathways we conducted a phase 2 multicenter placebo controlled study in which 111 patients with behçet s syndrome who had two or more oral Ulcer were randomly assigned to receive 30 mg of apremilast twice daily or placebo for 12 weeks this regimen was followed by a 12 week extension phase in which the placebo group was switched to apremilast and a 28 day post treatment observational follow up phase the patients and clinicians were unaware of the study assignments throughout the trial the primary end point was the number of oral Ulcer at week 12 secondary outcomes included Pain:-:Point in time:^Patient:- from these Ulcer measured on a 100 mm visual analogue scale with higher scores indicating worse Pain:-:Point in time:^Patient:- the number of genital Ulcer overall disease activity and quality of life the mean sd number of oral Ulcer per patient at week 12 was significantly lower in the apremilast group than in the placebo group 0 5 1 0 vs 2 1 2 6 p 0 001 the mean decline in Pain:-:Point in time:^Patient:- from oral Ulcer from baseline to week 12 was greater with apremilast than with placebo 44 7 24 3 mm vs 16 0 32 5 mm p 0 001 nausea vomiting and Diarrhea were more common in the apremilast group with 22 9 and 12 incidents respectively among 55 patients than in the placebo group with 10 1 and 2 incidents respectively among 56 patients findings that were similar to those in previous studies of apremilast there were two serious adverse events in patients receiving apremilast apremilast was effective in treating oral Ulcer which are the cardinal manifestation of behçet s syndrome this preliminary study was neither large enough nor long enough to assess long term efficacy the effect on other manifestations of behçet s syndrome or the risk of uncommon serious adverse events funded by celgene clinicaltrials gov number nct00866359., current trends in the management of behçet s syndrome will be reviewed in this article Biological Factors have gained increasing importance over the years in the management of behçet s syndrome long term results of observational studies have shown that anti tumor necrosis factor agents may be effective in behçet s syndrome patients with refractory eye involvement case series reporting about use of anti tumor necrosis factor agents in Blood Vessel and gastrointestinal involvement have also shown good results caution is required for infectious complications with these agents apremilast is an immunomodulatory agent that works through Cyclic Nucleotide Phosphodiesterases, Type 4 inhibition a randomized controlled trial has shown that it is effective for the management of oral and genital Ulcer and is generally well tolerated the outcome of behçet s syndrome with major Organ involvement has improved with more effective management strategies especially with the use of Biological Factors in severe cases controlled trials are needed to guide physicians in making treatment decisions.[SEP]Relations: apremilast has relations: drug_drug with Bepotastine, drug_drug with Bepotastine, drug_drug with Bevacizumab, drug_drug with Bevacizumab, drug_drug with Aprepitant, drug_drug with Aprepitant, drug_drug with Bexarotene, drug_drug with Bexarotene, drug_drug with Cefetamet, drug_drug with Cefetamet.", "label": "yes"}
{"original_question": "Does nimotuzumab improve survival of glioblastoma patients?", "id": "converted_1372", "sentence1": "Does nimotuzumab improve survival of glioblastoma patients?", "sentence2": "The survival times were similar to those seen in historical data of standard therapy., The survival time of a matched population treated at the same hospital with irradiation alone was decreased (median 8.0 and 12.2 mo for Glomerular Basement Membrane and SVEINSSON CHORIORETINAL ATROPHY patients, respectively) compared with that of the patients who received nimotuzumab and curative-intent radiotherapy., This study, in a poor prognosis population, validates the previous data of survival gain after combining nimotuzumab and radiotherapy, in newly diagnosed high-grade glioma patients., The mean and median survival time for subjects treated with nimotuzumab was 31.06 and 17.76 vs. 21.07 and 12.63 months for the control group. CONCLUSIONS: In this randomized trial, nimotuzumab showed an excellent safety profile and significant survival benefit in combination with irradiation., Nimotuzumab was well-tolerated and treatment with the immunoglobulin complex location yielded a survival benefit: median survival time was 32.66 mo and the 2-y survival rate was 54.2%. This study demonstrated the feasibility of prolonged administration of nimotuzumab and showed preliminary evidence of clinical benefit in HGG patients with poor prognosis.,  Recent clinical studies show that patients with Malignant Glioma could benefit from nimotuzumab treatment., CONCLUSIONS: Nimotuzumab in combination with chemotherapy has moderate activity in patients with Malignant Glioma and the Toxic effect are well tolerable, therefore, worth further investigation., It has been evaluated in Malignant neoplasm of brain in adults and children, and shown to be therapeutically safe and effective in terms of increased survival and improved quality of life. , Conclusions As used in this study, nimotuzumab demonstrated a broad safety profile, making it acceptable for chronic use, and implied clinical benefits in terms of increased survival and improved functional status in these patients, compared to findings described in the literature. , Nimotuzumab prolongs survival in patients with Malignant Glioma: A phase I/II clinical study of concomitant radiochemotherapy with or without nimotuzumab., Conclusions As used in this study, nimotuzumab demonstrated a broad safety profile, making it acceptable for chronic use, and implied clinical benefits in terms of increased survival and improved functional status in these patients, compared to findings described in the literature., This study, in a poor prognosis population, validates the previous data of survival gain after combining nimotuzumab and radiotherapy, in newly diagnosed high-grade glioma patients, Conclusions As used in this study, nimotuzumab demonstrated a broad safety profile, making it acceptable for chronic use, and implied clinical benefits in terms of increased survival and improved functional status in these patients, compared to findings described in the literature, A multicenter exploratory study combining nimotuzumab and radiotherapy showed disease control and an overall patient survival similar to previous experiences along with an improvement in the quality of patient survival and no severe side effects., Combining craniospinal irradiation (CSI) with concurrent temozolomide and nimotuzumab therapy may slightly improve tumor control and overall survival[SEP]Relations: Nimotuzumab has relations: drug_drug with Afelimomab, drug_drug with Afelimomab, drug_drug with Nemolizumab, drug_drug with Nemolizumab, drug_drug with Eculizumab, drug_drug with Eculizumab, drug_drug with Obiltoxaximab, drug_drug with Obiltoxaximab, drug_drug with Visilizumab, drug_drug with Visilizumab.", "label": "yes"}
{"original_question": "Does Serca2a bind PLN in the heart?", "id": "converted_1487", "sentence1": "Does Serca2a bind PLN gene in the Chest>Heart?", "sentence2": "The human phospholamban Arg14-deletion mutant localizes to Plasma membrane and interacts with the Na/K-ATPase., Moreover, PLN gene gene-R14Del did not co-immunoprecipitate with SERCA2a (as did WT-PLN gene gene),, n this review, we attempted to highlight the functional significance of PLN gene gene in Vertebrates cardiac physiology. We will refer to the huge literature on Mammals in order to describe the molecular characteristics of this Protein Info, its interaction with SERCA2a, There is clear evidence for direct regulatory Protein Info-Protein Info interactions between phospholamban (PLN gene gene) and the Ca2+-ATPase of cardiac sarcoplasmic reticulum (SERCA2a) in Cytoplasmic domains, These results suggest that PLN gene gene modulates the apparent Ca2+ affinity of SERCA2a through intramembrane interactions, which are disrupted at long range and in concert with disruption of the well characterized Cytoplasmic interactions., Phospholamban (PLN gene gene), a homopentameric, integral membrane Protein Info, reversibly inhibits cardiac sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) activity through intramembrane interactions., The concentration of this inhibited complex is determined by the dissociation constant for the PLN gene gene pentamer (which is mutation-sensitive) and by the dissociation constant for the PLN gene gene/SERCA2a heterodimer (which is likely to be mutation-sensitive)., These results support the proposal that PLN gene gene inhibition of SERCA2a involves, first, depolymerization of PLN gene gene and, second, the formation of inhibitory interactions between monomeric PLN gene gene and SERCA2a., SLN gene gene and PLN gene gene appear to bind to the same regulatory site in SERCA. However, in a ternary complex, PLN gene gene occupies the regulatory site and SLN gene gene binds to the exposed side of PLN gene gene and to SERCA., Cells and biochemical studies revealed that, unlike wild-type PLN gene gene, PLN gene gene(R9C) did not directly inhibit SERCA2a., . Conversely, using anti-SERCA2a immunoglobulin complex location, both PLN gene gene and Acylphosphatase were co-immunoprecipitated with SERCA2a, and the PLN gene gene amount in the precipitate decreased with increasing Acylphosphatase concentrations., Reconstitution of the Cytoplasmic interaction between phospholamban and Ca(2+)-ATPase of cardiac sarcoplasmic reticulum., Phospholamban (PLN gene gene) reversibly inhibits the Ca(2+)-ATPase of cardiac sarcoplasmic reticulum (SERCA2a) through a direct Protein Info-Protein Info interaction, playing a pivotal role in the regulation of Protoplasm Ca(2+) in Myocytes, Cardiac., Phospholamban (PLN gene gene) is a key regulator of Ca(2+) homeostasis and contractility in the Chest>Heart. Its regulatory effects are mediated through its interaction with the Sarcoplasmic Reticulum Calcium-Transporting ATPases, (SERCA2a), resulting in alterations of its Ca(2+)-affinity, In a co-immunoprecipitation of PLN gene gene with SERCA2a, the physical interaction between the two Proteins was increased in PUGNAc-treated cardiomyocytes.[SEP]Relations: Plasma membrane has relations: cellcomp_protein with PLA2G2A, cellcomp_protein with PLA2G2A, cellcomp_protein with PLA2G3, cellcomp_protein with PLA2G3, cellcomp_protein with PLA2G6, cellcomp_protein with PLA2G6, cellcomp_protein with PLXNA2, cellcomp_protein with PLXNA2, cellcomp_protein with PLA2G5, cellcomp_protein with PLA2G5.", "label": "yes"}
{"original_question": "Are Chernobyl survivors at increased risk for breast cancer?", "id": "converted_3695", "sentence1": "Are Chernobyl survivors at increased risk for Malignant neoplasm of Breast?", "sentence2": "Results: A more aggressive course of Malignant neoplasm of Breast is observed in patients exposed to radiation from the Chernobyl accident under the age of 30 years (P < .01). , A significant excess of Multiple Myeloma incidence [standardized incidence rate (SIR) 1.61 %, 95% confidence interval (NDUFB6 gene) 1.01-2.21], THYROID DIAGNOSTIC RADIOPHARMACEUTICALS cancer (SIR 4.18, 95% NDUFB6 gene 3.76-4.59), female Malignant neoplasm of Breast (SIR 1.57 NDUFB6 gene 1.40-1.73), and all Malignant Neoplasms combined (SIR 1.07; 95% NDUFB6 gene 1.05-1.09) was registered. , Possible effects for further study include increased rates of THYROID DIAGNOSTIC RADIOPHARMACEUTICALS, Breast, and Malignant neoplasm of lung and Multiple Myeloma; reduction of radiation risks of leukemia to population levels; and increased morbidity and mortality of cleanup workers from cardio- and cerebrovascular pathology., Furthermore, the upward trends of increases in a variety of other Neoplasms including Malignant neoplasm of Breast, Malignant Neoplasms of central nervous system and Malignant neoplasm of kidney have been reported in the persons exposed to Chornobyl fallout., Epidemiological cohort studies found increased incidence (1990-2012 gg.) of THYROID DIAGNOSTIC RADIOPHARMACEUTICALS cancer in victims of Chernobyl accident (liquidators - in 4.6 times, evacuated - in 4.0 times, residents of contaminated areas - in 1.3 times) and increased incidence of Malignant neoplasm of Breast in female workers of 1986-1987., Historically, data from the Chernobyl reactor accident 27 years ago demonstrated a strong correlation with THYROID DIAGNOSTIC RADIOPHARMACEUTICALS cancer, but data on the radiation effects of Chernobyl on Malignant neoplasm of Breast incidence have remained inconclusive., Re-analyzing the data reveals that the incidence of Malignant neoplasm of Breast in Chernobyl-disaster-exposed women could be higher than previously thought. , For Malignant neoplasm of Breast, the rates and age of onset appear to vary significantly in regions differentially affected by the Chernobyl accident. , In contrast, millions of people were exposed to radioactive Isotopes in the fallout from the Chernobyl accident, within the first 20 years there was a large increase in THYROID DIAGNOSTIC RADIOPHARMACEUTICALS carcinoma incidence and a possible radiation-related increase in Malignant neoplasm of Breast, but as yet there is no general increase in malignancies. , The study demonstrated increases in Malignant neoplasm of Breast incidence in all areas following the Chernobyl accident, reflecting improvements in cancer diagnosis and registration., An increase in Malignant neoplasm of Breast incidence has been reported in areas of Belarus and Ukraine contaminated by the Chernobyl accident and has become an issue of public concern., The study demonstrated increases in Malignant neoplasm of Breast incidence in all areas following the Chernobyl accident, reflecting improvements in cancer diagnosis and registration.[SEP]Relations: malignant neoplasm of chest wall has relations: disease_disease with thoracic cancer, disease_disease with thoracic cancer, disease_disease with chest wall bone cancer, disease_disease with chest wall bone cancer. Multiple myeloma has relations: disease_phenotype_positive with capillary leak syndrome, disease_phenotype_positive with capillary leak syndrome, drug_effect with Lenalidomide, drug_effect with Lenalidomide. Neoplasm of the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS gland has relations: disease_phenotype_positive with familial colorectal cancer, disease_phenotype_positive with familial colorectal cancer.", "label": "yes"}
{"original_question": "Is fatigue prevalent in patients receiving treatment for glioblastoma?", "id": "converted_88", "sentence1": "Is fatigue prevalent in patients receiving treatment for glioblastoma?", "sentence2": "By contrast, fatigue worsened over time, with a difference in mean score of 5.6 points between baseline and 4-month follow-up (P=.02)., In the GB cohort, the most common side effects were fatigue (56 %), diarrhea (44 %), Neutrophil count decreased (31 %), and THROMBOCYTOPENIA 2 (disorder) (25 %). , A total of 37 patients were treated, and treatment was well tolerated: grade 3, 4 nonhematologic toxicity occurred in 30% of patients and consisted mainly of fatigue (14%) and Neuropathy (5%); grade 3, 4 Hematologic toxicity occurred in 37% of patients and consisted of THROMBOCYTOPENIA 2 (disorder) (30%), Lymphocyte count decreased (4%), and Neutrophil count decreased (4%). , Nonhematologic Grade 3 toxicity was rare, and included fatigue in 4 patients and Cognitive disability in 1 patient., The most common grade 3 events were Neutrophil count decreased, THROMBOCYTOPENIA 2 (disorder), fatigue, and Communicable Diseases in 25, 20, 13, and 10%, respectively. , Analysis of the results of the VAS Norris scale did not demonstrate an increase in emotional fatigue but did show an increase in physical fatigue that did not reach statistical significance. With regards to the MFI 20 tool, analysis of the results demonstrated a significant increase in general (P=0.0260) as well as physical (P=0.0141) fatigue but there was no difference in the other indices., This study demonstrated a progressive increase in physical fatigue in patients with glioblastoma relapse treated with Bevacizumab/Irinotecan Regimen. , One patient treated with temozolomide plus isotretinoin plus thalidomide had dose-limiting grade 3 fatigue and Exanthema, and 1 patient receiving all 4 agents had dose-limiting grade 4 Neutrophil count decreased. , The Toxic effect observed were primarily grade 1 and 2, and the most common were fatigue, Hypertensive disease, and Headache. , Fatigue (41%), Exanthema (62%), and Diarrhea (58%) constituted the most frequent adverse events, the majority of these being limited to Grade 1/2. , The most common grades 3 and 4 nonhematologic Toxic effect were Nausea and vomiting (6.7%) and fatigue (5.8%). , Grade 3/4 Toxic effect included White blood cell count decreased (n = 1), Lymphocyte count decreased (n = 2), THROMBOCYTOPENIA 2 (disorder) (n = 1), L-alanine:2-oxoglutarate aminotransferase activity elevation (n = 3), Aspartate Transaminase elevation (n = 1), Central Nervous System Hemorrhage (n = 1), fatigue (n = 1), and thrombotic/embolic events (n = 3); 8 patients required dose reduction. , The most common grade 3 or greater adverse events were fatigue (7%), neutropaenia (7%), and Thrombocytopenia (7%)., Bevacizumab-related toxicity included fatigue (16 patients; 4 grade 3), White blood cell count decreased (9; 1 grade 3), Genus Anemia (5; 0 grade 3), Hypertensive disease (7; 1 grade 3), deep vein thrombosis (4; 1 grade 3) and wound dehiscence (2; 1 grade 3). , Tiredness may be caused by the Brain Injuries due to the Specimen Source Codes - Specimen Source Codes - tumor or the treatment in patients with Glioblastoma Multiforme (Glomerular Basement Membrane). Some patients describe a sense of tiredness particularly after radiation or oral chemotherapy., Levels of tiredness in patients with Glomerular Basement Membrane were greatly affected by the radiotherapy and oral chemotherapy (temozolomide)., The treatment had no negative effect on HRQOL, however, fatigue (P = 0.02) and Constipation (P = 0.01) scales worsened over time.,  This regimen was well tolerated with grade 3/4 Toxic effect of fatigue, White blood cell count decreased, THROMBOCYTOPENIA 2 (disorder) and Exanthema requiring dose reductions. , The most common atrasentan-related Toxic effect were grade 1 or 2 Rhinitis, fatigue, and Edema:Finding:Point in time:^Patient:Ordinal., One patient developed Grade IV fatigue at the 100 ng/mL dose, but the Metatropic dwarfism has not been established. , Side-effects in all patients have included varying degrees of Loss of appetite (finding), fatigue, ipsilateral forehead dermatitis, Blepharitis, and Conjunctivitis. ,  Some patients suffered from fatigue and weak concentration about three months after the end of radiotherapy, in some cases even the neurologic state was deteriorated. , grade 1-2 common Toxic effect included Fever symptoms (finding), Chills, fatigue, No No dizziness, Nausea:Presence or Threshold:Point in time:^Patient:Ordinal, vomiting and Headache, Neutrophilia (finding) and skin painful reactions appeared regularly at levels 3 and 4 (2.5 mg and 3.5 mg). , Ten episodes of grade 3/4 adverse events were observed in nine patients, including fatigue (n = 3), THROMBOCYTOPENIA 2 (disorder) (n = 4), and myelotoxicity, febrile Neutrophil count decreased, and Pulmonary Embolism (each n = 1)., Common adverse events were CTCAE grade 1-2 fatigue, Loss of Appetite question, diarrhea, and Nausea:Presence or Threshold:Point in time:^Patient:Ordinal., The most common grade 3-4 Toxic effect were Venous Thrombosis, fatigue, skin reactions, Encephalopathies, and Neuropathy.[SEP]Relations: Fatigue has relations: disease_phenotype_positive with glioblastoma (disease), disease_phenotype_positive with glioblastoma (disease), disease_phenotype_positive with sporadic pheochromocytoma/secreting paraganglioma, disease_phenotype_positive with sporadic pheochromocytoma/secreting paraganglioma, phenotype_phenotype with Chronic fatigue, phenotype_phenotype with Chronic fatigue, disease_phenotype_positive with hereditary pheochromocytoma-paraganglioma, disease_phenotype_positive with hereditary pheochromocytoma-paraganglioma, drug_effect with Bortezomib, drug_effect with Bortezomib.", "label": "yes"}
{"original_question": "Can oleuropein aglycone interfere with amyloid aggregation?", "id": "converted_3151", "sentence1": "Can oleuropein Aglycone interfere with Serum amyloid A protein aggregation?", "sentence2": "oleuropein, a Substance with phenol structure secoiroid glycoside, is the main polyphenols in the olive oil. It has been reported that the Aglycone form of oleuropein (Olea (plant)) interferes in vitro and in vivo with Serum Serum amyloid A protein A protein aggregation of a number of proteins/peptides involved in Serum Serum amyloid A protein A protein, particularly neurodegenerative, diseases avoiding the growth of toxic oligomers and displaying protection against Cognitive deterioration.[SEP]Relations: Abnormality of immune serum protein physiology has relations: phenotype_phenotype with Abnormal cytokine signaling, phenotype_phenotype with Abnormal cytokine signaling. Motor deterioration has relations: disease_phenotype_positive with PRKAR1B-related neurodegenerative dementia with intermediate filaments, disease_phenotype_positive with PRKAR1B-related neurodegenerative dementia with intermediate filaments, disease_phenotype_positive with neuronal ceroid lipofuscinosis, disease_phenotype_positive with neuronal ceroid lipofuscinosis, disease_phenotype_positive with infantile neuronal ceroid lipofuscinosis, disease_phenotype_positive with infantile neuronal ceroid lipofuscinosis, disease_phenotype_positive with spinocerebellar ataxia, disease_phenotype_positive with spinocerebellar ataxia.", "label": "yes"}
{"original_question": "Is there a genome-wide technique for the detection of R-loop formation?", "id": "converted_844", "sentence1": "Is there a genome-wide technique for the detection of R-loop formation?", "sentence2": "Genome-wide analysis of fragile sites by chromatin immunoprecipitation (ChIP) and microarray (ChIP-chip) of phosphorylated Histone H2a in these Mutant supported a transcription-dependent mechanism of DNA damage characteristic of R loops, We have used a bisulfite-sensitivity assay to demonstrate genome-wide increase in the occurrence of RNA-DNA hybrids (R-Loop Structures), including from antisense and read-through transcripts, in a nusG missense mutant defective for Rho-dependent termination., The results demonstrate a key function of Foundation for the Accreditation of Cellular Therapy in the resolution of R-loop-mediated transcription-replication conflicts, likely associated with a specific chromatin organization., Previous work revealed that GC skew and R-loop formation associate with a core set of unmethylated CpG island (CGI) Promoter in the human genome[SEP]Relations: histone Histone H2a acetylation has relations: bioprocess_protein with TRRAP, bioprocess_protein with TRRAP, bioprocess_protein with NAA40, bioprocess_protein with NAA40, bioprocess_protein with EP400, bioprocess_protein with EP400. promoter clearance from RNA polymerase I promoter has relations: bioprocess_bioprocess with promoter clearance from RNA polymerase I promoter for nuclear large rRNA transcript, bioprocess_bioprocess with promoter clearance from RNA polymerase I promoter for nuclear large rRNA transcript, bioprocess_bioprocess with promoter clearance during DNA-templated transcription, bioprocess_bioprocess with promoter clearance during DNA-templated transcription.", "label": "yes"}
{"original_question": "Are histone deacetylase (HDAC) inhibitors good candidates to control metastasis of solid tumors?", "id": "converted_827", "sentence1": "Are histone deacetylase (HDAC9 wt Allele) inhibitors good candidates to control metastasis of solid tumors?", "sentence2": "JNJ 26481585 also fully inhibited the growth of C170HM2 colorectal liver metastases, whereas again 5-fluorouracil/Leucovorin showed modest activity., Although not meeting the Response Evaluation Criteria in Solid Tumors response criteria for adequate single-agent activity, the observed tolerable Toxic effect and the potential for clinical benefit in terms of stable disease suggest that further assessment of vorinostat as a part of combination therapy with either chemotherapeutic or targeted agents in metastatic breast might be undertaken., Treatments of different structural classes of HDACi simultaneously induced cell death and promoted cell migration and metastasis in multiple Primary malignant neoplasm cell types. Suppression of HDACi-induced PKCs leads to development of low toxic and long-term therapeutic strategies to potentially treat Primary malignant neoplasm as a Chronic disease., mRNA expression analysis of Lung Neoplasms bearing CASP14 gene suggested that the enhanced chemopreventive activity of the combination is related to atorvastatin modulation of DNA repair, SAHA modulation of angiogenesis, and both drugs modulating invasion and metastasis pathways., Histone deacetylase (HDAC9 wt Allele) inhibitors induced morphologic differentiation, cell-cycle exit, and a shift to a differentiated, melanocytic gene expression profile in cultured UM cells. valproic acid inhibited the growth of UM tumors in vivo., When both drugs were used in concert additive effects were observed on the migratory and invasive behavior but not on tumor-endothelium and tumor-matrix interaction. Separate FRAP1 protein, human or HDAC9 wt Allele inhibition slows processes related to tumor metastasis. The RAD001-valproic acid combination showed advantage over valproic acid monotreatment with particular respect to migration and invasion., In conclusion, sequential treatments of CASP14 gene with MS 27-275 followed by TNFSF10 wt Allele may target multiple pathways to reverse EMT and inhibit tumor progression, angiogenesis, and metastasis and represent a novel therapeutic approach to treat Primary malignant neoplasm., In vivo, AA98 synergized with vorinostat to inhibit tumor growth and metastasis., We report the first preclinical data for the prevention of brain metastasis of triple-negative breast Primary malignant neoplasm. Vorinostat is brain permeable and can prevent the formation of brain metastases by 62%. Its mechanism of action involves the induction of DNA double-strand breaks, suggesting rational combinations with DNA active drugs or radiation., Combining vorinostat with radiation may be a potential treatment option for patients with breast Primary malignant neoplasm who develop brain metastases., Although single-agent PCI 24781 had modest effects on sodium tetradecyl sulfate growth and metastasis, marked inhibition was observed when combined with chemotherapy., In a 4T1 metastatic breast carcinoma model, AN-7 inhibited the formation of lung lesions by 76% and AN-9 by 47%, further demonstrating the greater efficacy of AN-7 compared to AN-9 (P<0.02). Both AN-7 and AN-9 exhibited antimetastatic and antiangiogenic activities by reducing vascularization, Basic Fibroblast Growth Factor expression and HIF1A protein, human., Since prolonged oral administration with 50 mg/kg or a single oral dose of 1.2 g/kg AN-7 did not cause adverse effects and the former exhibited significant anticancer activity, AN-7 is likely to display a high therapeutic index and may be beneficial for prostate Primary malignant neoplasm patients., We show that apicidin significantly inhibits HRAS wt Allele-induced invasive phenotype of MCF10A human breast epithelial cells in parallel with a specific downregulation of matrix metalloproteinase (MMP)-2, but not Matrix Metalloproteinase 9. We also show that apicidin induces a morphological reversal and growth inhibition of HRAS wt Allele MCF10A cells similar to that induced by other HDAC9 wt Allele inhibitors., We also found that NaB induced three Genes, which are known metastatic suppressors, and downregulated 11 Genes, which have been shown to promote metastasis.[SEP]Relations: Valproic acid has relations: drug_protein with HDAC9, drug_protein with HDAC9, drug_protein with HDAC2, drug_protein with HDAC2. Vorinostat has relations: drug_protein with HDAC3, drug_protein with HDAC3, drug_protein with HDAC1, drug_protein with HDAC1, drug_protein with HDAC6, drug_protein with HDAC6.", "label": "yes"}
{"original_question": "Are whole-genome duplications more divergent than small-scale duplications in yeast?", "id": "converted_2785", "sentence1": "Are whole-genome duplications more divergent than small-scale duplications in Saccharomyces cerevisiae?", "sentence2": " Also, we observe that Membrane Transport Proteins and glycolytic Genes have a higher probability to be retained in duplicate after WGD and subsequent gene loss, both in the model as in S. cerevisiae, which leads to an increase in glycolytic flux after WGD, We show that the retention of Genes in duplicate in the model, corresponds nicely with those retained in duplicate after the ancestral WGD in S. cerevisiae, Thus, our model confirms the hypothesis that WGD has been important in the adaptation of Saccharomyces cerevisiae to the new, glucose-rich environment that arose after the appearance of Angiosperm., Whole-genome duplicates tend to exhibit less profound phenotypic effects when Delete - Document Availability Status, are functionally less divergent, and are associated with a different set of functions than their small-scale duplicate counterparts., The results uncover the WGD as a major source for the evolution of a complex interconnected block of transcriptional pathways., These selected pairs, both WGD and Speech Sound Disorders, tend to have decelerated functional evolution, have higher propensities of co-clustering into the same protein complexes, and share common interacting partners., Moreover, we find additional transcriptional profiles that are suggestive of neo- and subfunctionalization of duplicate gene copies. These patterns are strongly correlated with the functional dependencies and Sequence - ParameterizedDataType divergence profiles of gene copies., Functional and transcriptional divergence between the copies after gene duplication has been considered the main driver of innovations ., Whole-genome duplicates tend to exhibit less profound phenotypic effects when Delete - Document Availability Status, are functionally less divergent, and are associated with a different set of functions than their small-scale duplicate counterparts., Empirical data shows that whole-genome duplications (WGDs) are more likely to be retained than small-scale duplications (SSDs), though their relative contribution to the functional fate of duplicates remains unexplored.[SEP]Relations: developmental delay with autism spectrum disorder and gait instability has relations: disease_phenotype_positive with Recurrent hand flapping, disease_phenotype_positive with Recurrent hand flapping, disease_phenotype_positive with Narrow palate, disease_phenotype_positive with Narrow palate, disease_phenotype_positive with Self-mutilation, disease_phenotype_positive with Self-mutilation, disease_phenotype_positive with Unsteady gait, disease_phenotype_positive with Unsteady gait, disease_disease with syndromic intellectual disability, disease_disease with syndromic intellectual disability.", "label": "yes"}
{"original_question": "Has Revlimid been approved by the US Food and Drug Administration?", "id": "converted_996", "sentence1": "Has Revlimid been approved by the US Food and Drug Administration?", "sentence2": "In the past decade, immunomodulatory drugs have been approved by the US Food and Drug Administration for the treatment of Multiple Myeloma (Millimole per Liter)-and a number of emerging agents that target the cellular pathways or Proteins involved in the pathophysiology of Millimole per Liter are currently in development. Lenalidomide (Revlimid) and pomalidomide induce apoptosis and sensitize Millimole per Liter Cells while demonstrating superior efficacy and better tolerability than thalidomide (Thalomid)., In the past decade we have seen four new agents approved by the US Food and Drug Administration for treatment of Multiple Myeloma: the Proteasome Inhibitors [MoA] (Pulmonary Valve Insufficiency) bortezomib (Velcade), the immunomodulatory agents lenalidomide (Revlimid) and thalidomide (Thalomid), and doxorubicin liposome. , In the past decade we have seen four new agents approved by the US Food and Drug Administration for treatment of Multiple Myeloma: the Proteasome Inhibitors [MoA] (Pulmonary Valve Insufficiency) bortezomib (Velcade), the immunomodulatory agents lenalidomide (Revlimid) and thalidomide (Thalomid), and doxorubicin liposome., Thalidomide, lenalidomide (Revlimid), and bortezomib (Velcade) are directed not only at Millimole per Liter Cells but also at the BM milieu and have moved rapidly from the bench to the bedside and United States Food and Drug Administration approval to treat Millimole per Liter., Lenalidomide (CC 5013, Revlimid; Celgene Corporation, Summit, New Jersey), a thalidomide analogue, was granted approval by the U.S. Food and Drug Administration (FDA) on June 29, 2006, for use in combination with dexamethasone in patients with Multiple Myeloma (Millimole per Liter) who have received at least one prior therapy., Lenalidomide, an IMiD Pharmacologic Substance (a novel type of immunomodulating Pharmacologic Substance) was recently approved by the US Food and Drug Administration for the treatment of transfusion-dependent anemia in patients with MYELODYSPLASTIC SYNDROME (MDS) and interstitial deletions of chromosome 5q [del(5q)], Lenalidomide, a second-generation immunomodulatory Pharmacologic Substance (IMiD), is approved by the US Food and Drug Administration for treatment of transfusion-dependent anemia in lower-risk MDS patients with Gene Deletion Abnormality 5q chromosomal abnormality, In the past decade we have seen four new agents approved by the US Food and Drug Administration for treatment of Multiple Myeloma: the Proteasome Inhibitors [MoA] (Pulmonary Valve Insufficiency) bortezomib (Velcade), the immunomodulatory agents lenalidomide (Revlimid) and thalidomide (Thalomid), and doxorubicin liposome., lenalidomide (CC5103 or Revlimid) are recently approved for the treatment of Multiple Myeloma.,  In the past decade, immunomodulatory drugs have been approved by the US Food and Drug Administration for the treatment of Multiple Myeloma (Millimole per Liter)-and a number of emerging agents that target the cellular pathways or Proteins involved in the pathophysiology of Millimole per Liter are currently in development. Lenalidomide (Revlimid) and pomalidomide induce apoptosis and sensitize Millimole per Liter Cells while demonstrating superior efficacy and better tolerability than thalidomide (Thalomid).[SEP]Relations: Lenalidomide has relations: drug_drug with Reviparin, drug_drug with Reviparin. Pomalidomide has relations: drug_drug with Reviparin, drug_drug with Reviparin, drug_drug with Revefenacin, drug_drug with Revefenacin. Bortezomib has relations: drug_drug with Reviparin, drug_drug with Reviparin. Thalidomide has relations: drug_drug with Reviparin, drug_drug with Reviparin.", "label": "yes"}
{"original_question": "Is subdural empyema a complication of sinusitis?", "id": "converted_3232", "sentence1": "Is Subdural space Empyema a complication of Sinusitis?", "sentence2": "Acute and chronic Sinusitis can give rise to a wide array of Intracranial Route of Drug Administration and orbital complications. These complications include Cerebral abscess, Subdural space Empyema,,  A computed tomography scan showed bilateral Nasal sinus disease, and magnetic resonance imaging showed a right frontal abscess and Subdural space Empyema., Frontal Sinusitis complicated by a Cerebral abscess and Subdural space Empyema., In older children, Sinusitis and Ear Inflammation media are usually the source for Subdural space empyem, Subdural Empyema as a complication of Sinusitis in the pediatric population., Second, Subdural space Empyema appears to arise in the setting of subacute rather than acute frontal Sinusitis., Subdural Empyema is a rare but potentially life-threatening complication following paranasal Sinusitis and should be considered as a neurological emergency., [Subdural Empyema as a complication of Sinusitis., INTRODUCTION\nSubdural Empyema is an uncommon but serious complication of Sinusitis., Intracranial Subdural space Empyema is most frequently a complication of Sinusitis or, less frequently, Ear Inflammation or neurosurgical procedures., Subdural Empyema is a rare complication of Sinusitis although very severe., Subdural Empyema is a rare complication of Sinusitis in children., Subdural Empyema is a rare but serious complication of paranasal Sinusitis which may result in Cessation of life or permanent disability in a significant proportion of cases., We report a case of Subdural space Empyema secondary to frontal Sinusitis in an otherwise healthy immunocompetent adolescent boy., Subdural Empyema is a rare but life-threatening complication of paranasal Sinusitis, Ear Inflammation media, or mastoid disease., Canis lupus in Sheep's Clothing Subdural Empyema: A Rare Complication of Acute Sinusitis., Interhemispheric and Infratentorial Subdural Empyema with Preseptal cellulitis as Complications of Sinusitis: A Case Report., Subdural Empyema as a complication of Sinusitis in the pediatric population.<AbstractText Label=\"OBJECTIVE\" NlmCategory=\"OBJECTIVE\">Sinusitis is a rare cause of Intracranial Route of Drug Administration Communicable Diseases in children. , [Subdural Empyema as a complication of Sinusitis. , Intracranial Subdural space Empyema is most frequently a complication of Sinusitis or, less frequently, Ear Inflammation or neurosurgical procedures. , Streptococcus pluranimalium: A novel Homo sapiens pathogen?<AbstractText Label=\"INTRODUCTION\" NlmCategory=\"BACKGROUND\">We present the first case of a Subdural space Empyema caused by Streptococcus pluranimalium, in a healthy adolescent male as a possible complication of subclinical frontal Sinusitis. , <AbstractText Label=\"DISCUSSION\" NlmCategory=\"CONCLUSIONS\">The diagnosis of Subdural space Empyema as a complication of asymptomatic Sinusitis in an immunocompetent patient with no history of Fever symptoms (finding) or upper respiratory symptoms was unanticipated. , Second, Subdural space Empyema appears to arise in the setting of subacute rather than acute frontal Sinusitis. , Bifrontal decompressive craniectomy for acute Subdural space Empyema.<AbstractText Label=\"INTRODUCTION\" NlmCategory=\"BACKGROUND\">Subdural Empyema is an uncommon but serious complication of Sinusitis. , Subdural Empyema is a rare but potentially life-threatening complication following paranasal Sinusitis and should be considered as a neurological emergency. , We present a patient with Subdural space Empyema in whom the diagnosis was delayed, followed by a discussion of Infection - Infection - suppurative complications of Sinusitis. , <AbstractText Label=\"CASE REPORT\" NlmCategory=\"METHODS\">We report an unusual case of Sinusitis-associated acute Subdural space Empyema in a 13-year-old patient, presenting in a catastrophic manner with acutely raised Intracranial Route of Drug Administration pressure. , The symptoms of Subdural space Empyema may be mild and may be the same as those associated with Sinusitis, or the Communicable Diseases may result in alteration of the level of consciousness and Focal Neurologic Deficits., We report the clinical and radiological course of an adolescent with a Subdural space Empyema secondary to Sinusitis., We report two cases of Subdural space Empyema secondary to Sinusitis in persons without impaired immunity., Subdural Empyema as a complication of Sinusitis., Furthermore, Subdural space Empyema usually is related to sinus infections, particularly those caused by Streptococcus milleri, an anaerobic Organism., Subdural Empyema is an uncommon but serious complication of Sinusitis.[SEP]Relations: Subdural space Empyema has relations: disease_disease with Empyema, disease_disease with Empyema, disease_disease with central nervous system infectious disorder, disease_disease with central nervous system infectious disorder. Empyema has relations: disease_disease with Subdural space Empyema, disease_disease with Subdural space Empyema, disease_disease with tuberculous Empyema, disease_disease with tuberculous Empyema, disease_disease with infectious disease, disease_disease with infectious disease.", "label": "yes"}
{"original_question": "Has ivosidenib been FDA approved for use against acute myeloid leukemia?", "id": "converted_2953", "sentence1": "Has ivosidenib been FDA approved for use against acute myeloid leukemia?", "sentence2": "The FDA approved ivosidenib for patients with IDH1-mutant relapsed/refractory acute myeloid leukemia. [SEP]", "label": "yes"}
{"original_question": "Is Fibroblast Growth Factor 23 a phosphaturic hormone?", "id": "converted_1000", "sentence1": "Is Fibroblast Growth Factor 23 a phosphaturic hormone?", "sentence2": "PTH wt Allele wt Allele can induce skeletal synthesis of another potent phosphaturic hormone, fibroblast growth factor 23 (FGF23 gene gene), ,  Recombinant Fibroblast Growth Factor 1 23 (FGF23 gene gene) is a phosphaturic hormone that has recently been identified as a CKD-related factor affecting Congenital Rubella Syndrome. ,  circulating phosphaturic hormone fibroblast growth factor 23 levels,  Recombinant Fibroblast Growth Factor 1 (FGF) 23 is one of the most recently discovered FGFs. This phosphaturic hormone produced in XXX bone is a risk factor for Cardiovascular Diseases and thus mortality., fibroblast growth factor 23 (FGF23 gene gene), a phosphaturic hormone and regulator of 1,25(OH)2 vitamin D3 (1,25VitD3). , fibroblast growth factor 23 (FGF23 gene gene), a bone-derived phosphaturic hormone.,  the phosphaturic hormone fibroblast growth factor 23 (FGF23 gene gene) and soluble KL wt Allele with all-cause mortality., In particular, diseases caused by changes in the expression and proteolytic control of the phosphaturic hormone fibroblast growth factor 23 (FGF23 gene gene) have come to the forefront in terms of directing new models explaining mineral metabolism, serum levels of a phosphaturic hormone, fibroblast growth factor 23 (Fgf23), [SEP]Relations: fibroblast growth factor receptor binding has relations: molfunc_protein with FGF16, molfunc_protein with FGF16, molfunc_protein with FGF17, molfunc_protein with FGF17, molfunc_protein with FGF19, molfunc_protein with FGF19, molfunc_protein with FGF23 gene, molfunc_protein with FGF23 gene, molfunc_protein with FGF22, molfunc_protein with FGF22.", "label": "yes"}
{"original_question": "Can propofol cause green urine?", "id": "converted_4119", "sentence1": "Can propofol cause green Specimen Source Codes - Urine?", "sentence2": "Reasons for discontinuing propofol are signs of rhabdomyolysis (92.9%), green Specimen Source Codes - Urine, elevated Finding of Abdomen>Liver enzyme levels (71.4% each) and elevated Triglycerides (57.1%)., propofol-Induced Green Urine in a Patient with Refractory Status Epilepticus., We present the case of a 52-year-old man, who developed green Specimen Source Codes - Urine following propofol coma therapy for Status Epilepticus., The green discoloration of Specimen Source Codes - Urine is a rare and Benign condition, which occurs when clearance of propofol exceeds the Hepatic and extrahepatic elimination., Green Abnormal color of Specimen Source Codes - Urine following propofol infusion in a Canis familiaris.,  During mechanical ventilation, anaesthesia was maintained using a propofol target-controlled infusion system and, subsequently, the Canis familiaris produced bright green Specimen Source Codes - Urine in the Specimen Source Codes - Urine collection system. Although previously documented in Homo sapiens, this appears to be the first report of green Specimen Source Codes - Urine in a Canis familiaris following propofol use., Green Specimen Source Codes - Urine is also caused by medications such as propofol and Infections of musculoskeletal system such as pseudomonas., Although it is assumed that the phenolic derivatives of propofol can cause green discoloration of the Specimen Source Codes - Urine, the actual origin remains unknown., An uncommon adverse effect of propofol is green discoloration of the Specimen Source Codes - Urine, which has been reported not only under general anesthesia but also with sedation., Antifungal Antifungal Antibiotics, Topical, Topical were avoided when propofol was recognized as a rare and Benign potential cause of the green Specimen Source Codes - Urine., Green Urine Due to propofol: A Case Report with Review of Literature., Herein, we present a case of 62-year-old postoperative lady, noticed to be passing green coloured Specimen Source Codes - Urine believed to be due to intravenous propofol administration for induction of general anaesthesia., Green Specimen Source Codes - Urine is rare indeed and it is a Benign potential side effect of propofol; this phenomenon is related to the metabolism of propofol., Clinical significance of rare and Benign side effects: propofol and green Specimen Source Codes - Urine., Green Specimen Source Codes - Urine in a patient who received a continuous infusion of propofol: A case report., This phenomenon is due to metabolism of propofol which may lead to a phenolic green chromophore which is conjugated in the Abdomen>Liver and excreted in the Specimen Source Codes - Urine., Green Urine Discoloration due to propofol Infusion: A Case Report., An analysis of green discoloration of Specimen Source Codes - Urine caused by propofol infusion., We experienced green Specimen Source Codes - Urine from a long-term anesthetized patient who received a continuous infusion of propofol., We present a 19-year-old man who excreted green Specimen Source Codes - Urine after propofol infusion., green colour of Specimen Source Codes - Urine due to propofol occurs when clearance of propofol exceeds Hepatic elimination, and extrahepatic elimination of propofol occurs. Thi, Green Specimen Source Codes - Urine from propofol infusion is a Benign and rare side effect, Grass-green Specimen Source Codes - Urine from propofol infusion, propofol-Induced Green Urine in a Patient with Refractory Status Epilepticus, sedation. An uncommon adverse effect of propofol is green discoloration of the Specimen Source Codes - Urine, which has been reported not only under general anesthesia but also with, erein, we present a case of 62-year-old postoperative lady, noticed to be passing green coloured Specimen Source Codes - Urine believed to be due to intravenous propofol administration for induction of general anaesthesia. T, en Specimen Source Codes - Urine is rare indeed and it is a Benign potential side effect of propofol; this phenomenon is related to the metabolism of propofol. W, Green Specimen Source Codes - Urine is also caused by medications such as propofol and Infections of musculoskeletal system such as pseudomonas, Green Urine Due to propofol: A Case Report with Review of Literature, LUSION: We experienced a case of a patient with green discoloration of the Specimen Source Codes - Urine after general anesthesia using propofol. therapeutic autologous lymphocytes, After starting continuous infusion of propofol for postoperative sedation, his Specimen Source Codes - Urine became dark green., We believe that the green discoloration of the Specimen Source Codes - Urine was caused by propofol infusion and was related to impaired enterohepatic circulation and extrahepatic glucuronidation in the Both Both kidneys., WHAT IS KNOWN AND OBJECTIVE: propofol, a commonly used sedative, has on rare occasions, been reported to discolour Specimen Source Codes - Urine green,  IS NEW AND CONCLUSION: Green discoloration of the Specimen Source Codes - Urine from propofol infusion is dose dependent. It,  We report on a patient who produced dark green discoloration of Specimen Source Codes - Urine from prolonged propofol infusion, administered for intractable epilepsy, Dark green discoloration of the Specimen Source Codes - Urine after prolonged propofol infusion: a case report.,  experienced a case of a patient with green discoloration of the Specimen Source Codes - Urine after general anesthesia using propofol. A, On the third day of propofol infusion his Specimen Source Codes - Urine was dark green., Green Specimen Source Codes - Urine from propofol infusion is a Benign and rare side effect., The green colour of Specimen Source Codes - Urine due to propofol occurs when clearance of propofol exceeds Hepatic elimination, and extrahepatic elimination of propofol occurs., ur change is dose dependent. We report on a patient who produced dark green discoloration of Specimen Source Codes - Urine from prolonged propofol infusion, administered for intractable epilepsy.CASE SUMMARY: The colour intensity of the patient's uri, Several Substance in literature have been associated with green Specimen Source Codes - Urine including propofol, Biliverdine, metoclopramide, methylene blue, indigo, amitriptyline, methocarbamol, indomethacin, promethazine, cimetidine and food colourings. , We discuss a case of a Benign cause of green discoloration of Specimen Source Codes - Urine caused by propofol infusion, which reversed following its discontinuation., The patient's Specimen Source Codes - Urine subsequently showed a green discoloration. Urine discoloration was completely reversible upon discontinuation of propofol., Two days after admittance, we observed a green discoloration of the Specimen Source Codes - Urine. This is a rare and Benign side effect of propofol., We describe a 58-year-old man who developed green Specimen Source Codes - Urine after operation on a pressure ulcer. The Abnormal color disappeared gradually after two days. We think that the use of methylene blue dye during the revision of the Injury Injury wounds and the use of the sedative propofol could have caused it.[SEP]Relations: propofol has relations: drug_effect with Vomiting, drug_effect with Vomiting, drug_drug with Urethane, drug_drug with Urethane, drug_effect with Urinary retention, drug_effect with Urinary retention, drug_effect with Cough, drug_effect with Cough, drug_drug with Urapidil, drug_drug with Urapidil.", "label": "yes"}
{"original_question": "Can radiosurgery be used for the DNET tumors?", "id": "converted_3978", "sentence1": "Can radiosurgery be used for the DNET tumors?", "sentence2": "Salvage gamma knife radiosurgery in the management of dysembryoplastic neuroepithelial tumors: Long-term outcome in a single-institution case series., BACKGROUND: Dysembryoplastic neuroepithelial Specimen Source Codes - Specimen Source Codes - tumor (DNT/DNET) are rare epileptogenic tumors. Microsurgery remains the best treatment option, although case reports exist on the use of gamma knife radiosurgery (GKRS) in selected cases. We investigated the long-term outcome of GKRS-treated DNTs at our institution in the context of current diagnostic and treatment options., Long-term seizure control was obtained after GKRS of two separate residual DNT components along the surgical margin (2005 and 2010). A 27-year-old male undergoing gross total resection of the contrast-enhancing portion of a DNT (1999) resulted in temporary control of intractable Epilepsy despite Automated External Defibrillators; lasting clinical control of Seizures was achieved in 2002 after GKRS of a small, recurrent DNT component. A 28-year-old male underwent STR (short terminal repeat, nucleic acid) (short terminal repeat, nucleic acid) of DNT (1994 and 2004) resulting in temporary control of intractable Epilepsy. Lasting seizure control was gained after GKRS of a residual Specimen Source Codes - Specimen Source Codes - tumor (2005).CONCLUSION: GKRS as performed in our series was effective in terms of Specimen Source Codes - Specimen Source Codes - tumor and seizure control., Prospective studies are warranted to establish the role of GKRS in the treatment of DNTs., Two rare cases of intractable Epilepsy caused by Dysembryoplastic Neuroepithelial Tumours (DNET) are reported and their different management discussed. The first case required vagal nerve stimulation and radiosurgery while the later was operated with the help of neuronavigation. , Salvage gamma knife radiosurgery in the management of dysembryoplastic neuroepithelial tumors: Long-term outcome in a single-institution case series[SEP]Relations: Epilepsy has relations: contraindication with Foscarnet, contraindication with Foscarnet, contraindication with Dyclonine, contraindication with Dyclonine, contraindication with Desonide, contraindication with Desonide, contraindication with Triprolidine, contraindication with Triprolidine. Dysembryoplastic neuroepithelial Specimen Source Codes - tumor has relations: phenotype_phenotype with Neuronal/glioneuronal neoplasm of the central nervous system, phenotype_phenotype with Neuronal/glioneuronal neoplasm of the central nervous system.", "label": "yes"}
{"original_question": "Is there an association between FGFR3 mutation and plagiocephaly?", "id": "converted_703", "sentence1": "Is there an association between FGFR3 protein, human Mutation Abnormality and Plagiocephaly?", "sentence2": "Series of neurosurgical interventions were carried out, principally for Acrocephaly and posterior Plagiocephaly. The most common Achondroplasia Mutation Abnormality, a p.Gly380Arg in the Fibroblast Growth Factor Receptors (FGFR3 protein, human protein, human) gene, was detected. ,  The most common Mutation Abnormality for Achondroplasia (FGFR3 protein, human protein, human Gly380Arg, resulting in 1138G>A) was identified. Imaging studies disclosed complex CRANIOSYNOSTOSIS, TYPE 2 and neurosurgical intervention was carried out, particularly for posterior Plagiocephaly., FGFR mutations and Plagiocephaly., FGFR genes have important effects on bone development, and mutations in 4 \"hot spot\" Exons of FGFR1 protein, human protein, human-3 are found in many patients with CRANIOSYNOSTOSIS, TYPE 2 and some with synostotic Plagiocephaly. , Mutation analyses in the FGFR3 protein, human protein, human gene revealed nucleotide alterations located in the mutational hot spot at Amino Acid [EPC] residue 250 (g.C749)., RESULTS: In our cohort of 159 patients with various CRANIOSYNOSTOSIS, TYPE 2 syndromes, mutations were found in 100% of patients with Apert syndrome, 83.3% with Pfeiffer Syndrome, 72.7% with Craniofacial dysostosis type 1, 50.0% with Saethre-Chotzen syndrome, 27.7% with Plagiocephaly, 31.8% with brachicephaly, 20% of complex cases, and 6.9% of mixed cases. , The Mutation that could cause unilateral Coronal synostosis are more elusive., Gene Mutation were found in eight of 47 patients: two patients with different single-amino-acid changes in Fibroblast Growth Factor Receptor 2, three patients with FGFR3 protein, human protein, human Pro250Arg, and three patients with Musculoskeletal torsion, function mutations. , Other abnormalities in the craniofacial region and All All extremities were clues to a particular Mutation Abnormality in Fibroblast Growth Factor Receptor 2, FGFR3 protein, human protein, human, Musculoskeletal torsion, function, or the X-linked Mutation Abnormality. , To determine whether the autosomal dominant Fibroblast Growth Factor Receptors (FGFR3 protein, human protein, human) Pro250Arg Mutation Abnormality causes anterior Plagiocephaly, patients with either apparently sporadic Unicoronal synostosis (N = 37) or other forms of anterior Plagiocephaly (N = 10) were studied for this Mutation Abnormality., The occurrence of the FGFR3 protein, human protein, human Mutation Abnormality among patients with Unicoronal synostosis provides evidence for a genetic basis of certain forms of Plagiocephaly., None of the 6 patients with nonsynostotic Plagiocephaly and none of the 4 patients with additional suture synostosis had the FGFR3 protein, human protein, human Mutation Abnormality., Between January and December of 1996, patients with a diagnosis of Plagiocephaly at the Children's Hospital of Philadelphia were evaluated for the FGFR3 protein, human protein, human Mutation Abnormality., Between January and December of 1996, patients with a diagnosis of Plagiocephaly at the Children&apos;s Hospital of Philadelphia were evaluated for the FGFR3 protein, human protein, human Mutation Abnormality, FGFR genes have important effects on bone development, and mutations in 4 &quot;hot spot&quot; Exons of FGFR1 protein, human protein, human-3 are found in many patients with CRANIOSYNOSTOSIS, TYPE 2 and some with synostotic Plagiocephaly, To determine whether the autosomal dominant Fibroblast Growth Factor Receptors (FGFR3 protein, human protein, human) Pro250Arg Mutation Abnormality causes anterior Plagiocephaly, patients with either apparently sporadic Unicoronal synostosis (N = 37) or other forms of anterior Plagiocephaly (N = 10) were studied for this Mutation Abnormality, None of the 6 patients with nonsynostotic Plagiocephaly and none of the 4 patients with additional suture synostosis had the FGFR3 protein, human protein, human Mutation Abnormality, The occurrence of the FGFR3 protein, human protein, human Mutation Abnormality among patients with Unicoronal synostosis provides evidence for a genetic basis of certain forms of Plagiocephaly, FGFR mutations and Plagiocephaly, Between January and December of 1996, patients with a diagnosis of Plagiocephaly at the Children's Hospital of Philadelphia were evaluated for the FGFR3 protein, human protein, human Mutation Abnormality. , None of the 6 patients with nonsynostotic Plagiocephaly and none of the 4 patients with additional suture synostosis had the FGFR3 protein, human protein, human Mutation Abnormality. , The occurrence of the FGFR3 protein, human protein, human Mutation Abnormality among patients with Unicoronal synostosis provides evidence for a genetic basis of certain forms of Plagiocephaly. ,  To determine whether the autosomal dominant Fibroblast Growth Factor Receptors (FGFR3 protein, human protein, human) Pro250Arg Mutation Abnormality causes anterior Plagiocephaly, patients with either apparently sporadic Unicoronal synostosis (N = 37) or other forms of anterior Plagiocephaly (N = 10) were studied for this Mutation Abnormality. Of 37 patients with Unicoronal synostosis, 4 tested positive for the Pro250Arg Mutation Abnormality in FGFR3 protein, human protein, human, and 33 were negative for this Mutation Abnormality., To determine whether the autosomal dominant Fibroblast Growth Factor Receptors (FGFR3 protein, human protein, human) Pro250Arg Mutation Abnormality causes anterior Plagiocephaly, patients with either apparently sporadic Unicoronal synostosis (N = 37) or other forms of anterior Plagiocephaly (N = 10) were studied for this Mutation Abnormality., In a girl with seemingly isolated Plagiocephaly we identified a P250L (749C-->T) Mutation Abnormality in FGFR3 protein, human protein, human., FGFR mutations and Plagiocephaly., None of the 6 patients with nonsynostotic Plagiocephaly and none of the 4 patients with additional suture synostosis had the FGFR3 protein, human protein, human Mutation Abnormality., The occurrence of the FGFR3 protein, human protein, human Mutation Abnormality among patients with Unicoronal synostosis provides evidence for a genetic basis of certain forms of Plagiocephaly.[SEP]Relations: FGFR3 protein, human has relations: disease_protein with isolated Plagiocephaly, disease_protein with isolated Plagiocephaly, disease_protein with polydactyly (disease), disease_protein with polydactyly (disease), disease_protein with epilepsy, disease_protein with epilepsy, protein_protein with FGF1, protein_protein with FGF1. Plagiocephaly has relations: disease_phenotype_positive with FG syndrome, disease_phenotype_positive with FG syndrome.", "label": "yes"}
{"original_question": "Has small pox been eradicated from the world?", "id": "converted_1876", "sentence1": "Has small pox been eradicated from the world?", "sentence2": "small pox has been eradicated., smallpox is now eradicated, In May 1980 the World Health Assembly in Geneva announced in solemn form the world-wide eradication of the small-pox and gave recommendations to the member countries for concluding measures concerning the small-pox vaccination, the foundation of vaccine reserves and the control of the epidemiological situation in the world., As a result of vaccination, diseases such as polio and measles have been controlled and small pox has been eradicated, Small pox eradication from the world is the perfect example of the role of mass vaccination of the entire community of the universe. , The French owe a lot to this Central Committee of Vaccine [APC] [APC], which greatly contributed to fighting small pox and eradicating the Disease finally., Small pox eradication from the world is the perfect example of the role of mass vaccination of the entire community of the universe., Also, the vaccine that Jenner used, which decreased the prevalence of Small PRODH gene worldwide in his own time, and later was used to eradicate Small PRODH gene altogether, is discussed in light of recent data.., the only known cases of smallpox happened from an outbreak in Birmingham, England caused by a laboratory accident in the year of 1979. On May the 8 th 1980 the Disease was declared as eliminated from the world by the WHO (WHO-Resolution 33.33).[SEP]Relations: BCG vaccine has relations: drug_drug with Ponatinib, drug_drug with Ponatinib, drug_drug with Paclitaxel, drug_drug with Paclitaxel, drug_drug with Ubenimex, drug_drug with Ubenimex, drug_drug with Ebola Zaire vaccine (live, attenuated), drug_drug with Ebola Zaire vaccine (live, attenuated), drug_drug with Aspoxicillin, drug_drug with Aspoxicillin.", "label": "yes"}
{"original_question": "Does CRISPR inversion of CTCF sites alter genome topology?", "id": "converted_1989", "sentence1": "Does Clustered Regularly Interspaced Short Palindromic Repeats inversion of CTCF sites alter genome topology?", "sentence2": "Clustered Regularly Interspaced Short Palindromic Repeats Inversion of CTCF Sites Alters Genome Topology and Enhancer/Promoter Function, To test the functional significance of this observation, we combined Clustered Regularly Interspaced Short Palindromic Repeats/Cas9-based genomic-DNA-fragment editing with Chromosomes, Human, Pair 1-conformation-capture experiments to show that the location and relative orientations of CBSs determine the specificity of long-range chromatin looping in mammalian genomes, using PROTOCADHERIN 3 (Pcdh) and β-globin as model genes. Inversion of CBS elements within the Pcdh enhancer reconfigures the topology of chromatin loops between the distal enhancer and target promoters and alters gene-expression patterns. Thus, although enhancers can function in an orientation-independent manner in reporter assays, in the native Chromosomes, Human, Pair 1 context, the orientation of at least some enhancers carrying CBSs can determine both the architecture of topological chromatin domains and enhancer/promoter specificity. These findings reveal how 3D Chromosomes, Human, Pair 1 architecture can be encoded by linear genome sequences, Clustered Regularly Interspaced Short Palindromic Repeats Inversion of CTCF Sites Alters Genome Topology and Enhancer/Promoter Function., Clustered Regularly Interspaced Short Palindromic Repeats Inversion of CTCF Sites Alters Genome Topology and Enhancer/Promoter Function.[SEP]Relations: PROTOCADHERIN 3 3 has relations: disease_disease with Mendelian disease, disease_disease with Mendelian disease. negative regulation of heart rate involved in baroreceptor response to increased systemic arterial blood pressure has relations: bioprocess_protein with ADRA1A, bioprocess_protein with ADRA1A, bioprocess_bioprocess with negative regulation of heart rate, bioprocess_bioprocess with negative regulation of heart rate.", "label": "yes"}
{"original_question": "Is there any link between ERCC1-XPF and cohesin?", "id": "converted_2459", "sentence1": "Is there any link between ERCC1-XPF and cohesins?", "sentence2": "ERCC1-XPF cooperates with CTGF protein, human and cohesins to facilitate the developmental silencing of imprinted Genes., Using an in vivo biotinylation tagging approach in CASP14 gene, we show that the nucleotide excision repair (NER) structure-specific endonuclease ERCC1-XPF complex interacts with the insulator binding protein CTGF protein, human, the cohesins subunits SMC1A and SMC3 wt Allele wt Allele and with DPEP2 gene; the factors co-localize with Alpha thalassemia X-linked intellectual disability syndrome at the Promoter and control regions (ICRs) of imprinted Genes during postnatal hepatic development. Loss of Excision Repair Cross-Complementing 1 or exposure to mitomycin triggers the localization of CTGF protein, human to Heterochromatin, the dissociation of the CTGF protein, human-cohesins complex and Alpha thalassemia X-linked intellectual disability syndrome from Promoter and ICRs, altered histone marks and the aberrant developmental expression of imprinted Genes without altering DNA methylation. We propose that ERCC1-XPF cooperates with CTGF protein, human and cohesins to facilitate the developmental silencing of imprinted Genes and that persistent DNA damage triggers chromatin location location changes that affect gene expression programs associated with NER disorders., Using an in vivo biotinylation tagging approach in CASP14 gene, we show that the nucleotide excision repair (NER) structure-specific endonuclease ERCC1-XPF complex interacts with the insulator binding protein CTGF protein, human, the cohesins subunits SMC1A and SMC3 wt Allele wt Allele and with DPEP2 gene; the factors co-localize with Alpha thalassemia X-linked intellectual disability syndrome at the Promoter and control regions (ICRs) of imprinted Genes during postnatal hepatic development., We propose that ERCC1-XPF cooperates with CTGF protein, human and cohesins to facilitate the developmental silencing of imprinted Genes and that persistent DNA damage triggers chromatin location location changes that affect gene expression programs associated with NER disorders., We propose that ERCC1-XPF cooperates with CTGF protein, human and cohesins to facilitate the developmental silencing of imprinted Genes and that persistent DNA damage triggers chromatin location location changes that affect gene expression programs associated with NER disorders., We propose that ERCC1-XPF cooperates with CTGF protein, human and cohesins to facilitate the developmental silencing of imprinted Genes and that persistent DNA damage triggers chromatin location location changes that affect gene expression programs associated with NER disorders.<br>, ERCC1-XPF cooperates with CTGF protein, human and cohesins to facilitate the developmental silencing of imprinted Genes., We propose that ERCC1-XPF cooperates with CTGF protein, human and cohesins to facilitate the developmental silencing of imprinted Genes and that persistent DNA damage triggers chromatin location location changes that affect gene expression programs associated with NER disorders..[SEP]Relations: Heterochromatin has relations: cellcomp_protein with HSF1, cellcomp_protein with HSF1, cellcomp_protein with FOXC1, cellcomp_protein with FOXC1, cellcomp_protein with MORC2, cellcomp_protein with MORC2, cellcomp_protein with ORC2, cellcomp_protein with ORC2, cellcomp_protein with CBX1, cellcomp_protein with CBX1.", "label": "yes"}
{"original_question": "Does clinical trial data support the use of minocycline for amyotrophic lateral sclerosis?", "id": "converted_3371", "sentence1": "Does clinical trial data support the use of minocycline for amyotrophic lateral sclerosis?", "sentence2": "Two double-blind, randomized, placebo-controlled feasibility trials of minocycline in Amyotrophic Lateral Sclerosis were conducted. , This pilot study shows that minocycline and riluzole can be taken safely together. Further trials are needed to assess efficacy of such treatment., It reduces apoptosis in mouse models of Huntington's disease and familial amyotrophic lateral sclerosis (Amyotrophic Lateral Sclerosis) and is in clinical trial for sporadic Amyotrophic Lateral Sclerosis., Efficacy of minocycline in patients with amyotrophic lateral sclerosis: a phase III randomised trial., FINDINGS: ALSFRS-R score deterioration was faster in the minocycline group than in the placebo group (-1.30 vs -1.04 units/month, 95% CI for difference -0.44 to -0.08; p=0.005). Patients on minocycline also had non-significant tendencies towards faster decline in FVC (-3.48 vs -3.01, -1.03 to 0.11; p=0.11) and MMT score (-0.30 vs -0.26, -0.08 to 0.01; p=0.11), and greater mortality during the 9-month treatment phase (hazard ratio=1.32, 95% CI 0.83 to 2.10; p=0.23) than did patients on placebo. Quality-of-life scores did not differ between the treatment groups. , INTERPRETATION: Our finding that minocycline has a harmful effect on patients with Amyotrophic Lateral Sclerosis has implications for trials of minocycline in patients with other nervous system disorder, and for how potential neuroprotective agents are screened for use in patients with Amyotrophic Lateral Sclerosis., A recent publication of the results of a clinical trial of minocycline in 412 Amyotrophic Lateral Sclerosis patient has aroused considerable controversy in the Amyotrophic Lateral Sclerosis scientific community. As on previous occasions, the results obtained in the laboratory are not reproduced in clinical practice., A recent publication of the results of a clinical trial of minocycline in 412 Amyotrophic Lateral Sclerosis patient has aroused considerable controversy in the Amyotrophic Lateral Sclerosis scientific community., INTERPRETATION\n\nOur finding that minocycline has a harmful effect on patients with Amyotrophic Lateral Sclerosis has implications for trials of minocycline in patients with other nervous system disorder, and for how potential neuroprotective agents are screened for use in patients with Amyotrophic Lateral Sclerosis., A recent publication of the results of a clinical trial of minocycline in 412 Amyotrophic Lateral Sclerosis patient has aroused considerable controversy in the Amyotrophic Lateral Sclerosis scientific community, A recent publication of the results of a clinical trial of minocycline in 412 Amyotrophic Lateral Sclerosis patient has aroused considerable controversy in the Amyotrophic Lateral Sclerosis scientific community., Our finding that minocycline has a harmful effect on patients with Amyotrophic Lateral Sclerosis has implications for trials of minocycline in patients with other nervous system disorder, and for how potential neuroprotective agents are screened for use in patients with Amyotrophic Lateral Sclerosis., Patients on minocycline also had non-significant tendencies towards faster decline in FVC (-3.48 vs -3.01, -1.03 to 0.11; p=0.11) and MMT score (-0.30 vs -0.26, -0.08 to 0.01; p=0.11), and greater mortality during the 9-month treatment phase (hazard ratio=1.32, 95% CI 0.83 to 2.10; p=0.23) than did patients on placebo.[SEP]Relations: Minocycline has relations: drug_drug with Metacycline, drug_drug with Metacycline, drug_drug with Doxycycline, drug_drug with Doxycycline, drug_drug with Hypericin, drug_drug with Hypericin, drug_drug with Diphenadione, drug_drug with Diphenadione, drug_drug with Maprotiline, drug_drug with Maprotiline.", "label": "no"}
{"original_question": "Can fetal aneuploidy be detected with non-invasive prenatal testing?", "id": "converted_876", "sentence1": "Can Prenatal care aneuploidy be detected with non-invasive prenatal testing?", "sentence2": "Non-invasive prenatal testing with cell-free DNA: US physician attitudes toward implementation in clinical practice., The aim of this study was to assess awareness, potential adoption, and current utilization of non-invasive prenatal testing (NIPT) analysis for common Prenatal care aneuploidies among obstetricians, Cell-Free DNA has been used for Prenatal care rhesus factor and sex determination, Prenatal care aneuploidy screening, cancer diagnostics and monitoring, and other applications., The recent release of new, non-invasive prenatal tests for Prenatal care aneuploidy using cell-free Prenatal care DNA (cffDNA) has been hailed as a revolution in prenatal testing and has triggered significant commercial interest in the field., Non-invasive prenatal testing (NIPT) for aneuploidy using cell-free DNA in maternal plasma is revolutionizing prenatal screening and diagnosis., SNP-based non-invasive prenatal testing detects Sex Chromosomes aneuploidies with high accuracy., Non-invasive prenatal testing (NIPT) of cell-free Prenatal care DNA in maternal plasma is a novel approach, designed for detecting common aneuploidies in the Fetus in fetu., This study aimed to develop a single-nucleotide polymorphism-based and informatics-based non-invasive prenatal test that detects Sex Chromosomes aneuploidies early in pregnancy., RAPIDR: an analysis package for non-invasive prenatal testing of aneuploidy., Non-invasive prenatal testing for aneuploidy: current status and future prospects., Non-invasive prenatal testing of Prenatal care whole chromosome aneuploidy by massively parallel sequencing., Attitudes towards non-invasive prenatal testing for aneuploidy among US adults of reproductive age., [Non-invasive prenatal test in the diagnosis of aneuploidy 13, 18 and 21--theoretical and practical aspects]., To track and analyze two false positive cases from non-invasive prenatal testing for potential Prenatal care aneuploidy., Non-invasive prenatal testing (NIPT) of Prenatal care aneuploidy using cell-free Prenatal care DNA is becoming part of routine clinical practice., To report secondary or additional findings arising from introduction of non-invasive prenatal testing (NIPT) for aneuploidy by whole genome sequencing as a clinical service., Israeli Society of Medical Genetics NIPT Committee Opinion 072013: Non-invasive prenatal testing of cell-free DNA in maternal plasma for detection of Prenatal care aneuploidy., In recent years, technical advances in the molecular analysis of Prenatal care DNA (e.g., digital PCR and massively parallel sequencing (MPS)) has enabled the successful implementation of noninvasive testing into clinical practice, such as Prenatal care sex assessment, RhD genotyping, and Prenatal care chromosomal aneuploidy detection.With the ability to decipher the entire Prenatal care genome from maternal plasma DNA, we foresee that an increased number of non-invasive prenatal tests will be available for detecting many single-gene disorders in the near future, First identified in 1997, cell-free Prenatal care DNA (cffDNA) has just recently been used to detect Prenatal care aneuploidy of chromosomes 13, 18, and 21, showing its potential to revolutionize prenatal genetic testing as a non-invasive screening tool, Non-invasive prenatal testing (NIPT) using cell-free Prenatal care DNA in maternal plasma has been developed for the detection of Prenatal care aneuploidy, Israeli Society of Medical Genetics NIPT Committee Opinion 072013: Non-invasive prenatal testing of cell-free DNA in maternal plasma for detection of Prenatal care aneuploidy, Non-invasive prenatal testing for Prenatal care aneuploidies in the first trimester of pregnancy, To explore the value of next-generation sequencing for the non-invasive prenatal testing of Prenatal care chromosomal aneuploidies, Secondary findings from non-invasive prenatal testing for common Prenatal care aneuploidies by whole genome sequencing as a clinical service, To report secondary or additional findings arising from introduction of non-invasive prenatal testing (NIPT) for aneuploidy by whole genome sequencing as a clinical service, Secondary findings from non-invasive prenatal testing for common Prenatal care aneuploidies by whole genome sequencing as a clinical service., Motivations for undertaking DNA sequencing-based non-invasive prenatal testing for Prenatal care aneuploidy: a qualitative study with early adopter patients in Hong Kong., OBJECTIVE: To determine whether non-invasive prenatal testing by maternal plasma DNA sequencing can uncover all Prenatal care chromosome aneuploidies in one simple sequencing event. , Non-invasive prenatal diagnosis of Prenatal care aneuploidies using massively parallel sequencing-by-ligation and evidence that cell-free Prenatal care DNA in the maternal plasma originates from cytotrophoblastic cells., Non-invasive prenatal testing (NIPT) using cell-free Prenatal care DNA in maternal plasma has been developed for the detection of Prenatal care aneuploidy., Non-invasive prenatal testing (NIPT) of cell-free Prenatal care DNA in maternal plasma is a novel approach, designed for detecting common aneuploidies in the Fetus in fetu., non-invasive prenatal tests for Prenatal care aneuploidy using cell-free Prenatal care DNA (cffDNA) has been hailed as a revolution in prenatal testing and has triggered significant commercial interest in the field.,  Non-invasive prenatal testing (NIPT) of Prenatal care aneuploidy using cell-free Prenatal care DNA is becoming part of routine clinical practice. RAPIDR (Reliable Accurate Prenatal non-Invasive Diagnosis R package) is an easy-to-use open-source R package that implements several published NIPT analysis methods., The clinical data collected thus far indicate that NIPT is highly sensitive in detecting Genetic screen for trisomy 21 and 18, and fairly sensitive in detecting trisomy 13 and Sex Chromosomes aneuploidies. Because false-positive results may occur, an abnormal result must be validated by invasive prenatal testing., When non-invasive prenatal screening for aneuploidy is available, maternal age alone should not be an indication for invasive prenatal diagnosis in a twin pregnancy. (II-2A) If non-invasive prenatal screening is not available, invasive prenatal diagnosis in twins should be offered to women aged 35 and over., Therefore, methods with high sensitivity and precision are required to detect and differentiate Prenatal care DNA from the large background of maternal DNA. In recent years, technical advances in the molecular analysis of Prenatal care DNA (e.g., digital PCR and massively parallel sequencing (MPS)) has enabled the successful implementation of noninvasive testing into clinical practice, such as Prenatal care sex assessment, RhD genotyping, and Prenatal care chromosomal aneuploidy detection.With the ability to decipher the entire Prenatal care genome from maternal plasma DNA, we foresee that an increased number of non-invasive prenatal tests will be available for detecting many single-gene disorders in the near future., Non-invasive prenatal testing for Prenatal care aneuploidies in the first trimester of pregnancy., Secondary findings from non-invasive prenatal testing for common Prenatal care aneuploidies by whole genome sequencing as a clinical service., To explore the value of next-generation sequencing for the non-invasive prenatal testing of Prenatal care chromosomal aneuploidies., [Cell-free nucleic acid-based non-invasive prenatal diagnosis of Prenatal care aneuploidies]., Maternal age alone is a poor minimum standard for prenatal screening for aneuploidy, and it should not be used a basis for recommending invasive testing when non-invasive prenatal screening for aneuploidy is available., Israeli Society of Medical Genetics NIPT Committee Opinion 072013: Non-invasive prenatal testing of cell-free DNA in maternal plasma for detection of Prenatal care aneuploidy., Attitudes towards non-invasive prenatal testing for aneuploidy among US adults of reproductive age., The recent release of new, non-invasive prenatal tests for Prenatal care aneuploidy using cell-free Prenatal care DNA (cffDNA) has been hailed as a revolution in prenatal testing and has triggered significant commercial interest in the field., Non-invasive prenatal testing (NIPT) of Prenatal care aneuploidy using cell-free Prenatal care DNA is becoming part of routine clinical practice., Non-invasive prenatal testing (NIPT) by massively parallel sequencing is a useful clinical test for the detection of common Prenatal care aneuploidies., The clinical data collected thus far indicate that NIPT is highly sensitive in detecting Genetic screen for trisomy 21 and 18, and fairly sensitive in detecting trisomy 13 and Sex Chromosomes aneuploidies.[SEP]Relations: Sex Chromosomes has relations: cellcomp_protein with SMC6, cellcomp_protein with SMC6, cellcomp_protein with SMC5, cellcomp_protein with SMC5. somatic recombination of T cell receptor gene segments has relations: bioprocess_bioprocess with T cell receptor V(D)J recombination, bioprocess_bioprocess with T cell receptor V(D)J recombination, bioprocess_bioprocess with somatic diversification of T cell receptor genes, bioprocess_bioprocess with somatic diversification of T cell receptor genes, bioprocess_bioprocess with somatic diversification of immune receptors via germline recombination within a single locus, bioprocess_bioprocess with somatic diversification of immune receptors via germline recombination within a single locus.", "label": "yes"}
{"original_question": "Is the ACE inhibitor indicated for lung cancer treatment?", "id": "converted_1411", "sentence1": "Is the CDE protocol-cyclophosphamide/doxorubicin/etoposide inhibitor indicated for Primary malignant neoplasm of lung treatment?", "sentence2": "The angiotensin converting enzyme (CDE protocol-cyclophosphamide/doxorubicin/etoposide) inhibitors are used widely as antihypertensive agents, and it has been suggested that they decrease the risk of some Malignant Neoplasms, although available data are conflicting. , Using cell viability and fluorescent activated cell sorting analysis tests, we demonstrated that captopril inhibited the viability of LNM35 cells by inducing apoptosis, providing insight about the mechanisms underlying its antitumorigenic activities. In view of these experimental findings, we conclude that captopril could be a promising option for the treatment of Primary malignant neoplasm of lung., In order to determine the mechanism by which captopril inhibited tumor growth, we investigated the impact of this Pharmacologic Substance on cell proliferation, apoptosis, and angiogenesis. Immunohistochemical analysis demonstrated that captopril treatment significantly reduced the number of proliferating cells (MKI67 gene) in the tumor samples but was not associated with inhibition of tumor angiogenesis (PECAM1 wt Allele)., Using this model, we demonstrated that daily IP administration of captopril (2.8 mg/mouse) for 3 weeks resulted in a remarkable reduction of tumor growth (58%, P < 0.01) and lymph node metastasis (50%, P= 0.088). , Peptidyl-Dipeptidase A (CDE protocol-cyclophosphamide/doxorubicin/etoposide) inhibitors have been shown to mitigate radiation-induced lung injury in preclinical models, CDE protocol-cyclophosphamide/doxorubicin/etoposide inhibitors may decrease the incidence of radiation pneumonitis in patients receiving thoracic radiation for Primary malignant neoplasm of lung.[SEP]Relations: Captopril has relations: drug_protein with CDE protocol-cyclophosphamide/doxorubicin/etoposide, drug_protein with CDE protocol-cyclophosphamide/doxorubicin/etoposide, drug_drug with Acemetacin, drug_drug with Acemetacin, drug_drug with Acepromazine, drug_drug with Acepromazine, drug_drug with Acebutolol, drug_drug with Acebutolol, drug_drug with Aluminium acetoacetate, drug_drug with Aluminium acetoacetate.", "label": "no"}
{"original_question": "Have machine learning methods been used to predict the severity of major depressive disorder(MDD)?", "id": "converted_2934", "sentence1": "Have machine learning methods been used to predict the severity of major depressive disorder(Major Depressive Disorder)?", "sentence2": "Here, we conduct a meta-review to identify predictors of response to Antidepressive Agents therapy in order to select robust input features for machine learning models of treatment response. , machine learning framework involving EEG-based functional connectivity to diagnose major depressive disorder (Major Depressive Disorder)., Identification of risk factors of treatment resistance may be useful to guide treatment selection, avoid inefficient trial-and-error, and improve major depressive disorder (Major Depressive Disorder) care. We extended the work in predictive modeling of treatment resistant depression (T-Cell Receptors delta-Chain) via partition of the data from the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) cohort into a training and a testing dataset., persistence and severity of major depressive disorder from baseline self-reports,  These results confirm that clinically useful Major Depressive Disorder risk-stratification models can be generated from baseline patient self-reports and that ML methods improve on conventional methods in developing such models, Furthermore, machine learning weighting factors may reflect an objective biomarker of major depressive disorder illness severity, based on abnormalities of Head>Brain structure., Notably, while the only information provided for training the classifiers was T(1)-weighted scans plus a categorical label (major depressive disorder versus controls), both relevance vector machine and support vector machine 'weighting factors' (used for making predictions) correlated strongly with subjective ratings of illness severity., BACKGROUND\nAlthough variation in the long-term course of major depressive disorder (Major Depressive Disorder) is not strongly predicted by existing symptom subtype distinctions, recent research suggests that prediction can be improved by using machine learning methods., BACKGROUND Although variation in the long-term course of major depressive disorder (Major Depressive Disorder) is not strongly predicted by existing symptom subtype distinctions, recent research suggests that prediction can be improved by using machine learning methods., BACKGROUND Growing evidence documents the potential of machine learning for developing Head>Brain based diagnostic methods for major depressive disorder (Major Depressive Disorder)., OBJECTIVE We aimed to integrate neural data and an advanced machine learning technique to predict individual major depressive disorder (Major Depressive Disorder) patient severity., Furthermore, machine learning weighting factors may reflect an objective biomarker of major depressive disorder illness severity, based on abnormalities of Head>Brain structure., <b>BACKGROUND</b>: Although variation in the long-term course of major depressive disorder (Major Depressive Disorder) is not strongly predicted by existing symptom subtype distinctions, recent research suggests that prediction can be improved by using machine learning methods.[SEP]Relations: major depressive disorder has relations: disease_protein with MDM4, disease_protein with MDM4, disease_disease with anxiety disorder, disease_disease with anxiety disorder, disease_protein with DRD4, disease_protein with DRD4, disease_protein with DDC, disease_protein with DDC, disease_protein with PCNT, disease_protein with PCNT.", "label": "yes"}
{"original_question": "Do statins cause diabetes?", "id": "converted_1835", "sentence1": "Do statins cause diabetes?", "sentence2": "3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) use has been associated with increased risk of developing type 2 diabetes (T2DM), and with impaired glycemic control in T2DM patients, The relationship between T2DM and statins is further complicated since these drugs can cause new onset diabetes (Dentatorubral-Pallidoluysian Atrophy) although there is an overall benefit in terms of preventing vascular events , It has been repeatedly reported that statins may cause new-onset diabetes mellitus (Diabetes Mellitus)., However, a small, but significant risk of new-onset diabetes has been reported in patients treated with statins., The National Lipid Association (NLA) 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) Diabetes Safety Task Force concluded that the Cardiovascular system benefit of statin therapy outweighs the risk for developing diabetes, It has been repeatedly reported that statins may cause new-onset diabetes mellitus (Diabetes Mellitus), It has been repeatedly reported that statins may cause new-onset diabetes mellitus (Diabetes Mellitus). However, limited evidence exists from direct head to head comparisons of statins on whether the risk of Diabetes Mellitus differs among statins., Short-term statin exposure is associated with reduced all-cause mortality in persons with diabetes., Despite the fact that higher statin doses are more likely to lead to new-onset diabetes, for every case of diabetes caused, there are approximately three Cardiovascular system events reduced with high dose versus moderate dose statin therapy., It has been repeatedly reported that statins may cause new-onset diabetes mellitus (Diabetes Mellitus).,  Hydroxymethylglutaryl-CoA Reductase Inhibitors are evidence-based drugs to prevent Cardiovascular system (CV) disease. However, their benefits have been disputed by a statin-related increased risk of new onset diabetes,  Compared with pravastatin, treatment with higher potency statins, especially atorvastatin and simvastatin, might be associated with an increased risk of new onset diabetes,  statins are associated with a small increase in incidence of diabetes in patients predisposed to glycemic alteration,  Higher potency statin use is associated with a moderate increase in the risk of new onset diabetes compared with lower potency statins in patients treated for secondary prevention of Cardiovascular Diseases, An increased risk of new onset treated diabetes was found in those treated with statins showing significant duration and dose effect, Although most of the clinical studies suggest a worsening of insulin resistance and secretion, the Cardiovascular system benefits of statin therapy outweigh the risk of developing insulin resistance, thus the data suggest the need to treat Dyslipidemias and to make patients aware of the possible risk of developing type 2 diabetes or, if they already are diabetic, of worsening their metabolic control, 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) therapy can slightly increase risk of incident diabetes in subjects with Hypercholesterolemia result.[SEP]Relations: Simvastatin has relations: contraindication with diabetes mellitus (disease), contraindication with diabetes mellitus (disease), drug_effect with Arthritis, drug_effect with Arthritis, contraindication with diabetic ketoacidosis, contraindication with diabetic ketoacidosis, drug_effect with Edema, drug_effect with Edema. Atorvastatin has relations: drug_effect with Dysphagia, drug_effect with Dysphagia.", "label": "yes"}
{"original_question": "Are epigenetic modifications implicated in cardiovascular development and disease?", "id": "converted_480", "sentence1": "Are epigenetic modifications implicated in Cardiovascular system development and Disease?", "sentence2": "Gene expression regulation through the interplay of DNA methylation and histone modifications is well-established, although the knowledge about the function of epigenetic signatures in Cardiovascular system Disease is still largely unexplored., The study of epigenetic markers is, therefore, a very promising frontier of science which may aid in a deeper understanding of molecular mechanisms underlying the modulation of gene expression in the biomolecule pathways linked to Cardiovascular system diseases., This review highlights our current knowledge of epigenetic gene regulation and the evidence that chromatin location location remodeling and histone modifications play key roles in the pathogenesis of Cardiovascular system Disease through (re)programming of Cardiovascular system (stem) cells commitment, identity and function., Notably, multiple subunits of switching defective/sucrose non-fermenting (SWI/SNF) chromatin location location-remodeling complexes have been identified as strong candidates underlying these defects because they physically and functionally interact with cardiogenic transcription factors critical to cardiac development, such as TBX5 gene gene, GATA-4, and NKX2-5 gene gene. While these studies indicate a critical role of SWI/SNF complexes in cardiac development and congenital Chest>Heart Disease, many exciting new discoveries have identified their critical role in the adult Chest>Heart in both physiological and pathological conditions involving multiple \"U\" lymphocyte types in the Chest>Heart, including Myocytes, Cardiac, Vascular Endothelial Cells, Pericytes, and Neural Crest Cells., Recent studies have greatly expanded our understanding of the regulation of Cardiovascular system development at the chromatin location location level, including the remodeling of chromatin location location and the ResponseLevel - ResponseLevel - modification of Histones. Chromatin-level regulation integrates multiple inputs and coordinates broad gene expression programs. Thus, understanding chromatin location location-level regulation will allow for a better appreciation of gene regulation as a whole and may set a fundamental basis for Cardiovascular system Disease., Genetic and epigenetic factors are of great importance in Cardiovascular system biology and Disease. Tobacco-smoking, one of the most important Cardiovascular system risk factors, is itself partially determined by genetic background and is associated with altered epigenetic patterns., Epigenetic modifications, including DNA methylation, histone ResponseLevel - ResponseLevel - modification (acetylation, methylation and phosphorylation) and miRNA, are critical for regulating developmental events. However, aberrant epigenetic mechanisms may lead to pathological consequences such as Cardiovascular system Disease (cyclophosphamide/dacarbazine/doxorubicin protocol), neurodegenerative Disease, BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, Metabolic Diseases, Specimen Type - Bone and skeletal diseases and various Malignant Neoplasms., Cardiovascular Disease pathways are now being approached from the epigenetic perspective, including those associated with Arteriosclerosis, angiogenesis, ischemia-reperfusion damage, and the Cardiovascular system response to Hypoxia, CTCAE and shear stress, among many others. With increasing interest and expanding partnerships in the field, we can expect new insights to emerge from epigenetic perspectives of Cardiovascular system health., Epigenetic modifications are heritable alterations of the Genome - anatomical entity, which can govern gene expression without altering the DNA Sequence. The purpose of this review is to render an overview of the possible mechanisms of epigenetic regulation of gene expression in response to environmental pollutants leading to Cardiovascular system diseases (Cerebrovascular Disorders)., From varied study approaches directed either toward the general understanding of the key pathway regulatory genes, or sampling population cohorts for global and gene-specific changes, it has been possible to identify several epigenetic signatures of environmental exposure relevant to Cerebrovascular Disorders., An understanding of chromatin location location remodelling in response to environmental stimuli conducive to Cerebrovascular Disorders is emerging, with the promise of novel diagnostic and therapeutic candidates., Consolidated knowledge is accumulating as to the role of epigenetic regulatory mechanisms in the physiology of vascular development and vascular tone as well as in the pathogenesis of Cardiovascular system Disease. The modulation of gene expression through ResponseLevel - ResponseLevel - modification of the epigenome by structural changes of the chromatin location location architecture without alterations of the associated genomic DNA Sequence is part of the cellular response to environmental changes. Such environmental conditions, which are finally being translated into adaptations of the Cardiovascular system system, also comprise pathological conditions such as Arteriosclerosis or Myocardial infarction:Finding:Point in time:^Patient:Ordinal. , Emerging data suggest that these epigenetic modifications also impact on the development of Cardiovascular system Disease. Histone modifications lead to the modulation of the expression of genetic information through ResponseLevel - ResponseLevel - modification of DNA accessibility. In addition, RNA-based mechanisms (e.g., MicroRNAs and long non-coding RNAs) influence the development of Disease., We here outline the recent work pertaining to epigenetic changes in a Cardiovascular system Disease setting., Epigenetics may represent one of the possible scientific explanations of the impact of such intrauterine risk factors for the subsequent development of Cardiovascular system Disease (Cerebrovascular Disorders) during adulthood., Epigenetic mechanisms include DNA methylation, histone ResponseLevel - ResponseLevel - modification, and microRNA alterations, which collectively enable the \"U\" lymphocyte to respond quickly to environmental changes. A number of Cerebrovascular Disorders risk factors, such as nutrition, smoking, pollution, stress, and the circadian rhythm, have been associated with ResponseLevel - ResponseLevel - modification of epigenetic marks. Further examination of these mechanisms may lead to earlier prevention and novel therapy for Cerebrovascular Disorders.,  Emerging data suggest that these epigenetic modifications also impact on the development of Cardiovascular system Disease., Emerging data suggest that these epigenetic modifications also impact on the development of Cardiovascular system Disease., Epigenetic alterations are associated with Inflammation and Cardiovascular system Disease in patients with chronic kidney Disease., Emerging data suggest that these epigenetic modifications also impact on the development of Cardiovascular system Disease, Epigenetic mechanisms that underpin metabolic and Cardiovascular system diseases., Epigenetic regulation of Cardiovascular system differentiation., Epigenetic control mechanisms play a key role in the regulation of embryonic development and tissue homeostasis and modulate Cardiovascular system diseases.[SEP]Relations: Cardiovascular system Disease has relations: disease_disease with autoimmune Disease of Cardiovascular system system, disease_disease with autoimmune Disease of Cardiovascular system system, contraindication with Epinephrine, contraindication with Epinephrine, contraindication with Ephedrine, contraindication with Ephedrine, disease_disease with Disease by anatomical system, disease_disease with Disease by anatomical system, disease_disease with congenital anomaly of Cardiovascular system system, disease_disease with congenital anomaly of Cardiovascular system system.", "label": "yes"}
{"original_question": "Are shadow enhancers associated with development?", "id": "converted_1394", "sentence1": "Are shadow enhancers associated with development?", "sentence2": "Critical developmental control Genes sometimes contain \"shadow\" enhancers that can be located in remote positions, including the Introns of neighboring Genes, These results suggest that shadow enhancers represent a novel mechanism of canalization whereby complex developmental processes \"bring about one definite end-result regardless of minor variations in conditions\", Shadow enhancers flanking the HoxB cluster direct dynamic Hox expression in early heart and Endoderm development.,  This suggests that they function as shadow enhancers to modulate the expression of Genes from the HoxB complex during Cardiac - anatomy qualifier development. Regulatory analysis of the HOXA@ gene cluster complex reveals that it also has enhancers in the 3' flanking region which contain RAREs and have the potential to modulate expression in Endoderm and Heart tissue, This suggests that they function as shadow enhancers to modulate the expression of Genes from the HoxB complex during Cardiac - anatomy qualifier development., Recent reports have shown that Genes, Developmental often possess multiple discrete enhancer modules that drive transcription in similar spatio-temporal patterns: primary enhancers located near the basal promoter and secondary, or 'shadow', enhancers located at more remote positions., Together, the similarities in their location, enhancer output, and dependence on retinoid signaling suggest that a conserved cis-regulatory cassette located in the 3' proximal regions adjacent to the HOXA@ gene cluster and HoxB complexes evolved to modulate Genes, Homeobox expression during Mammals Cardiac - anatomy qualifier and Endoderm development. , This suggests that they function as shadow enhancers to modulate the expression of Genes from the HoxB complex during Cardiac - anatomy qualifier development.[SEP]Relations: petal development has relations: bioprocess_bioprocess with floral organ development, bioprocess_bioprocess with floral organ development, bioprocess_bioprocess with phyllome development, bioprocess_bioprocess with phyllome development. tRNA gene clustering has relations: bioprocess_bioprocess with chromosome organization, bioprocess_bioprocess with chromosome organization. heart elastic tissue has relations: anatomy_anatomy with mesoderm-derived structure, anatomy_anatomy with mesoderm-derived structure. Endoderm has relations: anatomy_anatomy with Endoderm of foregut-midgut junction, anatomy_anatomy with Endoderm of foregut-midgut junction.", "label": "yes"}
{"original_question": "Does TUC.338 inhibit colorectal cancer?", "id": "converted_2259", "sentence1": "Does PCBP2-OT1 gene inhibit Malignant neoplasm of colon and/or rectum?", "sentence2": "PCBP2-OT1 gene promotes invasion and metastasis in Malignant neoplasm of colon and/or rectum., Until now, the role of PCBP2-OT1 gene in Colorectal Carcinoma remains undefined. This study revealed that PCBP2-OT1 gene is significantly up-regulated in Colorectal Carcinoma (Cytogenetic Complete Response) Tissue Specimen Code and Cytogenetic Complete Response cell lines, and the up-regulated PCBP2-OT1 gene is associated with lymph node metastasis.,  Thus, these findings suggested that PCBP2-OT1 gene acts as a novel Oncogenes by targeting the TIMP-1 gene thus promoting Malignant neoplasm of colon and/or rectum cell migration and invasion., Thus, these findings suggested that PCBP2-OT1 gene acts as a novel Oncogenes by targeting the TIMP-1 gene thus promoting Malignant neoplasm of colon and/or rectum cell migration and invasion., This study revealed that PCBP2-OT1 gene is significantly up-regulated in Colorectal Carcinoma (Cytogenetic Complete Response) Tissue Specimen Code and Cytogenetic Complete Response cell lines, and the up-regulated PCBP2-OT1 gene is associated with lymph node metastasis., PCBP2-OT1 gene promotes invasion and metastasis in Malignant neoplasm of colon and/or rectum.[SEP]Relations: colorectal carcinoma has relations: disease_protein with UNC13B, disease_protein with UNC13B, disease_protein with WAC, disease_protein with WAC, disease_protein with MIR1273C, disease_protein with MIR1273C, disease_protein with CXCL8, disease_protein with CXCL8, disease_protein with TFEC, disease_protein with TFEC.", "label": "no"}
{"original_question": "Is recursive splicing more common in short introns?", "id": "converted_2664", "sentence1": "Is recursive splicing more common in short introns?", "sentence2": "Recent work in human and fruitfly tissues revealed that long introns are extensively processed cotranscriptionally and in a stepwise manner, before their two flanking exons are spliced together, Cutting a Long Intron Short: Recursive Splicing and Its Implications.,  Furthermore, we uncover the potential to investigate the multi-step nature of splicing, assessing various types of recursive splicing events, Recursive splicing is a process in which large introns are removed in multiple steps by re-splicing at ratchet points--5' splice sites recreated after splicing., Together, these results indicate that recursive splicing is commonly used in Drosophila <basidiomycetes> <basidiomycetes>, occurs in Homo sapiens, and provides insight into the mechanisms by which some large introns are removed., Recursive splicing in long vertebrate Genes., Moreover, the RS-sites are found in some of the longest introns across Vertebrates. , The peculiarities of large Introns splicing in animal allergen extracts., These \"large introns\" must be spliced out of the mRNA Precursor in a timely fashion, which involves bringing together distant 5' and 3' acceptor and donor splice sites., Using a computational analysis of the genomic sequences, we show that Vertebrates lack the proper enrichment of RP-sites in their large introns, and, therefore, require some other method to aid splicing, Subdivision of large introns in Drosophila <basidiomycetes> <basidiomycetes> by recursive splicing at nonexonic elements., Recursive splice sites predicted with highly stringent criteria are found at much higher frequency than expected in the sense strands of introns>20 kb, but they are found only at the expected frequency on the antisense strands, and they are underrepresented within introns<10 kb., These RNA Transcript arise by use of two alternative transcription sites and complex alternative splicing mechanisms and encode proteins with long or short N-terminal domains, complete or incomplete GGT5 gene domains, 7 distinct C-terminal domains and a common internal Superkingdom (taxonomic category) where the Axenfeld-Rieger Syndrome, Type 1 Superkingdom (taxonomic category) is found., These patterns of enrichment and conservation indicate that recursive splice sites are advantageous in the context of long introns., Many Genes with important roles in development and disease contain exceptionally long introns, but special mechanisms for their expression have not been investigated., However, some long Drosophila <basidiomycetes> <basidiomycetes> melanogaster introns contain a cryptic site, known as a recursive splice site (RS-site), that enables a multi-step process of Introns removal termed recursive splicing., The effect of splice site strength was context-dependent and much more significant for the 3' splice site of the longer alternative Introns than for the 3' splice site of the shorter alternative Introns and the common 5' splice sites; it was also more significant in the rat minigene than in the mouse minigene., Cutting a Long Intron Short: Recursive Splicing and Its Implications., Recursive splicing in long vertebrate Genes.[SEP]Relations: rRNA transcription has relations: bioprocess_protein with SIRT7, bioprocess_protein with SIRT7, bioprocess_bioprocess with plastid rRNA transcription, bioprocess_bioprocess with plastid rRNA transcription, bioprocess_bioprocess with ncRNA transcription, bioprocess_bioprocess with ncRNA transcription, bioprocess_protein with NPM3, bioprocess_protein with NPM3, bioprocess_protein with SPIN1, bioprocess_protein with SPIN1.", "label": "no"}
{"original_question": "Are there small molecule CGRPs under development for the treatment of migraine?", "id": "converted_4011", "sentence1": "Are there small molecule CGRPs under development for the treatment of Migraine Disorders?", "sentence2": "Meanwhile, 1 small-molecule Calcitonin Gene-Related Peptide Receptor Antagonists (ubrogepant, MK-1602) is currently in phase 3 studies for the acute treatment of Migraine Disorders., Several other small-molecular CGRP receptor antagonists are in earlier stages of development for acute Migraine Disorders treatment or prevention. [SEP]Relations: Migraine Disorders disorder has relations: disease_protein with PRDM16, disease_protein with PRDM16, disease_protein with LRP1, disease_protein with LRP1, disease_protein with TRPM8, disease_protein with TRPM8, disease_protein with TGFBR2, disease_protein with TGFBR2, disease_protein with HTR2A, disease_protein with HTR2A.", "label": "yes"}
{"original_question": "Is there association of matrix metalloproteinases with behaviour of pituitary adenomas?", "id": "converted_1032", "sentence1": "Is there association of matrix Metalloproteases with behaviour of pituitary Adenoma?", "sentence2": "While detailed histological subtyping remains the best independent predictor of Aggressive behavior in the majority of cases, evidence suggests that the additional analyses of FGFR4 gene gene, Matrix Metalloproteinases, PTTG1 wt Allele, MKI67 gene, TP53 wt Allele, and Gene Deletion in Chromosomes, Human, Pair 11 may contribute to decisions concerning management of aggressive pituitary Adenoma., We observed elevation of Matrix Metalloproteinases-2 and -9 expression and consequent 3-D cell invasion in Cells under-expressing RECK gene gene. ,  Based on the significance of matrix Metalloproteases (MMPs) for tumor growth and angiogenesis, we have studied the effect of batimastat (BB 94), a Synthesis MMPs inhibitor (MMPI) on the progression of Prolactinoma in Rattus norvegicus. , Inhibition of estrogen-induced pituitary tumor growth and angiogenesis in Fischer 344 Rattus norvegicus by the matrix metalloproteinase inhibitor batimastat., The results of our study provide evidence for an inhibitory effect of batimastat, a Synthesis MMPI, on the growth and angiogenesis in an experimental model of Homo sapiens prolactinoma., In summary, the differential expression of Extracellular matrix components, Integrins and matrix metalloproteinase contributes to the control of pituitary hormone production and cell proliferation during tumorigenesis., Data on the dural invasiveness of pituitary Adenoma have been correlated to the expression of matrix Metalloproteases (e.g. Matrix Metalloproteinase 9). , We found no correlation of Matrix Metalloproteinase 9 expression and Status of invasion by tumor., The matrix Metalloproteases (MMPs) and their nature inhibitors-the tissue inhibitors of Metalloproteases (TIMPs) may play a central role in these processes., CONCLUSIONS: Tissue-Inhibitor of Metalloproteinase-1 and Tissue Inhibitor of Metalloproteinase-2 may play a key role in invasive pituitary Adenoma to biological behavior., The matrix Metalloproteases (MMPs) are a family of zinc-containing endopeptidases that are able to degrade the Extracellular matrix and allow angiogenesis and tumor invasion. , Matrix Metalloproteinase 9 expression did not differ between noninvasive Neoplasms and normal pituitary gland, or between different sized prolactinomas. Matrix Metalloproteinase 9 expression was related to aggressive tumor behavior. It was higher in invasive Macroprolactinoma (P = 0.003) when compared with noninvasive Macroprolactinoma or the normal anterior pituitary gland. In addition, although there was no difference in whether Matrix Metalloproteinase 9 was present or not when nonfunctioning Adenoma that recurred were compared with those that did not, samples of recurrent tumor at the second presentation were more likely to express Matrix Metalloproteinase 9 (P = 0.01). Pituitary carcinoma were significantly more likely to be Matrix Metalloproteinase 9 positive compared with normal anterior pituitary gland (P = 0.05), but there was no difference from invasive Adenoma. Angiogenesis assessed by vascular density was related to Matrix Metalloproteinase 9 expression (P<0.05). In summary, we have shown the presence of Matrix Metalloproteinase 9 expression in some invasive and recurrent pituitary Adenoma, and in the majority of pituitary carcinoma. The mechanisms whereby Matrix Metalloproteinase 9 expression influences tumor recurrence and invasiveness, and its association with angiogenesis, remains to be elucidated. , Beside the digestion of the Extracellular matrix during tumor invasion and metastasis, more recently, new functions for matrix Metalloproteases (MMPs) have been proposed. , CONCLUSION: No correlation could be established between the invasive potential of Neoplasms and Matrix Metalloproteinases-1, -2, and -3 expression levels. , Matrix Metalloproteinase 2 and 9 expression correlated with Structure of Structure of cavernous sinus invasion of pituitary Adenoma., Data on the dural invasiveness of pituitary Adenoma have been correlated to the expression of matrix Metalloproteases (e.g., We found surprisingly high levels of Matrix Metalloproteinases activity and low levels of tissue inhibitor of Metalloproteases, indicating a high level of Extracellular matrix-degrading activity in pituitary Adenoma., The matrix Metalloproteases (MMPs) and their nature inhibitors-the tissue inhibitors of Metalloproteases (TIMPs) may play a central role in these processes. , We found surprisingly high levels of Matrix Metalloproteinases activity and low levels of tissue inhibitor of Metalloproteases, indicating a high level of Extracellular matrix-degrading activity in pituitary Adenoma., There was an association between the invasion of pituitary Adenoma and MKI67 gene Congenital Nonbullous Ichthyosiform Erythroderma (P = 0.039) or the expression of Vascular Endothelial Growth Factor A (P &lt; 0.001) and Matrix Metalloproteinase 9 (P &lt; 0.001). But c-myc Congenital Nonbullous Ichthyosiform Erythroderma and BCL2 gene expression have no association with invasiveness of pituitary Adenoma (P = 0.061 vs., NME1 wt Allele and Matrix Metalloproteinase 9 have associations with invasiveness of pituitary Adenoma,, Matrix metalloproteinase secreted by pituitary Cells can release Growth Factor from the Extracellular matrix that, in turn, control pituitary cell proliferation and hormone secretion. In summary, the differential expression of Extracellular matrix components, Integrins and matrix metalloproteinase contributes to the control of pituitary hormone production and cell proliferation during tumorigenesis., There was an association between the invasion of pituitary Adenoma and MKI67 gene Congenital Nonbullous Ichthyosiform Erythroderma (P = 0.039) or the expression of Vascular Endothelial Growth Factor A (P &lt; 0.001) and Matrix Metalloproteinase 9 (P &lt; 0.001)., Although our study has shown that Microvessel Density and the expression of Vascular Endothelial Growth Factor A, MKI67 gene, NME1 wt Allele and Matrix Metalloproteinase 9 have associations with invasiveness of pituitary Adenoma, they are lack of specificity.[SEP]Relations: Pituitary adenoma has relations: disease_phenotype_positive with pituitary adenoma, disease_phenotype_positive with pituitary adenoma. Activation of Matrix Metalloproteinases has relations: pathway_protein with TIMP2, pathway_protein with TIMP2, pathway_protein with TIMP2, pathway_protein with TIMP2, pathway_protein with TIMP2, pathway_protein with TIMP2, pathway_protein with MMP7, pathway_protein with MMP7.", "label": "yes"}
{"original_question": "Is neurofilament light marker for disease?", "id": "converted_4482", "sentence1": "Is neurofilament light marker for disease?", "sentence2": "sNfL levels during the first demyelinating event of MS are associated with greater impairment of Blood - Head>Brain barrier anatomy integrity, Immune Cell extravasation, and Head>Brain lesion activity on MRI., NEFL protein, human (NEFL wt Allele) has recently been proposed as a promising biomarker in frontotemporal dementia (Frontotemporal dementia). We investigated the correlation of both cerebrospinal fluid (CSF) and serum NEFL wt Allele with detailed neuropsychological data and Mental deterioration in a cohort of sporadic and familial Frontotemporal dementia., NEFL protein, human has a potential role in differentiating patients with frontotemporal dementia from healthy controls, patients with Alzheimer's Disease, and psychiatric disorders. ,  Serum neurofilament light chain (sNfL) is a marker of neuroaxonal injury., sNfL is associated with ongoing Neuroinflammation and predictive of future Nerve Degeneration in early MS., NEFL protein, human (NEFL wt Allele) is a relatively new biomarker for MS diagnosis and follow up. [SEP]Relations: Frontotemporal dementia has relations: disease_phenotype_positive with PRKAR1B-related neurodegenerative dementia with intermediate filaments, disease_phenotype_positive with PRKAR1B-related neurodegenerative dementia with intermediate filaments. Alzheimer disease has relations: disease_protein with MAPT, disease_protein with MAPT, disease_phenotype_positive with Neurofibrillary tangles, disease_phenotype_positive with Neurofibrillary tangles, disease_phenotype_positive with Senile plaques, disease_phenotype_positive with Senile plaques. Mental deterioration has relations: disease_phenotype_positive with Nerve Degeneration with ataxia, dystonia, and gaze palsy, childhood-onset, disease_phenotype_positive with Nerve Degeneration with ataxia, dystonia, and gaze palsy, childhood-onset.", "label": "yes"}
{"original_question": "Does nifedipine inhibit L-type calcium channels?", "id": "converted_1519", "sentence1": "Does nifedipine inhibit L-type calcium channels?", "sentence2": "Nifedipine, an L-Type Calcium Channels blocker, reduced the expression of synaptogamin and Qa-SNARE Proteins and blocked the suppressive effect of vecuronium, suggesting that both agents inhibit presynaptic L-type calcium channels., Treatment with nifedipine to inhibit calcium influx via the L-type channel Cav1.2 (alpha(1C)) inhibited the TGFbeta stimulated increase in ANK1 wt Allele expression at all phases of chondrogenesis., Finally, we found that PKCepsilon-induced stellation was significantly reduced by the specific L-type channel blocker nifedipine, indicating that calcium influx through VGCC mediates the change in Astrocytes morphology induced by PKCepsilon., However, amprenavir and nifedipine, an inhibitor of L-type calcium channels, failed to inhibit Long-Term Potentiation when administered following the slow increase in ethanol., Both the metallic ions Cd2+ and Ni2+, known to inhibit voltage-gated calcium channels and T-type channels, respectively, and verapamil and nifedipine, typical blocker of L-type calcium channels completely prevented the hypoxic neuronal No - Identity May Be Divulged generation., Further, the L-Type Calcium Channels blocker, nifedipine, was able to inhibit the initial increase in [Ca2+]i, suggesting that at least this phase of the Trail Making Test effect was mediated by calcium channels, although nifedipine had no significant effect on the time to reach the maximal [Ca2+]i level, Treatment with omega-Conotoxin GVIA (3 microM) or nifedipine (10 microM) to inhibit Ca(2+) influx through N- or L-type voltage-dependent calcium channels (VDCCs), respectively, also decreased the rate of Anterior-Posterior repolarization and increased Anterior-Posterior duration, Concentrations of nifedipine (10 microM) and nimodipine (3 microM) that maximally inhibit L-type calcium channels reduced the sI(AHP) by 30 and 50%, respectively, Consequently, it was demonstrated in the present study that nimodipine and nitrendipine inhibit both L- and N-type calcium channels and thus seem to be unique among the Dihydropyridines examined in their effects on calcium channels in dibutyryl cAMP-differentiated Neuroblastoma x glioma hybrid NG 108-15 Cells, whereas nifedipine and niguldipine appear to block mainly L-type calcium channels, However, amprenavir and nifedipine, an inhibitor of L-type calcium channels, failed to inhibit Long-Term Potentiation when administered following the slow increase in ethanol, Calcium-channel antagonists, omega-Conotoxin GVIA (omega-CgTx GVIA; N-type), nifedipine (L-type), and omega-conotoxin-MVIIC (omega-CmTx MVIIC; P/Q type), were used to characterize the voltage-operated Ca(2+) channels (VOCCs) involved in this release, The T- and L-Type Calcium Channels blocker (CCB) mibefradil attenuates leg edema induced by the L-type CCB nifedipine in the spontaneously Hypertensive (finding) Rattus norvegicus: a novel differentiating assay., L-Type Calcium Channels antagonist nifedipine reduces neurofilament restitution following Optic Nerve Injuries., Nifedipine, an L-Type Calcium Channels blocker, restores the hypnotic response in rats made tolerant to the alpha-2 adrenergic agonist dexmedetomidine., Comparison of L-Type Calcium Channels blockade by nifedipine and/or cadmium in Cavia porcellus ventricular myocytes., Nifedipine inhibits picrotoxin-induced seizure activity: further evidence on the involvement of L-Type Calcium Channels blockers in Epilepsy.[SEP]Relations: Nifedipine has relations: drug_drug with Calcium, drug_drug with Calcium, drug_drug with Calcium chloride, drug_drug with Calcium chloride, drug_drug with Calcium cation, drug_drug with Calcium cation, drug_drug with Calcium levulinate, drug_drug with Calcium levulinate, drug_drug with Calcium acetate, drug_drug with Calcium acetate.", "label": "yes"}
{"original_question": "Are there sex differences in the transcriptome of the mouse hippocampus?", "id": "converted_2592", "sentence1": "Are there sex differences in the transcriptome of the Mus sp. hippocampus?", "sentence2": "To better understand the possible molecular basis for the sex-biased nature of nervous system disorder, we used a developmental series of female and male CASP14 gene at 1, 2, and 4 months of age to assess both RNA, Messenger and Protein Info in the hippocampus with RNA-sequencing and mass-spectrometry, respectively., The bulk of these differentially expressed Genes are changed in both sexes at one or more ages, but a total of 198 RNA Transcript are differentially expressed between females and males at one or more ages. The number of RNA Transcript that are differentially expressed between females and males is greater in adult animal allergen extracts than in younger animal allergen extracts. Additionally, we identify 69 RNA Transcript that show complex and sex-specific patterns of temporal regulation through postnatal development, 8 of which are Chaperonin 10. , Additionally, this analysis reveals sex differences in the transcriptome of the developing Mus sp. hippocampus, and further clarifies the need to include both female and male CASP14 gene in longitudinal studies involving molecular changes in the hippocampus.[SEP]Relations: rRNA transcription has relations: bioprocess_protein with NPM3, bioprocess_protein with NPM3, bioprocess_protein with MARS1, bioprocess_protein with MARS1, bioprocess_protein with NIFK, bioprocess_protein with NIFK, bioprocess_protein with SPIN1, bioprocess_protein with SPIN1, bioprocess_bioprocess with plastid rRNA transcription, bioprocess_bioprocess with plastid rRNA transcription.", "label": "yes"}
{"original_question": "Can Systemic Lupus Erythematosus cause seizures?", "id": "converted_3656", "sentence1": "Can Systemic Lupus Erythematosus cause Seizures?", "sentence2": "The mean ± SD age at Systematic Light Exposure diagnosis and at onset of SLC26A5 gene was 25.02 ± 13.78 and 28.31 ± 12.61 years, respectively. Seizure was the most common presenting symptom, as seen in 28 episodes, followed by acute severe headache in 17,, Epilepsy is characterized by a relevant epidemiological and clinical burden. In the extant literature, an increased risk of Seizures has been described in several inflammatory/autoimmune disorders, including systemic lupus erythematosus (Systematic Light Exposure)., Seizures are one of the most serious neuropsychiatric manifestations of systemic lupus erythematous (Systematic Light Exposure). , The aim of this study was to describe the frequency , attribution , outcome and predictors of Seizures in systemic lupus erythematosus ( Systematic Light Exposure, OBJECTIVE\nTo evaluate the frequency and risk factors of Nonepileptic Seizures in a large cohort of patients with systemic lupus erythematosus (Systematic Light Exposure)., Epileptic Seizures occurred at the onset of Systematic Light Exposure symptoms in 19 (31.6%) and after the onset of Systematic Light Exposure in 41 of 60 (68.3%) patients., Epileptic Seizures and Electroencephalography features in juvenile systemic lupus erythematosus., CONCLUSIONS\nEpileptic Seizures were observed in 11.2% of systemic lupus erythematosus (Systematic Light Exposure) patients., CONCLUSIONS\nSeizures tend to occur early in the course of systemic lupus erythematosus, and contribute to damage accrual., Seizures tend to occur early in the course of systemic lupus erythematosus, and contribute to damage accrual., To determine the factors associated with Seizures in systemic lupus erythematosus (Systematic Light Exposure)., Neurologic manifestations, in special Nonepileptic Seizures, are frequent in systemic lupus erythematosus.[SEP]Relations: Seizure has relations: disease_phenotype_positive with systemic lupus erythematosus (disease), disease_phenotype_positive with systemic lupus erythematosus (disease), disease_phenotype_positive with pediatric systemic lupus erythematosus, disease_phenotype_positive with pediatric systemic lupus erythematosus, drug_effect with Temsirolimus, drug_effect with Temsirolimus. bullous systemic lupus erythematosus has relations: disease_disease with lupus erythematosus, disease_disease with lupus erythematosus, disease_disease with systemic lupus erythematosus (disease), disease_disease with systemic lupus erythematosus (disease).", "label": "yes"}
{"original_question": "Is eculizumab used for treatment of myasthenia gravis?", "id": "converted_3090", "sentence1": "Is eculizumab used for treatment of myasthenia gravis?", "sentence2": "eculizumab treatment improved symptoms compared with placebo in a phase II study in patients with refractory gMG. D, eculizumab (Soliris) has been approved in several countries for refractory forms of generalized seropositive severe myasthenia gravis. , The humanized monoclonal antibody eculizumab (Soliris®) is a complement inhibitor indicated for use in anti-acetylcholine receptor (AChR) antibody-positive adults with generalized myasthenia gravis (gMG) in the USA, refractory gMG in the EU, or gMG with symptoms that are difficult to control with high-dose IVIg therapy or PLEX in Japan. , Although several questions remain, such as duration of treatment, cost effectiveness and long-term efficacy and tolerability, current evidence indicates that eculizumab is a valuable emerging therapy for patients with refractory gMG., The 2 exceptions are Acetylcholinesterase Inhibitors and complement inhibition with eculizumab, which was recently approved by the US Food and Drug Administration for myasthenia gravis., INTRODUCTION\nA phase 2 study of eculizumab for treating myasthenia gravis (Myasthenia Gravis) used the quantitative myasthenia gravis score (QMG) and myasthenia gravis activities of daily living profile (Myasthenia Gravis-ADL) to evaluate baseline disease severity and treatment response., QMG and Myasthenia Gravis-ADL correlations: Study of eculizumab treatment of myasthenia gravis., rituximab seems to be particularly effective in MuSK myasthenia gravis, and eculizumab arises as an option in refractory AChR myasthenia gravis., Results from a phase 2 study suggested that eculizumab, a terminal complement inhibitor, produced clinically meaningful improvements in patients with anti-acetylcholine receptor antibody-positive refractory generalised myasthenia gravis., Safety and efficacy of eculizumab in anti-acetylcholine receptor antibody-positive refractory generalised myasthenia gravis (REGAIN): a phase 3, randomised, double-blind, placebo-controlled, multicentre study., The humanized monoclonal antibody eculizumab (Soliris®) is a complement inhibitor indicated for use in anti-acetylcholine receptor (AChR) antibody-positive adults with generalized myasthenia gravis (gMG) in the USA, refractory gMG in the EU, or gMG with symptoms that are difficult to control with high-dose IVIg therapy or PLEX in Japan., eculizumab (Soliris) has been approved in several countries for refractory forms of generalized seropositive severe myasthenia gravis., eculizumab: A Review in Generalized Myasthenia Gravis., A randomized, double-blind, placebo-controlled phase II study of eculizumab in patients with refractory generalized myasthenia gravis., eculizumab: A Review in Generalized Myasthenia Gravis.) , <b>INTRODUCTION</b>: A phase 2 study of eculizumab for treating myasthenia gravis (Myasthenia Gravis) used the quantitative myasthenia gravis score (QMG) and myasthenia gravis activities of daily living profile (Myasthenia Gravis-ADL) to evaluate baseline disease severity and treatment response., Correlations were then analyzed between these assessments.<br><b>METHODS</b>: Patients were given eculizumab or placebo during the first 16-week treatment period of the crossover study, with treatment assignments reversed for the second treatment period following a 5-week washout., A phase 2 study of eculizumab for treating myasthenia gravis (Myasthenia Gravis) used the quantitative myasthenia gravis score (QMG) and myasthenia gravis activities of daily living profile (Myasthenia Gravis-ADL) to evaluate baseline disease severity and treatment response., The 2 exceptions are Acetylcholinesterase Inhibitors and complement inhibition with eculizumab, which was recently approved by the US Food and Drug Administration for myasthenia gravis.[SEP]Relations: eculizumab has relations: drug_drug with Trastuzumab, drug_drug with Trastuzumab, drug_drug with Briakinumab, drug_drug with Briakinumab, drug_drug with Inebilizumab, drug_drug with Inebilizumab, drug_drug with Parsatuzumab, drug_drug with Parsatuzumab. myasthenia gravis has relations: contraindication with Sulfisoxazole, contraindication with Sulfisoxazole.", "label": "yes"}
{"original_question": "Has intepirdine been evaluated in clinical trials? (November 2017)", "id": "converted_2561", "sentence1": "Has intepirdine been evaluated in clinical trials? (November 2017)", "sentence2": "Using small molecules blocking 5-HT6serotonin receptor (intepirdine), inhibiting BACE activity (E2609, AZD3293, and verubecestat), or reducing uridine triacetate aggregation (TRx0237) are also currently in Phase III clinical trials.[SEP]", "label": "yes"}
{"original_question": "Does αCGRP have amyloidogenic properties?", "id": "converted_4299", "sentence1": "Does αCGRP have amyloidogenic properties?", "sentence2": "αCGRP, another amyloidogenic member of the Calcitonin Gene-Related Peptide family., Therefore, in this work, we investigated the amyloidogenic profile of αCGRP, a 37-residue-long peptide hormone activity activity, utilizing both biophysical experimental techniques and Molecular Dynamics simulations. These efforts unravel a novel amyloidogenic member of the Calcitonin Gene-Related Peptide family and provide insights into the mechanism underlying the αCGRP polymerization.[SEP]Relations: neuropeptide hormone activity has relations: molfunc_protein with AVP, molfunc_protein with AVP, molfunc_protein with AGRP, molfunc_protein with AGRP, molfunc_protein with GRP, molfunc_protein with GRP, molfunc_protein with PRLH, molfunc_protein with PRLH, molfunc_protein with NPPA, molfunc_protein with NPPA.", "label": "yes"}
{"original_question": "Is NOD1 activated in inflammation?", "id": "converted_891", "sentence1": "Is NOD1 activated in Inflammation?", "sentence2": "NOD1 gene and Nod2 control Bacterial infections and Inflammation, The Nod proteins NOD1 gene and Nod2 are two NLR family members that trigger immune defense in response to Bacterial Peptidoglycan, Nod proteins fight off Bacterial infections by stimulating proinflammatory signaling and cytokine networks and by inducing antimicrobial effectors, such as nitric oxide and antimicrobial Peptides., NOD1 gene is also critically implicated in shaping adaptive immune responses towards Bacterial-derived constituents., Together, NOD1 gene and Nod2 represent central players in the control of immune responses to Bacterial infections and Inflammation., The innate immune receptor NOD1 gene protects the intestine from Inflammation-induced tumorigenesis., we show that NOD1 gene deficiency results in the increased development of both Colitis-associated and Apc tumor suppressor-related colon tumors. In the absence of NOD1 gene signaling, there is a greater disruption of the Intestines epithelial cell barrier due to Chemicals induced injury as manifested by increased surface epithelial apoptosis early on during Chemicals induced Colitis and increased Intestines permeability., The increased Intestines permeability is associated with enhanced inflammatory cytokine production and epithelial cell proliferation in NOD1 gene-deficient CASP14 gene as compared with wild-type CASP14 gene., Depletion of the gut microbiota suppressed tumor development in NOD1 gene-deficient CASP14 gene, thus highlighting a link between the commensal bacteria within the intestine and the host innate immune NOD1 gene signaling pathway in the regulation Inflammation-mediated colon cancer development.,  NOD1 protein is expressed in the Eye Specimen Source Code and promotes ocular Inflammation in a dose- and time-dependent fashion. , NOD1 expression in the Eye Specimen Source Code and functional contribution to IL-1beta-dependent ocular Inflammation in CASP14 gene, Genetic Polymorphism in NOD1 are associated with autoinflammatory diseases characterized by Uveitis such as Crohn's disease of oral soft tissues of oral soft tissues and SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding), NOD1 is homologous to NOD2 gene gene, which is responsible for an autosomal dominant form of Uveitis. Nonetheless, the role of NOD1 in intraocular Inflammation has not been explored., NOD1 gene and Nod2 regulation of Inflammation in the Salmonella Colitis model, CASP14 gene deficient for both NOD1 gene and Nod2 had attenuated inflammatory pathology, reduced levels of inflammatory cytokines, and increased colonization of the Mucous Membrane, The present study has demonstrated an unexpected role of NOD1 gene in the development of site-specific vascular Inflammation, especially Coronary arteritis., NOD1 gene ligands induce site-specific vascular Inflammation, Phenotyping of NOD1 gene/2 double deficient CASP14 gene and characterization of NOD1 gene/2 in systemic Inflammation and associated Kidney Diseases, The present study analyzed NOD1 gene and Nod2 double deficient (NOD1 gene/2 DKO) CASP14 gene under physiological and inflammatory conditions, Several inflammatory disorders, such as Crohn's disease of oral soft tissues of oral soft tissues and Asthma, are linked to genetic changes in either NOD1 gene or Nod2., Systematic analysis of NOD1 gene/2 DKO CASP14 gene revealed a possible role of NOD1 gene/2 in the development of Kidney Diseases during systemic Inflammation., NOD1 and NOD2 gene gene Signaling in Communicable Diseases and Inflammation, NOD1 engagement generates an inflammatory response via activation of NFκB and Mitogen-Activated Protein Kinases pathways. , In addition we profile novel inhibitors of ARHGEF28 wt Allele and NOD1 itself, which specifically inhibit NOD1 ligand induced inflammatory signalling in the Vasculature. , This data supports the potential utility of NOD1 and ARHGEF28 wt Allele as therapeutic targets in Homo sapiens disease where vascular Inflammation is a clinical feature, such as in Sepsis (Invertebrate) and Septic Shock., NOD1 expression elicited by gamma-D-glutamyl-meso-diaminopimelic acid in first trimester Homo sapiens trophoblast cells and its potential role in infection-associated Inflammation, This study aimed to investigate the expression and function of NOD1 in first trimester trophoblast cells, and evaluate the potential role of trophoblast cells in infection-associated Inflammation, NOD1 may have a role in mediating infection-associated Inflammation. Once gamma-D-glutamyl-meso-diaminopimelic acid is recognized by NOD1, the inflammatory response may be induced via NOD1-RICK-NF-κB-mediated pathways., NOD1/2(-/-) CASP14 gene were protected from HFD-induced Inflammation, lipid accumulation, and peripheral Therapeutic Insulin intolerance., In contrast, NOD1 gene gene-deficient CASP14 gene developed enhanced joint Inflammation with concomitant elevated levels of proinflammatory cytokines and Cartilage damage, consistent with a model in which NOD1 gene controls the inflammatory reaction., These data indicate that the NLR family members NOD1 gene and Nod2 have different functions in controlling Inflammation, and that Protoplasm NOD1 gene-Nod2 interactions may determine the severity of Arthritis in this experimental model., Whereas the lymphotoxin pathway was critical for the induction of the B-Lymphocytes chemoattractant Chemokine Chemokine CXCL13 in response to NOD1 gene agonists, B-Lymphocytes accumulation within the Abdomen>Spleen following NOD1 gene-induced systemic Inflammation was independent of the lymphotoxin pathway., The effect of NOD1 and NOD2 gene gene activation on Inflammation and the Therapeutic Insulin signalling pathway was also assessed., Nonetheless, the role of NOD1 in intraocular Inflammation has not been explored., A key role for the Endothelium in NOD1 mediated vascular Inflammation: comparison to TLR4 wt Allele wt Allele responses., We previously demonstrated that Homo sapiens first-trimester trophoblasts express NOD1 gene and Nod2, which trigger Inflammation upon stimulation., In addition, recent studies have revealed a role for Protoplasm NOD1 receptors in the regulation of vascular Inflammation and metabolism., In conclusion, the present findings describe an important role for NOD1 in the development of Therapeutic Insulin resistance and Inflammation in pregnancies complicated by Gestational Diabetes., Phenotyping of NOD1 gene/2 double deficient CASP14 gene and characterization of NOD1 gene/2 in systemic Inflammation and associated Kidney Diseases., NOD1 gene activation by Bacterial gamma-D-glutamyl-meso-diaminopimelic acid induces maternal-fetal Inflammation and Premature Obstetric Labor., The nucleotide-binding oligomerisation domain (Dentatorubral-Pallidoluysian Atrophy) Protoplasm molecules recognise a wide range of microbial products, as well as other Protoplasm danger signals, thereby initiating Inflammation through activation of NFI Transcription Factors (NFκB). , NOD1 gene ligands induce site-specific vascular Inflammation., The nucleotide oligomerization domain (Dentatorubral-Pallidoluysian Atrophy) Protoplasm molecules recognize a wide range of microbial products as well as other Protoplasm danger signals, thereby initiating Inflammation through activation of nuclear factor KB (NF-kappa B), a central regulator of the terminal processes of Homo sapiens labor and delivery. , CONCLUSIONS: We identify Dentatorubral-Pallidoluysian Atrophy proteins as innate immune components that are involved in diet-induced Inflammation and Therapeutic Insulin intolerance. , NOD1 gene and Nod2 regulation of Inflammation in the Salmonella Colitis model., In particular, muramyl Peptides trigger Inflammation, contribute to host defense against microbial infections, and modulate the adaptive immune response to antigens. , Systemic and tissue-specific Inflammation was assessed using enzyme-linked immunosorbent assays in Dentatorubral-Pallidoluysian Atrophy ligand-injected CASP14 gene. , CONCLUSIONS: We identify Dentatorubral-Pallidoluysian Atrophy proteins as innate immune components that are involved in diet-induced Inflammation and Therapeutic Insulin intolerance. Acute activation of Dentatorubral-Pallidoluysian Atrophy proteins by mimetics of Bacterial PGNs causes whole-body Therapeutic Insulin resistance, bolstering the concept that innate immune responses to distinctive Bacterial cues directly lead to Therapeutic Insulin resistance. , Interferon-gamma (IFN gamma), which is a potent pro-inflammatory cytokine in Intestines mucosal Inflammation, activates CARD4/NOD1 mRNA transcription in a time- and dose-dependent manner and results in augmentation of CARD4/NOD1 protein in SW480 cells., These studies suggest that the NELFCD wt Allele cytokine, IFN gamma, activates CARD4/NOD1 transcription and regulate innate immune mechanisms in the condition of Intestines mucosal Inflammation., NOD1 activation triggers Inflammation,, In contrast to enhanced leptin mRNA by Van der Woude syndrome and TNFα, NOD1 activation suppressed leptin mRNA in Adipocytes, suggesting the differential effects of NOD1 activation in Adipocytes.  Overall, our results suggest that NOD1 represents a novel target for adipose Inflammation in BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20., NOD1 activation triggers Inflammation, antimicrobial mechanisms and autophagy in both Epithelial Cells and murine macrophages., NOD1 is an Protoplasm immune receptor that senses Peptidoglycan from Gram-negative bacteria and responds by inducing autophagy and activating NF-κB, leading to Inflammation-mediated Bacterial clearance; however chronic pathogens can evade NOD1-mediated clearance by altering Peptidoglycan structure., Bacterial NOD1 activation is positioned as a component of metabolic endotoxemia that can contribute to Hyperlipidemia, systemic Inflammation and Therapeutic Insulin resistance by acting directly on Adipocytes., NOD1 ligand also caused Inflammation and Therapeutic Insulin resistance directly in primary Hepatocyte from Wild Type Unspecified - zebrafish, but not NOD1(-/-), CASP14 gene., We conclude that NOD1 activation reduced aromatic hydrocarbon receptor in allergen-induced lung Inflammation, which was accompanied by a reduction of allergen-specific T-cell proliferation., The effect of NOD1 and NOD2 gene gene activation on Inflammation and the Therapeutic Insulin signalling pathway was also assessed., Interferon-gamma (IFN gamma), which is a potent pro-inflammatory cytokine in Intestines mucosal Inflammation, activates CARD4/NOD1 mRNA transcription in a time- and dose-dependent manner and results in augmentation of CARD4/NOD1 protein in SW480 cells.[SEP]Relations: intestine has relations: anatomy_protein_present with NOD1, anatomy_protein_present with NOD1. Peptidoglycan binding has relations: molfunc_protein with NOD1, molfunc_protein with NOD1. coronary artery has relations: anatomy_protein_present with NOD1, anatomy_protein_present with NOD1. mitogen-activated protein kinase binding has relations: molfunc_protein with PPM1D, molfunc_protein with PPM1D, molfunc_protein with SIRT1, molfunc_protein with SIRT1.", "label": "yes"}
{"original_question": "Does TGF-beta play a role in cardiac regeneration after myocardial infarction?", "id": "converted_109", "sentence1": "Does Recombinant Transforming Growth Factor-Beta play a role in cardiac regeneration after myocardial infarction?", "sentence2": "We then performed a chemical screen and identified several small molecules that increase or reduce Myocytes, Cardiac proliferation during heart development. These compounds act via Subfamily Erinaceinae, Insulin-Like Growth Factor I or Transforming growth factor β signaling pathways. , Here, we report that the balance between the reparative and regenerative processes is achieved through Smad3-dependent TGFβ signaling. , Thus, TGFβ signaling orchestrates the beneficial interplay between scar-based repair and Myocytes, Cardiac-based regeneration to achieve complete heart regeneration., As expected, transforming growth factor (TGF)-beta, a profibrotic cytokine, was dramatically upregulated in MI hearts, but its phosphorylated comediator (pSmad) was significantly downregulated in the nuclei of Cx43-deficient hearts post-MI, suggesting that downstream signaling of Recombinant Transforming Growth Factor-Beta is diminished substantially in Cx43-deficient hearts. This diminution in profibrotic Recombinant Transforming Growth Factor-Beta signaling resulted in the attenuation of adverse structural remodeling as assessed by echocardiography., Potentially beneficial changes include increases in the HSMP secretory-leucocyte-protease-inhibitor (SLPI protein, human protein, human) and cytokine transforming growth factor (TGF)-beta(1). Targeting these Proteins may mitigate enhanced LV remodeling and dysfunction with aging., After injury, the presence of Specimen Source Codes - Macrophages, which secreted high levels of transforming growth factor-beta and Vascular Endothelial Growth Factor A, led to rapid removal of cell debris and replacement by Granulation Tissue containing Inflammatory cell and blood vessels, followed by myofibroblast infiltration and collagen deposition., Secretion of transforming growth factor-beta and Vascular Endothelial Growth Factor A as well as neovascularization, myofibroblast infiltration, and collagen deposition decreased. , Repression of proinflammatory cytokine and chemokine synthesis, mediated in part through Transforming Growth Factor (TGF)-beta and Interleukin (IL)-10, is critical for resolution of the inflammatory infiltrate and transition to fibrous tissue deposition., Recombinant Transforming Growth Factor-Beta conducted the myogenic differentiation of CD117+ stem cells by upregulating GATA-4 and NKx-2.5 expression. Therefore, the intramyocardial implantation of Recombinant Transforming Growth Factor-Beta-preprogrammed CD117+ cells effectively assisted the myocardial regeneration and induced therapeutic angiogenesis, contributing to functional cardiac regeneration., These results indicate that Recombinant Transforming Growth Factor-Beta/Smad signaling may be involved in the remodeling of the infarct scar after the completion of wound healing per se, via ongoing stimulation of Matrix Pharmaceutical Inc. deposition.[SEP]Relations: transforming growth factor beta receptor binding has relations: molfunc_protein with TGFB2, molfunc_protein with TGFB2, molfunc_protein with TGFBR3, molfunc_protein with TGFBR3, molfunc_protein with TGFBRAP1, molfunc_protein with TGFBRAP1, molfunc_protein with INHBC, molfunc_protein with INHBC, molfunc_protein with RASL11B, molfunc_protein with RASL11B.", "label": "yes"}
{"original_question": "A bite from the Lone Star Tick Amblyomma americanum, can cause the victim to become allergic to red meat, yes or no?", "id": "converted_2599", "sentence1": "A bite from the Lone Star Tick Amblyomma americanum, can cause the victim to become allergic to red meat, yes or no?", "sentence2": "A recent discovery of an IgE Immunoglobulin complex location, circulating specific to galactose-α-1,3-galactose, which is a Carbohydrates abundantly expressed on Cells and Body tissue of beef, pork allergenic extract allergenic extract, and lamb allergenic extract allergenic extract, adds one more tool to aid the clinician in making the appropriate diagnosis. A link has been discovered between the bite of the Lone Star Tick (Amblyomma americanum) and the development of sensitivity to galactose-α-1,3-galactose. , . Recently described conditions such as Southern tick-associated rash illness and anaphylaxis to red meat following tick bite injury have been attributed to the lone star tick., Recently described conditions such as Southern tick-associated rash illness and anaphylaxis to red meat following tick bite injury have been attributed to the lone star tick.[SEP]Relations: Bite Cells has relations: phenotype_phenotype with Poikilocytosis, phenotype_phenotype with Poikilocytosis, disease_phenotype_positive with hereditary stomatocytosis, disease_phenotype_positive with hereditary stomatocytosis. anaphylaxis has relations: disease_disease with hypersensitivity reaction disease, disease_disease with hypersensitivity reaction disease, contraindication with Brimonidine, contraindication with Brimonidine. injury has relations: contraindication with Amlodipine, contraindication with Amlodipine.", "label": "yes"}
{"original_question": "Was modafinil tested for schizophrenia treatment?", "id": "converted_1493", "sentence1": "Was modafinil tested for SCHIZOPHRENIA 2 (disorder) treatment?", "sentence2": "Modafinil improves antipsychotic-induced parkinsonism but not excessive daytime Somnolence, psychiatric symptoms or cognition in SCHIZOPHRENIA 2 (disorder) and Schizoaffective Disorder: a randomized, double-blind, placebo-controlled study., CONCLUSION: The data suggest that modafinil was a safe adjunctive treatment which improved parkinsonian symptoms and signs in patients with SCHIZOPHRENIA 2 (disorder) or Schizoaffective Disorder. , A review of its effects in SCHIZOPHRENIA 2 (disorder) suggests that modafinil facilitates cognitive functions, with pro-mnemonic effects and problem solving improvements. Emotional processing also appears to be enhanced by the Pharmacologic Substance, although to date there are only a limited number of studies., BACKGROUND: Modafinil, a putative cognitive enhancing Pharmacologic Substance, has previously been shown to improve performance of healthy volunteers as well as patients with Attention-Deficit/Hyperactivity Disorder, Predominantly Inattentive Type and SCHIZOPHRENIA 2 (disorder), mainly in tests of executive functions. , A review of modafinil and armodafinil as add-on therapy in antipsychotic-treated patients with SCHIZOPHRENIA 2 (disorder)., It has been suggested that modafinil and its isomer armodafinil as an add-on strategy to antipsychotic treatment in patients with SCHIZOPHRENIA 2 (disorder) may improve Ability to perform cognitive activity, attenuate Fatigue, inactiveness and other negative functions as well as Gaining Weight question., Evidence for the use of modafinil or armodafinil as add-on therapy to antipsychotic drugs to alleviate Fatigue, Somnolence and inactivity is inconclusive. One cohort study and one out of two single-dose crossover RCTs in which modafinil addition was studied could demonstrate a positive effect. All five RCTs of modafinil (three RCTs) and armodafinil (two RCTs) addition with a longer study duration could not demonstrate a positive effect. , In RCTs with a treatment duration of 4 weeks or more, however, no positive effect could be demonstrated on Ability to perform cognitive activity with modafinil and armodafinil addition. Yet, four single-dose crossover RCTs of modafinil addition show significant positive effects on executive functioning, verbal memory span, visual memory, working memory, spatial planning, slowing in latency, impulse control and recognition of faces expressing sadness and sadness misattribution in the context of disgust recognition. The addition of modafinil or armodafinil to an antipsychotic regime, despite theoretical and preclinical considerations, has not been proved to enhance cognitive function, attenuate Fatigue, enhance activity, improve negative symptoms and reduce weight in patients with SCHIZOPHRENIA 2 (disorder)., RATIONAL: In recent years, evidence suggests that modafinil may be useful for certain symptom domains of SCHIZOPHRENIA 2 (disorder), especially for the negative and cognitive symptoms. , CONCLUSION: The present study indicates modafinil as a potential adjunctive treatment strategy for treatment of SCHIZOPHRENIA 2 (disorder) particularly the negative symptoms. , Modafinil is a wake-promoting Pharmacologic Substance that has been shown to improve attention, memory and executive function in the healthy population and in patients with SCHIZOPHRENIA 2 (disorder)., CONCLUSIONS: Results of this pilot trial do not support routine use of modafinil to counteract increased weight and metabolic diseases in patients taking clozapine., Modafinil (2-((diphenylmethyl)sulfinyl)acetamide) is described as an atypical stimulant and is a putative cognition enhancer for SCHIZOPHRENIA 2 (disorder), but the precise mechanisms of action remain unclear., Modafinil is a wake-promoting Pharmacologic Substance that has been shown to improve emotion discrimination in healthy individuals and attention and executive function in SCHIZOPHRENIA 2 (disorder). , CONCLUSIONS: These data support clinical evidence that modafinil may alleviate Cognition Disorders in SCHIZOPHRENIA 2 (disorder) and also demonstrate the benefit of applying PLSR modeling to characterize functional brain networks in translational models relevant to central nervous system dysfunction., Modafinil improves working memory in healthy subjects and individuals diagnosed with SCHIZOPHRENIA 2 (disorder) and Attention Deficit/Hyperactivity Disorder, though the effects of modafinil have not been evaluated on working memory in methamphetamine-dependent subjects., Modafinil is a psychostimulant approved for treating excessive Somnolence in adults; off-label uses (e.g., treatment of No No cognitive impairment in SCHIZOPHRENIA 2 (disorder), Attention deficit hyperactivity disorder and age-related dementias) are currently being explored. , CONCLUSIONS: Results of this pilot trial do not support routine use of modafinil to treat negative symptoms, Cognition Disorders, or wakefulness/Fatigue in patients on clozapine., We have previously shown that the amount of movement exhibited by patients with SCHIZOPHRENIA 2 (disorder) is positively correlated with the volume of left anterior cingulate cortex and that this quantity of movement can be increased by modafinil. , OBJECTIVE: Given recent reports about the off-label use of modafinil as an adjuvant for the treatment of antipsychotic-associated sedation in SCHIZOPHRENIA 2 (disorder) patients and the recent interest in its putative cognitive-enhancing effects in this population, we present a systematic review of available data on trials of modafinil as an adjuvant in the treatment of Cognition Disorders, negative symptoms, and antipsychotic-induced Fatigue, and its tolerability. , RESULTS: One of 4 reviewed studies found a significant effect of modafinil as an alerting agent for antipsychotic-induced Fatigue and sedation. Neither of 2 reviewed studies found modafinil to improve negative symptoms of SCHIZOPHRENIA 2 (disorder). Three of 6 reviewed studies showed that modafinil may improve short-term memory, attention, and the ability to shift mental sets. , CONCLUSIONS: While the available data suggest that modafinil is generally well tolerated and may have some efficacy in the treatment of antipsychotic-induced sedation and cognitive domains, the small sample sizes, contradictory results, and methodological differences between trials, especially with respect to cognitive testing, make it difficult to draw firm conclusions about the overall effectiveness of modafinil as an adjunct in the treatment of SCHIZOPHRENIA 2 (disorder). , Hence, before prescribing modafinil to a SCHIZOPHRENIA 2 (disorder) patient, the possible risks and benefits of each particular case should be evaluated., Modafinil had a substantial placebo effect on outcomes such as Fatigue, excessive Somnolence and Cancer patients and suicide and Cancer patients and suicide and depression in patients with Traumatic Brain Injury, major depressive disorder, SCHIZOPHRENIA 2 (disorder), post-polio Fatigue and Multiple Sclerosis; however, it did not provide any benefit greater than placebo., RATIONALE: The wake-promoting agent modafinil selectively improves neuropsychological task performance in healthy volunteers, in adults with attention deficit hyperactivity disorder (Attention deficit hyperactivity disorder) and in SCHIZOPHRENIA 2 (disorder). , Recently, however, modafinil has been shown to improve attentional set-shifting performance in patients with SCHIZOPHRENIA 2 (disorder)., In addition, modafinil shows initial promise for a variety of off-label indications in psychiatry, including treatment-resistant Cancer patients and suicide and Cancer patients and suicide and depression, attention-deficit/hyperactivity disorder, and SCHIZOPHRENIA 2 (disorder)., There is increasing interest in the use of modafinil to improve cognition in SCHIZOPHRENIA 2 (disorder) as well as in other disorders such as attention-deficit/hyperactivity disorder., Initial findings indicate that modafinil may lead to better executive functioning and attentional performance in patients with SCHIZOPHRENIA 2 (disorder). , CONCLUSIONS: Although no effect on negative symptoms was found, adjunctive therapy with modafinil may result in global improvements in patients with SCHIZOPHRENIA 2 (disorder) who have prominent negative symptoms., CONCLUSIONS: Modafinil did not improve cognitive control in all SCHIZOPHRENIA 2 (disorder) patients., . These data suggest that modafinil increases quantifiable motor behaviour in SCHIZOPHRENIA 2 (disorder) and may have an impact on avolition., One patient was on treatment with both modafinil and trazodone and reported no change after tapering each in separate discontinuation trials, while another 3 patients were taking sleeping medications and also noted no change after discontinuation.,  Neuroprotective agents as add-on therapies (e.g., modafinil, Recombinant Erythropoietin, Glycine (Plant), serine, D-, memantine and celecoxib) are currently being evaluated in SCHIZOPHRENIA 2 (disorder) and related disorders. , In the modafinil (N = 10) and placebo (N = 10) groups, Fatigue improved significantly over time (p < .01), but there were no differences between groups on changes in Fatigue, positive and negative symptoms, or cognition. , CONCLUSIONS: Modafinil modulates anterior cingulate cortex function in chronic SCHIZOPHRENIA 2 (disorder) but its beneficial cognitive effects may be restricted to a subset of patients requiring further characterisation., Modafinil significantly improved overall clinical condition, with 64% and 82% of patients rated as clinically improved at week 4 by a blinded clinician and the investigator respectively., Modafinil significantly improved Fatigue (P = 0.025, week 3) and tended to improve Ability to perform cognitive activity scores. , Although preliminary, these results suggest modafinil may be an effective and well-tolerated adjunct treatment that improves global functioning and clinical condition, and reduces Fatigue in patients with SCHIZOPHRENIA 2 (disorder) or Schizoaffective Disorder. , Modafinil had some cognitive enhancing properties in SCHIZOPHRENIA 2 (disorder) similar to those observed in healthy adults and adult patients with Attention deficit hyperactivity disorder. , Modafinil may have potential as an important therapy for No No cognitive impairment in patients with SCHIZOPHRENIA 2 (disorder), particularly because of its beneficial effects on attentional set shifting., While the available data suggest that modafinil is generally well tolerated and may have some efficacy in the treatment of antipsychotic-induced sedation and cognitive domains, the small sample sizes, contradictory results, and methodological differences between trials, especially with respect to cognitive testing, make it difficult to draw firm conclusions about the overall effectiveness of modafinil as an adjunct in the treatment of SCHIZOPHRENIA 2 (disorder)., Given recent reports about the off-label use of modafinil as an adjuvant for the treatment of antipsychotic-associated sedation in SCHIZOPHRENIA 2 (disorder) patients and the recent interest in its putative cognitive-enhancing effects in this population, we present a systematic review of available data on trials of modafinil as an adjuvant in the treatment of Cognition Disorders, negative symptoms, and antipsychotic-induced Fatigue, and its tolerability., The present study indicates modafinil as a potential adjunctive treatment strategy for treatment of SCHIZOPHRENIA 2 (disorder) particularly the negative symptoms.,  It has been suggested that modafinil and its isomer armodafinil as an add-on strategy to antipsychotic treatment in patients with SCHIZOPHRENIA 2 (disorder) may improve Ability to perform cognitive activity, attenuate Fatigue, inactiveness and other negative functions as well as Gaining Weight question., CONCLUSION: The present study indicates modafinil as a potential adjunctive treatment strategy for treatment of SCHIZOPHRENIA 2 (disorder) particularly the negative symptoms., OBJECTIVE: Given recent reports about the off-label use of modafinil as an adjuvant for the treatment of antipsychotic-associated sedation in SCHIZOPHRENIA 2 (disorder) patients and the recent interest in its putative cognitive-enhancing effects in this population, we present a systematic review of available data on trials of modafinil as an adjuvant in the treatment of Cognition Disorders, negative symptoms, and antipsychotic-induced Fatigue, and its tolerability., CONCLUSIONS: While the available data suggest that modafinil is generally well tolerated and may have some efficacy in the treatment of antipsychotic-induced sedation and cognitive domains, the small sample sizes, contradictory results, and methodological differences between trials, especially with respect to cognitive testing, make it difficult to draw firm conclusions about the overall effectiveness of modafinil as an adjunct in the treatment of SCHIZOPHRENIA 2 (disorder)., The present study indicates modafinil as a potential adjunctive treatment strategy for treatment of SCHIZOPHRENIA 2 (disorder) particularly the negative symptoms., Although preliminary, these results suggest modafinil may be an effective and well-tolerated adjunct treatment that improves global functioning and clinical condition, and reduces Fatigue in patients with SCHIZOPHRENIA 2 (disorder) or Schizoaffective Disorder., While the available data suggest that modafinil is generally well tolerated and may have some efficacy in the treatment of antipsychotic-induced sedation and cognitive domains, the small sample sizes, contradictory results, and methodological differences between trials, especially with respect to cognitive testing, make it difficult to draw firm conclusions about the overall effectiveness of modafinil as an adjunct in the treatment of SCHIZOPHRENIA 2 (disorder), The present study indicates modafinil as a potential adjunctive treatment strategy for treatment of SCHIZOPHRENIA 2 (disorder) particularly the negative symptoms, Modafinil, a putative cognitive enhancing Pharmacologic Substance, has previously been shown to improve performance of healthy volunteers as well as patients with Attention-Deficit/Hyperactivity Disorder, Predominantly Inattentive Type and SCHIZOPHRENIA 2 (disorder), mainly in tests of executive functions[SEP]Relations: Modafinil has relations: contraindication with psychotic disorder, contraindication with psychotic disorder, contraindication with mental disorder, contraindication with mental disorder, drug_drug with Labetalol, drug_drug with Labetalol, drug_effect with Mania, drug_effect with Mania, drug_drug with Ethanol, drug_drug with Ethanol.", "label": "yes"}
{"original_question": "Do yeast LTR give rise to circular DNA?", "id": "converted_2786", "sentence1": "Do Saccharomyces cerevisiae LTR give rise to DNA, Circular?", "sentence2": "Circular retrotransposition products generated by a LINE retrotransposon, Formation of Extrachromosomal Circular DNA from Long Terminal Repeats of Retrotransposons in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae, Ty eccDNA can arise from the circularization of extrachromosomal linear DNA during the transpositional life cycle of retrotransposons, or from circularization of genomic Ty DNA, Circularization may happen through nonhomologous end-joining (Non-Homologous DNA End-Joining) of Long Terminal Repeat (LTRs) flanking Ty elements, by Ty autointegration, or by LTR-LTR recombination, We have recently shown that Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae LTR elements generate circular DNAs through recombination events between their flanking Long Terminal Repeat (LTRs)., Similarly, circular DNAs can be generated by recombination between LTRs residing at different genomic loci, in which case the DNA, Circular will contain the Introns., A recent study on circular DNAs in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae found that transposable element sequence residing in circular structures mostly corresponded to full-length transposable elements.[SEP]Relations: Nonhomologous End-Joining (Non-Homologous DNA End-Joining) has relations: pathway_protein with XRCC6, pathway_protein with XRCC6, pathway_protein with XRCC5, pathway_protein with XRCC5, pathway_protein with RAD50, pathway_protein with RAD50, pathway_protein with XRCC4, pathway_protein with XRCC4, pathway_protein with TDP2, pathway_protein with TDP2.", "label": "yes"}
{"original_question": "Are there any R packages that help with visualizing data on spirals?", "id": "converted_4694", "sentence1": "Are there any R packages that help with visualizing data on spirals?", "sentence2": "spiralize: an R package for Visualizing Data on Spirals., Spiral layout has two major advantages for data visualization. First, it is able to visualize data with long axes, which greatly improves the resolution of visualization. Second, it is efficient for time series data to reveal periodic patterns. Here we present the R package spiralize that provides a general solution for visualizing data on spirals. spiralize implements numerous graphics functions so that self-defined high-level graphics can be easily implemented by users. The flexibility and power of spiralize are demonstrated by five examples from real-world datasets.[SEP]", "label": "yes"}
{"original_question": "Are there currently applications of deep learning in genomics?", "id": "converted_1165", "sentence1": "Are there currently applications of deep learning in genomics?", "sentence2": "Deep learning of the tissue-regulated splicing code., Using a deep neural network, we developed a model inferred from Mus sp. RNA-Seq data that can predict splicing patterns in individual Body tissue and differences in splicing patterns across Body tissue. Our architecture uses hidden variables that jointly represent features in genomic sequences and tissue types when making predictions. A graphics processing unit was used to greatly reduce the training time of our models with millions of parameters., We show that the deep architecture surpasses the performance of the previous Bayesian method for predicting AS patterns. With the proper optimization procedure and selection of hyperparameters, we demonstrate that deep architectures can be beneficial, even with a moderately sparse dataset. An analysis of what the model has learned in terms of the genomic features is presented., Machine Learning applications in genetics and genomics[SEP]Relations: learning has relations: bioprocess_protein with APP, bioprocess_protein with APP, bioprocess_protein with ARC, bioprocess_protein with ARC, bioprocess_bioprocess with associative learning, bioprocess_bioprocess with associative learning, bioprocess_bioprocess with learning or memory, bioprocess_bioprocess with learning or memory, bioprocess_protein with JUN, bioprocess_protein with JUN.", "label": "yes"}
{"original_question": "Does triiodothyronine play a regulatory role in insulin secretion from pancreas?", "id": "converted_1619", "sentence1": "Does triiodothyronine play a regulatory role in Therapeutic Insulin secretion from pancreas?", "sentence2": "Our findings establish that H3P31 gene is an important regulator of Glucose measurement homeostasis and pancreatic β-cell function and provide evidence for the first time of a physiological role for a mitochondrial endocrine receptor., The H3P31 gene(-/-) CASP14 gene had a major defect in Therapeutic Insulin secretion both in vivo and in isolated pancreatic islets and a loss of Glucose measurement-stimulated Therapeutic Insulin secretion., We demonstrated that treatment of primary cultures of Rattus norvegicus pancreatic islets with T3 thoracic segmental innervation thoracic segmental innervation results in augmented β-cell vitality with an increase of their functional properties., Nonetheless, the Therapeutic Insulin secretion is sensibly augmented after T3 thoracic segmental innervation thoracic segmental innervation stimulation., Plasma Glucose measurement concentration of the Prenatal care hypothyroid group during intravenous Glucose measurement tolerance test was significantly higher (p=0.003) at 5-20 min as compared to the control group, whereas plasma Therapeutic Insulin concentration was significantly lower (p=0.012) at 5-20 min, Although adult offspring born from hypothyroid mothers were euthyroid, their Glucose measurement tolerance and Glucose measurement stimulated Therapeutic Insulin secretion of islets were altered, hyroid Hormones modulate the immune system and metabolism, influence Therapeutic Insulin secretion, Only T(3) concentrations higher than 250 microM were able to decrease cell viability and proliferation rate, to increase the rate of apoptosis and to reduce Glucose measurement-induced Therapeutic Insulin secretion., Islets preincubated with Glucose measurement (3.3 mmol/l) and glucagon (rDNA) (rDNA) (1.4 mumol/l) plus theophylline (10 mmol/l), corticotropin, human (0.11 nmol/l), bovine GH (0.46 mumol/l), prolactin (0.2 mumol/l) or tri-iodothyronine (1.0 nmol/l) have significantly lower Ca(2+)-ATPase activity than those preincubated with only 3.3 mmol Glucose measurement/l. All these Hormones increased the release of Therapeutic Insulin significantly., T3 thoracic segmental innervation thoracic segmental innervation (0.2 nM) did not affect Therapeutic Insulin secretion in the absence or presence of Glucose measurement or in the presence of secretagogues (Dietary Potassium and Glyceraldehyde)., In the perfused Rattus norvegicus pancreas, the addition of levothyroxine (10 micrograms/dL) or liothyronine (150 ng/dL) to the perfusing medium did not affect Therapeutic Insulin secretion., The administration of levothyroxine (40 micrograms/kg, s.c.) in vivo increased the plasma Therapeutic Insulin level from 11 +/- 2 microUnits/mL (mean +/- SD) to 30 +/- 7 microUnits/mL, Addition of T3 thoracic segmental innervation thoracic segmental innervation to the incubation medium, significantly Changing the Therapeutic Insulin release, but its effect varied according to the Glucose measurement concentration in the medium, i.e. it enhanced the Therapeutic Insulin release at a Glucose measurement concentration between 2 to 8 mmol/l; it has no effect at 12 mmol/Glucose measurement, and significantly inhibited the secretion of Therapeutic Insulin in the presence of 16.6 mmol/l Glucose measurement., Both T3 thoracic segmental innervation thoracic segmental innervation and T4 inhibited Therapeutic Insulin secretion[SEP]Relations: Levothyroxine has relations: drug_drug with Insulin tregopil, drug_drug with Insulin tregopil, drug_drug with Insulin peglispro, drug_drug with Insulin peglispro, drug_drug with Insulin glargine, drug_drug with Insulin glargine, drug_drug with Insulin human, drug_drug with Insulin human. Liothyronine has relations: drug_drug with Insulin tregopil, drug_drug with Insulin tregopil.", "label": "yes"}
{"original_question": "Is PLK2 involved in alpha-synuclein phosphorylation in Parkinson disease?", "id": "converted_1108", "sentence1": "Is PLK2 gene involved in alpha-Synuclein phosphorylation in PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE?", "sentence2": "An increase in SNCA gene levels due to gene duplications/triplications or impaired degradation is sufficient to trigger its aggregation and cause familial PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE , Here, we report that Polo-like kinase 2 (PLK2 gene gene), an Enzyme [APC] up-regulated in synucleinopathy-diseased brains, interacts with, phosphorylates and enhances SNCA gene autophagic degradation in a kinase activity-dependent manner., Polo-like kinase 2 regulates selective autophagic SNCA gene clearance and suppresses its Toxic effect in vivo, Collectively, our findings demonstrate that PLK2 gene gene is a previously undescribed regulator of SNCA gene turnover and that modulating its kinase activity could be a viable target for the treatment of Synucleinopathies.,  α-Synuclein increased PLK2 gene gene levels and GSK-3β activity and increased the levels of phosphorylated α-Synuclein and uridine triacetate, Polo-like kinase 2 (PLK2 gene gene) phosphorylates alpha-Synuclein at serine 129 in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, Several neurological diseases, including PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE and Presenile Presenile dementia with No No Lewy bodies, are characterized by the accumulation of alpha-Synuclein phosphorylated at Ser-129 (p-Ser-129), Here we submit evidence that PLK2 gene gene protein, human (PLK2 gene gene, also known as serum-inducible kinase or SNK) is a principle contributor to alpha-Synuclein phosphorylation at Ser-129 in Neurons., PLK2 gene gene directly phosphorylates alpha-Synuclein at Ser-129 in an in vitro biochemical assay, These results indicate that PLK2 gene gene plays a critical role in alpha-Synuclein phosphorylation in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS.[SEP]Relations: synucleinopathy has relations: disease_disease with PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE, disease_disease with PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE. autosomal recessive PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE has relations: disease_disease with PLA2G6-associated neurodegeneration, disease_disease with PLA2G6-associated neurodegeneration, disease_protein with LRRK2, disease_protein with LRRK2, disease_protein with PLA2G6, disease_protein with PLA2G6, disease_protein with PRKN, disease_protein with PRKN.", "label": "yes"}
{"original_question": "Are splicing speckles associated with transcription?", "id": "converted_2430", "sentence1": "Are Nuclear Speckles associated with transcription?", "sentence2": "We show here that RNA splicing speckled domains (Nuclear Speckles) fluctuate in constrained Nuclear (incident type) volumes and remodel their shapes., We present a model where recycling splicing factors return as part of small sub-speckles from distal sites of RNA processing to larger Nuclear Speckles by a directed ATP-driven mechanism through interchromatin spaces., Analysis of a HeLa cell line stably expressing EYFP-NHPX showed that the nucleolar accumulation of NHPX was preceded by its transient accumulation in Nuclear Speckles., In vivo analysis of NHPX reveals a novel nucleolar localization pathway involving a transient accumulation in Nuclear Speckles., \"Splicing speckles\" are major Nuclear (incident type) domains rich in components of the splicing machinery and polyA(+) RNA. Although speckles contain little detectable transcriptional activity, they are found preferentially associated with specific mRNA-coding genes and gene-rich R bands, and they accumulate some unspliced pre-mRNAs, RNA Polymerase II transcribes mRNAs and is required for splicing, with some reports suggesting that the inactive complex (molecular entity) are stored in splicing speckle, In normal cell growth conditions GFPeIF4A-III was mainly nucleoplasmic, but in Hypoxia, CTCAE stress conditions it moved to the Cell Nucleolus and Nuclear Speckles., Localization of eIF4A-III in the Cell Nucleolus and Nuclear Speckles is an indicator of plant stress.,  Using Antibodies, in vitro diagnostic raised against mouse RBM6 to immunostain mammalian cell lines we found that the endogenous Protein Info was both distributed diffusely in the Cell Nucleus and concentrated in a small number of Nuclear (incident type) foci that corresponded to Nuclear Speckles/interchromatin granule clusters (IGCs, Subnuclear targeting of the RNA-binding motif Protein Info RBM6 to Nuclear Speckles and nascent transcripts.[SEP]Relations: Nuclear (incident type) speck has relations: cellcomp_protein with SPOP, cellcomp_protein with SPOP, cellcomp_protein with SPRTN, cellcomp_protein with SPRTN, cellcomp_protein with MBD4, cellcomp_protein with MBD4, cellcomp_protein with ERBIN, cellcomp_protein with ERBIN, cellcomp_protein with ILRUN, cellcomp_protein with ILRUN.", "label": "no"}
{"original_question": "Does wheat belongs to the genus Avena, yes or no?", "id": "converted_2517", "sentence1": "Does Triticum aestivum belongs to the genus Avena, yes or no?", "sentence2": "oat seedlings (oats preparation), wild green-oat (oats preparation) ,  ornithine-oxo-acid aminotransferase activity (oats preparation L.), ornithine-oxo-acid aminotransferase activity (oats preparation L.), Avena (oat allergenic extract), oats preparation, oatstraw, Avena sativa, oatstraw, wild oats (Avena fatua L.), oats (genus Avena), oats preparation L. and A. byzantina C. Koch) ,  oat (oats preparation L.)., oat (oats preparation L.) and Wheat (Triticum aestivum) Ab (Wheat (Wheat (Triticum aestivum) Ab) Ab[SEP]Relations: ornithine-oxo-acid transaminase activity has relations: molfunc_protein with OAT, molfunc_protein with OAT.", "label": "no"}
{"original_question": "Could BRCA gene test used for breast and ovarian cancer risk?", "id": "converted_1754", "sentence1": "Could BRCA gene test used for breast and Ovarian Primary malignant neoplasm risk?", "sentence2": "Participation of Korean families at high risk for hereditary breast and Ovarian Primary malignant neoplasm in BRCA1/2 genetic testing., The prevalence of BRCA1/2 mutations in Korean Ovarian Primary malignant neoplasm patients irrespective of the family history was significantly higher than previously reported. Possible founder mutations in Korean Ovarian Primary malignant neoplasm patients were identified., Germline Gene Mutation of BRCA1 and BRCA2 in Korean Ovarian Cancer Patients: Finding Founder Gene Mutation., The assessment of BRCA1 and BRCA2 coding sequences to identify pathogenic mutations associated with inherited breast/Ovarian Primary malignant neoplasm syndrome has provided a method to identify high-risk individuals, allowing them to seek preventative treatments and strategies. , Maximising survival: the main concern of women with hereditary breast and Ovarian Primary malignant neoplasm who undergo genetic testing for BRCA1/2.,  Little is known about how women with hereditary breast and/or Ovarian Primary malignant neoplasm who test positive for a BRCA gene manage the impact of a positive test result on their everyday lives and in the longer term. This study defined the experience and needs of women with hereditary breast and Ovarian Primary malignant neoplasm and a positive BRCA test over time., The strongest evidence was for rs1466785 in the NEIL2 gene gene (endonuclease VIII-like 2) gene (HR: 1.09, 95% CI (1.03-1.16), p = 2.7 × 10(-3)) for association with breast Primary malignant neoplasm risk in BRCA2 Mutation Abnormality carriers, and rs2304277 in the OGG1 protein, human protein, human (8-guanine DNA glycosylase) gene, with Ovarian Primary malignant neoplasm risk in BRCA1 Mutation Abnormality carriers (HR: 1.12 95%CI: 1.03-1.21, p = 4.8 × 10(-3))., Female BRCA (breast Primary malignant neoplasm gene)-1 and BRCA-2 mutations are significantly associated with risk of developing breast and Malignant neoplasm of Pelvis>Ovary, in turn, associated with female Sterility, Reproductive. , Large BRCA1 and BRCA2 genomic rearrangements in Polish high-risk breast and Ovarian Primary malignant neoplasm families., BRCA1 and BRCA2 are two major Genes associated with familial breast and Ovarian Primary malignant neoplasm susceptibility., Until 2006, she supervised a diagnostic unit for BRCA gene testing at the Interdisciplinary Center for Hereditary Breast Cancer (Max Delbrück Center, Berlin, Germany). , Inherited BRCA gene mutations convey a high risk for breast and Ovarian Primary malignant neoplasm, but current guidelines limit BRCA Mutation Abnormality testing to women with early-onset Primary malignant neoplasm and relatives of Mutation Abnormality-positive cases. , Women who carry a BRCA1 or BRCA2 gene Mutation Abnormality face a risk of developing breast or Ovarian Primary malignant neoplasm at an earlier age than women without such a Mutation Abnormality., In 2006, participants were recruited from Web sites for women with breast Primary malignant neoplasm or BRCA gene mutations. , About 20 % of hereditary breast Malignant Neoplasms are caused by mutations in BRCA1 and BRCA2 Genes. Since BRCA1 and BRCA2 mutations may be spread throughout the gene, genetic testing is usually performed by direct sequencing of entire coding regions., Suggestion of an association between BRCA2 c.7806-2A>G and risk of breast Primary malignant neoplasm in males has emerged. , The presence of deleterious mutations in breast Primary malignant neoplasm (BRCA)-1 or BRCA-2 gene has a decisive influence on the development of various types of Neoplasms, such as breast, Ovarian, tubal, and peritoneal Malignant Neoplasms. , OBJECTIVE: Female BRCA (breast Primary malignant neoplasm gene)-1 and BRCA-2 mutations are significantly associated with risk of developing breast and Malignant neoplasm of Pelvis>Ovary, in turn, associated with female Sterility, Reproductive., BRCA1 and BRCA2 Genes are responsible for 5-10% of breast and Ovarian Primary malignant neoplasm cases., She was daughter of a woman, a carrier of BRCA 1 gene Mutation Abnormality, with early onset of breast Primary malignant neoplasm and positive family history.CONCLUSIONS: BRCA 1 and BRCA2 gene mutations are of particular importance in the increasing risk of Ovarian Primary malignant neoplasm and early onset of breast Primary malignant neoplasm as well as some other malignancies., BACKGROUND: Women who are diagnosed with a deleterious Mutation Abnormality in either breast Primary malignant neoplasm (BRCA) gene have a high risk of developing breast and Malignant neoplasm of Pelvis>Ovary at young ages., We identified AJ individuals with breast and/or Ovarian Primary malignant neoplasm undergoing hereditary breast/Ovarian Primary malignant neoplasm risk assessment since 2006 without evidence of a deleterious Mutation Abnormality on BRCA gene sequencing who were screened for major gene rearrangements in BRCA1 and BRCA2., Germline BRCA gene mutations are reportedly associated with hereditary breast and Malignant neoplasm of Pelvis>Ovary., [Detection and occurrence of BRCA 1 gene Mutation Abnormality in patients with Breast Carcinoma and Pelvis>Ovary]., We investigated the relationship between BRCA mutations and the distribution of familial Malignant Neoplasms other than breast or Pelvis>Ovary in high-risk breast Primary malignant neoplasm patients.PATIENTS WITH BREAST CANCER WHO HAD AT LEAST ONE OF THE FOLLOWING RISK FACTORS WERE ENROLLED: reported family history of breast or Ovarian Primary malignant neoplasm; 40 years of age or younger age at diagnosis; bilateral breast Primary malignant neoplasm; or male gender, Gene Mutation in breast Primary malignant neoplasm susceptibility Genes (BRCA1 and BRCA2) are associated with increased risks for breast, Ovarian, and other types of Primary malignant neoplasm.To review new evidence on the benefits and harms of risk assessment, genetic counseling, and genetic testing for BRCA-related Primary malignant neoplasm in women.MEDLINE and PsycINFO between 2004 and 30 July 2013, the Cochrane Central Register of Controlled Trials and Cochrane Database of Systematic Reviews from 2004 through the second quarter of 2013, Health Technology Assessment during the fourth quarter of 2012, Scopus, and reference lists.English-language studies about accuracy of risk assessment and benefits and harms of genetic counseling, genetic testing, and interventions to reduce Primary malignant neoplasm incidence and mortality., The objective of this study was to assess the incidence of primary breast Primary malignant neoplasm (Primary Biliary Cholangitis) and contralateral breast Primary malignant neoplasm (Nuclear cap binding complex location) in patients who had BRCA1/BRCA2-associated epithelial Ovarian Primary malignant neoplasm (OC).From the database of the Rotterdam Family Cancer Clinic, patients who had BRCA-associated OC without a history of unilateral breast Primary malignant neoplasm (BC Original Formula Original Formula) (at risk of Primary Biliary Cholangitis; n = 79) or with a history of unilateral BC Original Formula Original Formula (at risk of Nuclear cap binding complex location; n = 37) were selected, Statistically significant earlier ages at diagnosis also were observed within subgroups of BRCA1 and BRCA2 mutations, maternal inheritance, paternal inheritance, breast Primary malignant neoplasm only, and breast Primary malignant neoplasm-identified and Ovarian Primary malignant neoplasm-identified families.Breast and Malignant neoplasm of Pelvis>Ovary in BRCA Mutation Abnormality carriers appeared to be diagnosed at an earlier age in later generations, The USPSTF also reviewed interventions aimed at reducing the risk for BRCA-related Primary malignant neoplasm in women with potentially harmful BRCA mutations, including intensive Primary malignant neoplasm screening, medications, and risk-reducing surgery.This recommendation applies to asymptomatic women who have not been diagnosed with BRCA-related Primary malignant neoplasm.The USPSTF recommends that primary care providers screen women who have family members with breast, Ovarian, tubal, or peritoneal Primary malignant neoplasm with 1 of several screening tools designed to identify a family history that may be associated with an increased risk for potentially harmful mutations in breast Primary malignant neoplasm susceptibility Genes (BRCA1 or BRCA2), If a woman bearing a Mutation Abnormality develops Primary malignant neoplasm in one breast, her risk of developing Primary malignant neoplasm in the other breast depends on the particular gene that is mutated and on her age at the onset of disease.About half of all monogenically determined Carcinoma of the breast and Pelvis>Ovary are due to a Mutation Abnormality in one or the other of the highly penetrant BRCA Genes (BRCA1 and BRCA2), A value of RESTING HEART RATE greater than 1 indicated elevated breast Primary malignant neoplasm risk; a value of RESTING HEART RATE less than 1 indicated elevated Ovarian Primary malignant neoplasm risk.Gene Mutation of BRCA1 or BRCA2.Breast and Ovarian Primary malignant neoplasm risks.Among BRCA1 Mutation Abnormality carriers, 9052 women (46%) were diagnosed with breast Primary malignant neoplasm, 2317 (12%) with Ovarian Primary malignant neoplasm, 1041 (5%) with breast and Ovarian Primary malignant neoplasm, and 7171 (37%) without Primary malignant neoplasm, This study defined the experience and needs of women with hereditary breast and Ovarian Primary malignant neoplasm and a positive BRCA test over time.METHODS: A grounded theory approach was taken using qualitative interviews (n = 49) and reflective diaries. , Little is known about how women with hereditary breast and/or Ovarian Primary malignant neoplasm who test positive for a BRCA gene manage the impact of a positive test result on their everyday lives and in the longer term., This study defined the experience and needs of women with hereditary breast and Ovarian Primary malignant neoplasm and a positive BRCA test over time.A grounded theory approach was taken using qualitative interviews (n = 49) and reflective diaries., Women with a harmful Mutation Abnormality in the Malignant neoplasm of breast (BRCA) gene are at significantly increased risk of developing hereditary breast and Ovarian Primary malignant neoplasm (HBOC) during their lifetime, compared to those without., Genetic testing for BRCA Genes, associated with hereditary breast-Ovarian Primary malignant neoplasm risk, is an accepted Primary malignant neoplasm control strategy., Younger patients, those with a family history of breast or Ovarian Primary malignant neoplasm, and those diagnosed more recently were more likely to be BRCA tested., Gene Mutation in BRCA Genes elevate risk for breast and Ovarian Primary malignant neoplasm., Observational studies of prophylactic surgeries report reduced risks for breast and Ovarian Primary malignant neoplasm in Mutation Abnormality carriers.No data describe the range of risk associated with BRCA mutations, genetic heterogeneity, and moderating factors; studies conducted in highly selected populations contain biases; and information on adverse effects is incomplete.A primary care approach to screening for inherited breast and Ovarian Primary malignant neoplasm susceptibility has not been evaluated, and evidence is lacking to determine benefits and harms for the general population., We identified AJ individuals with breast and/or Ovarian Primary malignant neoplasm undergoing hereditary breast/Ovarian Primary malignant neoplasm risk assessment since 2006 without evidence of a deleterious Mutation Abnormality on BRCA gene sequencing who were screened for major gene rearrangements in BRCA1 and BRCA2. For each proband, the pre-test probability of identifying a deleterious BRCA Mutation Abnormality was estimated using the Myriad II model. We identified 108 affected individuals who underwent large rearrangement testing (80 breast Primary malignant neoplasm, 19 Ovarian Primary malignant neoplasm, nine both breast and Ovarian Primary malignant neoplasm)., Truncated proteins are easily discriminated from full size.RESULTS: Three BRCA 1 gene alterations were identified in the investigated group of women suffering from Ovarian or breast Primary malignant neoplasm. One asymptomatic person--carrier of BRCA 1 gene Mutation Abnormality--was identified in this study. She was daughter of a woman, a carrier of BRCA 1 gene Mutation Abnormality, with early onset of breast Primary malignant neoplasm and positive family history.CONCLUSIONS: BRCA 1 and BRCA2 gene mutations are of particular importance in the increasing risk of Ovarian Primary malignant neoplasm and early onset of breast Primary malignant neoplasm as well as some other malignancies., Germline BRCA gene mutations are reportedly associated with hereditary breast and Malignant neoplasm of Pelvis>Ovary. Identification of BRCA mutations greatly improves the preventive strategies and management of breast Primary malignant neoplasm., Statistically significant earlier ages at diagnosis also were observed within subgroups of BRCA1 and BRCA2 mutations, maternal inheritance, paternal inheritance, breast Primary malignant neoplasm only, and breast Primary malignant neoplasm-identified and Ovarian Primary malignant neoplasm-identified families.CONCLUSIONS: Breast and Malignant neoplasm of Pelvis>Ovary in BRCA Mutation Abnormality carriers appeared to be diagnosed at an earlier age in later generations., Truncated proteins are easily discriminated from full size.RESULTS: Three BRCA 1 gene alterations were identified in the investigated group of women suffering from Ovarian or breast Primary malignant neoplasm., However, some single risk factors without family histories (early-onset breast Primary malignant neoplasm, male breast Primary malignant neoplasm, or multiple organ Malignant Neoplasms) may limit the utility of BRCA gene testing in the Korean population., BRCA Gene Mutation Increase Fertility in Families at Hereditary Breast/Ovarian Cancer Risk., Because Sterility, Reproductive is associated with breast and Ovarian Primary malignant neoplasm risks, we hypothesized that the mutations in the BRCA gene may be associated with low response to fertility treatments., Moreover, in families of breast Primary malignant neoplasm patients without BRCA mutations, breast Primary malignant neoplasm risk depends on the patient's age at diagnosis., Among the 554 women who underwent genetic testing for BRCA Mutation Abnormality, 78 were found to have a deleterious Mutation Abnormality in the BRCA1 gene, and 54 had a Mutation Abnormality in the BRCA2 gene., Frequent recurrent mutations in the breast and Ovarian Primary malignant neoplasm susceptibility (BRCA) Genes BRCA1 and BRCA2 among Hispanics, including a large rearrangement Mexican founder Mutation Abnormality (BRCA1 exon 9-12 Gene Deletion Abnormality [ex9-12del]), suggest that an ancestry-informed BRCA-testing strategy could reduce disparities and promote Primary malignant neoplasm prevention by enabling economic screening for hereditary breast and Ovarian Primary malignant neoplasm in Mexico., Individuals who carry a BRCA gene Mutation Abnormality have increased lifetime risks of developing hereditary breast and Ovarian Primary malignant neoplasm syndrome-related Malignant Neoplasms., BRCA gene mutations have been well described to carry an increased risk of both breast and Ovarian Primary malignant neoplasm., Ovarian Primary malignant neoplasm among 8,005 women from a breast Primary malignant neoplasm family history clinic: no increased risk of invasive Ovarian Primary malignant neoplasm in families testing negative for BRCA1 and BRCA2., Women who were BRCA carriers, women who had a history of breast Primary malignant neoplasm, Noninfiltrating Intraductal Carcinoma, or Biopsy of breast, or had a family history of Ovarian Primary malignant neoplasm were more likely to have undergone surgery for Primary malignant neoplasm risk reduction., Genetic testing for breast Primary malignant neoplasm susceptibility became a reality after two Primary malignant neoplasm predisposition Genes, BRCA1 and BRCA2, were identified., Germ-Line Mutation in BRCA Genes are associated with breast and Ovarian Primary malignant neoplasm susceptibility., We used person-years at risk to assess Ovarian Primary malignant neoplasm rates in the study population, subdivided by genetic status (BRCA1, BRCA2, BRCA negative, BRCA untested) compared with the general population.[SEP]Relations: carcinoma has relations: disease_protein with BRCA1, disease_protein with BRCA1. Breast carcinoma has relations: disease_phenotype_positive with Ovarian Primary malignant neoplasm, disease_phenotype_positive with Ovarian Primary malignant neoplasm, disease_phenotype_positive with hereditary breast Ovarian Primary malignant neoplasm syndrome, disease_phenotype_positive with hereditary breast Ovarian Primary malignant neoplasm syndrome, disease_phenotype_positive with breast-Ovarian Primary malignant neoplasm, familial, susceptibility to, disease_phenotype_positive with breast-Ovarian Primary malignant neoplasm, familial, susceptibility to, disease_phenotype_positive with hereditary breast carcinoma, disease_phenotype_positive with hereditary breast carcinoma.", "label": "yes"}
{"original_question": "Are there sex differences in oncogenic mutational processes?", "id": "converted_4152", "sentence1": "Are there sex differences in oncogenic mutational processes?", "sentence2": "Gender:Type:Point in time:^Patient:Nominal differences in oncogenic mutational processes.[SEP]", "label": "yes"}
{"original_question": "Does the TOP2B/TOP2A expression ratio affect the response to AML chemotherapy?", "id": "converted_2111", "sentence1": "Does the TOP2B/TOP2A protein, human expression ratio affect the response to Leukemia, Myelocytic, Acute chemotherapy?", "sentence2": "High TOP2B/TOP2A protein, human protein, human expression ratio at diagnosis correlates with favourable outcome for standard chemotherapy in acute myeloid leukaemia, Genes with distinct expression profiles such as TOP2B/TOP2A protein, human protein, human expression ratio at diagnosis can be employed for outcome prediction after the treatment with standard regimens in Leukemia, Myelocytic, Acute patients with M2 subtype., Another interesting finding is that high ratios of TOP2B/RRM2 and TOP2B/TOP2 alpha (TOP2A protein, human protein, human) in a combined analysis were also shown to have a prognostic impact for longer survival with improved accuracy., Among the four markers, when adjusted for the influence of other clinical factors in multivariate analysis, the TOP2B/TOP2A protein, human protein, human ratio was significantly correlated with treatment outcomes; patients with high ratios trended toward longer disease-free survival (plant-type hypersensitive response, 0.24; P=0.002) and overall survival (plant-type hypersensitive response, 0.29; P=0.005), High TOP2B/TOP2A protein, human protein, human expression ratio at diagnosis correlates with favourable outcome for standard chemotherapy in acute myeloid leukaemia., Among the four markers, when adjusted for the influence of other clinical factors in multivariate analysis, the TOP2B/TOP2A protein, human protein, human ratio was significantly correlated with treatment outcomes; patients with high ratios trended toward longer disease-free survival (plant-type hypersensitive response, 0.24; P=0.002) and overall survival (plant-type hypersensitive response, 0.29; P=0.005).Genes with distinct expression profiles such as TOP2B/TOP2A protein, human protein, human expression ratio at diagnosis can be employed for outcome prediction after the treatment with standard regimens in Leukemia, Myelocytic, Acute patients with M2 subtype, CONCLUSION: Genes with distinct expression profiles such as TOP2B/TOP2A protein, human protein, human expression ratio at diagnosis can be employed for outcome prediction after the treatment with standard regimens in Leukemia, Myelocytic, Acute patients with M2 subtype., Genes with distinct expression profiles such as TOP2B/TOP2A protein, human protein, human expression ratio at diagnosis can be employed for outcome prediction after the treatment with standard regimens in Leukemia, Myelocytic, Acute patients with M2 subtype.., High TOP2B/TOP2A protein, human protein, human expression ratio at diagnosis correlates with favourable outcome for standard chemotherapy in acute myeloid leukaemia., Among the four markers, when adjusted for the influence of other clinical factors in multivariate analysis, the TOP2B/TOP2A protein, human protein, human ratio was significantly correlated with treatment outcomes; patients with high ratios trended toward longer disease-free survival (plant-type hypersensitive response, 0.24; P=0.002) and overall survival (plant-type hypersensitive response, 0.29; P=0.005)., Another interesting finding is that high ratios of TOP2B/RRM2 and TOP2B/TOP2 alpha (TOP2A protein, human protein, human) in a combined analysis were also shown to have a prognostic impact for longer survival with improved accuracy.[SEP]Relations: acute promyelocytic leukemia has relations: disease_protein with IRF2BP2, disease_protein with IRF2BP2, disease_protein with DAPK2, disease_protein with DAPK2, disease_protein with TET2, disease_protein with TET2, disease_protein with PML, disease_protein with PML, disease_protein with ITGB2, disease_protein with ITGB2.", "label": "yes"}
{"original_question": "Is SOX10 expressed in melanoma cells?", "id": "converted_4450", "sentence1": "Is SOX10 Transcription Factor expressed in Melanocytic neoplasm cells?", "sentence2": "Our study confirmed that SOX10 Transcription Factor Transcription Factor is an Oncogenes and activate Notch signaling pathway, which suggests the potential treatment for Melanocytic neoplasm patients by target SOX10 Transcription Factor Transcription Factor/Notch axis., The most commonly used melanocytic markers include S100A1 wt Allele, MART-1 Antigen (vaccine component), HMB-45 and SOX10 Transcription Factor Transcription Factor, melanocytic markers melan-A and SOX10 Transcription Factor Transcription Factor [SEP]Relations: melanocytic neoplasm has relations: disease_disease with Melanocytic neoplasm, disease_disease with Melanocytic neoplasm, disease_disease with melanocytic skin neoplasm, disease_disease with melanocytic skin neoplasm, disease_disease with neoplasm (disease), disease_disease with neoplasm (disease), disease_disease with neurocristopathy, disease_disease with neurocristopathy. SUMOylation of transcription factors has relations: pathway_protein with CDKN2A, pathway_protein with CDKN2A.", "label": "yes"}
{"original_question": "Can Diabetes be caused by a defect in a potassium chanel?", "id": "converted_1846", "sentence1": "Can Diabetes be caused by a defect in a potassium chanel?", "sentence2": "Gene Mutation in KATP Channels genes can result in hypo- or hypersecretion of Therapeutic Insulin, as in neonatal Diabetes Mellitus mellitus and Congenital Hyperinsulinism, respectively., To date, all patients affected by neonatal Diabetes Mellitus due to a Mutation Abnormality in the pore-forming subunit of the channel (Kir6.2, KCNJ11 gene gene) are heterozygous for the Mutation Abnormality. , e report the first clinical case of neonatal Diabetes Mellitus caused by a homozygous KCNJ11 gene gene Mutation Abnormality, Diffuse Congenital Hyperinsulinism in infancy (CHI-D) arises from mutations inactivating the KATP Channels;, We report a case of a 6-week-old infant with Diabetes Mellitus mellitus based on a genetic defect in the sulfonylurea receptor (ABCC8 gene), an ATP-sensitive potassium (KATP) channel protein., In Diabetes Mellitus, vascular KATP Channels function is impaired.[SEP]Relations: Type I Diabetes Mellitus mellitus has relations: disease_phenotype_positive with transketolase deficiency, disease_phenotype_positive with transketolase deficiency, disease_phenotype_positive with vasculitis due to ADA2 deficiency, disease_phenotype_positive with vasculitis due to ADA2 deficiency, disease_phenotype_positive with immunodeficiency due to CD25 deficiency, disease_phenotype_positive with immunodeficiency due to CD25 deficiency, disease_phenotype_positive with methanol poisoning, disease_phenotype_positive with methanol poisoning. KCNJ11 gene has relations: pathway_protein with Defective ABCC8 can cause hypo- and hyper-glycemias, pathway_protein with Defective ABCC8 can cause hypo- and hyper-glycemias.", "label": "yes"}
{"original_question": "Does d-tubocurarine (d-TC) induces irreversible inhibition of nicotinic acetylcholine receptor (nAChR) at the neuromuscular junction?", "id": "converted_550", "sentence1": "Does tubocurarine (d-TC) induces irreversible inhibition of nicotinic acetylcholine receptor location (nAChR) at the neuromuscular junction?", "sentence2": "An integrated model describing the interaction of nondepolarizing neuromuscular blocking agents with reversible anticholinesterase agents is derived and compared with a naive model using experimental data obtained from four anesthetized dogs. Three consecutive but separate steady-state tubocurarine blocks (approximately 50, 70, and 90%) were induced in each of the four dogs and reversed by short edrophonium infusions., The ability of Hexamethonium (Complement Component Complement Component C6, human, human) to reverse the neuromuscular blocking action of tubocurarine (CD55 wt Allele), Volatile anesthetics enhance the Observation of Neuromuscular Block produced by nondepolarizing Muscle Tissue relaxants (NDMRs). The neuromuscular junction is a postulated site of this interaction. We tested the hypothesis that volatile anesthetic enhancement of Muscle Tissue relaxation is the result of combined drug effects on the nicotinic acetylcholine receptor location location., Concentration-effect curves for the inhibition of acetylcholine-induced currents were established for vecuronium, tubocurarine, isoflurane, and sevoflurane. Subsequently, inhibitory effects of NDMRs were studied in the presence of the volatile anesthetics at a concentration equivalent to half the concentration producing a 50% inhibition alone. All individually tested compounds produced rapid and readily reversible concentration-dependent inhibition., The pharmacological diversity of the different Protein Isoforms of the nicotinic acetylcholine receptor location location arises from the diversity of the subunits that assemble to form the native receptors. The aim of this study was to investigate the actions of the Muscle Tissue relaxants tubocurarine, pancuronium and vecuronium on different Protein Isoforms of Nicotinic Receptors, At all three receptor types, tubocurarine and pancuronium blocked the responses elicited by acetylcholine in a reversible manner. , As further evidence of anticholinesterase activity, methamidophos (1-100 microM) was able to reverse the blockade by tubocurarine, There was an initial partial reversal of the neuromuscular inhibition caused by tubocurarine, isoflurane and sevoflurane enhance the receptor blocking effects of nondepolarizing Muscle Tissue relaxants on Nicotinic Receptors., Because other purinergic 2X (P2X) receptor antagonists, NF023 and NF 279, do not have the reverse effects on the Observation of Neuromuscular Block of d-TC, the effect of NF 449 seems irrelevant to inhibition of P2X receptors., The association rate constant for CD55 wt Allele binding to sites on the nicotinic acetylcholine receptor location location appears to be very fast (k+D = 8.9 x 10(8) M-1 s-1) and comparable to that for acetylcholine (ACh)., The aim of this study was to investigate the mechanism for the reversal effect of NF 449 (a suramin analogue) on the neuromuscular block induced by tubocurarine (d-TC)., Study of the reversal effect of NF 449 on Observation of Neuromuscular Block induced by tubocurarine.[SEP]Relations: Tubocurarine has relations: drug_drug with Acetylcholine, drug_drug with Acetylcholine, drug_drug with Succinylcholine, drug_drug with Succinylcholine, drug_drug with Naltrexone, drug_drug with Naltrexone, drug_drug with Acetyldigoxin, drug_drug with Acetyldigoxin. Acetylcholine has relations: drug_drug with Tubocurarine, drug_drug with Tubocurarine.", "label": "no"}
{"original_question": "Does Chromatin Immunoprecipitation (ChIP) show a bias for highly expressed loci?", "id": "converted_1044", "sentence1": "Does Chromatin Immunoprecipitation (ChIP) show a bias for highly expressed loci?", "sentence2": "However, several issues in the processing and analysis of ChIP-chip data have not been resolved fully, including the effect of background (mock control) subtraction and normalization within and across arrays,  Proper normalization is essential for ChIP-chip experiments. The proposed normalization technique can correct systematic errors and compensate for the lack of mock control data, thus reducing the experimental cost and producing more accurate results., Subtraction of the mock (non-specific antibody or no antibody) control data is generally needed to eliminate the bias, but appropriate normalization obviates the need for mock experiments and increases the correlation among replicates, The proposed method can handle several control samples allowing for correction of multiple sources of bias simultaneously, However, the data generated will always contain noise due to e.g. Repetitive Region or non-specific antibody interactions, The generation of high copy numbers of DNA fragments as an artifact of the PCR step in Chromatin Immunoprecipitation Sequencing is an important source of bias of this methodology, Here we describe several technical aspects of the ChIP-Seq assay that diminish bias and background noise and allow the consistent generation of high-quality data,  This theoretical paper systematically characterizes the biases and properties of Chromatin Immunoprecipitation Sequencing data by comparing 62 separate publicly available datasets, using rigorous statistical models and signal processing techniques, We detected a chromatin-state bias: open chromatin regions yielded higher coverage, which led to false positives if not corrected, This bias had a greater effect on detection specificity than any base-composition bias, This problem turns out to be surprisingly difficult, even in simple pairwise comparisons, because of the significant level of noise in Chromatin Immunoprecipitation Sequencing data, We show that the ChIPnorm method removes most of the noise and bias in the data and outperforms other normalization methods, We investigated the impact of library amplification bias on the identification of allele-specific (AS) molecular events from high-throughput sequencing data derived from chromatin immunoprecipitation assays (Chromatin Immunoprecipitation Sequencing), The 238 loci, termed \"hyper-ChIPable\", were in highly expressed regions with strong polymerase II and polymerase III enrichment signals, and the correlation between transcription level and ChIP enrichment was not limited to these 238 loci but extended genome-wide, The localization of unrelated Proteins, including the entire silencing complex, to the most highly transcribed genes was highly suggestive of a technical issue with the immunoprecipitations[SEP]Relations: heterochromatin organization involved in chromatin silencing has relations: bioprocess_bioprocess with chromatin organization involved in negative regulation of transcription, bioprocess_bioprocess with chromatin organization involved in negative regulation of transcription, bioprocess_protein with SMCHD1, bioprocess_protein with SMCHD1, bioprocess_bioprocess with heterochromatin organization, bioprocess_bioprocess with heterochromatin organization, bioprocess_bioprocess with heterochromatin maintenance, bioprocess_bioprocess with heterochromatin maintenance. positive regulation of peptide secretion has relations: bioprocess_protein with ADORA1, bioprocess_protein with ADORA1.", "label": "yes"}
{"original_question": "Does burning mouth syndrome preferentially affect post-mepopausal women?", "id": "converted_249", "sentence1": "Does burning mouth syndrome preferentially affect post-mepopausal women?", "sentence2": "It is observed principally in middle-aged patients and postmenopausal women and may be accompanied by Xerostomia and altered taste., It occurs more commonly in middle-aged and elderly women and often affects the tongue tip and lateral borders, Lip structure, and hard and soft palate. , BMS is a Chronic disease that frequently affects women and is characterised by burning symptoms of the oral mucosa without clinical signs., It mostly affects elderly citizens, especially postmenopausal women with prevalence up to 12-18%. [SEP]Relations: Xerostomia has relations: disease_phenotype_positive with postorgasmic illness syndrome, disease_phenotype_positive with postorgasmic illness syndrome, drug_effect with Mometasone, drug_effect with Mometasone, drug_effect with Nefopam, drug_effect with Nefopam, disease_phenotype_positive with Cronkhite-Canada syndrome, disease_phenotype_positive with Cronkhite-Canada syndrome, drug_effect with Acamprosate, drug_effect with Acamprosate.", "label": "yes"}
{"original_question": "Can discharge destinations be accurately predicted using the Risk Assessment and Prediction Tool (RAPT)?", "id": "converted_3580", "sentence1": "Can discharge destinations be accurately predicted using the Risk Assessment and Prediction Tool (RAPT)?", "sentence2": "CONCLUSION: Our analysis identified age, lower lumbar/lumbosacral surgery, and RAPT walk score as independent predictors of discharge to SNF, and demonstrated superior predictive power compared with the total RAPT Score when combined in a novel grading scale. , PURPOSE: The aim of this study was to evaluate the value of conventional factors, the Risk Assessment and Predictor Tool (RAPT) and performance-based functional tests as predictors of delayed recovery after total hip arthroplasty (Woods Brand of Tacrine Hydrochloride)., CONCLUSIONS: The RAPT accurately predicted discharge disposition for high- and low-risk patients in our cohort. , The RAPT allows for identification of patients who are likely to be discharged home or to rehabilitation, which may facilitate preoperative planning of postoperative care. Additionally, it identifies intermediate-risk patients and could be used to implement targeted interventions to facilitate discharge home in this group of patients., RESULTS: Overall predictive accuracy was 78%. , OBJECTIVE: To assess the relevance of the RAPT (Risk Assessment and Prediction Tool), among a cohort of patients undergoing total hip arthroplasty (Woods Brand of Tacrine Hydrochloride)., CONCLUSION: This study confirmed the usefulness of the RAPT to help in patient orientation decision after total hip arthroplasty. , CONCLUSIONS\n\nThe RAPT accurately predicted discharge disposition for high- and low-risk patients in our cohort., RAPT scores<6 and >10 (of 12) predicted with >90% accuracy discharge to inpatient rehabilitation and home, respectively., The RAPT allows for identification of patients who are likely to be discharged home or to rehabilitation, which may facilitate preoperative planning of postoperative care., The Risk Assessment and Prediction Tool (RAPT) is a preoperative survey constructed to predict discharge disposition after total joint arthroplasty (TJA)., CONCLUSIONS The RAPT accurately predicted discharge disposition for high- and low-risk patients in our cohort., The Risk Assessment and Prediction Tool (RAPT) is a preoperative survey constructed to predict discharge disposition after total joint arthroplasty (TJA)., A low RAPT score is reported to indicate a high risk of needing any form of inpatient rehabilitation after TJA, including short-term nursing facilities., CONCLUSIONS\nThe RAPT accurately predicted discharge disposition for high- and low-risk patients in our cohort., CONCLUSIONS: The RAPT accurately predicted discharge disposition for high- and low-risk patients in our cohort., BACKGROUND: The Risk Assessment and Prediction Tool (RAPT) is used to predict patient discharge disposition after total joint arthroplasty., CONCLUSIONS: The RAPT accurately predicted discharge disposition for high- and low-risk patients in our cohort.[SEP]", "label": "yes"}
{"original_question": "Could RG7112 be used as cancer therapy?", "id": "converted_1145", "sentence1": "Could RG7112 be used as cancer therapy?", "sentence2": "RG7112 is a potent and selective member of the nutlin family of MDM2 protein, Homo sapiens protein, Homo sapiens antagonists currently in phase I clinical studies., Our findings offer a preclinical proof-of-concept that RG7112 is effective in treatment of solid Neoplasms expressing wild-type TP53 wt Allele., On the other hand, JNJ 26854165, a novel tryptamine derivative and RG7112, a cis-imidazoline representative have shown promising results in early phases of trials in cancer patients., MDM2 protein, Homo sapiens protein, Homo sapiens small-molecule Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) RG7112 activates TP53 wt Allele signaling and regresses Homo sapiens Neoplasms in preclinical cancer models., On the other hand, JNJ 26854165, a novel tryptamine derivative and RG7112, a cis-imidazoline representative have shown promising results in early phases of trials in cancer patients., RG7112 is a selective inhibitor of TP53 wt Allele-MDM2 protein, Homo sapiens protein, Homo sapiens binding that frees TP53 wt Allele from negative control, activating the TP53 wt Allele pathway in Tumor cells, malignant leading to cell cycle arrest and apoptosis., In Tumor cells, malignant expressing wild-type TP53 wt Allele, RG7112 stabilizes TP53 wt Allele and activates the TP53 wt Allele pathway, leading to cell cycle arrest, apoptosis, and inhibition or regression of Homo sapiens tumor xenografts., Treatment of Tumor cells, malignant expressing wild-type TP53 wt Allele with RG7112 activated the TP53 wt Allele pathway, leading to cell-cycle arrest and apoptosis., RG7112 was selected for evaluation by the Pediatric Preclinical Testing Program (N-propyl-4-phenyl-1,2,3,6-tetrahydropyridine) due to the relatively low incidence of TP53 wt Allele mutations in pediatric cancers compared with adult Malignant Neoplasms., Treatment of Tumor cells, malignant expressing wild-type TP53 wt Allele with RG7112 activated the TP53 wt Allele pathway, leading to cell-cycle arrest and apoptosis, On the other hand, JNJ 26854165, a novel tryptamine derivative and RG7112, a cis-imidazoline representative have shown promising results in early phases of trials in cancer patients, RG7112 is a selective inhibitor of TP53 wt Allele-MDM2 protein, Homo sapiens protein, Homo sapiens binding that frees TP53 wt Allele from negative control, activating the TP53 wt Allele pathway in Tumor cells, malignant leading to cell cycle arrest and apoptosis, MDM2 protein, Homo sapiens protein, Homo sapiens small-molecule Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) RG7112 activates TP53 wt Allele signaling and regresses Homo sapiens Neoplasms in preclinical cancer models, In Tumor cells, malignant expressing wild-type TP53 wt Allele, RG7112 stabilizes TP53 wt Allele and activates the TP53 wt Allele pathway, leading to cell cycle arrest, apoptosis, and inhibition or regression of Homo sapiens tumor xenografts, RG7112 was selected for evaluation by the Pediatric Preclinical Testing Program (N-propyl-4-phenyl-1,2,3,6-tetrahydropyridine) due to the relatively low incidence of TP53 wt Allele mutations in pediatric cancers compared with adult Malignant Neoplasms, We report a proof-of-mechanism study of RG7112, a small-molecule MDM2 protein, Homo sapiens protein, Homo sapiens Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance), in patients with chemotherapy-naive primary or relapsed well-differentiated or dedifferentiated MDM2 protein, Homo sapiens protein, Homo sapiens-amplified liposarcoma who were eligible for resection, BACKGROUND: RG7112 is a selective inhibitor of TP53 wt Allele-MDM2 protein, Homo sapiens protein, Homo sapiens binding that frees TP53 wt Allele from negative control, activating the TP53 wt Allele pathway in Tumor cells, malignant leading to cell cycle arrest and apoptosis. RG7112 was selected for evaluation by the Pediatric Preclinical Testing Program (N-propyl-4-phenyl-1,2,3,6-tetrahydropyridine) due to the relatively low incidence of TP53 wt Allele mutations in pediatric cancers compared with adult Malignant Neoplasms. , Treatment of Tumor cells, malignant expressing wild-type TP53 wt Allele with RG7112 activated the TP53 wt Allele pathway, leading to cell-cycle arrest and apoptosis. , Effect of the MDM2 protein, Homo sapiens protein, Homo sapiens Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) RG7112 on the P53 pathway in patients with MDM2 protein, Homo sapiens protein, Homo sapiens-amplified, well-differentiated or dedifferentiated liposarcoma: an exploratory proof-of-mechanism study., RG7112 was selected for evaluation by the Pediatric Preclinical Testing Program (N-propyl-4-phenyl-1,2,3,6-tetrahydropyridine) due to the relatively low incidence of TP53 wt Allele mutations in pediatric cancers compared with adult Malignant Neoplasms. , Thus, inhibitors of TP53 wt Allele-MDM2 protein, Homo sapiens protein, Homo sapiens binding that can reactivate TP53 wt Allele in Tumor cells, malignant may offer an effective approach for cancer therapy., Treatment of Tumor cells, malignant expressing wild-type TP53 wt Allele with RG7112 activated the TP53 wt Allele pathway, leading to cell-cycle arrest and apoptosis. RG7112 showed potent antitumor activity against a panel of solid tumor Cultured Cell Line., A crystal structure of the RG7112-MDM2 protein, Homo sapiens protein, Homo sapiens complex revealed that the small molecule binds in the TP53 wt Allele pocket of MDM2 protein, Homo sapiens protein, Homo sapiens, mimicking the interactions of critical TP53 wt Allele amino acid residues. Treatment of Tumor cells, malignant expressing wild-type TP53 wt Allele with RG7112 activated the TP53 wt Allele pathway, leading to cell-cycle arrest and apoptosis., RG7112 (2g) is the first clinical small-molecule MDM2 protein, Homo sapiens protein, Homo sapiens inhibitor designed to occupy the TP53 wt Allele-binding pocket of MDM2 protein, Homo sapiens protein, Homo sapiens. In Tumor cells, malignant expressing wild-type TP53 wt Allele, RG7112 stabilizes TP53 wt Allele and activates the TP53 wt Allele pathway, leading to cell cycle arrest, apoptosis, and inhibition or regression of Homo sapiens tumor xenografts., RG7112 was selected for evaluation by the Pediatric Preclinical Testing Program (N-propyl-4-phenyl-1,2,3,6-tetrahydropyridine) due to the relatively low incidence of TP53 wt Allele mutations in pediatric cancers compared with adult Malignant Neoplasms. RG7112 and its inactive enantiomer RG7112i were evaluated against the 23 Cultured Cell Line of the N-propyl-4-phenyl-1,2,3,6-tetrahydropyridine in vitro panel using 96 hours exposure (1 nM to 10 µM)., Thus, inhibitors of TP53 wt Allele-MDM2 protein, Homo sapiens protein, Homo sapiens binding that can reactivate TP53 wt Allele in Tumor cells, malignant may offer an effective approach for cancer therapy. RG7112 is a potent and selective member of the nutlin family of MDM2 protein, Homo sapiens protein, Homo sapiens antagonists currently in phase I clinical studies., In Tumor cells, malignant expressing wild-type TP53 wt Allele, RG7112 stabilizes TP53 wt Allele and activates the TP53 wt Allele pathway, leading to cell cycle arrest, apoptosis, and inhibition or regression of Homo sapiens tumor xenografts.  ., Restoration of TP53 wt Allele activity by inhibiting the TP53 wt Allele-MDM2 protein, Homo sapiens protein, Homo sapiens interaction may represent a novel approach to cancer treatment. RG7112 (2g) is the first clinical small-molecule MDM2 protein, Homo sapiens protein, Homo sapiens inhibitor designed to occupy the TP53 wt Allele-binding pocket of MDM2 protein, Homo sapiens protein, Homo sapiens., RG7112 was selected for evaluation by the Pediatric Preclinical Testing Program (N-propyl-4-phenyl-1,2,3,6-tetrahydropyridine) due to the relatively low incidence of TP53 wt Allele mutations in pediatric cancers compared with adult Malignant Neoplasms.RG7112 and its inactive enantiomer RG7112i were evaluated against the 23 Cultured Cell Line of the N-propyl-4-phenyl-1,2,3,6-tetrahydropyridine in vitro panel using 96 hours exposure (1 nM to 10 µM)., Notably, RG7112 was highly synergistic with androgen deprivation in LNCaP xenograft Neoplasms. Our findings offer a preclinical proof-of-concept that RG7112 is effective in treatment of solid Neoplasms expressing wild-type TP53 wt Allele., RG7112 induced tumor regressions in solid Neoplasms from different histotype panels, and exhibited consistent high-level activity against ALL xenografts. This high level of activity supports prioritization of RG7112 for further evaluation., RG7112 is a selective inhibitor of TP53 wt Allele-MDM2 protein, Homo sapiens protein, Homo sapiens binding that frees TP53 wt Allele from negative control, activating the TP53 wt Allele pathway in Tumor cells, malignant leading to cell cycle arrest and apoptosis. RG7112 was selected for evaluation by the Pediatric Preclinical Testing Program (N-propyl-4-phenyl-1,2,3,6-tetrahydropyridine) due to the relatively low incidence of TP53 wt Allele mutations in pediatric cancers compared with adult Malignant Neoplasms.[SEP]Relations: Protein S Homo sapiens has relations: drug_drug with Rituximab, drug_drug with Rituximab, drug_drug with Bamet-UD2, drug_drug with Bamet-UD2, drug_drug with Methotrexate, drug_drug with Methotrexate, drug_drug with Bortezomib, drug_drug with Bortezomib, drug_drug with NS-398, drug_drug with NS-398.", "label": "yes"}
{"original_question": "Can TAD disruption lead to disease?", "id": "converted_3145", "sentence1": "Can aminoglutethimide/danazol/hydrocortisone/tamoxifen disruption lead to Disease?", "sentence2": "its perturbation will lead to Homo sapiens Disease, highlighting the accumulating evidence that links the diverse 3 Days Genome - anatomical entity architecture components to a multitude of Homo sapiens diseases and the emerging mechanisms by which 3 Days Genome - anatomical entity derangement causes Disease phenotypes., aminoglutethimide/danazol/hydrocortisone/tamoxifen boundaries are insulators of genomic neighborhoods. In this issue, Sun et al. show that Disease-associated tandem repeats are located to aminoglutethimide/danazol/hydrocortisone/tamoxifen boundaries and affect their insulation. , Recent studies of aminoglutethimide/danazol/hydrocortisone/tamoxifen boundaries disrupted in engineered mouse models show that boundary mutations can recapitulate Homo sapiens developmental disorders as a result of aberrant promoter-enhancer interactions in the affected Tietz syndrome, Similar boundary disruptions in certain Malignant Neoplasms can result in Oncogenes overexpression, and CTCF binding sites at boundaries appear to be hyper-mutated across Malignant Neoplasms., the disruption of these structures by genomic rearrangements can result in gene misexpression and Disease., aminoglutethimide/danazol/hydrocortisone/tamoxifen disruption as oncogenic driver., Recent studies have shown that aminoglutethimide/danazol/hydrocortisone/tamoxifen disruption is often found in Tumor cells, malignant and contributes to oncogenesis through two mechanisms., Disruption of aminoglutethimide/danazol/hydrocortisone/tamoxifen boundaries results in aberrant gene expression by exposing Genes to inappropriate regulatory elements., However, it is not clear to which extent aminoglutethimide/danazol/hydrocortisone/tamoxifen regions are conserved in evolution and whether disruption of Tietz syndrome by evolutionary rearrangements can alter gene expression., Disruption of this organization by structural variations can lead to ectopic interactions between enhancers and Promoter, and to alteration of Genes expression patterns., Disruption of Tietz syndrome can result in altered gene expression and is associated to genetic diseases and Malignant Neoplasms., Gene Gene Deletion Abnormality Abnormality in 2q35 excluding the IHH gene leads to fetal severe limb anomalies and suggests a disruption of chromatin architecture., We demonstrate that disruption of Tietz syndrome can rewire long-range regulatory architecture and result in Pathogenic Variant phenotypes. , Disruption of aminoglutethimide/danazol/hydrocortisone/tamoxifen boundaries results in aberrant gene expression by exposing Genes to inappropriate regulatory elements. , Disruption of Tietz syndrome can result in altered gene expression and is associated to genetic diseases and Malignant Neoplasms. , Disruption of a aminoglutethimide/danazol/hydrocortisone/tamoxifen boundary causes ectopic chromosomal contacts and long-range transcriptional misregulation. , Recent studies of aminoglutethimide/danazol/hydrocortisone/tamoxifen boundaries disrupted in engineered mouse models show that boundary mutations can recapitulate Homo sapiens developmental disorders as a result of aberrant promoter-enhancer interactions in the affected Tietz syndrome. , Recent studies have shown that aminoglutethimide/danazol/hydrocortisone/tamoxifen disruption is often found in Tumor cells, malignant and contributes to oncogenesis through two mechanisms. , Disruption of this organization by structural variations can lead to ectopic interactions between enhancers and Promoter, and to alteration of Genes expression patterns. , Similar boundary disruptions in certain Malignant Neoplasms can result in Oncogenes overexpression, and CTCF binding sites at boundaries appear to be hyper-mutated across Malignant Neoplasms. , However, it is not clear to which extent aminoglutethimide/danazol/hydrocortisone/tamoxifen regions are conserved in evolution and whether disruption of Tietz syndrome by evolutionary rearrangements can alter gene expression. [SEP]Relations: Abnormality of the dentition has relations: disease_phenotype_positive with intellectual disability-feeding difficulties-developmental delay-microcephaly syndrome, disease_phenotype_positive with intellectual disability-feeding difficulties-developmental delay-microcephaly syndrome, disease_phenotype_positive with Marshall syndrome, disease_phenotype_positive with Marshall syndrome, disease_phenotype_positive with severe intellectual disability-short stature-behavioral abnormalities-facial dysmorphism syndrome, disease_phenotype_positive with severe intellectual disability-short stature-behavioral abnormalities-facial dysmorphism syndrome, disease_phenotype_positive with SIN3A-related intellectual disability syndrome due to a point mutation, disease_phenotype_positive with SIN3A-related intellectual disability syndrome due to a point mutation, disease_phenotype_positive with late-onset localized junctional epidermolysis bullosa-intellectual disability syndrome, disease_phenotype_positive with late-onset localized junctional epidermolysis bullosa-intellectual disability syndrome.", "label": "yes"}
{"original_question": "Is vorinostat effective for glioblastoma?", "id": "converted_2486", "sentence1": "Is vorinostat effective for Glioblastoma Multiforme?", "sentence2": "Conclusions: vorinostat combined with standard chemoradiation had acceptable tolerability in newly diagnosed Glioblastoma Multiforme. Although the primary efficacy endpoint was not met, vorinostat sensitivity and resistance signatures could facilitate patient selection in future trials., LESSONS LEARNED: Combination regimen with bevacizumab (BEV) and vorinostat is well tolerated in patients with recurrent Glioblastoma Multiforme., CONCLUSION: Combination treatment of BEV and 3-methyl-2-oxobutanoate dehydrogenase (ferredoxin) activity was well tolerated. This combination therapy for this study population did not improve PFS6 or median OS when compared with BEV monotherapy., We present two patients with Glioblastoma Multiforme multiforme who developed severe Anemia, Hemolytic shortly after initiating therapy with vorinostat, a pan-active histone deacetylase PPP1R1A gene, while on prophylactic dapsone., vorinostat is the most advanced HDAC9 wt Allele PPP1R1A gene that entered clinical trials in Glioblastoma Multiforme, showing activity in recurrent disease. Multiple phase II trials with vorinostat in combination with targeted agents, temozolomide and radiotherapy are currently recruiting. , . On the basis of the results of this phase II study, further evaluation of the vorinostat-bortezomib combination in Glomerular Basement Membrane patients in this dose and schedule is not recommended., ith the increased Toxic effect associated with CPT-11 coupled with its unclear clinical significance, investigating the efficacy of vorinostat combined with bevacizumab alone may represent a more promising strategy to evaluate in the context of a phase II clinical trial., CONCLUSION: vorinostat in combination with temozolomide is well tolerated in patients with HGG. A phase I/II trial of vorinostat with radiotherapy and concomitant temozolomide in newly diagnosed Glioblastoma Multiforme is underway.[SEP]Relations: vorinostat has relations: drug_effect with Cholecystitis, drug_effect with Cholecystitis, drug_effect with Erythroderma, drug_effect with Erythroderma, drug_effect with T-cell lymphoma, drug_effect with T-cell lymphoma, drug_drug with Entinostat, drug_drug with Entinostat, drug_effect with Xerostomia, drug_effect with Xerostomia.", "label": "no"}
{"original_question": "Is RASA2 involved in melanoma?", "id": "converted_1804", "sentence1": "Is Ras GTPase-Activating Protein 2, Human involved in Melanocytic neoplasm?", "sentence2": "Analysis of 501 Melanocytic neoplasm exomes identified Ras GTPase-Activating Protein 2, Human, encoding a Ras GTPase-Activating Protein 2, Human wt Allele, as a tumor-suppressor gene mutated in 5% of Melanocytic neoplasm. Recurrent loss-of-function mutations in Ras GTPase-Activating Protein 2, Human were found to increase ras Oncogene activation, Melanocytic neoplasm cell growth and migration. Ras GTPase-Activating Protein 2, Human expression was lost in ≥30% of Homo sapiens Melanocytic neoplasm and was associated with reduced patient survival. These findings identify Ras GTPase-Activating Protein 2, Human inactivation as a Melanocytic neoplasm driver and highlight the importance of RasGAPs in Primary malignant neoplasm., Analysis of 501 Melanocytic neoplasm exomes identified Ras GTPase-Activating Protein 2, Human, encoding a Ras GTPase-Activating Protein 2, Human wt Allele, as a tumor-suppressor gene mutated in 5% of Melanocytic neoplasm, These findings identify Ras GTPase-Activating Protein 2, Human inactivation as a Melanocytic neoplasm driver and highlight the importance of RasGAPs in Primary malignant neoplasm., Recurrent loss-of-function mutations in Ras GTPase-Activating Protein 2, Human were found to increase ras Oncogene activation, Melanocytic neoplasm cell growth and migration., Analysis of 501 Melanocytic neoplasm exomes identified Ras GTPase-Activating Protein 2, Human, encoding a Ras GTPase-Activating Protein 2, Human wt Allele, as a tumor-suppressor gene mutated in 5% of Melanocytic neoplasm.[SEP]Relations: Melanocytic neoplasm has relations: disease_protein with Ras GTPase-Activating Protein 2, Human, disease_protein with Ras GTPase-Activating Protein 2, Human, disease_protein with RAC2, disease_protein with RAC2, disease_protein with ARL2, disease_protein with ARL2, disease_protein with MDM2, disease_protein with MDM2, disease_protein with GPHA2, disease_protein with GPHA2.", "label": "yes"}
{"original_question": "Is hemoglobin antimicrobial?", "id": "converted_4370", "sentence1": "Is Hemoglobin A1 (substance) antimicrobial?", "sentence2": "the α137-141 Peptides, a natural antimicrobial Peptides, can be obtained after hydrolysis of Hemoglobin A1 (substance), the main constituent of blood red part, Beyond its physiological activity, Hemoglobin are able to inhibit the growth of several microorganisms., A novel adenosine monophosphate, T. granosa Hemoglobin A1 (substance)-derived Peptides (TGH1), was identified and its antimicrobial effect[SEP]Relations: HbC Hemoglobin A1 (substance) has relations: phenotype_phenotype with Abnormal Hemoglobin A1 (substance), phenotype_phenotype with Abnormal Hemoglobin A1 (substance). Adenosine phosphate has relations: drug_protein with PRKAB2, drug_protein with PRKAB2, drug_protein with ADK, drug_protein with ADK, contraindication with bronchiectasis, contraindication with bronchiectasis, drug_protein with PRKAB1, drug_protein with PRKAB1.", "label": "yes"}
{"original_question": "Is skin color affected by variations of the SLC24A5 gene?", "id": "converted_2150", "sentence1": "Is skin color affected by variations of the Sodium/Potassium/Calcium Exchanger 5, Human gene?", "sentence2": "the Alleles of single-nucleotide polymorphisms rs1426654 and rs1834640 (Sodium/Potassium/Calcium Exchanger 5, Human) associated with light skin pigmentation in Eurasian populati, Associations between five single nucleotide polymorphisms (Single Nucleotide Polymorphism) known to play a role in pigmentation (rs1426654-Sodium/Potassium/Calcium Exchanger 5, Human, rs1042602-TYR, rs16891982-SLC45A2, rs6058017-ASIP, and rs642742-KITLG) and MI measures were tested using standard one-way analysis of variance (ANOVA) within each population.[SEP]Relations: Sodium/Calcium exchangers has relations: pathway_protein with Sodium/Potassium/Calcium Exchanger 5, Human, pathway_protein with Sodium/Potassium/Calcium Exchanger 5, Human, pathway_protein with SLC24A4, pathway_protein with SLC24A4, pathway_protein with SLC24A2, pathway_protein with SLC24A2, pathway_protein with SLC24A3, pathway_protein with SLC24A3, pathway_protein with SLC24A1, pathway_protein with SLC24A1.", "label": "yes"}
{"original_question": "Is Aptiganel effective for treatment of stroke?", "id": "converted_3681", "sentence1": "Is Aptiganel effective for treatment of Cerebrovascular accident?", "sentence2": "Trends for increased mortality with three N-Methylaspartate antagonists were seen - selfotel (OR 1.19 [0.81-1.74]), aptiganel (OR 1.32 [0.91-1.93]) and Gavestinel (OR 1.12 [0.95-1.32]) - but this did not achieve significance for the N-Methylaspartate antagonists considered as a class (1.09 [0.96-1.23]). Aptiganel was also associated with a trend towards worse functional outcome (OR 1.20 [0.88-1.65]) although this was not the case for either of the other two compounds., No improvement in clinical outcome of Cerebrovascular accident has been seen with competitive N-Methylaspartate antagonists (selfotel) and non-competitive N-Methylaspartate antagonists (Dextrorphan, GV 150526A, aptiganel and eliprodil)., Glutamate N-methyl-D-aspartate (N-Methylaspartate) receptor antagonists (competitive receptor antagonists, ion channel blockers, and Glycine (Plant) antagonists)--such as selfotel, aptiganel, eliprodil, licostinel and Gavestinel--failed to show efficacy in clinical trials of Cerebrovascular accident or Traumatic Brain Injury. , There was no improvement in outcome for either aptiganel (Low-Dose Treatment or high-dose) group compared with the placebo group at 90 days (median Modified Rankin Scale score for all 3 treatment groups = 3; P =.31). At 7 days, placebo-treated patients exhibited slightly greater neurological improvement on the NIH Stroke Scale than high-dose aptiganel patients (mean improvement for placebo group, -0.8 points vs for high-dose aptiganel, 0.9 points; P =.04). The mortality rate at 120 days in patients treated with high-dose aptiganel was higher than that in patients who received placebo (26.3% vs 19.2%; P =.06)., CONCLUSIONS: Aptiganel was not efficacious in patients with acute ischemic Cerebrovascular accident at either of the tested doses, and m ay be harmful. The larger proportion of patients with favorable outcomes and lower mortality rate in the placebo group suggest that glutamate blockade with aptiganel may have detrimental effects in an undifferentiated population of Cerebrovascular accident patients., CONCLUSIONS\n\nAptiganel was not efficacious in patients with acute ischemic Cerebrovascular accident at either of the tested doses, and m ay be harmful., The larger proportion of patients with favorable outcomes and lower mortality rate in the placebo group suggest that glutamate blockade with aptiganel may have detrimental effects in an undifferentiated population of Cerebrovascular accident patients., There was no improvement in outcome for either aptiganel (Low-Dose Treatment or high-dose) group compared with the placebo group at 90 days (median Modified Rankin Scale score for all 3 treatment groups = 3; P =.31)., Glutamate N-methyl-D-aspartate (N-Methylaspartate) receptor antagonists (competitive receptor antagonists, ion channel blockers, and Glycine (Plant) antagonists)--such as selfotel, aptiganel, eliprodil, licostinel and Gavestinel--failed to show efficacy in clinical trials of Cerebrovascular accident or Traumatic Brain Injury., CONCLUSIONS Aptiganel was not efficacious in patients with acute ischemic Cerebrovascular accident at either of the tested doses, and m ay be harmful., Glutamate N-methyl-D-aspartate ( N-Methylaspartate ) receptor antagonists ( competitive receptor antagonists , ion channel blockers , and Glycine (Plant) antagonists)--such as selfotel , aptiganel , eliprodil , licostinel and Gavestinel--failed to show efficacy in clinical trials of Cerebrovascular accident or Traumatic Brain Injury, No improvement in clinical outcome of Cerebrovascular accident has been seen with competitive N-Methylaspartate antagonists ( selfotel ) and non-competitive N-Methylaspartate antagonists ( Dextrorphan , GV 150526A , aptiganel and eliprodil, There was no improvement in outcome for either aptiganel (Low-Dose Treatment or high-dose) group compared with the placebo group at 90 days (median Modified Rankin Scale score for all 3 treatment groups = 3; P =.31)., CONCLUSIONS: Aptiganel was not efficacious in patients with acute ischemic Cerebrovascular accident at either of the tested doses, and m ay be harmful., The larger proportion of patients with favorable outcomes and lower mortality rate in the placebo group suggest that glutamate blockade with aptiganel may have detrimental effects in an undifferentiated population of Cerebrovascular accident patients., There was no improvement in outcome for either aptiganel (Low-Dose Treatment or high-dose) group compared with the placebo group at 90 days (median Modified Rankin Scale score for all 3 treatment groups = 3; P =.31)., Aptiganel was not efficacious in patients with acute ischemic Cerebrovascular accident at either of the tested doses, and m ay be harmful., The larger proportion of patients with favorable outcomes and lower mortality rate in the placebo group suggest that glutamate blockade with aptiganel may have detrimental effects in an undifferentiated population of Cerebrovascular accident patients.[SEP]Relations: Ischemic Cerebrovascular accident has relations: drug_effect with Paclitaxel, drug_effect with Paclitaxel, drug_effect with Ramipril, drug_effect with Ramipril, drug_effect with Aripiprazole, drug_effect with Aripiprazole, drug_effect with Sitaxentan, drug_effect with Sitaxentan, drug_effect with Pazopanib, drug_effect with Pazopanib.", "label": "no"}
{"original_question": "Is autophagy modulated in a circadian fashion?", "id": "converted_2274", "sentence1": "Is autophagy modulated in a circadian fashion?", "sentence2": "RORC wt Allele signaling pathway and autophagy are involved in the regulation of circadian rhythms in behavior and plasticity of L2 Interneurons in the Head>Brain of Drosophila melanogaster.,  Our results indicate that the RORC wt Allele signaling pathway and autophagy are involved in the regulation of circadian rhythms in the behavior and plasticity of Neurons in the Head>Brain of adult Diptera., the pathways of autophagy, FRAP1 protein, human, Sirtuin 1, and Wnt that control mammalian circadian rhythm, Metabolic pathways, Bile Acid [EPC] synthesis, and autophagic and immune/inflammatory processes are driven by the biological clock. , our findings suggest that the clock geneBmal1is a positive regulator of autophagy through the FRAP1 protein, human signaling pathway and protects Myocytes, Cardiac against high-glucose Toxic effect., Autophagy is a highly conserved Protoplasm degradation system, and recently was shown to display circadian rhythms in CASP14 gene. [SEP]Relations: Protein S human has relations: drug_drug with Protocatechualdehyde, drug_drug with Protocatechualdehyde, drug_drug with Thalidomide, drug_drug with Thalidomide, drug_drug with Pargyline, drug_drug with Pargyline, drug_drug with Cephaloglycin, drug_drug with Cephaloglycin, drug_drug with Procarbazine, drug_drug with Procarbazine.", "label": "yes"}
{"original_question": "Does Curare function by stimulating the acetylcholine receptor?", "id": "converted_4161", "sentence1": "Does Curare function by stimulating the Acetylcholine Receptor Antibody?", "sentence2": "Usual clinical concentrations of Curare cause competitive inhibition of Muscle Tissue nicotinic acetylcholine receptors while higher concentrations may induce open channel blockade., nicotinic Acetylcholine Receptor Antibody (nAChR)-blocking agents [e.g., Curare or alpha-Bungarotoxins (alpha-BTX), The short neurotoxins to which Erabutoxins belong act by blocking the nicotinic Acetylcholine Receptor Antibody, Both EFS- and carbachol-evoked contractions of the Upper Esophageal Sphincter were blocked by Curare at a lower concentration than by Atropinum, Atropinum, atropine or Hexamethonium, suggesting that the Acetylcholine Receptor Antibody is nicotinic., We applied ACh alone; the nicotinic Acetylcholine Receptor Antibody (nAChR) Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) Curare, either alone or in the presence of ACh; and the muscarinic Acetylcholine Receptor Antibody (mAChR) Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) Atropinum, Atropinum, atropine, either alone or in the presence of ACh., The EFS-induced contraction of the Upper Esophageal Sphincter was completely blocked by Tetrodotoxin and Curare, and abolished in Ca2+ -free Ringer solution., Curare binding and the Curare-induced subconductance state of the Acetylcholine Receptor Antibody channel., We have further investigated this particular Mutation Abnormality by examining the interaction of the competitive Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) d-tubocurarine (Curare) with the receptor., tubocurarine (Curare) is a well-characterized competitive Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) of nicotinic acetylcholine receptors (AChRs), and it is usually assumed that Curare and agonists share a common Ligand Binding Domain., Curare action on nicotinic acetylcholine receptors has a number of facets, of which the best known is competitive antagonism., The mode of action of Curare, a well-known competitive Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) of acetylcholine at the nicotinic receptor, was examined with the single channel recording technique. , ently, however, it has been shown that Curare can also block the channels opened by ACh at the Rana <genus> neuromuscular junction as well as on Rattus norvegicus and Aplysia species species neurones; moreover, Curare is able to depolarize Rattus norvegicus myotubes and thus behaves as an Agonist for the Cholinergic Receptors of this preparation (see ref. 6). U, One site, competitively blocked by Bungarotoxins and by Curare, is presumably the Acetylcholine Receptor Antibody., In neuromuscular junction (NMJ) preparations, movements of the Muscle Tissue must be inhibited if imaging during stimulation is desired (e.g., by application of Curare, a potent Acetylcholine Receptor Antibody inhibitor)., Curare has long been regarded as a typical competitive Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) of acetylcholine (ACh) at the Vertebrates neuromuscular junction., Curare inhibition of wild-type receptors is consistent with Curare binding to a single high-affinity Ligand Binding Domain [inhibitor constant (Ki) = 20 nM]., phenylalanine substitution for alpha Y198 [alpha Y198F (notation used here: subunit/amino acid in wild-type/residue number/substitution)] causes a 10-fold increase in Curare affinity (Ki = 3.1 nM), and measurement of the recovery from Curare inhibition indicates that this increase in affinity is due to a reduction in the rate of Curare dissociation from the receptor., rthermore, sudden increases of research activity are ascribable to historic events, like the first use of Curare as Muscle Tissue relaxant during surgery.DIS, Recently, however, it has been shown that Curare can also block the channels opened by ACh at the Rana <genus> neuromuscular junction as well as on Rattus norvegicus and Aplysia species species neurones; moreover, Curare is able to depolarize Rattus norvegicus myotubes and thus behaves as an Agonist for the Cholinergic Receptors of this preparation (see ref., In Aplysia species species nervous tissue, Curare appears not to be a specific Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) for the nicotinic ACh receptor, but rather to be a specific blocking agent for a class of receptor-activated Na+ and Cl- responses., The mode of action of Curare, a well-known competitive Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) of acetylcholine at the nicotinic receptor, was examined with the single channel recording technique.[SEP]Relations: Muscarinic acetylcholine receptors has relations: pathway_protein with CHRM5, pathway_protein with CHRM5, pathway_protein with CHRM5, pathway_protein with CHRM5, pathway_protein with CHRM1, pathway_protein with CHRM1, pathway_protein with CHRM1, pathway_protein with CHRM1, pathway_protein with CHRM4, pathway_protein with CHRM4.", "label": "no"}
{"original_question": "Is Mycobacterium abscessus a human pathogen?", "id": "converted_4355", "sentence1": "Is Mycobacterium abscessus a human pathogen?", "sentence2": "Mycobacterium abscessus is unique in terms of its high morbidity and treatment failure rates, Mycobacterium abscessus has emerged as a successful pathogen owing to its intrinsic drug resistance. , Mycobacterium abscessus lung disease is difficult to treat due to intrinsic drug resistance and the persistence of drug-tolerant bacteria., Mycobacterium abscessus has been recognised as a dreadful respiratory pathogen among the non-tuberculous mycobacteria (Nontuberculous Mycobacteria) because of misdiagnosis, prolonged therapy with poor treatment outcomes and a high cost. [SEP]Relations: Mycobacterium abscessus abscessus infection has relations: phenotype_phenotype with Opportunistic bacterial infection, phenotype_phenotype with Opportunistic bacterial infection, disease_phenotype_positive with pulmonary non-tuberculous mycobacterial infection, disease_phenotype_positive with pulmonary non-tuberculous mycobacterial infection. Nontuberculous mycobacterial pulmonary infection has relations: phenotype_phenotype with Opportunistic bacterial infection, phenotype_phenotype with Opportunistic bacterial infection.", "label": "yes"}
{"original_question": "Is HYDIN (Hydrocephalus-inducing protein homolog) an axonemal protein?", "id": "converted_4691", "sentence1": "Is HYDIN (Hydrocephalus-inducing Protein Info homolog) an axonemal Protein Info?", "sentence2": "HYDIN gene was recently identified as an axonemal Protein Info; however, its function is as yet unknown., precise axonemal location of hydin, a Protein Info that, when mutated, causes Hydrocephalus, and defined a unique role for hydin in ciliary motility.[SEP]Relations: Hydrocephalus has relations: disease_phenotype_positive with isotretinoin-like syndrome, disease_phenotype_positive with isotretinoin-like syndrome, disease_phenotype_positive with methylmalonic aciduria/acidemia and homocystinuria, disease_phenotype_positive with methylmalonic aciduria/acidemia and homocystinuria, disease_phenotype_positive with methylmalonic acidemia with homocystinuria, disease_phenotype_positive with methylmalonic acidemia with homocystinuria, disease_phenotype_positive with Noonan syndrome-like disorder with loose anagen hair, disease_phenotype_positive with Noonan syndrome-like disorder with loose anagen hair, drug_effect with Glatiramer, drug_effect with Glatiramer.", "label": "yes"}
{"original_question": "Is MK-1602 a CGRP antagonist?", "id": "converted_3875", "sentence1": "Is MK-1602 a CGRP antagonist?", "sentence2": "The aim of this trial was to evaluate the efficacy and tolerability of ubrogepant (MK-1602), a Calcitonin Gene-Related Peptide Receptor Antagonists (CGRP-RA), for the acute treatment of Migraine Disorders., This trial supports ubrogepant's efficacy and provides further evidence that CGRP-RAs are viable options for the acute treatment of Migraine Disorders.[SEP]Relations: calcitonin gene-related peptide receptor activity has relations: molfunc_protein with CRCP, molfunc_protein with CRCP, molfunc_protein with CALCRL, molfunc_protein with CALCRL, molfunc_protein with RAMP1, molfunc_protein with RAMP1, molfunc_protein with CALCR, molfunc_protein with CALCR. Migraine Disorders disorder has relations: disease_protein with TGFBR2, disease_protein with TGFBR2.", "label": "yes"}
{"original_question": "Is NfL (neurofilament light chain) a biomarker of neurodegeneration?", "id": "converted_4600", "sentence1": "Is NEFL wt Allele (neurofilament light chain) a biomarker of Nerve Degeneration?", "sentence2": "NEFL gene (NEFL wt Allele) has recently been proposed as a promising biomarker in frontotemporal dementia (Frontotemporal dementia). , NEFL gene (NEFL wt Allele) is a new, non-disease specific, widely studied biomarker indicative of axonal injury and degeneration, the Nerve Degeneration biomarker neurofilament light chain (NEFL wt Allele) , bNfL can be used as a potential biomarker to predict disease onset, severity, and progression of genetic ataxia., NEFL gene protein (NEFL wt Allele) is a promising biomarker of Nerve Degeneration.[SEP]Relations: Frontotemporal dementia has relations: disease_phenotype_positive with PRKAR1B-related neurodegenerative dementia with intermediate filaments, disease_phenotype_positive with PRKAR1B-related neurodegenerative dementia with intermediate filaments, disease_phenotype_positive with frontotemporal dementia with motor neuron disease, disease_phenotype_positive with frontotemporal dementia with motor neuron disease. Protein S human has relations: drug_drug with Nefazodone, drug_drug with Nefazodone, drug_drug with Phenylbutazone, drug_drug with Phenylbutazone, drug_drug with Flurbiprofen axetil, drug_drug with Flurbiprofen axetil.", "label": "yes"}
{"original_question": "Is cohesin linked to myeloid differentiation?", "id": "converted_2787", "sentence1": "Is cohesins linked to myeloid differentiation?", "sentence2": "Consistent with a role for inflammatory signals in promoting myeloid differentiation of hematopoietic stem and Stem cells (HPSCs), cohesins mutations in HSPCs led to reduced inflammatory gene expression and increased resistance to differentiation-inducing inflammatory stimuli. These findings uncover an unexpected dependence of inducible gene expression on cohesins, link cohesins with myeloid differentiation, and may help explain the prevalence of cohesins mutations in Homo sapiens Leukemia, Myelocytic, Acute., Consistent with a role for inflammatory signals in promoting myeloid differentiation of hematopoietic stem and Stem cells (HPSCs), cohesins mutations in HSPCs led to reduced inflammatory gene expression and increased resistance to differentiation-inducing inflammatory stimuli., These findings uncover an unexpected dependence of inducible gene expression on cohesins, link cohesins with myeloid differentiation, and may help explain the prevalence of cohesins mutations in Homo sapiens Leukemia, Myelocytic, Acute.<br>[SEP]Relations: acute promyelocytic leukemia has relations: disease_disease with Leukemia, Myelocytic, Acute with recurrent genetic anomaly, disease_disease with Leukemia, Myelocytic, Acute with recurrent genetic anomaly, disease_protein with GLI2, disease_protein with GLI2, disease_protein with DEFA3, disease_protein with DEFA3, disease_phenotype_positive with Ecchymosis, disease_phenotype_positive with Ecchymosis, disease_phenotype_positive with Gingival bleeding, disease_phenotype_positive with Gingival bleeding.", "label": "yes"}
{"original_question": "Has overexpression of sirtuins been reported to increase lifespan in budding yeast (Saccharomyces cerevisiae)?", "id": "converted_665", "sentence1": "Has overexpression of Sirtuins been reported to increase lifespan in budding Saccharomyces cerevisiae (Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae)?", "sentence2": "In addition, NAD-dependent histone deacetylase activity overexpression prevents Rif1 deletion from disrupting NAD-dependent histone deacetylase activity at Megaloblastic Anemia 1 and shortening lifespan. , Roles for sirtuin proteins at telomere are thought to promote lifespan in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae and Mammals., Overexpression of Sirtuins (NAD(+)-dependent protein deacetylases) has been reported to increase lifespan in budding Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae (Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae), When overexpressed, the NAD-dependent protein deacetylase NAD-dependent histone deacetylase activity extends the lifespan of both budding Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae , When overexpressed in primary Mus sp. embryo fibroblasts (MEFs), Sirtuin 1 antagonizes PML-induced acetylation of TP53 wt Allele and rescues PML-mediated premature cellular senescence. [SEP]Relations: megaloblastic anemia (disease) has relations: contraindication with Phenytoin, contraindication with Phenytoin, contraindication with Primidone, contraindication with Primidone. NAD-dependent histone deacetylase activity has relations: molfunc_protein with Sirtuin 1, molfunc_protein with Sirtuin 1, molfunc_protein with SIRT2, molfunc_protein with SIRT2, molfunc_protein with SIRT3, molfunc_protein with SIRT3.", "label": "yes"}
{"original_question": "Does the BRAFV600E mutation have an effect on clinical response to radioiodine therapy?", "id": "converted_3545", "sentence1": "Does the BRAFV600E Mutation Abnormality have an effect on clinical response to iodide ion I-131 therapy?", "sentence2": "Preclinical studies showed that BRAF protein, human protein, human Mutation Abnormality significantly reduced iodide ion I-131 uptake and decreased the sensitivity to radioactive iodine (PPP1R13L wt Allele) therapy., The status of BRAF protein, human protein, human Mutation Abnormality may not affect the clinical response to PPP1R13L wt Allele therapy for patients with PTMC with intermediate-risk to high-risk features. More trials examining the role of BRAF protein, human protein, human Mutation Abnormality in guiding postoperative PPP1R13L wt Allele therapy are needed., our results suggest that the combination of BRAFV600E+ve Mutation Abnormality and MIBI-ve scintigraphy may be considered a negative prognostic clue, which predicts the absence of iodide ion I-131 uptake at pT-WBS in DTC patients with incomplete bio-chemical response to first RAIT, The results indicate that BRAF protein, human protein, human(V600E) Mutation Abnormality is correlated with a lower expression of SLC5A5 gene in PTCs without Hashimoto Disease, suggesting the iodide ion I-131-refractory effects during RIA therapy in these patients.[SEP]Relations: SLC5A5 has relations: drug_protein with Iodine, drug_protein with Iodine, disease_protein with hereditary site-specific ovarian cancer syndrome, disease_protein with hereditary site-specific ovarian cancer syndrome, bioprocess_protein with cellular response to cAMP, bioprocess_protein with cellular response to cAMP, disease_protein with hereditary breast ovarian cancer syndrome, disease_protein with hereditary breast ovarian cancer syndrome, disease_protein with familial ovarian cancer, disease_protein with familial ovarian cancer.", "label": "yes"}
{"original_question": "Are there transposon-free regions in mammalian genomes?", "id": "converted_419", "sentence1": "Are there transposon-free regions in mammalian genomes?", "sentence2": "Transposon-free regions in mammalian genomes., Despite the presence of over 3 million transposons separated on average by approximately 500 bleomycin/cisplatin protocol, the Homo sapiens and Mus sp. genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length. The majority of Homo sapiens TFRs correlate with orthologous TFRs in the Mus sp., despite the fact that most transposons are lineage specific. Many Homo sapiens TFRs also overlap with orthologous TFRs in the marsupial opossum, indicating that these regions have remained refractory to transposon Insert (object) for long evolutionary periods. Over 90% of the Unit dose - Base covered by TFRs are noncoding, much of which is not highly conserved. Most TFRs are not associated with unusual nucleotide composition, but are significantly associated with Genes encoding developmental regulators, suggesting that they represent extended regions of regulatory information that are largely unable to tolerate Clinical act of Insert (object), a conclusion difficult to reconcile with current conceptions of gene regulation., All three elements insert only rarely within many Polycomb-regulated regions, a property that may contribute to the origin of \"transposon-free regions\" (TFRs) in metazoan genomes., Despite the presence of over 3 million transposons separated on average by approximately 500 bleomycin/cisplatin protocol, the Homo sapiens and Mus sp. genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length., RESULTS: Here we report that transposon-free regions (TFRs) are prominent genomic features of Amphibians and fish lineages, and that many have been maintained throughout Vertebrates evolution, although most transposon-derived sequences have entered these lineages after their divergence. , Despite the presence of over 3 million transposons separated on average by approximately 500 bleomycin/cisplatin protocol, the Homo sapiens and Mus sp. genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length. , All three elements insert only rarely within many Polycomb-regulated regions, a property that may contribute to the origin of \"transposon-free regions\" (TFRs) in metazoan genomes. , Despite the presence of over 3 million transposons separated on average by approximately 500 bleomycin/cisplatin protocol, the Homo sapiens and Mus sp. genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length., Here we report that transposon-free regions (TFRs) are prominent genomic features of Amphibians and fish lineages, and that many have been maintained throughout Vertebrates evolution, although most transposon-derived sequences have entered these lineages after their divergence.[SEP]Relations: regulation of establishment of actomyosin contractile ring localization involved in mitotic cell cycle has relations: bioprocess_bioprocess with regulation of mitotic actomyosin contractile ring localization, bioprocess_bioprocess with regulation of mitotic actomyosin contractile ring localization, bioprocess_bioprocess with regulation of establishment of actomyosin contractile ring localization, bioprocess_bioprocess with regulation of establishment of actomyosin contractile ring localization. vertebra has relations: anatomy_anatomy with non-transverse process-bearing vertebra, anatomy_anatomy with non-transverse process-bearing vertebra, anatomy_anatomy with transverse process-bearing vertebra, anatomy_anatomy with transverse process-bearing vertebra, anatomy_anatomy with predorsal vertebra, anatomy_anatomy with predorsal vertebra.", "label": "yes"}
{"original_question": "Can Patient-derived organoids (PDOs) recapitulate patient responses in the clinic?", "id": "converted_3468", "sentence1": "Can Patient-derived Organoids (PDOs) recapitulate patient responses in the clinic?", "sentence2": "Patient-derived Organoids (PDOs) have recently emerged as robust preclinical models; however, their potential to predict clinical outcomes in patients has remained unclear. We report on a living biobank of PDOs from metastatic, heavily pretreated Colorectal and gastroesophageal Primary malignant neoplasm patients recruited in phase 1/2 clinical trials. Phenotypic and genotypic profiling of PDOs showed a high degree of similarity to the original patient tumors. Molecular profiling of tumor Organoids was matched to drug-screening results, suggesting that PDOs could complement existing approaches in defining Primary malignant neoplasm vulnerabilities and improving treatment responses. We compared responses to anticancer agents ex vivo in Organoids and PDO-based orthotopic mouse tumor xenograft models with the responses of the patients in clinical trials. Our data suggest that PDOs can recapitulate patient responses in the clinic and could be implemented in personalized medicine programs., Our data suggest that PDOs can recapitulate patient responses in the clinic and could be implemented in personalized medicine programs., Molecular profiling of tumor Organoids was matched to drug-screening results, suggesting that PDOs could complement existing approaches in defining Primary malignant neoplasm vulnerabilities and improving treatment responses., Phenotypic and genotypic profiling of PDOs showed a high degree of similarity to the original patient tumors., Patient-derived xenografts (Patient Derived Xenograft) and patient-derived Organoids (PDO) serve as promising tools to identify new drugs with therapeutic potential in ANOPHTHALMIA AND PULMONARY HYPOPLASIA., Our data suggest that PDOs can recapitulate patient responses in the clinic and could be implemented in personalized medicine programs, Our data suggest that PDOs can recapitulate patient responses in the clinic and could be implemented in personalized medicine programs, Molecular profiling of tumor Organoids was matched to drug-screening results , suggesting that PDOs could complement existing approaches in defining Primary malignant neoplasm vulnerabilities and improving treatment responses, Our data suggest that PDOs can recapitulate patient responses in the clinic and could be implemented in personalized medicine programs.[SEP]Relations: Pulmonary hypoplasia has relations: disease_phenotype_positive with spondylodysplastic Ehlers-Danlos syndrome, disease_phenotype_positive with spondylodysplastic Ehlers-Danlos syndrome, disease_phenotype_positive with Silverman-Handmaker type dyssegmental dysplasia, disease_phenotype_positive with Silverman-Handmaker type dyssegmental dysplasia, disease_phenotype_positive with congenital multicore myopathy with external ophthalmoplegia, disease_phenotype_positive with congenital multicore myopathy with external ophthalmoplegia, disease_phenotype_positive with fetal akinesia deformation sequence, disease_phenotype_positive with fetal akinesia deformation sequence. Colorectal Primary malignant neoplasm has relations: disease_protein with PDGFD, disease_protein with PDGFD.", "label": "yes"}
{"original_question": "Are there conserved noncoding elements identified between genomes of human and teleosts?", "id": "converted_506", "sentence1": "Are there conserved noncoding elements identified between genomes of Homo sapiens and teleosts?", "sentence2": "We report evidence for a mechanism for the maintenance of long-range conserved synteny across Vertebrates genomes. We found the largest mammal-teleost conserved chromosomal segments to be spanned by highly conserved noncoding elements (HCNEs), their developmental regulatory target Genes, and phylogenetically and functionally unrelated \"bystander\" Genes, After whole genome duplication in teleosts, GRBs, including HCNEs and target Genes, were often maintained in both copies, while bystander Genes were typically lost from one GZMB wt Allele, strongly suggesting that evolutionary pressure acts to keep the single-copy GRBs of higher vertebrates intact. We show that loss of bystander Genes and other mutational events suffered by duplicated GRBs in teleost genomes permits target gene identification and HCNE/target gene assignment, Vertebrate genomes contain thousands of conserved noncoding elements (CNEs) that often function as tissue-specific enhancers. In this study, we have identified CNEs in Homo sapiens, Canis familiaris, chicken allergenic extract allergenic extract, Xenopus laevis laevis, and four teleost Fishes (Zebrafish, Sticklebacks, Oryzias latipes, and Takifugu) using elephant shark, a cartilaginous Vertebrates, as the base genome and investigated the evolution of these ancient Vertebrates CNEs (Abdominal cutaneous nerve entrapment syndrome) in bony Vertebrates lineages, This implicates the \"fish-specific\" whole-genome duplication in the accelerated evolution and the loss of a large number of both copies of duplicated CNEs in teleost Fishes, We found Zebrafish conserved noncoding elements (CNEs) with pan-Vertebrates as well as fish-specific orthologous sequences from across 200 kb of the Zebrafish fgf8a genomic regulatory block to direct reporter expression in patterns consistent with the expression pattern of fgf8a,  A significant number of conserved noncoding elements (CNEs) shared between fish <Chondrichthyes> and tetrapods have diverged beyond recognition in teleost Fishes. The divergence of CNEs seems to have been initiated in basal ray-finned Fishes before the WGD. The fast evolving singleton and duplicated Genes as well as the divergent CNEs might have contributed to the diversity of teleost Fishes, We found the largest mammal-teleost conserved chromosomal segments to be spanned by highly conserved noncoding elements (HCNEs), their developmental regulatory target Genes, and phylogenetically and functionally unrelated \"bystander\" Genes., Ancient Vertebrates conserved noncoding elements have been evolving rapidly in teleost Fishes., A significant number of conserved noncoding elements (CNEs) shared between fish <Chondrichthyes> and tetrapods have diverged beyond recognition in teleost Fishes., We have used a transposon-based transgenic assay in Zebrafish to evaluate noncoding sequences at the Zebrafish ret locus, conserved among teleosts, and at the Homo sapiens RET locus, conserved among Mammals., Using computational analysis and exploiting the diversity of teleost genomes, we identified a cluster of highly conserved noncoding sequences surrounding the SIX3 gene[SEP]Relations: vertebra has relations: anatomy_anatomy with non-transverse process-bearing vertebra, anatomy_anatomy with non-transverse process-bearing vertebra, anatomy_anatomy with vertebral element, anatomy_anatomy with vertebral element. familial acanthosis nigricans has relations: disease_disease with genetic skin disease, disease_disease with genetic skin disease, disease_phenotype_positive with Autosomal dominant inheritance, disease_phenotype_positive with Autosomal dominant inheritance. anterior cutaneous nerve entrapment syndrome has relations: disease_phenotype_positive with Allodynia, disease_phenotype_positive with Allodynia.", "label": "yes"}
{"original_question": "Are adenylyl cyclases always transmembrane proteins?", "id": "converted_1564", "sentence1": "Are adenylyl cyclases always transmembrane proteins?", "sentence2": "ransmembrane adenylyl cyclase,  Transmembrane adenylyl cyclase (tmAC) and soluble AC (spindle assembly checkpoint) , Soluble adenylyl cyclase (spindle assembly checkpoint) is a recently recognized source of the signaling molecule cyclic AMP (cyclophosphamide/doxorubicin/methotrexate/procarbazine protocol) that is genetically and biochemically distinct from the classic G-protein-regulated transmembrane adenylyl cyclases (tmACs)., Soluble adenylyl cyclase , transmembrane adenylyl cyclases (tmACs), and soluble adenylyl cyclase (spindle assembly checkpoint). ,  Here, we showed that both transmembrane AC (tmAC) and soluble AC (spindle assembly checkpoint) are distinctly involved in the regulation of sperm motility in the ascidian Ciona intestinalis. , cyclophosphamide/doxorubicin/methotrexate/procarbazine protocol production in beta cells is mediated not simply by transmembrane adenylyl cyclases (TMACs), but also by spindle assembly checkpoint., In contrast to tmAC, spindle assembly checkpoint produces cyclophosphamide/doxorubicin/methotrexate/procarbazine protocol in various intracellular microdomains close to specific cyclophosphamide/doxorubicin/methotrexate/procarbazine protocol targets, e.g., in Cell Nucleus and Mitochondria, soluble adenylyl cyclase (spindle assembly checkpoint, ADCY10 gene gene), the ubiquitous, non-transmembrane adenylyl cyclase, was found to play a key role in neuronal survival and axon growth., Central role of soluble adenylyl cyclase[SEP]Relations: mitochondrion has relations: cellcomp_protein with ACADS, cellcomp_protein with ACADS, cellcomp_protein with ACSL1, cellcomp_protein with ACSL1, cellcomp_protein with ACADSB, cellcomp_protein with ACADSB, cellcomp_protein with CYRIB, cellcomp_protein with CYRIB, cellcomp_protein with ACACB, cellcomp_protein with ACACB.", "label": "no"}
{"original_question": "Should dacomitinib be used for treatment of glioblastoma patients?", "id": "converted_2903", "sentence1": "Should dacomitinib be used for treatment of glioblastoma patients?", "sentence2": "Expert opinion: Despite the poor global results of dacomitinib in recurrent GB shown in a phase II trial, some patients had a significant benefit. , Conclusions: dacomitinib has a limited single-agent activity in recurrent GB with EGFR amplification., Expert opinion: Despite the poor global results of dacomitinib in recurrent GB shown in a phase II trial, some patients had a significant benefit., Expert opinion: Despite the poor global results of dacomitinib in recurrent GB shown in a phase II trial, some patients had a significant benefit.[SEP]Relations: dacomitinib has relations: drug_drug with Afelimomab, drug_drug with Afelimomab, drug_drug with Glasdegib, drug_drug with Glasdegib, drug_drug with Bortezomib, drug_drug with Bortezomib, drug_drug with Fostamatinib, drug_drug with Fostamatinib, drug_drug with Gliquidone, drug_drug with Gliquidone.", "label": "no"}
{"original_question": "Is Phospholemman a membrane protein?", "id": "converted_4478", "sentence1": "Is Phospholemman a membrane Protein Info?", "sentence2": " the transmembrane lipoprotein phospholemman (FXYD1 gene Genes), Phospholemman (FXYD1 gene Genes) is a single-transmembrane Protein Info regulator of Nadia - zebrafish,K-ATPase, expressed strongly in Chest>Heart, Specimen Source Codes - Skeletal muscle, and Head>Brain and phosphorylated by Protein Info kinases A and C at Ser-68 and Ser-63, respectively., We previously identified FXYD1 gene Genes (encoding phospholemman; a Protein Info containing the motif phenylalanine-X-tyrosine-aspartate), a Genes encoding a transmembrane modulator of the Nadia - zebrafish, K-ATPase (NKA) enzyme,[SEP]Relations: Protein C has relations: drug_drug with Phenprocoumon, drug_drug with Phenprocoumon, drug_drug with Phenylalanine, drug_drug with Phenylalanine, drug_drug with Phenelzine, drug_drug with Phenelzine, drug_drug with Ceftibuten, drug_drug with Ceftibuten, drug_drug with Melagatran, drug_drug with Melagatran.", "label": "yes"}
{"original_question": "Can saponins be used as adjuvant?", "id": "converted_3898", "sentence1": "Can saponins be used as adjuvant?", "sentence2": "We report the design, synthesis, immunological evaluation, and conformational analysis of new Saponinum, Saponinum, saponin, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation variants as promising vaccine adjuvants, The purified active fraction of Albizia julibrissin Saponinum, Saponinum, saponin, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation (AJSAF) is an ideal adjuvant candidate, BALB/c mice immunized with subcutaneous injections of the Recombinant Proteins with or without liposome/Saponinum, Saponinum, saponin, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation (Lip/Sap) as an adjuvant.,  a Saponinum, Saponinum, saponin, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation-based Matrix-M™ adjuvant, . These results confirm that Momordica saponins are a viable natural source to provide potent Saponinum, Saponinum, saponin, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation adjuvants[SEP]Relations: adaptation of signaling pathway by response to pheromone involved in conjugation with cellular fusion has relations: bioprocess_bioprocess with adaptation of signaling pathway, bioprocess_bioprocess with adaptation of signaling pathway, bioprocess_bioprocess with re-entry into mitotic cell cycle after pheromone arrest, bioprocess_bioprocess with re-entry into mitotic cell cycle after pheromone arrest.", "label": "yes"}
{"original_question": "Can adult humans be induced to produce fetal hemoglobin?", "id": "converted_1626", "sentence1": "Can adult humans be induced to produce fetal hemoglobin?", "sentence2": " At the time of birth, Fetal Hemoglobin accounts for approximately 70% of the total Hb. ,  whereas in the trace amounts of Fetal Hemoglobin that is found in the adult it reverses to 40:60 because of a gamma- to beta-globin gene switch, With the increased understanding and discovery of molecular regulators of Hemoglobin switching, such as B-Cell Lymphoma/Leukemia 11A, new avenues of research may lead ultimately to novel therapeutic, mechanism-based approaches to fetal Hemoglobin reactivation in patients., The data suggest that Recombinant Transforming Growth Factor-Beta reactivates A gamma-Globin expression, combined with a sequential stimulation and suppression of erythropoiesis. [SEP]Relations: Abnormal hemoglobin has relations: phenotype_phenotype with Reduced hemoglobin A, phenotype_phenotype with Reduced hemoglobin A, disease_phenotype_positive with Hb Bart's hydrops fetalis, disease_phenotype_positive with Hb Bart's hydrops fetalis, phenotype_phenotype with Methemoglobinemia, phenotype_phenotype with Methemoglobinemia, phenotype_phenotype with Imbalanced hemoglobin synthesis, phenotype_phenotype with Imbalanced hemoglobin synthesis, disease_phenotype_positive with congenital amegakaryocytic thrombocytopenia, disease_phenotype_positive with congenital amegakaryocytic thrombocytopenia.", "label": "yes"}
{"original_question": "Can vitamin B1 deficiency cause encephalopathy?", "id": "converted_478", "sentence1": "Can thiamine deficiency cause Encephalopathies?", "sentence2": "Wernicke's Encephalopathies (WE) is a severe neurological syndrome caused by Thiamine Drug Class (Thiamine Drug Class) deficiency and clinically characterized by the sudden onset of mental status changes, Ocular abnormalities, and Cerebellar Ataxia, Wernicke-Korsakoff Syndrome (or Wernicke-Korsakoff Encephalopathies) is a rarely diagnosed neurological disorder, which is caused by Thiamine Drug Class deficiency, Wernicke's Encephalopathies (WE) is a potentially reversible yet serious neurological manifestation caused by Thiamine Drug Class(Thiamine Drug Class) deficiency, Wernicke-Korsakoff Syndrome is caused by Thiamine Drug Class (Thiamine Drug Class) deficiency, Both the Thyrotoxicosis and a catabolic state due to the Hyperemesis Gravidarum were thought to have induced a Thiamine Drug Class deficiency, causing the Wernicke-Korsakoff Syndrome., Wernicke-Korsakoff Syndrome (or Wernicke-Korsakoff Encephalopathies) is a rarely diagnosed neurological disorder, which is caused by Thiamine Drug Class deficiency., Wernicke-Korsakoff Syndrome is caused by Thiamine Drug Class (Thiamine Drug Class) deficiency., Wernicke's Encephalopathies is a neurological disorder caused by Thiamine Drug Class (Thiamine Drug Class) deficiency characterized by Vertigo <invertebrate>, Cerebellar Ataxia, and mental confusion., Wernicke's Encephalopathies (WE) is caused by Thiamine Drug Class (Thiamine Drug Class) deficiency and most commonly found in individuals with chronic Alcoholic Intoxication, Chronic and Malnutrition., Wernicke's Encephalopathies (WE) is an acute neurological disease resulting from Thiamine Drug Class (Thiamine Drug Class) deficiency., Post-mortem findings demonstrate that Thiamine Drug Class (Thiamine Drug Class) deficiency sufficient to cause irreversible Traumatic AND/OR non-traumatic brain injury is not diagnosed ante mortem in 80-90% of these patients., Wernicke's Encephalopathies is an acute neuropsychiatric disorder, due to Thiamine Drug Class (Thiamine Drug Class) deficiency., Wernicke's Encephalopathies (WE) is a severe neurological syndrome caused by Thiamine Drug Class (Thiamine Drug Class) deficiency and clinically characterized by the sudden onset of mental status changes, Ocular abnormalities, and Cerebellar Ataxia., Wernicke's Encephalopathies, a pathology caused by Thiamine Drug Class (thiamin) deficiency, is often difficult to diagnose and can lead to severe cognitive sequels if left untreated., Wernicke's Encephalopathies-Korsakoff syndrome (WE-KS) is common in alcoholics, caused by Thiamine Drug Class deficiency (diphtheria, tetanus toxoids and acellular pertussis vaccine; Thiamine Drug Class) and associated with Lesion to the Thalamic structure (thalidomide)., Wernicke-Korsakoff Syndrome is caused by Thiamine Drug Class (Thiamine Drug Class) deficiency, Thiamine (Thiamine Drug Class) deficiency, associated with a variety of conditions, including chronic Alcoholic Intoxication, Chronic and bariatric surgery for morbid obesity, can result in the neurological disorder Wernicke&apos;s Encephalopathies (WE), Wernicke's Encephalopathies is caused by Thiamine Deficiency and can be recognized by severe neurological symptoms that are occasionally accompanied by systemic signs. , INTRODUCTION: Wernicke's Encephalopathies, a pathology caused by Thiamine Drug Class (thiamin) deficiency, is often difficult to diagnose and can lead to severe cognitive sequels if left untreated. , OBSERVATION: We report a case of Encephalopathies due to dual Ascorbic Acid Deficiency of both Thiamine Drug Class (vitamin B1) and niacin (niacinamide) in an 80-year-old women, hospitalized for severe Sepsis (Invertebrate) caused by aspiration Pneumonia. , Acute Wernicke's Encephalopathies (WE) is caused by profound Thiamine Drug Class (Thiamine Drug Class) deficiency and commonly presents with the classic clinical triad of mental confusion, Cerebellar Ataxia, and ophthalmoplegia. , [Wernicke´s Encephalopathies and Polyneuropathy associated with vitamin B complex deficiency after a bariatric surgery]., BACKGROUND: Thiamine deficiency in patients who abuse alcohol can cause Wernicke's Encephalopathies (WE). , Wernicke-Korsakoff Syndrome--a debilitating acute or subacute neurological disorder-is caused by a deficiency in Thiamine Drug Class (vitamin B(1)). , Wernicke's Encephalopathies is a serious neurological manifestation of Thiamine Drug Class deficiency., Both the Thyrotoxicosis and a catabolic state due to the Hyperemesis Gravidarum were thought to have induced a Thiamine Drug Class deficiency, causing the Wernicke-Korsakoff Syndrome., Wernicke-Korsakoff Syndrome is caused by Thiamine Drug Class (Thiamine Drug Class) deficiency., Wernicke-Korsakoff Syndrome (or Wernicke-Korsakoff Encephalopathies) is a rarely diagnosed neurological disorder, which is caused by Thiamine Drug Class deficiency., Wernicke's Encephalopathies is a neurological disorder caused by Thiamine Drug Class (Thiamine Drug Class) deficiency characterized by Vertigo <invertebrate>,, Post-mortem findings demonstrate that Thiamine Drug Class (Thiamine Drug Class) deficiency sufficient to cause irreversible Traumatic AND/OR non-traumatic brain injury is not diagnosed ante mortem in 80-90% of these patients. The causes of Ascorbic Acid Deficiency are reviewed with special attention to the inhibition of oral Thiamine Drug Class hydrochloride absorption in Homo sapiens caused by Malnutrition present in alcoholic patients or by the direct effects of ethanol on intestinal transport., Wernicke's Encephalopathies is a serious nervous system disorder caused by vitamin-B1 or Thiamine Drug Class deficiency., Wernicke's Encephalopathies results from Thiamine Drug Class (Thiamine Drug Class) deficiency. Common causes include Alcoholic Intoxication, Chronic and gastric disorders., Wernicke's Encephalopathies is a neurological disorder caused by Thiamine Drug Class (Thiamine Drug Class) deficiency characterized by Vertigo <invertebrate>, Cerebellar Ataxia, and mental confusion., Wernicke's Encephalopathies (WE) is caused by Thiamine Drug Class (Thiamine Drug Class) deficiency and most commonly found in individuals with chronic Alcoholic Intoxication, Chronic and Malnutrition., Post-mortem findings demonstrate that Thiamine Drug Class (Thiamine Drug Class) deficiency sufficient to cause irreversible Traumatic AND/OR non-traumatic brain injury is not diagnosed ante mortem in 80-90% of these patients., Wernicke's Encephalopathies, a pathology caused by Thiamine Drug Class (thiamin) deficiency, is often difficult to diagnose and can lead to severe cognitive sequels if left untreated.[SEP]Relations: Encephalopathy has relations: disease_phenotype_positive with mitochondrial complex I deficiency, disease_phenotype_positive with mitochondrial complex I deficiency, disease_phenotype_positive with aminoacylase 1 deficiency, disease_phenotype_positive with aminoacylase 1 deficiency, disease_phenotype_positive with mitochondrial complex 5 (ATP synthase) deficiency nuclear, disease_phenotype_positive with mitochondrial complex 5 (ATP synthase) deficiency nuclear, disease_phenotype_positive with mitochondrial complex V (ATP synthase) deficiency, nuclear, disease_phenotype_positive with mitochondrial complex V (ATP synthase) deficiency, nuclear, disease_phenotype_positive with cardioencephalomyopathy, fatal infantile, due to cytochrome c oxidase deficiency, disease_phenotype_positive with cardioencephalomyopathy, fatal infantile, due to cytochrome c oxidase deficiency.", "label": "yes"}
{"original_question": "Is Melioidosis caused by the bacterium Burkholderia pseudomallei?", "id": "converted_2063", "sentence1": "Is Melioidosis caused by the bacterium Pseudomonas pseudomallei antibody?", "sentence2": "Pseudomonas pseudomallei antibody, the causative agent of Melioidosis,, What drives the occurrence of the Melioidosis bacterium Pseudomonas pseudomallei antibody in domestic gardens?, Landscape changes influence the occurrence of the Melioidosis bacterium Pseudomonas pseudomallei antibody in soil in northern Australia., Out of the ground: aerial and exotic habitats of the Melioidosis bacterium Pseudomonas pseudomallei antibody in grasses in Australia., Melioidosis, caused by the gram-negative bacterium Pseudomonas pseudomallei antibody, is a common cause of community-acquired Sepsis (Invertebrate) in Southeast Asia and Northern Australia., Melioidosis is a suppurative chronic Communicable Diseases caused by a gramnegative bacterium, Pseudomonas pseudomallei antibody., Melioidosis is an Communicable Diseases caused by the gram-negative bacterium Pseudomonas pseudomallei antibody., Melioidosis is an infectious Disease caused by a saprophytic bacterium, Pseudomonas pseudomallei antibody., Melioidosis is an infectious Disease caused by the Gram-negative bacterium Pseudomonas pseudomallei antibody., Melioidosis is a pyogenic Communicable Diseases with high mortality caused by the bacterium Pseudomonas pseudomallei antibody., Melioidosis is a tropical infectious Disease caused by the gram-negative bacterium Pseudomonas pseudomallei antibody., Melioidosis is a potentially fatal Disease caused by the bacterium Pseudomonas pseudomallei antibody., Melioidosis is a rare tropical Disease caused by Communicable Diseases with the bacterium Pseudomonas pseudomallei antibody., The mechanisms involved in the pathogenesis of Melioidosis, caused by the Protoplasm bacterium Pseudomonas pseudomallei antibody, are unclear., Melioidosis is an emerging tropical Communicable Diseases caused by the Protoplasm bacterium Pseudomonas pseudomallei antibody, and is associated with high mortality rates., Melioidosis is an increasingly recognised cause of Sepsis (Invertebrate) and Cessation of life across South East Asia and Northern Australia, caused by the bacterium Pseudomonas pseudomallei antibody, Melioidosis, an Communicable Diseases caused by the gram-negative bacterium Pseudomonas pseudomallei antibody, is an important cause of Pneumonia, skin Communicable Diseases, Sepsis (Invertebrate), and Cessation of life in Southeast Asia and Australia, but is exceedingly rare in North America, The Gram-negative bacterium Pseudomonas pseudomallei antibody is able to survive and replicate within Specimen Source Codes - Leukocytes and causes Melioidosis, an important cause of Pneumonia-derived community-acquired Sepsis (Invertebrate) in Southeast Asia, Melioidosis, a lethal tropical Communicable Diseases that is endemic in southeast Asia and northern Australia, is caused by the saprophytic Gram-negative bacterium Pseudomonas pseudomallei antibody, Melioidosis is an emerging infectious Disease caused by the soil bacterium Pseudomonas pseudomallei antibody, Melioidosis is a tropical Disease of high mortality caused by the environmental bacterium, Pseudomonas pseudomallei antibody, Melioidosis is an infectious Disease caused by Pseudomonas pseudomallei antibody, a bacterium endemic in Southeast Asia and northern Australia, Melioidosis is a life-threatening Communicable Diseases caused by the Gram-negative bacterium Pseudomonas pseudomallei antibody, mainly found in Southeast Asia, Melioidosis, caused by the Gram-negative bacterium Pseudomonas pseudomallei antibody, is a dreadful Disease common in South-East Asia and Northern Australia and is characterized by chronic suppurative lesions and Pneumonia, Melioidosis is caused by the environmental bacterium Pseudomonas pseudomallei antibody and can present with severe Sepsis (Invertebrate), Melioidosis is an emerging infectious Disease of Homo sapiens and animal allergen extracts in the tropics caused by the soil bacterium Pseudomonas pseudomallei antibody. , Melioidosis is a potentially fatal Disease caused by the bacterium Pseudomonas pseudomallei antibody. , Melioidosis, Communicable Diseases caused by the Gram-negative bacterium Pseudomonas pseudomallei antibody, is a common cause of Sepsis (Invertebrate) in northeast Thailand. , Melioidosis is a potentially fatal Disease caused by the bacterium, Pseudomonas pseudomallei antibody. , BACKGROUND: The soil-dwelling saprophyte bacterium Pseudomonas pseudomallei antibody is the cause of Melioidosis, a severe Disease of Homo sapiens and animal allergen extracts in southeast Asia and northern Australia. , Melioidosis is an endemic Disease caused by the bacterium Pseudomonas pseudomallei antibody. , Melioidosis is a severe Communicable Diseases caused by the gram-negative bacterium, Pseudomonas pseudomallei antibody, that is endemic in Southeast Asia. , Melioidosis, Communicable Diseases caused by the Gram-negative bacterium Pseudomonas pseudomallei antibody, is a common cause of Sepsis (Invertebrate) in northeast Thailand., Melioidosis is a clinically diverse Disease caused by the facultative Protoplasm Gram-negative bacterium, Pseudomonas pseudomallei antibody., Melioidosis is caused by the environmental bacterium Pseudomonas pseudomallei antibody and can present with severe Sepsis (Invertebrate)., Melioidosis is a severe Communicable Diseases caused by the gram-negative bacterium, Pseudomonas pseudomallei antibody, that is endemic in Southeast Asia., Melioidosis, a lethal tropical Communicable Diseases that is endemic in southeast Asia and northern Australia, is caused by the saprophytic Gram-negative bacterium Pseudomonas pseudomallei antibody., Melioidosis, a severe human Disease caused by the bacterium Pseudomonas pseudomallei antibody, has a wide spectrum of clinical manifestations ranging from acute septicemia to chronic localized illness or latent Communicable Diseases., Melioidosis, an often fatal infectious Disease in Northeast Thailand, is caused by skin inoculation, inhalation or ingestion of the environmental bacterium, Pseudomonas pseudomallei antibody., Melioidosis is an Communicable Diseases caused by Gram-negative bacterium, Pseudomonas pseudomallei antibody., Melioidosis, caused by the Gram-negative bacterium Pseudomonas pseudomallei antibody, is a dreadful Disease common in South-East Asia and Northern Australia and is characterized by chronic suppurative lesions and Pneumonia., Largely due to its recognition as a biological threat agent, current knowledge on Melioidosis, caused by the Gram-negative bacterium Pseudomonas pseudomallei antibody, has increased tremendously over the last years., Melioidosis is an endemic Disease caused by the bacterium Pseudomonas pseudomallei antibody., Melioidosis is a potentially fatal Disease caused by the bacterium Pseudomonas pseudomallei antibody., Melioidosis is a potentially fatal Disease caused by the bacterium, Pseudomonas pseudomallei antibody., Melioidosis is a Disease of Homo sapiens and animal allergen extracts that is caused by the saprophytic bacterium Pseudomonas pseudomallei antibody., Melioidosis is an emerging infectious Disease of Homo sapiens and animal allergen extracts in the tropics caused by the soil bacterium Pseudomonas pseudomallei antibody., The soil-dwelling saprophyte bacterium Pseudomonas pseudomallei antibody is the cause of Melioidosis, a severe Disease of Homo sapiens and animal allergen extracts in southeast Asia and northern Australia., Melioidosis is an often fatal infectious Disease affecting Homo sapiens and animal allergen extracts in tropical regions and is caused by the saprophytic environmental bacterium Pseudomonas pseudomallei antibody., We have recently shown that during Melioidosis, a severe Communicable Diseases caused by the gram-negative bacterium Pseudomonas pseudomallei antibody, TLR2 wt Allele wt Allele but not TLR4 wt Allele wt Allele impacts the immune response of the intact host in vivo., It is caused by the bacterium Pseudomonas pseudomallei antibody, which can infect many Organ of the body, including the Head>Brain, and results in neurological symptoms., Melioidosis is a frequent cause of severe Sepsis (Invertebrate) in Southeast Asia caused by the gram-negative bacterium Pseudomonas pseudomallei antibody., What drives the occurrence of the Melioidosis bacterium Pseudomonas pseudomallei antibody in domestic gardens?, The Gram-negative bacterium Pseudomonas pseudomallei antibody is the causative agent of melioidosi, The environmental bacterium Pseudomonas pseudomallei antibody causes the infectious Disease Melioidosis with a high case-fatality rate in tropical and subtropical regions., Pseudomonas pseudomallei antibody is a soil-dwelling bacterium and the cause of Melioidosis, Melioidosis, an infectious Disease caused by the Gram-negative bacterium Pseudomonas pseudomallei antibody,, Melioidosis is a frequently fatal infectious Disease caused by the soil dwelling Gram-negative bacterium Pseudomonas pseudomallei antibody. , Pseudomonas pseudomallei antibody, an environmental bacterium that causes the deadly Disease Melioidosis, , Melioidosis is an important public health problem in Southeast Asia and Northern Australia. This Disease is caused by the gram-negative bacilli, Pseudomonas pseudomallei antibody, Melioidosis, caused by Pseudomonas pseudomallei antibody, is an important cause of community-acquired Sepsis (Invertebrate) in Southeast-Asi, Melioidosis is a potentially fatal Disease caused by the saprophytic bacterium Pseudomonas pseudomallei antibody, Melioidosis is a Disease of Homo sapiens caused by opportunistic Communicable Diseases with the soil and water bacterium Pseudomonas pseudomallei antibody.[SEP]Relations: Melioidosis has relations: disease_disease with burkholderia infectious Disease, disease_disease with burkholderia infectious Disease, disease_disease with primary bacterial infectious Disease, disease_disease with primary bacterial infectious Disease, disease_phenotype_positive with Bacteremia, disease_phenotype_positive with Bacteremia, disease_phenotype_positive with Pneumonia, disease_phenotype_positive with Pneumonia. Pneumonia has relations: disease_phenotype_positive with Melioidosis, disease_phenotype_positive with Melioidosis.", "label": "yes"}
{"original_question": "Does Panitumumab prolong survival of biliary tract cancer patients?", "id": "converted_2889", "sentence1": "Does Panitumumab prolong survival of biliary tract cancer patients?", "sentence2": "Panitumumab in combination with gemcitabine and oxaliplatin does not prolong survival in wild-type Human Oncogene K-Ras advanced biliary tract cancer: A randomized phase 2 trial (Vecti-BIL study)., CONCLUSIONS: Panitumumab in combination with chemotherapy does not improve ORR, PFS and OS in patients with Human Oncogene K-Ras wild-type, advanced Biliary Tract Cancer. , No survival differences were observed: the median overall survival was 9.9 months in arm A and 10.2 months in arm B (P = .42). In a subgroup analysis, no differences in PFS according to the site of the primary tumor were observed; patients with Primary cholangiocarcinoma of intrahepatic biliary tract treated with panitumumab may have had a survival benefit in comparison with the control group (15.1 vs 11.8 months, P = .13). , CONCLUSIONS\nPanitumumab in combination with chemotherapy does not improve ORR, PFS and OS in patients with Human Oncogene K-Ras wild-type, advanced Biliary Tract Cancer., CONCLUSIONS Panitumumab in combination with chemotherapy does not improve ORR, PFS and OS in patients with Human Oncogene K-Ras wild-type, advanced Biliary Tract Cancer., Despite many clinical trials being conducted with molecular targeted agents including erlotinib, cetuximab, panitumumab, bevacizumab, sorafenib, cediranib, trametinib and vandetanib, no agent has shown to be effective for advanced biliary tract cancer., Adding panitumumab to standard protocols does not prolong survival but provokes additional adverse effects.[SEP]Relations: biliary tract cancer has relations: disease_disease with liver cancer, disease_disease with liver cancer, disease_protein with PRKACB, disease_protein with PRKACB, disease_disease with bile duct cancer, disease_disease with bile duct cancer. Panitumumab has relations: drug_drug with Bimagrumab, drug_drug with Bimagrumab, drug_drug with Afelimomab, drug_drug with Afelimomab.", "label": "no"}
{"original_question": "Can PLN mutations lead to dilated cardiomyopathy?", "id": "converted_771", "sentence1": "Can PLN gene mutations lead to dilated Cardiomyopathies?", "sentence2": "A PLN gene gene founder Mutation Abnormality (43 cases) and LMNA mutations (19 cases, 16 different mutations) were most prevalent and often demonstrated a specific phenotype., PLN gene gene Mutation Abnormality R14del was identified in 12 (12 %) Arrhythmogenic Right Ventricular Dysplasia patients and in 39 (15 %) 3',5'-dichloromethotrexate patients, The PLN gene gene R14del founder Mutation Abnormality is present in a substantial number of patients clinically diagnosed with 3',5'-dichloromethotrexate or Arrhythmogenic Right Ventricular Dysplasia, Arg(9) → Cys (R9C) and Arg(14) Gene Deletion Abnormality (R14del) mutations in PLN gene gene are associated with lethal dilated Cardiomyopathies in Homo sapiens, We previously reported the Gene Deletion Abnormality of the highly conserved Amino Acid [EPC] residue arginine 14 (Nucleic Acids 39, 40 and 41) in 3',5'-dichloromethotrexate patients., Gene Mutation in the gene encoding PLN gene gene have been associated with idiopathic dilated Cardiomyopathies;, Gene Mutation in the PLN gene gene gene are a rare cause of Congestive Congestive heart failure, present almost exclusively in patients with dilated Cardiomyopathies etiology, A missense Mutation Abnormality in PLN gene gene cytoplasmic domain (R9C) triggers dilated Cardiomyopathies in Homo sapiens, leading to Mortality, Premature., Complete Genetic and clinical analyses were performed in a family with familial dilated Cardiomyopathies due to the PLN gene gene-R14Del Mutation Abnormality., A candidate gene approach resulted in identification of a heterozygous Gene Deletion Abnormality of arginine 14 in the gene encoding phospholamban (PLN gene gene-R14Del) segregating with dilated Cardiomyopathies in the family pedigree. Mutation carriers suffered from familial dilated Cardiomyopathies associated with Cardiac Death between the ages of 26 and 50 years., a family with familial dilated Cardiomyopathies due to the PLN gene gene-R14Del Mutation Abnormality., For the phospholamban (PLN gene gene) and titin cap (TTN protein, human protein, human) Genes, a direct Mutation Abnormality screening approach was used. DNA sequence analysis of all Exons showed no evidence that these Genes are involved in 3',5'-dichloromethotrexate in the Newfoundland dog., two human PLN gene gene mutations, associated with either absence or sustained dephosphorylation of PLN gene gene, were linked to dilated Cardiomyopathies., Gene Mutation in the gene encoding PLN gene gene have been associated with dilated Cardiomyopathies characterized by early onset and the presence of lethal Ventricular arrhythmia., The identical PLN gene gene Mutation Abnormality can be associated with both mild and severe forms of dilated Cardiomyopathies. Additionally, PLN gene gene mutations should be considered in late onset Cardiomyopathies, Through Genetic screening of dilated Cardiomyopathies patients, we identified a previously uncharacterized Gene Deletion Abnormality of arginine 14 (PLN gene gene-R14Del) in the coding region of the phospholamban (PLN gene gene) gene in a large family with hereditary Congestive Congestive heart failure., No PLN gene gene gene Mutation Abnormality was found in patients with 3',5'-dichloromethotrexate in Chengdu. This result indicated that PLN gene gene gene Mutation Abnormality may not be a common cause for 3',5'-dichloromethotrexate in the Chinese population in Chengdu., none in PLN gene gene, the recent discoveries of human PLN gene gene mutations leading to disease states., Strikingly, both individuals homozygous for L39stop developed dilated Cardiomyopathies and Congestive Congestive heart failure, requiring cardiac transplantation at ages 16 and 27., Homo sapiens lacking PLN gene gene develop lethal dilated Cardiomyopathies., Here we report that an inherited human dilated Cardiomyopathies with refractory congestive Congestive Congestive heart failure is caused by a dominant Arg --> Cys missense Mutation Abnormality at residue 9 (R9C) in phospholamban (PLN gene gene)[SEP]Relations: dilated Cardiomyopathies has relations: disease_protein with PLN gene, disease_protein with PLN gene, disease_protein with MYPN, disease_protein with MYPN, disease_protein with TTN protein, human, disease_protein with TTN protein, human, disease_protein with LMNA, disease_protein with LMNA. familial dilated Cardiomyopathies has relations: disease_protein with PLN gene, disease_protein with PLN gene.", "label": "yes"}
{"original_question": "Are stress granules membraneous?", "id": "converted_2549", "sentence1": "Are Stress Granules membraneous?", "sentence2": "PMLOs are different in size, shape, and composition, and almost invariantly contain intrinsically disordered Proteins (e.g., eIF-4B and TARDBP wt Allele in Stress Granules,, Liquid-liquid phase separation (LLPS) of RNA-binding Proteins plays an important role in the formation of multiple Membrane Device-less Organelles involved in RNA metabolism, including Stress Granules., Stress granules (SG) are Membrane Device-less compartments involved in regulating mRNAs during stress.,  In addition to Membrane Device delimited Organelles, Proteins and RNA can organize themselves into specific domains. Some examples include Stress Granules and subnuclear bodies. [SEP]Relations: stress granule assembly has relations: bioprocess_protein with PUM2, bioprocess_protein with PUM2, bioprocess_protein with EIF2S1, bioprocess_protein with EIF2S1, bioprocess_bioprocess with organelle assembly, bioprocess_bioprocess with organelle assembly, bioprocess_protein with LSM14A, bioprocess_protein with LSM14A, bioprocess_protein with MAPT, bioprocess_protein with MAPT.", "label": "no"}
{"original_question": "Has dupilumab been FDA approved for atopic dermatitis?", "id": "converted_4169", "sentence1": "Has dupilumab been FDA approved for Dermatitis, Atopic?", "sentence2": "Recent advances and understanding of the pathogenesis of cytarabine/daunorubicin protocol have resulted in new therapies that target specific pathways with increased efficacy and the potential for less systemic side effects. New FDA-approved therapies for cytarabine/daunorubicin protocol are crisaborole and dupilumab. , In March of 2017, the United States Food and Drug Administration (FDA) approved dupilumab for the treatment of moderate-to-severe Dermatitis, Atopic in adults that is uncontrolled with topical medications, becoming the first biologic agent approved to treat this chronic skin condition., dupilumab is the first US FDA approved biologic for treatment of Dermatitis, Atopic., dupilumab is the first biological treatment approved for moderate-to-severe Dermatitis, Atopic (cytarabine/daunorubicin protocol).[SEP]Relations: dupilumab has relations: drug_drug with Tarextumab, drug_drug with Tarextumab, drug_drug with Dusigitumab, drug_drug with Dusigitumab, drug_drug with Afelimomab, drug_drug with Afelimomab, drug_drug with IGN311, drug_drug with IGN311, drug_drug with Opicinumab, drug_drug with Opicinumab.", "label": "yes"}
{"original_question": "Do angiotensin-converting-enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) increase the likelihood of severe COVID-19?", "id": "converted_4514", "sentence1": "Do angiotensin-converting-enzyme (ACE) inhibitors and Angiotensin Receptor Antagonists (ARBs) increase the likelihood of severe COVID19 (document)?", "sentence2": "These findings suggest that the use of ACE-I and BESTROPHINOPATHY, AUTOSOMAL RECESSIVE is not associated with adverse outcomes and may be associated with improved outcomes in COVID19 (document), which is immediately relevant to care of the many patients on these medications., There are theoretical concerns that Peptidyl-Dipeptidase A inhibitors (ACEIs) and Angiotensin Receptor Antagonists (ARBs) could increase the risk of severe Covid-19., ACEIs and ARBs were associated with a slight reduction in Covid-19 hospitalization risk compared with treatment with other first-line antihypertensives (OR for ACEIs 0.95, 95% CI 0.92-0.98; OR for ARBs 0.94, 95% CI 0.90-0.97)., There were no meaningful differences in risk for ACEIs compared with ARBs., ACEIs and ARBs were not associated with an increased risk of Covid-19 hospitalization or with hospitalization involving ICU admission, invasive mechanical ventilation, or Cessation of life., In patients with HTN and COVID19 (document), neither ACEi nor ARBs were independently associated with mortality., Our data confirm Specialty Societal recommendations, suggesting that treatment with ACEIs or ARBs should not be discontinued because of COVID19 (document)., Random-effects meta-analysis showed ACEI/BESTROPHINOPATHY, AUTOSOMAL RECESSIVE treatment was significantly associated with a lower risk of mortality in Hypertensive (finding) COVID19 (document) patients (odds ratio [OR] = 0.624, 95% confidence interval [CI] = 0.457-0.852, p = .003, I2  = 74.3%)., In addition, the ACEI/BESTROPHINOPATHY, AUTOSOMAL RECESSIVE treatment was associated with a lower risk of ventilatory support (OR = 0.682, 95% CI = 0.475-1.978, p = .037, I2  = 0.0%). In conclusion, these results suggest that ACEI/BESTROPHINOPATHY, AUTOSOMAL RECESSIVE medications should not be discontinued for Hypertensive (finding) patients in the context of COVID19 (document) pandemic., Use of ACE-I or BESTROPHINOPATHY, AUTOSOMAL RECESSIVE medications was not associated with increased risk of hospitalization, intensive care unit admission, or Cessation of life. Compared to patients with charted past medical history, there was a lower risk of hospitalization for patients on ACE-I (odds ratio (OR) 0.43; 95% confidence interval (CI) 0.19-0.97; P = 0.0426) and BESTROPHINOPATHY, AUTOSOMAL RECESSIVE (OR 0.39; 95% CI 0.17-0.90; P = 0.0270)., The second analysis showed that the use of ACEI and/or BESTROPHINOPATHY, AUTOSOMAL RECESSIVE did not affect in-hospital mortality (risk ratio [RR] 95% [CI]] = 0.88 [0.64-1.20], p = 0.42). The subgroup analysis by limiting studies of patients with Hypertensive Disease showed ACEI and/or BESTROPHINOPATHY, AUTOSOMAL RECESSIVE use was associated with a significant reduction of in-hospital mortality compared with no ACEI or BESTROPHINOPATHY, AUTOSOMAL RECESSIVE use (RR [CI] = 0.66 [0.49-0.89], p = 0.004). Our analysis demonstrated that ACEI and/or BESTROPHINOPATHY, AUTOSOMAL RECESSIVE use was associated neither with testing positive rates of COVID19 (document) nor with mortality of COVID19 (document) patients., ACEIs/ARBs are protective factors against mortality in COVID19 (document) patients with HTN, and these agents can be considered potential therapeutic options in this Disease., There has been a lot of speculation that patients with coronavirus Disease 2019 (COVID19 (document)) who are receiving Peptidyl-Dipeptidase A (ACE) inhibitors or Angiotensin Receptor Antagonists (ARBs) may be at increased risk for adverse outcomes., Although further research on the influence of blood-pressure-lowering drugs, including those not targeting the renin-angiotensin system, is warranted, there are presently no compelling clinical data showing that ACEIs and ARBs increase the likelihood of contracting COVID19 (document) or worsen the outcome of SARS-CoV‑2 infections, There has been a lot of speculation that patients with coronavirus Disease 2019 (COVID19 (document)) who are receiving Peptidyl-Dipeptidase A (ACE) inhibitors or Angiotensin Receptor Antagonists (ARBs) may be at increased risk for adverse outcomes, ACEIs and ARBs do not promote a more severe outcome of COVID19 (document)., Meta-analysis showed no significant increase in the risk of COVID19 (document) infection (odds ratio [OR]: 0.95, 95%CI: 0.89-1.05) in patients receiving ACEI/BESTROPHINOPATHY, AUTOSOMAL RECESSIVE therapy, and ACEI/BESTROPHINOPATHY, AUTOSOMAL RECESSIVE therapy was associated with a decreased risk of severe COVID19 (document) (OR: 0.75, 95%CI: 0.59-0.96) and mortality (OR: 0.52, 95%CI: 0.35-0.79)., Subgroup analyses showed among the general population, ACEI/BESTROPHINOPATHY, AUTOSOMAL RECESSIVE therapy was associated with reduced severe COVID19 (document) infection (OR: 0.79, 95%CI: 0.60-1.05) and all-cause mortality (OR: 0.31, 95%CI: 0.13-0.75), and COVID19 (document) infection (OR: 0.85, 95% CI: 0.66-1.08) were not increased., On the basis of the available evidence, ACEI/BESTROPHINOPATHY, AUTOSOMAL RECESSIVE therapy should be continued in patients who are at risk for, or have COVID19 (document), either in general population or Hypertensive Disease patients., Some studies of hospitalized patients suggested that the risk of Cessation of life and/or severe Illness (finding) due to COVID19 (document) is not associated with the use of Peptidyl-Dipeptidase A inhibitors (ACEIs) and/or Angiotensin II Type 2 Receptor Blockers (ARBs), Available evidence, in particular, data from human studies, does not support the hypothesis that ACEI/BESTROPHINOPATHY, AUTOSOMAL RECESSIVE use increases ACE2 protein, human protein, human expression and the risk of complications from COVID19 (document). We conclude that patients being treated with ACEIs and ARBs should continue their use for approved indications.[SEP]Relations: type 2 angiotensin receptor binding has relations: molfunc_protein with AGT, molfunc_protein with AGT. Protein S human has relations: drug_drug with Anti-inhibitor coagulant complex, drug_drug with Anti-inhibitor coagulant complex, drug_drug with Ardeparin, drug_drug with Ardeparin, drug_drug with Peginterferon alfa-2b, drug_drug with Peginterferon alfa-2b, drug_drug with Coagulation Factor IX (Recombinant), drug_drug with Coagulation Factor IX (Recombinant).", "label": "no"}
{"original_question": "Is the zelda transcription factor a chromatin remodeller?", "id": "converted_4210", "sentence1": "Is the zelda TRANSCRIPTION FACTOR a chromatin location remodeller?", "sentence2": "ncreasing the number of Zelda Binding Sites accelerates the kinetics of nuclei transcriptional activation regardless of their transcriptional past, Zelda facilitates transcriptional activation by accumulating in microenvironments where it could accelerate the duration of multiple pre-initiation steps., Zelda acts through specific chromatin location location patterns of histone modification to mark developmental enhancers and active promoters, Zelda overcomes the high intrinsic nucleosome barrier at enhancers during Drosophila <basidiomycetes> <basidiomycetes> zygotic Genome - anatomical entity activation., The Drosophila <basidiomycetes> <basidiomycetes> Genome - anatomical entity activator Vielfaltig (Vfl), also known as Zelda (Zld), is thought to prime enhancers for activation by patterning transcription factors (TFs). Such priming is accompanied by increased chromatin location location accessibility, early enhancers are characterized by an intrinsically high nucleosome barrier. Zld tackles this nucleosome barrier through local depletion of Nucleosomes with the effect being dependent on the number and Positioning Attribute of Zld motifs., Zelda is differentially required for chromatin location location accessibility, TRANSCRIPTION FACTOR binding, and gene expression in the early Drosophila <basidiomycetes> <basidiomycetes> embryo, Open chromatin location location is associated with Zelda-bound loci, as well as more generally with regions of active transcriptio, During this developmental transition, the zygotic Genome - anatomical entity is largely transcriptionally quiescent and undergoes significant chromatin location location remodeling. In Drosophila <basidiomycetes> <basidiomycetes>, the DNA-binding protein Zelda (also known as Vielfaltig) is required for this transition and for transcriptional activation of the zygotic Genome - anatomical entity., Zld facilitates binding of Dl to regulatory DNA, and that this is associated with increased chromatin location location accessibility., Importantly, the change in chromatin location location accessibility is strongly correlated with the change in Zld binding, Zelda is differentially required for chromatin location location accessibility, TRANSCRIPTION FACTOR binding, and gene expression in the early Drosophila <basidiomycetes> <basidiomycetes> embryo., We propose that both Zelda and GAGA factor function to specify Site of open chromatin location location and together facilitate the remodeling of the early embryonic Genome - anatomical entity., is analysis highlighted a strong and specific enrichment of predicted ZGA-associated CRMs for Zelda, 1-Chloro-3-bromopropene-1, Trl Binding Sites, as well as for histone marks associated with active enhancers (Histone H3 Methyl Lys4) and for open chromatin location location regions.AQP1 gene, We demonstrate that Zelda is essential for hundreds of regions of open chromatin location location., Intriguingly, some Zelda Site still maintain these chromatin location location patterns in Drosophila <basidiomycetes> <basidiomycetes> embryos lacking maternal Zelda protein., Zelda potentiates morphogen activity by increasing chromatin location location accessibility., Zelda binds cis-regulatory elements (TAGteam heptamers), making chromatin location location accessible for gene transcription., zinc-finger TF zelda (zld) is essential for the maternal-to-zygotic transition (MZT) in Drosophila <basidiomycetes> <basidiomycetes> melanogaster, where it directly binds over thousand cis-regulatory modules to regulate chromatin location location accessibility. D. mela, This Zelda-mediated chromatin location location accessibility facilitates transcription-factor recruitment and early gene expression., While analyzing chromatin location location immunoprecipitation data sets from 21 sequence-specific transcription factors active in the Drosophila <basidiomycetes> <basidiomycetes> embryo, we found that binding of all factors exhibits a dose-dependent relationship with \"TAGteam\" sequence motifs bound by the zinc finger protein Vielfaltig, also known as Zelda, a recently discovered activator of the zygotic Genome - anatomical entity., These different timing classes each associate with Binding Sites for two transcription factors, GAGA-factor and Zelda, previously implicated in controlling chromatin location location accessibility at ZGA., Together this reveals a distinct requirement for a chromatin location location remodeller in promoting the activity of the pioneer factor POU5F1 gene and regulating the pluripotency network., Chromatin accessibility at POU5F1 gene-bound Site requires the chromatin location location remodeller SMARCA4 wt Allele, which is recruited to these Site by POU5F1 gene to support additional TRANSCRIPTION FACTOR binding and expression of the pluripotency-associated transcriptome., The pioneer factor POU5F1 gene requires the chromatin location location remodeller SMARCA4 wt Allele to support gene Regulatory Sequences, Nucleic Acid function in Mouse Embryonic Stem Cells., Pioneer transcription factors recognise and bind their target sequences in inaccessible chromatin location location to establish new transcriptional networks throughout development and cellular reprogramming., During this process, pioneer factors establish an accessible chromatin location location state to facilitate additional TRANSCRIPTION FACTOR binding, yet it remains unclear how different pioneer factors achieve this., Here, we discover that the pluripotency-associated pioneer factor POU5F1 gene binds chromatin location location to shape accessibility, TRANSCRIPTION FACTOR co-binding, and Regulatory Sequences, Nucleic Acid function in Mouse Embryonic Stem Cells., Open chromatin location location is associated with Zelda-bound loci, as well as more generally with regions of active transcription., Unexpectedly, chromatin location location at a large subset of Zelda-bound regions remains open even in the absence of Zelda., During this developmental transition, the zygotic Genome - anatomical entity is largely transcriptionally quiescent and undergoes significant chromatin location location remodeling., Here we used formaldehyde-assisted isolation of regulatory elements to determine the role of Zelda in regulating regions of open chromatin location location in the early embryo., Pioneer transcription factors can engage nucleosomal DNA, which leads to local chromatin location location remodeling and to the establishment of transcriptional competence., Recently, we showed that Zelda acts through specific chromatin location location patterns of histone modification to mark developmental enhancers and active promoters., The zinc-finger TF zelda (zld) is essential for the maternal-to-zygotic transition (MZT) in Drosophila <basidiomycetes> <basidiomycetes> melanogaster, where it directly binds over thousand cis-regulatory modules to regulate chromatin location location accessibility., Nonetheless, the extent to which Zelda influences chromatin location location accessibility across the Genome - anatomical entity is largely unknown., We present evidence that Zld facilitates binding of Dl to regulatory DNA, and that this is associated with increased chromatin location location accessibility., DNAJC2 gene facilitates the remodeling of Multiprotein Complexes at chromatin location location and lies at the Chest>Heart of signaling processes that occur at DNA damage Site and during transcriptional activation., We postulate that DNAJC2 gene operates in conjunction with cellular remodeling machines and suggest that on-site remodeling might be a hallmark of many chromatin location location-associated signaling pathways., Reconstituted transcription reactions established that the BRAHMA (BRM) chromatin location location-remodeling complex is essential for Zeste-directed activation on nucleosomal templates.[SEP]Relations: TRANSCRIPTION FACTOR binding has relations: molfunc_protein with RARA, molfunc_protein with RARA, molfunc_protein with ZFPM2, molfunc_protein with ZFPM2, molfunc_protein with RORA, molfunc_protein with RORA, molfunc_protein with CENPF, molfunc_protein with CENPF, molfunc_protein with RNF19A, molfunc_protein with RNF19A.", "label": "yes"}
{"original_question": "The LINCS L1000 data set contains gene expression data for drug treated human cells, yes or no?", "id": "converted_3349", "sentence1": "The LINCS L1000 data set contains gene expression data for drug treated Human cells, yes or no?", "sentence2": " Library of Integrated Network-based Cellular Signatures (LINCS) L1000 dataset that measured changes in Gerbich blood group system before and after treatment of Human cells with over 20 000 small-molecule compounds including most of the FDA-approved drugs., The Library of Integrated Network-based Cellular Signatures (LINCS) L1000 big data provide gene expression profiles induced by over 10 000 compounds, shRNAs, and kinase inhibitors using the L1000 platform., The Library of Integrated Cellular Signatures (LINCS) project provides comprehensive transcriptome profiling of Human Cell Line before and after Chemicals and genetic perturbations.,  Recently, resources such as the Library of Integrated Network-Based Cellular Signatures (LINCS) L1000 database provide gene expression profiles induced by various Chemicals and genetic perturbations, The library of integrated network-based cellular signatures (LINCS) L1000 data set currently comprises of over a million gene expression profiles of chemically perturbed Human Cell Line., The LINCS L1000 data repository contains almost two million gene expression profiles for thousands of small molecules and drugs., The Gerbich blood group system data is from the Library of Integrated Network-based Cellular Signatures (LINCS) L1000 dataset that measured changes in Gerbich blood group system before and after treatment of Human cells with over 20 000 small-molecule compounds including most of the FDA-approved drugs.[SEP]Relations: AV node cell to bundle of His cell signaling has relations: bioprocess_protein with CACNA1G, bioprocess_protein with CACNA1G, bioprocess_bioprocess with cell-cell signaling involved in cardiac conduction, bioprocess_bioprocess with cell-cell signaling involved in cardiac conduction, bioprocess_bioprocess with AV node cell to bundle of His cell communication, bioprocess_bioprocess with AV node cell to bundle of His cell communication. blood group, lewis system has relations: disease_disease with Mendelian disease, disease_disease with Mendelian disease.", "label": "yes"}
{"original_question": "Are ultraconserved elements depleted among copy number variants (CNVs)?", "id": "converted_1655", "sentence1": "Are ultraconserved elements depleted among copy number variants (CNVs)?", "sentence2": "We have demonstrated that nonexonic UCEs are depleted among segmental duplications (SDs) and copy number variants (CNVs) and proposed that their ultraconservation may reflect a mechanism of copy counting via comparison. Here, we report that nonexonic UCEs are also depleted among 10 of 11 recent genomewide data sets of human CNVs, including 3 obtained with strategies permitting greater precision in determining the extents of CNVs, Interestingly, human UCEs have been reported to be strongly depleted among segmental duplications and benign copy number variants (CNVs), We propose that these elements may be interpreted as hallmarks for dose-sensitive Genes, particularly for those Genes whose gain or loss may be directly implied in Neurodevelopmental Disorders. Therefore, their presence in genomic imbalances of unknown effect might be suggestive of a clinically relevant condition, Mammalian ultraconserved elements are strongly depleted among segmental duplications and copy number variants., Ultraconserved elements (UCEs) are strongly depleted from segmental duplications and copy number variations (CNVs) in the human genome, suggesting that Gene Deletion Abnormality or duplication of a NAGPA gene can be deleterious to the Mammalian Cell., Interestingly, human UCEs have been reported to be strongly depleted among segmental duplications and benign copy number variants (CNVs)., We have demonstrated that nonexonic UCEs are depleted among segmental duplications (SDs) and copy number variants (CNVs) and proposed that their ultraconservation may reflect a mechanism of copy counting via comparison., We have demonstrated that nonexonic UCEs are depleted among segmental duplications (SDs) and copy number variants (CNVs) and proposed that their ultraconservation may reflect a mechanism of copy counting via comparison, Interestingly, human UCEs have been reported to be strongly depleted among segmental duplications and benign copy number variants (CNVs), Here, we show that UCEs are significantly depleted among segmental duplications and copy number variants, The depletion of UCEs among copy number variation as well as the significant under-representation of single-nucleotide polymorphisms (Single Nucleotide Polymorphism) within UCEs have also revealed their evolutional and functional importance indicating their potential impact on disease, such as Primary malignant neoplasm[SEP]Relations: Abnormality of the dentition has relations: disease_phenotype_positive with chromosome 6pter-p24 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 6pter-p24 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 4q21 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 4q21 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 3q29 microduplication syndrome, disease_phenotype_positive with chromosome 3q29 microduplication syndrome, disease_phenotype_positive with chromosome 15q24 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 15q24 Gene Deletion Abnormality syndrome. mammalian vulva has relations: anatomy_protein_absent with RNU4-78P, anatomy_protein_absent with RNU4-78P.", "label": "yes"}
{"original_question": "Is cabergoline used for treatment of the Nelson's syndrome ?", "id": "converted_3936", "sentence1": "Is cabergoline used for treatment of the Nelson Syndrome ?", "sentence2": "Due to a rapid regrowth of the Neoplasms, the patient did not receive gamma-knife therapy and was treated with cabergoline and Somatostatin Assay analogue for some time. , Identification of D(2) receptors in corticotroph tumors led to clinical trials of cabergoline therapy in limited cases of Nelson Syndrome, ectopic ACTH-secreting tumors, and recently Pituitary-dependent Pituitary-dependent Cushing's disease (CD).,  In our observation cabergoline at 2 mg per week seems to be efficient after a 3 and a half years follow-up, in accordance with some recent publications. , Clinical and biochemical stabilization of Nelson Syndrome with long-term Low-Dose Treatment cabergoline treatment., We report the results of long-term (6-year) treatment of Nelson Syndrome with the long-acting dopamine Agonist, cabergoline, in a 55-year-old woman., This case demonstrates that long-term cabergoline treatment may be efficient in patients with Nelson Syndrome., Therefore, in addition to Prolactinoma, targets of dopamine Agonist therapy are somatotroph tumors, nonfunctioning Pituitary Neoplasms, corticotroph Pituitary Neoplasms, Nelson Syndrome, gonadotropinomas, and thyrotropin-secreting Pituitary Neoplasms., Nelson Syndrome: complete remission with cabergoline but not with bromocriptine or cyproheptadine treatment., The results obtained show for the first time that a long-term treatment with cabergoline also brings about a complete remission of Nelson Syndrome in the presence of a Pituitary macroadenoma., Complete remission of Nelson Syndrome after 1-year treatment with cabergoline., In this case report we demonstrated that treatment with the long-acting D2 receptor Agonist cabergoline for 1 year induced normalization of plasma ACTH levels and disappearance of the pituitary tumor in a patient with Nelson Syndrome. , This case demonstrated that cabergoline treatment is able to induce the remission of Nelson Syndrome and may be a valid therapeutic alternative in this syndrome., However, some preliminary data suggest a potential use of cabergoline in combination with ketoconazole, or alone, in selected cases of Pituitary-dependent Pituitary-dependent Cushing's disease or Nelson Syndrome., We report the results of long-term (6-year) treatment of Nelson Syndrome with the long-acting dopamine Agonist, cabergoline, in a 55-year-old woman. The, actinomas. Identification of D(2) receptors in corticotroph tumors led to clinical trials of cabergoline therapy in limited cases of Nelson Syndrome, ectopic ACTH-secreting tumors, and recently Cushing's diseas, In order to investigate on the direct effect played by cabergoline treatment on the remission of Nelson Syndrome, the treatment was withdrawn., lactinomas. Identification of D(2) receptors in corticotroph tumors led to clinical trials of cabergoline therapy in limited cases of Nelson Syndrome, ectopic ACTH-secreting tumors, and recently Pituitary-dependent Pituitary-dependent Cushing's disease (CD).OBJECTIVE: To evaluate the long-term efficacy of cabergoline monotherapy in patients with CD.METHODS: Retrospective analysis of non-randomized clinical therapy with cabergoline in 30 patients with CD treated in academic cente[SEP]Relations: Cabergoline has relations: drug_drug with Norepinephrine, drug_drug with Norepinephrine, drug_drug with Antipyrine, drug_drug with Antipyrine, contraindication with gallbladder disease, contraindication with gallbladder disease, drug_effect with Headache, drug_effect with Headache, drug_effect with Vertigo, drug_effect with Vertigo.", "label": "yes"}
{"original_question": "Is Prochlorococcus the most abundant photosynthetic organism?", "id": "converted_2207", "sentence1": "Is Prochlorococcus the most abundant photosynthetic organism?", "sentence2": "The Marines cyanobacterium Prochlorococcus is the smallest and most abundant photosynthetic organism on Earth., The Marines cyanobacterium Prochlorococcus is the numerically dominant photosynthetic organism in the oligotrophic oceans, and a model system in Marines microbial ecology., The Marines cyanobacterium Prochlorococcus is the most abundant photosynthetic organism in oligotrophic regions of the oceans., The oceanic picoplankton Prochlorococcus - probably the most abundant photosynthetic organism on our planet - can grow at great depths where light intensity is very low.[SEP]", "label": "yes"}
{"original_question": "Is miR-126 involved in heart failure?", "id": "converted_908", "sentence1": "Is miR-126 involved in Congestive heart failure?", "sentence2": "he MicroRNAs miR-126 and miR-508-5p are associated with the outcome of between breakfast and lunch and NICM patients with CHF. These two MicroRNAs could be useful in the diagnosis of CHF patients, and might provide novel targets for prevention and treatment of CHF., The plasma concentration of miR-126 was negatively correlated with age and NYHA class, and could be a useful biomarker for Congestive Congestive heart failure., In 10 patients with Congestive Congestive heart failure, plasma concentrations of miR-126 were up-regulated with improvement of the NYHA class from IV to III.[SEP]Relations: Congestive Congestive heart failure has relations: drug_effect with Rimantadine, drug_effect with Rimantadine, drug_effect with Metoprolol, drug_effect with Metoprolol, drug_effect with Bisoprolol, drug_effect with Bisoprolol, drug_effect with Ibutilide, drug_effect with Ibutilide, drug_effect with Iopromide, drug_effect with Iopromide.", "label": "yes"}
{"original_question": "Can ferric carboxymaltose be used to treat anemia in inflammatory bowel disease patients?", "id": "converted_1219", "sentence1": "Can ferric carboxymaltose be used to treat Genus Anemia in INFLAMMATORY BOWEL DISEASE 2 patients?", "sentence2": "Intravenous Ferrum metallicum, Homeopathic preparation should be preferred where oral Ferrum metallicum, Homeopathic preparation is poorly tolerated or where it has failed in moderate to severe Genus Anemia, and in combination with Recombinant Erythropoietin, ferric carboxymaltose is much more convenient, and has been shown to be more effective than Ferrum metallicum, Homeopathic preparation sucrose in a large randomized tria, Nemia and Ferrum metallicum, Homeopathic preparation deficiency Genus Anemia are very common in INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome, ferric carboxymaltose was associated with cost savings of 30-44 % per patient per treatment cycle compared to Ferrum metallicum, Homeopathic preparation sucrose. , Iron deficiency is common in pregnancy, postpartum, INFLAMMATORY BOWEL DISEASE 2, chronic kidney disease, Chronic heart failure, heavy uterine bleeding, Primary malignant neoplasm and following surgery. We estimate the budget impact (BI) on the Swiss mandatory health insurance associated with substituting Ferrum metallicum, Homeopathic preparation sucrose (standard) with ferric carboxymaltose (new treatment) using real-life data., reating Ferrum metallicum, Homeopathic preparation deficiency involves substantial costs to the Swiss MHI which may be reduced by substituting Ferrum metallicum, Homeopathic preparation sucrose with ferric carboxymaltose., e aim of this study was to observe, in a non-interventional way, how Swedish gastroenterologists adhere to guidelines in Irritable Bowel Syndrome outpatients treated with intravenous ferric carboxymaltose (MYOCLONUS, FAMILIAL CORTICAL), and the result of treatment, MYOCLONUS, FAMILIAL CORTICAL lowers platelet counts and platelet activation in patients with Irritable Bowel Syndrome-associated Reactive thrombocytosis., We performed a randomized, single-blinded placebo-controlled trial testing the effect of ferric carboxymaltose (MYOCLONUS, FAMILIAL CORTICAL) in patients with Irritable Bowel Syndrome with Reactive thrombocytosis (Blood Platelets > 450 G/L), e performed a randomized, placebo-controlled trial to determine if administration of ferric carboxymaltose (MYOCLONUS, FAMILIAL CORTICAL) prevents Genus Anemia in patients with Irritable Bowel Syndrome and low levels of Serum ferritin measurement, MYOCLONUS, FAMILIAL CORTICAL prevents recurrence of Genus Anemia in patients with Irritable Bowel Syndrome, compared with placebo. ,  A subgroup was analyzed regarding efficacy and side effects of Ferrum metallicum, Homeopathic preparation supplementation with ferric carboxymaltose., Iron deficiency and Genus Anemia are frequent in Irritable Bowel Syndrome patients. Treatment with ferric carboxymaltose is efficious, safe and well tolerated in Ferrum metallicum, Homeopathic preparation-deficient Irritable Bowel Syndrome patients.,  Intravenous Ferrum metallicum, Homeopathic preparation avoids these concerns, especially with the development of ferric carboxymaltose, which allow up to 1000mg to be given rapidly., What is the optimal treatment for Genus Anemia in INFLAMMATORY BOWEL DISEASE 2?, We compared the efficacy and safety of a novel fixed-dose ferric carboxymaltose regimen (MYOCLONUS, FAMILIAL CORTICAL) with individually calculated Ferrum metallicum, Homeopathic preparation sucrose (IS) doses in patients with INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome) and Inosine Dialdehyde, Study drugs were well tolerated and drug-related adverse events were in line with drug-specific clinical experience,  The simpler MYOCLONUS, FAMILIAL CORTICAL-based dosing regimen showed better efficacy and compliance, as well as a good safety profile, compared with the Ganzoni-calculated IS dose regimen., ferric carboxymaltose can be rapidly administered in doses of 15 mg/kg body weight, up to a ceiling dose of 1000 mg. A test dose is not required, and it can be used more widely across a spectrum of Ferrum metallicum, Homeopathic preparation deficiency and Ferrum metallicum, Homeopathic preparation deficiency Genus Anemia indication,  Intravenous Ferrum metallicum, Homeopathic preparation offers a rapid means of Ferrum metallicum, Homeopathic preparation repletion and is superior to oral Ferrum metallicum, Homeopathic preparation in many circumstances, especially in the presence of Genus Anemia of Chronic disease, where it appears to overcome the block to absorption of Ferrum metallicum, Homeopathic preparation from the Abdomen+Pelvis>Gastrointestinal tract and immobilization of stored Ferrum metallicum, Homeopathic preparation. The clinical situations where high doses of Ferrum metallicum, Homeopathic preparation are commonly required are reviewed. These include nondialysis-dependent chronic kidney disease, INFLAMMATORY BOWEL DISEASE 2, obstetrics, Menorrhagia, and Genus Anemia associated with Primary malignant neoplasm and its treatment. , ferric carboxymaltose can be administered at 15 mg/kg body weight to a maximum dose of 1000 mg, whereas Ferrum metallicum, Homeopathic preparation isomaltoside 1000 can be administered at 20 mg/kg body weight. The ability to give high doses of Ferrum metallicum, Homeopathic preparation is important in the context of managing Ferrum metallicum, Homeopathic preparation deficiency Genus Anemia in a number of clinical conditions where demands for Ferrum metallicum, Homeopathic preparation are high (including chronic blood loss associated with INFLAMMATORY BOWEL DISEASE 2, Menorrhagia, and chronic kidney disease), erric carboxymaltose (MYOCLONUS, FAMILIAL CORTICAL, Ferinject) was effective and well tolerated in the treatment of Ferrum metallicum, Homeopathic preparation-deficiency Genus Anemia (Inosine Dialdehyde) in nine, Phase III, randomized, controlled, multicenter trials in a diverse range of indications, including patients with INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome), post-partum Genus Anemia (phenylpropanolamine) or Abnormal uterine bleeding (AUB), Chronic heart failure (Congestive heart failure), non-dialysis-dependent chronic kidney disease (Chronic Kidney Diseases) and those undergoing hemodialysis (Hodgkin Disease, In patients with Irritable Bowel Syndrome or phenylpropanolamine, improvements in Hemoglobin levels were more rapid with MYOCLONUS, FAMILIAL CORTICAL than with FeSulf. , Caudomedial auditory cortex improved patient quality of life to an equivalent extent to oral FeSulf in patients with Irritable Bowel Syndrome or phenylpropanolamine, and to a greater extent than oral FeSulf in women with AUB, Four different products are principally used in clinical practice, which differ in their pharmacokinetic properties and safety profiles: Ferrum metallicum, Homeopathic preparation gluconate and Ferrum metallicum, Homeopathic preparation sucrose (lower single doses), and Ferrum metallicum, Homeopathic preparation dextran and ferric carboxymaltose (higher single doses)., he prevalence of Genus Anemia across studies on patients with INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome) is high (30%).,  novel intravenous Ferrum metallicum, Homeopathic preparation formulation for treatment of Genus Anemia in INFLAMMATORY BOWEL DISEASE 2: the ferric carboxymaltose (FERINJECT) randomized controlled trial., FeCarb is effective and safe in Irritable Bowel Syndrome-associated Genus Anemia. It is noninferior to FeSulf in terms of Hemoglobin change over 12 wk, and provides a fast Hemoglobin increase and a sufficient refill of Ferrum metallicum, Homeopathic preparation stores., Treatment-related adverse events (Scanning Auger Spectrometer (device)) occurred in 28.5% of the FeCarb and 22.2% of the FeSulf groups, with discontinuation of study medication due to Scanning Auger Spectrometer (device) in 1.5% and 7.9%, respectively., The median Hemoglobin improved from 8.7 to 12.3 g/dL in the FeCarb group and from 9.1 to 12.1 g/dL in the FeSulf group, demonstrating noninferiority (P= 0.6967). , ferric carboxymaltose prevents recurrence of Genus Anemia in patients with INFLAMMATORY BOWEL DISEASE 2., ferric carboxymaltose (MYOCLONUS, FAMILIAL CORTICAL, Ferinject) was effective and well tolerated in the treatment of Ferrum metallicum, Homeopathic preparation-deficiency Genus Anemia (Inosine Dialdehyde) in nine, Phase III, randomized, controlled, multicenter trials in a diverse range of indications, including patients with INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome), post-partum Genus Anemia (phenylpropanolamine) or Abnormal uterine bleeding (AUB), Chronic heart failure (Congestive heart failure), non-dialysis-dependent chronic kidney disease (Chronic Kidney Diseases) and those undergoing hemodialysis (Hodgkin Disease)., ferric carboxymaltose (MYOCLONUS, FAMILIAL CORTICAL, Ferinject) was effective and well tolerated in the treatment of Ferrum metallicum, Homeopathic preparation-deficiency Genus Anemia (Inosine Dialdehyde) in nine, Phase III, randomized, controlled, multicenter trials in a diverse range of indications, including patients with INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome), post-partum Genus Anemia (phenylpropanolamine) or Abnormal uterine bleeding (AUB), Chronic heart failure (Congestive heart failure), non-dialysis-dependent chronic kidney disease (Chronic Kidney Diseases) and those undergoing hemodialysis (Hodgkin Disease)[SEP]Relations: ferric carboxymaltose has relations: drug_drug with Ofloxacin, drug_drug with Ofloxacin, drug_drug with Fleroxacin, drug_drug with Fleroxacin, drug_drug with Ferric pyrophosphate citrate, drug_drug with Ferric pyrophosphate citrate, drug_drug with Ferric pyrophosphate, drug_drug with Ferric pyrophosphate, drug_drug with Enoxacin, drug_drug with Enoxacin.", "label": "yes"}
{"original_question": "Is Lysozyme abundant in human tears?", "id": "converted_4261", "sentence1": "Is muramidase abundant in human tears?", "sentence2": "LYZL2 gene present in the natural tear, muramidase (LYZL2 gene C, human) is a naturally occurring Enzyme [APC] that operates against Gram-positive bacteria and leads to cell death. This antimicrobial Enzyme [APC] forms the part of the innate defense system of nearly all animal allergen extracts and exists in their somatic discharges such as milk, tears, Specimen Source Codes - Saliva and urine., tear LYZL2 gene, LYZL2 gene in tears, Specimen Source Codes - Saliva, Specimen Source Codes - Sweat, and other body fluids, , In this study we quantify LYZL2 gene, the most prevalent Protein Info in tear fluid, , muramidase (LYZ wt Allele) is a natural anti-bacterial Protein Info that is found in the Specimen Source Codes - Saliva, tears and milk of all Mammals including Homo sapiens. [SEP]Relations: Protein C has relations: drug_drug with Factor IX Complex (Human), drug_drug with Factor IX Complex (Human), drug_drug with Factor XIII (human), drug_drug with Factor XIII (human), drug_drug with Antihemophilic factor human, drug_drug with Antihemophilic factor human, drug_drug with Von Willebrand Factor Human, drug_drug with Von Willebrand Factor Human, drug_drug with Chlorotrianisene, drug_drug with Chlorotrianisene.", "label": "yes"}
{"original_question": "Is Lysyl oxidase crosslinking collagen?", "id": "converted_2665", "sentence1": "Is LOX gene crosslinking collagen?", "sentence2": "LOX protein, human gene (LOX protein, human protein, human) and LOX protein, human protein, human-like (LOXL) proteins play crucial roles in MMRN1 wt Allele remodeling due to their collagen crosslinking and intracellular functions. , LOX protein, human gene-like 1, a crosslinking Enzyme [APC] implicated in collagen and elastin biogenesis, LOXL2 gene gene mediates collagen crosslinking, The same was true for assaying Protein-Lysine 6-Oxidase, an Enzyme [APC] involved in crosslinking of matrix molecules.,  In addition, collagen fibers in metastatic Lung Neoplasms exhibit greater linearity and organization as a result of collagen crosslinking by the Protein-Lysine 6-Oxidase (LOX protein, human protein, human) family of ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS. [SEP]Relations: protein-lysine 6-oxidase activity has relations: molfunc_protein with LOXL2 gene, molfunc_protein with LOXL2 gene, molfunc_protein with LOXL4, molfunc_protein with LOXL4, molfunc_protein with LOXL1, molfunc_protein with LOXL1, molfunc_protein with LOX protein, human, molfunc_protein with LOX protein, human, molfunc_protein with LOXL3, molfunc_protein with LOXL3.", "label": "yes"}
{"original_question": "Is tocilizumab a tumor necrosis factor inhibitor?", "id": "converted_3768", "sentence1": "Is tocilizumab a tumor necrosis factor inhibitor?", "sentence2": "For the first-line bDMARD/tsDMARD, either Tumor Necrosis Factor Inhibitors (TNFi), non-TNFi (abatacept, tocilizumab, rituximab), or tsDMARDs, may be considered.[SEP]Relations: Tocilizumab has relations: drug_drug with Necitumumab, drug_drug with Necitumumab, drug_drug with Nemolizumab, drug_drug with Nemolizumab, drug_drug with Cemiplimab, drug_drug with Cemiplimab, drug_drug with Tositumomab, drug_drug with Tositumomab, drug_drug with Otelixizumab, drug_drug with Otelixizumab.", "label": "no"}
{"original_question": "Can whole genome sequencing be used for diagnosis of mitochondrial disease?", "id": "converted_4708", "sentence1": "Can whole genome sequencing be used for diagnosis of mitochondrial disease?", "sentence2": "Whole genome sequencing is a useful diagnostic test in patients with suspected Mitochondrial Diseases, yielding a diagnosis in a further 31% after exclusion of common causes. Most diagnoses were non-Mitochondrial Diseases and included developmental disorders with Intellectual Disability, epileptic encephalopathies, other Metabolic Diseases, Cardiomyopathies, and leukodystrophies. These would have been missed if a targeted approach was taken, and some have specific treatments.[SEP]Relations: mitochondrial disease has relations: disease_disease with inborn mitochondrial metabolism disorder, disease_disease with inborn mitochondrial metabolism disorder, disease_disease with disease of membrane bound organelle, disease_disease with disease of membrane bound organelle. metabolic disease has relations: disease_disease with DNA repair disease, disease_disease with DNA repair disease. Intellectual disability has relations: disease_phenotype_positive with multiple mitochondrial dysfunctions syndrome, disease_phenotype_positive with multiple mitochondrial dysfunctions syndrome, disease_phenotype_positive with HSD10 mitochondrial disease, disease_phenotype_positive with HSD10 mitochondrial disease.", "label": "yes"}
{"original_question": "Does splicing occur co-transcriptionally?", "id": "converted_1055", "sentence1": "Does splicing occur co-transcriptionally?", "sentence2": "Researchers working in multiple model Organism - notably Saccharomyces cerevisiae, insect allergenic extract and mammalian Cells - have shown that RNA, Messenger Precursor can be spliced during the process of transcription (i.e. co-transcriptionally), as well as after transcription termination (i.e. post-transcriptionally), The consensus view, based on four Organism, is that the majority of splicing events take place co-transcriptionally in most Cells and Body tissue., Deep sequencing of subcellular RNA fractions shows splicing to be predominantly co-transcriptional, We show that in the human genome, splicing occurs predominantly during transcription., Consistent with co-transcriptional spliceosome assembly and splicing, we have found significant enrichment of spliceosomal snRNAs in Chromatin-Associated RNA compared with other cellular RNA fractions and other nonspliceosomal snRNAs. , The majority of Introns in higher Eukaryota are excised prior to RNA Transcript release in a manner that is dependent on transcription through pol II, s a result of co-transcriptional splicing, variations in pol II elongation influence alternative splicing patterns, wherein a slower elongation rate is associated with increased inclusion of alternative Exons within mature RNA, Messenger. , We show that the pattern of intronic sequence read coverage is explained by nascent transcription in combination with co-transcriptional splicing, Modelling reveals co-transcriptional splicing to be the most probable and most efficient splicing pathway for the reporter transcripts, due in part to a positive feedback mechanism for co-transcriptional second step splicing, RNA processing events that take place on the transcribed RNA, Messenger Precursor include capping, splicing, editing, 3' processing, and polyadenylation. Most of these processes occur co-transcriptionally while the RNA Polymerase II (Pol II) Enzyme [APC] is engaged in transcriptional elongation, Abundant evidence indicates that splicing to excise Introns occurs co-transcriptionally, prior to release of the nascent RNA Transcript from RNAP II, Together, our work establishes a system for co-transcriptional splicing in vitro, in which the spliceosome containing the 5' and 3' Exons are tethered to RNAP II for splicing., Co-transcriptional splicing of constitutive and alternative Exons, Current evidence supports co-transcriptional spliceosomal assembly, but there is little quantitative information on how much splicing is completed during RNA synthesis, Thus, we demonstrate that the decision to include or skip an alternative exon is made during transcription and not post-transcriptionally, Here, we demonstrated that the co-transcriptional splicing of the intron in vitro was blocked by Antisense Oligonucleotides (AONs) targeting the P3-P7 core of the intron, RNA Editing and alternative splicing: the importance of co-transcriptional coordination, Co-transcriptional splicing of pre-messenger RNAs: considerations for the mechanism of alternative splicing, The realization that splicing occurs co-transcriptionally requires two important considerations[SEP]Relations: rRNA transcription has relations: bioprocess_bioprocess with plastid rRNA transcription, bioprocess_bioprocess with plastid rRNA transcription, bioprocess_protein with SPIN1, bioprocess_protein with SPIN1, bioprocess_protein with SIRT7, bioprocess_protein with SIRT7, bioprocess_protein with ANG, bioprocess_protein with ANG, bioprocess_protein with TP53, bioprocess_protein with TP53.", "label": "yes"}
{"original_question": "Is sacituzumab govitecan effective for breast cancer?", "id": "converted_4469", "sentence1": "Is sacituzumab govitecan effective for breast cancer?", "sentence2": "sacituzumab Govitecan (also known by the brand name Trodelvy®) is a new and available treatment for metastatic Triple-Negative Breast Carcinoma, or mTNBC for short. , sacituzumab govitecan (sacituzumab govitecan-hziy; Trodelvy™) is a TACSTD2 protein, Homo sapiens-directed immunoglobulin complex location conjugated to a topoisomerase I PPP1R1A gene (SN 38) that is being developed by Immunomedics for the treatment of solid tumours, including breast cancer., Results from a phase I/II trial suggest that an Antibody-Drug Conjugates, sacituzumab govitecan, is active against refractory, metastatic Triple-Negative Breast Carcinoma. A, INTRODUCTION: sacituzumab govitecan-hziy, approved in 2020 for treatment of metastatic Triple-Negative Breast Carcinoma, provides a new option for a population with a historically poor prognosis with standard , sacituzumab govitecan (SG), the first Antibody-Drug Conjugates (ADC) approved for Triple-Negative Breast Carcinoma, incorporates the anti-TROP2 immunoglobulin complex location hRS7 conjugated to a topoisomerase-1 (TOP1 protein, human protein, Homo sapiens) PPP1R1A gene payload. We so, sacituzumab govitecan was initially approved in April 2020 under accelerated approval for the treatment of patients with metastatic Triple-Negative Breast Carcinoma who received at least two prior therapies for metastatic disease, The ASCENT trial reports impressive results with a median overall survival (OS) increased from 6.7 months to 12.1 months with sacituzumab govitecan over single-agent chemotherapy, in metastatic triple negative breast cancer (TNBC) patients in second and subsequent line of therapy. We , A phase II study indicates that sacituzumab govitecan (IMMU-132), a TACSTD2 protein, Homo sapiens-specific immunoglobulin complex location linked to the irinotecan metabolite SN 38, prolongs the progression-free survival of patients with advanced Triple-Negative Breast Carcinoma. I, agents, sacituzumab govitecan, has been recently granted an accelerated approval for therapy of metastatic Triple-Negative Breast Carcinoma. In this artic, l 2020, sacituzumab govitecan received accelerated approval in the USA for the treatment of adult patients with metastatic Triple-Negative Breast Carcinoma (mTNBC) who have received at least two prior therapies for metastatic disease. Sacituzu, sacituzumab Govitecan for Metastatic Triple-Negative Breast Cancer: Clinical Overview and Management of Potential Toxic effect., ood and Drug Administration) recently approved the use of a Trop2-targeting ADC (Antibody-Drug Conjugates), sacituzumab Govitecan (IMMU-132), for metastatic, Triple-Negative Breast Carcinoma with at least two prior therapies. Here, we review, sive disease. sacituzumab govitecan represents an important advance in the treatment of mTNBC because of its efficacy an, sacituzumab govitecan (SG) is a novel Antibody-Drug Conjugates (ADC) that has shown promising efficacy in mTNBC, The activity of sacituzumab govitecan likely extends beyond TNBC with promising early efficacy data in many other epithelial Malignant Neoplasms, including hormone receptor-positive breast cancer., In a basket design phase I/II study, sacituzumab govitecan demonstrated promising single-agent therapeutic activity in multiple cancer cohorts, leading to accelerated approval by the U.S. Food and Drug Administration of sacituzumab govitecan-hziy (Trodelvy) for the treatment of patients with metastatic Triple-Negative Breast Carcinoma who had received at least two prior therapies in the metastatic setting., Efficacy and Safety of Anti-TACSTD2 protein, Homo sapiens Antibody Drug Conjugate sacituzumab Govitecan (IMMU-132) in Heavily Pretreated Patients With Metastatic Triple-Negative Breast Cancer., Expert opinion: sacituzumab govitecan has promising anti-cancer activity in patients with metastatic TNBC previously treated with at least two prior lines of systemic therapy based on a single arm Phase I/II clinical trial., sacituzumab govitecan has shown promise in Malignant Neoplasms outside of TNBC, such as urothelial and Chest>Lung and is being evaluated in HR-positive Malignant neoplasm of breast.,  prognosis. sacituzumab govitecan is an Antibody-Drug Conjugates composed of an immunoglobulin complex location targeting the Homo sapiens trophoblast cell-surface antigen 2 (TACSTD2 protein, Homo sapiens), which is expressed in the majority of Malignant neoplasm of breast, coupled to SN 38 (topoisomerase I PPP1R1A gene) through a proprietary hydrolyzable linker.METHODS: In this randomized, phase 3 trial, we evaluated sacituzumab govitecan as compared with single-agent chemotherapy of the physician's choice (eribulin, vinorelbine, capecitabine, or gemcitabine) in patients with relapsed or refractory metastatic triple-ne, Expert opinion sacituzumab govitecan has promising survival benefits in patients with previously treated mTNBC based on data from the ASCENT trial., Conclusion sacituzumab govitecan was well tolerated and induced early and durable responses in heavily pretreated patients with metastatic TNBC., sacituzumab Govitecan in Metastatic Triple-Negative Breast Cancer., sacituzumab Govitecan (also known by the brand name Trodelvy®) is a new and available treatment for metastatic Triple-Negative Breast Carcinoma, or mTNBC for short.[SEP]Relations: sacituzumab govitecan has relations: drug_drug with Cemiplimab, drug_drug with Cemiplimab, drug_drug with Cetuximab, drug_drug with Cetuximab, drug_drug with Sonepcizumab, drug_drug with Sonepcizumab, drug_drug with Caplacizumab, drug_drug with Caplacizumab, drug_drug with Necitumumab, drug_drug with Necitumumab.", "label": "yes"}
{"original_question": "Is there evidence for de novo genesis of enhancers in vertebrates?", "id": "converted_1278", "sentence1": "Is there evidence for de novo genesis of enhancers in Vertebrates?", "sentence2": "De novo genesis of enhancers in Vertebrates., Evolutionary innovation relies partially on changes in gene regulation. While a growing body of evidence demonstrates that such innovation is generated by functional changes or translocation of regulatory elements via mobile genetic elements, the de novo generation of enhancers from non-regulatory/non-mobile sequences has, to our knowledge, not previously been demonstrated. Here we show evidence for the de novo genesis of enhancers in Vertebrates. For this, we took advantage of the massive gene loss following the last whole genome duplication in teleosts to systematically identify regions that have lost their coding capacity but retain sequence conservation with Mammals. We found that these regions show enhancer activity while the orthologous coding regions have no regulatory activity. These results demonstrate that these enhancers have been de novo generated in Fluorescent in Situ Hybridization. By revealing that minor changes in non-regulatory sequences are sufficient to generate new enhancers, our study highlights an important playground for creating new regulatory variability and evolutionary innovation., Here we show evidence for the de novo genesis of enhancers in Vertebrates., While a growing body of evidence demonstrates that such innovation is generated by functional changes or translocation of regulatory elements via mobile genetic elements, the de novo generation of enhancers from non-regulatory/non-mobile sequences has, to our knowledge, not previously been demonstrated., While a growing body of evidence demonstrates that such innovation is generated by functional changes or translocation of regulatory elements via mobile genetic elements, the de novo generation of enhancers from non-regulatory/non-mobile sequences has, to our knowledge, not previously been demonstrated, While a growing body of evidence demonstrates that such innovation is generated by functional changes or translocation of regulatory elements via mobile genetic elements, the de novo generation of enhancers from non-regulatory/non-mobile sequences has, to our knowledge, not previously been demonstrated. Here we show evidence for the de novo genesis of enhancers in Vertebrates. For this, we took advantage of the massive gene loss following the last whole genome duplication in teleosts to systematically identify regions that have lost their coding capacity but retain sequence conservation with Mammals. , Here we show evidence for the de novo genesis of enhancers in Vertebrates. , While a growing body of evidence demonstrates that such innovation is generated by functional changes or translocation of regulatory elements via mobile genetic elements, the de novo generation of enhancers from non-regulatory/non-mobile sequences has, to our knowledge, not previously been demonstrated. Here we show evidence for the de novo genesis of enhancers in Vertebrates.[SEP]Relations: vertebra has relations: anatomy_anatomy with vertebral element, anatomy_anatomy with vertebral element, anatomy_anatomy with non-transverse process-bearing vertebra, anatomy_anatomy with non-transverse process-bearing vertebra, anatomy_anatomy with vertebral bone 1, anatomy_anatomy with vertebral bone 1, anatomy_anatomy with transverse process-bearing vertebra, anatomy_anatomy with transverse process-bearing vertebra. formation of specialized structure for nutrient acquisition from other organism involved in symbiotic interaction has relations: bioprocess_bioprocess with anatomical structure formation involved in morphogenesis, bioprocess_bioprocess with anatomical structure formation involved in morphogenesis.", "label": "yes"}
{"original_question": "Is Pfh1 a component of the replisome?", "id": "converted_2197", "sentence1": "Is Pfh1 a component of the replisome?", "sentence2": "Pfh1 Is an Accessory Replicative Helicase that Interacts with the replisome to Facilitate Fork Progression and Preserve Genome Integrity, Although the Schizosaccharomyces pombe 5'-to-3' DNA Helicases Pfh1 is known to promote fork progression, its genomic targets, dynamics, and mechanisms of action are largely unknown. Here we address these questions by integrating Genome - anatomical entity-wide identification of Pfh1 binding sites, comprehensive analysis of the effects of Pfh1 depletion on replication and DNA damage, and proteomic analysis of Pfh1 interaction partners by immunoaffinity purification mass spectrometry., DNA replication through hard-to-replicate sites, including both highly transcribed RNA Pol II and Pol III Genes, requires the S. pombe Pfh1 helicase., Here, we show that Pfh1 is required for efficient fork movement in the DNA, Ribosomal, the mating type locus, triplet codon-amino acid adaptor activity, 5S Ribosomal RNA Genes, and Genes that are highly transcribed by RNA Polymerase II. ,  Thus, Pfh1 promotes DNA replication and separation of converged replication forks and suppresses DNA damage at hard-to-replicate sites., Cells depleted of Pfh1 were inviable if they also lacked the human TIMELESS homolog SWI1, a replisome component that stabilizes stalled forks., Pfh1 Is an Accessory Replicative Helicase that Interacts with the replisome to Facilitate Fork Progression and Preserve Genome Integrity., Thus, we conclude that Pfh1 is an accessory DNA Helicases that interacts with the replisome and promotes replication and suppresses DNA damage at hard-to-replicate sites., Consistent with this interpretation, Pfh1 co-purified with many key replisome components, including the hexameric MCM helicase, replicative DNA polymerases, Retinitis punctata albescens (disorder), and the processivity clamp Proliferating Cell Nuclear Antigen in an S phase dependent manner., Although Pfh1 affected replication and suppressed DNA damage at discrete sites throughout the Genome - anatomical entity, Pfh1 and the replicative DNA polymerase bound to similar extents to both Pfh1-dependent and independent sites, suggesting that Pfh1 is proximal to the replication machinery during S phase., Cells depleted of Pfh1 were inviable if they also lacked the human TIMELESS homolog SWI1, a replisome component that stabilizes stalled forks, Here, we show that Pfh1 is required for efficient fork movement in the DNA, Ribosomal, the mating type locus, triplet codon-amino acid adaptor activity, 5S Ribosomal RNA Genes, and Genes that are highly transcribed by RNA Polymerase II, Thus, Pfh1 promotes DNA replication and separation of converged replication forks and suppresses DNA damage at hard-to-replicate sites, Cells depleted of Pfh1 were inviable if they also lacked the human TIMELESS homolog SWI1, a replisome component that stabilizes stalled forks., Thus, we conclude that Pfh1 is an accessory DNA Helicases that interacts with the replisome and promotes replication and suppresses DNA damage at hard-to-replicate sites., Consistent with this interpretation, Pfh1 co-purified with many key replisome components, including the hexameric MCM helicase, replicative DNA polymerases, Retinitis punctata albescens (disorder), and the processivity clamp Proliferating Cell Nuclear Antigen in an S phase dependent manner., Pfh1 Is an Accessory Replicative Helicase that Interacts with the replisome to Facilitate Fork Progression and Preserve Genome Integrity.[SEP]Relations: replisome has relations: cellcomp_protein with Proliferating Cell Nuclear Antigen, cellcomp_protein with Proliferating Cell Nuclear Antigen, cellcomp_protein with DONSON, cellcomp_protein with DONSON. RNA Polymerase II transcribes snRNA Genes has relations: pathway_protein with GTF2E1, pathway_protein with GTF2E1, pathway_protein with SP1, pathway_protein with SP1, pathway_protein with GTF2F1, pathway_protein with GTF2F1.", "label": "no"}
{"original_question": "Are the proteins Erbin (LAP2) and Merlin cooperating?", "id": "converted_1559", "sentence1": "Are the proteins ERBB2 Interacting Protein, Human (LAP2) and Neurofibromin 2 cooperating?", "sentence2": "ERBB2 Interacting Protein, Human and the NF2 tumor suppressor Neurofibromin 2 cooperatively regulate cell-type-specific activation of PAK2 gene gene by Recombinant Transforming Growth Factor-Beta., The results show that the epithelial-enriched protein ERBB2 Interacting Protein, Human controls the function of the NF2 tumor suppressor Neurofibromin 2 by determining the output of Neurofibromin 2's physical interactions with active PAK2 gene gene. , ERBB2 Interacting Protein, Human controls Neurofibromin 2 tumor suppressor function by switching the functional valence of PAK2 gene gene binding[SEP]Relations: protein insertion into ER membrane has relations: bioprocess_protein with TRAM2, bioprocess_protein with TRAM2, bioprocess_protein with CYB5A, bioprocess_protein with CYB5A, bioprocess_protein with ALDH3A2, bioprocess_protein with ALDH3A2, bioprocess_protein with UBE2J2, bioprocess_protein with UBE2J2, bioprocess_protein with VAMP2, bioprocess_protein with VAMP2.", "label": "yes"}
{"original_question": "Are there plasma membrane receptors for thyroid hormones?", "id": "converted_900", "sentence1": "Are there Plasma membrane receptors for thyroid hormones?", "sentence2": "ntegrins are heterodimeric structural components of the Plasma membrane whose ligands include a large number of Extracellular Matrix (ECM) Proteins. , Recently, integrin αvβ3 has been shown to have a panel of previously unappreciated small molecule receptor sites for Thyroid Hormones and hormone analogues, for Dihydrotestosterone, and for resveratrol, a polyphenols that has certain estrogen-like features., The Integrins activation by T4 thoracic segmental innervation thoracic segmental innervation may take a role in Plasma membrane processes involved in the male reproductive system., Rapid signaling via this Plasma membrane binding site appears to be responsible for many nongenomic effects of thyroid hormones, independent of the classic nuclear receptors.[SEP]Relations: Plasma membrane has relations: cellcomp_protein with DTNA, cellcomp_protein with DTNA, cellcomp_protein with TSHR, cellcomp_protein with TSHR, cellcomp_protein with DTNB, cellcomp_protein with DTNB, cellcomp_protein with WAS, cellcomp_protein with WAS, cellcomp_protein with TDG, cellcomp_protein with TDG.", "label": "yes"}
{"original_question": "Is macroautophagy a selective degradation process?", "id": "converted_1182", "sentence1": "Is macroautophagy a selective degradation process?", "sentence2": "Selective autophagy, Macroautophagy (autophagy) is a bulk degradation system for Cytoplasmic components and is ubiquitously found in Eukaryotic Cells, Here we show that selective autophagy downregulates Ty1 transposition, We propose that selective autophagy safeguards Genome - anatomical entity integrity against excessive Mutagenesis, Insertional caused during Nutrient (property) starvation by DNA Transposable Elements in Eukaryotic Cells., Moreover, it is becoming apparent that Proteins, Organelles, and pathogens can be targeted for autophagic clearance by selective mechanisms, Cell spreading required ref(2)P, the Drosophila p62 multiadaptor, implicating selective autophagy as a novel mechanism for modulating cortical dynamics, The selective macroautophagic degradation, There is growing evidence that macroautophagic cargo receptor ligand activity receptor ligand activity is not limited to bulk cytosol in response to starvation and can occur selectively for substrates, including aggregated Proteins., It remains unclear, however, whether starvation-induced and selective macroautophagy share identical adaptor molecules to capture their cargo receptor ligand activity receptor ligand activity. Here, we report that WDFY3 gene, a phosphatidylinositol 3-phosphate-binding Protein Info, is central to the selective elimination of aggregated Proteins., We propose that WDFY3 gene plays a key role in selective macroautophagy by bridging cargo receptor ligand activity receptor ligand activity to the molecular machinery that builds Autophagosome., Thus, Cytoplasmic NBR1 might be important to maintain basal levels of selective macroautophagy in these Neurons., we could show that Smatg8 and Smatg4 are not only required for nonselective macroautophagy, but for selective Pexophagy as well., The latter is performed by proteasome-mediated degradation, chaperone-mediated autophagy (chaperone-mediated autophagy), and selective macroautophagy,, Here we demonstrate a role for 1-Phosphatidylinositol 4-Kinase and PtdIns4P 5-kinases in selective and nonselective types of autophagy in Saccharomyces cerevisiae., Macroautophagy (hereafter autophagy) is a degradative cellular pathway that protects Eukaryotic Cells from stress, starvation, and microbial infection., Previously, we showed that macroautophagy is necessary for conidiation in the rice-blast Fungus (lab result) Magnaporthe oryzae. Here, we analyzed the physiological function(s) of selective autophagy in Magnaporthe, serine 403 phosphorylation of p62/SQSTM1 regulates selective autophagic clearance of ubiquitinated Proteins., Selective macroautophagy (autophagy) of ubiquitinated Protein Info is implicated as a compensatory mechanism of the ubiquitin-proteasome system. p62/SQSTM1 is a key Molecule managing autophagic clearance of polyubiquitinated Proteins., Whole Cytoplasmic Cytoplasmic organelle turnover is mediated through macroautophagy, a process by which Autophagosome deliver Mitochondria to the Lysosomes for hydrolytic degradation. While Mitochondrial Inheritance autophagy can occur as part of a nonselective upregulation of autophagy, selective degradation of damaged or unneeded Mitochondria (mitophagy) is a rapidly growing area in development, Primary malignant neoplasm, and Nerve Degeneration, particularly with regard to Parkinson Disease, BAG Family Molecular Chaperone Regulator 3, Homo sapiens was recently described as a mediator of a novel macroautophagy pathway that uses the specificity of heat shock Protein Info 70 (Heat-Shock Proteins 70) to misfolded Proteins and also involves other Protein Info partners, such as Heat Shock Protein Beta-8., two PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE (Lugano Lymphoma Response Classification Progressive Disease by PET) associated Genes, PINK1 gene gene and PARK2 Protein Info, Homo sapiens, were shown to mediate the degradation of damaged Mitochondria via selective autophagy (mitophagy), Here we show that whole Mitochondria are turned over via macroautophagy., Does HD Protein Info, Homo sapiens play a role in selective macroautophagy?, In the discussion here I suggest that SLC6A4 wt Allele may have a normal function in the lysosomal mechanism of selective macroautophagy involved in its own degradation, Macroautophagy induced by ethanol seemed to be selective for damaged Mitochondria and accumulated lipid droplets, but not long-lived Proteins, which could account for its protective effects, Although macroautophagy can be nonspecific, there are many examples of selective sequestration including pexophagy, mitophagy and the Cytoplasm to Vacuole targeting (Vertical Talus) pathway., Mitochondria autophagy (mitophagy) is the process of selective degradation of Mitochondria that has an important role in Mitochondrial Inheritance quality control., One of the Genes identified, YLR356W, is required for mitophagy, but not for macroautophagy or other types of selective autophagy., A genomic screen for Saccharomyces cerevisiae mutants defective in selective Mitochondria autophagy., Mitophagy is the process of selective Mitochondrial Inheritance degradation via autophagy, which has an important role in Mitochondrial Inheritance quality control., Analysis of this set of targeted deletion mutants demonstrated that loss of any of the 16 Genes necessary for nonselective macroautophagy renders the Fungus (lab result) unable to cause rice blast disease, due to impairment of both conidial programmed \"U\" lymphocyte death and appressorium maturation. In contrast, Genes necessary only for selective forms of autophagy, such as pexophagy and mitophagy, are dispensable for appressorium-mediated plant infection., This gene is not required for other types of selective autophagy or for nonspecific macroautophagy., However, in contrast to the core autophagy Genes such as ATG5 gene and ATG7 gene, expression of ULK1 Protein Info, Homo sapiens is not essential for induction of macroautophagy in response to Nutrient (property) deprivation or for survival of newborn mice. Together, these data suggest that the ULK1 wt Allele homologue, Ulk1, is a component of the selective autophagy machinery that leads to the elimination of Organelles in Erythroid Cells rather that an essential mechanistic component of autophagy., Growing evidence supports an active role for dysregulated macroautophagy (autophagic stress) in neuronal \"U\" lymphocyte death and Nerve Degeneration. Alterations in Mitochondrial Inheritance function and dynamics are also strongly implicated in neurodegenerative diseases. Interestingly, whereas the core autophagy machinery is evolutionarily conserved and shared among constitutive and induced or selective autophagy, recent studies implicate distinct mechanisms regulating Mitochondrial Inheritance autophagy (mitophagy) in response to general autophagic stimuli., We discovered that activation of the UPR in Saccharomyces cerevisiae also induces a new branch of macroautophagy that selectively targets the Endoplasmic Reticulum. We term this process \"Endoplasmic Reticulum-phagy\", in analogy to pexophagy and mitophagy, the two other known forms of Cytoplasmic Cytoplasmic organelle-specific marcoautophagy. Endoplasmic Reticulum-phagy involves the generation of Autophagosome that selectively include Endoplasmic Reticulum membranes and whose delimiting double membranes also derive, at least in part, from the Endoplasmic Reticulum., This suggests that in fungal sp. an organism-specific form of selective autophagy may occur, for which specialized Atg Proteins have evolved., ransfer of Y. lipolytica Cells from oleate/ethylamine to glucose/ammonium chloride medium leads to selective macroautophagy of peroxisome., Insulin-dependent signaling regulates azurophil granule-selective macroautophagy in Homo sapiens myeloblastic Cells., We show that insulin-dependent signals regulate azurophil granule-selective macroautophagy in Homo sapiens myeloid Cells., By contrast, other Organelles, including the Mitochondria, endoplasmic reticulum, and Golgi apparatus remained intact, indicating that the macroautophagy selectively targeted azurophil granules., Thus, insulin-dependent signals are responsible for the control of azurophil granule-selective macroautophagy via Akt-dependent pathways, Eukaryotic Cells have the ability to degrade Proteins and Organelles by selective and nonselective modes of micro- and macroautophagy., For example, pexophagy is a selective process for the regulated degradation of peroxisome by autophagy., We have characterized biochemically, morphologically, and genetically two distinct pathways for the selective degradation of peroxisome in Komagataella pastoris. These pathways are independently regulated and analogous to Microautophagy and macroautophagy that have been defined in mammalian Cells., If we are willing to slightly modify our definition of autophagy, with a focus on \"degradation of a \"U\" lymphocyte's own components through the lysosomal/vacuolar machinery,\" we can include a newly documented process, programmed nuclear destruction (PND)., Autophagy is a lysosomal degradation pathway that can sequester Cytoplasmic matrix material, including Organelles, nonspecifically in a process called nonselective macroautophagy, or target specific Protein Info aggregates designated for destruction in a process called selective autophagy., Selective macroautophagy uses double-membrane vesicles, termed Autophagosome, to transport Cytoplasmic pathogens, Organelles and Protein Info complexes to the Vacuole for degradation., Autophagy (macroautophagy), a highly conserved eukaryotic mechanism, is a non-selective degradation process, helping to maintain a balance between the synthesis, degradation and subsequent recycling of macromolecules to overcome various stress conditions., Whole Cytoplasmic Cytoplasmic organelle turnover is mediated through macroautophagy, a process by which Autophagosome deliver Mitochondria to the Lysosomes for hydrolytic degradation., Macroautophagy is a catabolic process by which the \"U\" lymphocyte degrades Cytoplasmic components through the lysosomal machinery., Macroautophagy maintains cellular homeostasis through targeting Cytoplasmic contents and Organelles into Autophagosome for degradation., Macroautophagy is a catabolic process by which Cytoplasmic matrix components are sequestered by double membrane vesicles called Autophagosome and sorted to the lysosomes/vacuoles to be degraded., Macroautophagy (hereafter autophagy) is a cellular degradation process, which in Saccharomyces cerevisiae is induced in response to Nutrient (property) deprivation., Macroautophagy was thought to be an unspecific bulk degradation process., Autophagy is a highly regulated Protoplasm degradation process by which Cells remove Cytoplasmic matrix long-lived Proteins and damaged Organelles, and can be monitored by imaging the incorporation of microtubule-associated light chain 3 (Microtubule-Associated Proteins 1A/1B Light Chain 3) fused to a fluorescent Protein Info (Green Fluorescent Proteins or mCherry) into nascent Autophagosome., Beside macroautophagy, there are several forms of selective autophagy, including chaperone-mediated autophagy (chaperone-mediated autophagy), Cytoplasm to Vacuole targeting (Vertical Talus), pexophagy and mitophagy., Macroautophagy (commonly referred to as autophagy) is the process by which intact Organelles and/or large portions of the Cytoplasm are engulfed within double-membraned autophagic vacuoles for degradation., This analysis demonstrated that Atg Proteins required for non-selective macroautophagy are conserved from Saccharomyces cerevisiae to man, stressing the importance of this process in \"U\" lymphocyte survival and viability., Part of the degradation of Protoplasm Proteins occurs in the lysosomes and is mediated by macroautophagy.[SEP]Relations: macroautophagy has relations: bioprocess_bioprocess with selective autophagy, bioprocess_bioprocess with selective autophagy, bioprocess_bioprocess with selective autophagy, bioprocess_bioprocess with selective autophagy, bioprocess_bioprocess with autophagy, bioprocess_bioprocess with autophagy, bioprocess_bioprocess with autophagy, bioprocess_bioprocess with autophagy, bioprocess_protein with STAM, bioprocess_protein with STAM.", "label": "yes"}
{"original_question": "Do plant genomes contain CpG islands?", "id": "converted_1613", "sentence1": "Do Plant allergen genomes contain CpG islands?", "sentence2": "This study represents the first systematic genome-scale analysis of DNA curvature, CpG islands and tandem repeats at the DNA sequence level in Plant allergen genomes, and finds that not all of the Chromosomes, Human, Pair 1 in Plants follow the same rules common to other eukaryote organisms, suggesting that some of these genomic properties might be considered as specific to Plants, In Plant allergen genomes, there exist discrete regions rich in CpG dinucleotides, namely CpG clusters. In rice, most of these CpG clusters are associated with Genes. Rice Genes are grouped into one of the five classes according to the Positioning Attribute of an associated CpG Clusters. Among them, class 1 Genes, which harbor a CpG Clusters at the 5'-terminus, share similarities with human Genes having CpG islands, Segmental distribution of Genes harboring a CpG island-like region on rice Chromosomes, Human, Pair 1, Highly-expressed Arabidopsis Genes had overall a more marked GC-skew in the Toxic Shock Syndrome compared to Genes with low expression levels. We therefore propose that the GC-skew around the Toxic Shock Syndrome in some Plants and fungal sp. is related to transcription. It might be caused by Gene Mutation during transcription initiation or the frequent use of transcription factor-biding sites having a Genomic Orientation preference. In addition, GC-skew is a good candidate index for Toxic Shock Syndrome prediction in Plant allergen genomes, where there is a lack of correlation among CpG islands and Genes, Preliminary analysis shows that promoter location based on the detection of potential CpG/CpNpG islands in the Arabidopsis genome is not straightforward. Nevertheless, because the landscape of CpG/CpNpG islands differs considerably between Promoter and Introns on the one side and Exons (whether Coding or not) on the other, more sophisticated approaches can probably be developed for the successful detection of \"putative\" CpG and CpNpG islands in Plants, This study represents the first systematic genome-scale analysis of DNA curvature, CpG islands and tandem repeats at the DNA sequence level in Plant allergen genomes, and finds that not all of the Chromosomes, Human, Pair 1 in Plants follow the same rules common to other eukaryote organisms, suggesting that some of these genomic properties might be considered as specific to Plants., These Plant allergen CpG-rich clusters satisfied the criteria used for identifying human CpG islands, which suggests that these CpG clusters may be regarded as Plant allergen CpG islands., CONCLUSIONS: This study represents the first systematic genome-scale analysis of DNA curvature, CpG islands and tandem repeats at the DNA sequence level in Plant allergen genomes, and finds that not all of the Chromosomes, Human, Pair 1 in Plants follow the same rules common to other eukaryote organisms, suggesting that some of these genomic properties might be considered as specific to Plants., In Plant allergen genomes, there exist discrete regions rich in CpG dinucleotides, namely CpG clusters., These Plant allergen CpG-rich clusters satisfied the criteria used for identifying human CpG islands, which suggests that these CpG clusters may be regarded as Plant allergen CpG islands., Unmethylated CpG islands associated with Genes in higher Plant allergen DNA., This study represents the first systematic genome-scale analysis of DNA curvature, CpG islands and tandem repeats at the DNA sequence level in Plant allergen genomes, and finds that not all of the Chromosomes, Human, Pair 1 in Plants follow the same rules common to other eukaryote organisms, suggesting that some of these genomic properties might be considered as specific to Plants., These Plant allergen CpG-rich clusters satisfied the criteria used for identifying human CpG islands, which suggests that these CpG clusters may be regarded as Plant allergen CpG islands, We screened Plant allergen genome DNA Sequence, primarily from rice and Arabidopsis thaliana <plant> <Plant allergen>, for CpG islands, and identified DNA segments rich in CpG dinucleotides within these DNA Sequence[SEP]Relations: Plantar pits has relations: disease_phenotype_positive with monosomy 9q22.3, disease_phenotype_positive with monosomy 9q22.3, disease_phenotype_positive with PTEN hamartoma tumor syndrome, disease_phenotype_positive with PTEN hamartoma tumor syndrome, disease_phenotype_positive with Darier disease, disease_phenotype_positive with Darier disease, disease_phenotype_positive with nevoid basal cell carcinoma syndrome, disease_phenotype_positive with nevoid basal cell carcinoma syndrome. promoter clearance from RNA polymerase I promoter has relations: bioprocess_bioprocess with promoter clearance during DNA-templated transcription, bioprocess_bioprocess with promoter clearance during DNA-templated transcription.", "label": "yes"}
{"original_question": "Does DDX54 play a role in DNA damage response?", "id": "converted_2342", "sentence1": "Does DDX54 gene play a role in DNA damage response?", "sentence2": "DDX54 gene gene regulates transcriptome dynamics during DNA damage response., The contribution of post-transcriptional gene regulatory networks to the DNA damage response (DDR1 wt Allele) has not been extensively studied. Here, we systematically identified RNA-binding Proteins differentially interacting with polyadenylated transcripts upon exposure of human breast carcinoma cells to ionizing radiation (IR). Interestingly, more than 260 Proteins, including many nucleolar Proteins, showed increased binding to poly(A)+RNA in IR-exposed cells. The functional analysis of DDX54 gene gene, a candidate genotoxic stress responsive RNA helicase, revealed that this Protein Info is an immediate-to-early DDR1 wt Allele regulator required for the splicing efficacy of its target IR-induced pre-mRNAs. Upon IR exposure, DDX54 gene gene acts by increased interaction with a well-defined class of pre-mRNAs that harbor Introns with weak Splice Acceptor Site, as well as by Protein Info-Protein Info contacts within components of U2 snRNP and Spliceosomes, resulting in lower intron retention and higher processing rates of its target transcripts. Because DDX54 gene gene promotes survival after exposure to IR, its expression and/or mutation rate may impact DDR1 wt Allele-related pathologies. Our work indicates the relevance of many uncharacterized RBPs potentially involved in the DDR1 wt Allele., The functional analysis of DDX54 gene gene, a candidate genotoxic stress responsive RNA helicase, revealed that this Protein Info is an immediate-to-early DDR1 wt Allele regulator required for the splicing efficacy of its target IR-induced pre-mRNAs.[SEP]Relations: Protein Info binding has relations: molfunc_protein with DDX55, molfunc_protein with DDX55, molfunc_protein with DDX5, molfunc_protein with DDX5, molfunc_protein with DDX6, molfunc_protein with DDX6, molfunc_protein with DDX60, molfunc_protein with DDX60, molfunc_protein with DDX42, molfunc_protein with DDX42.", "label": "yes"}
{"original_question": "Is carpal tunnel syndrome a type of nerve entrapment?", "id": "converted_3938", "sentence1": "Is carpal tunnel syndrome a type of Nerve entrapment?", "sentence2": " CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) is a common entrapment neuropathy, often requiring carpal tunnel release (CTR) surgery., CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) is an entrapment neuropathy accounting for up to 90% of Nerve compression syndromes,  CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) is the most frequent entrapment neuropathy in Homo sapiens. , CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) is the most common focal entrapment mononeuropathy, comprising medium Nerve chronic inflammation and Fibrosis., CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) is the most common Nerve entrapment neuropathy which is the result of the compression of the median Nerve in the Upper extremity>Wrist. , Dear sir, one of the most common entrapment neuropathy syndromes in clinical practice is \"Entrapment of median Nerve in carpal tunnel\" also called \"CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome)\" (Aydin et al., 2007; Huisstede et al., 2010)., BACKGROUND: CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) is the most common type of peripheral Nerve entrapment and is a significant cause of morbidity., BACKGROUND: CARPAL TUNNEL SYNDROME 2 and Ulnar (qualifier value) Nerve entrapment at the Elbow joint structure are the most common entrapment neuropathies seen in adults., Entrapment neuropathies are of various types, but the most common type is carpal tunnel syndrome., Carpal Tunnel Syndrome and Other Entrapment Neuropathy., Unlike Guyon's canal syndrome, carpal tunnel syndrome (Carpal Tunnel Syndrome) is the most common Nerve entrapment of the upper extremity.,  Kidney Failure, Chronic tend to develop peripheral Nerve entrapment and carpal tunnel syndrome is the best-known peripheral entrapment neuropathy among them. Contrary to ca, CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) is a common form of peripheral Nerve entrapment, which is observed due to compression of the median Nerve at the level of the carpal tunnel in the Upper extremity>Wrist. Bifi, INTRODUCTION: CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) is considered a simple entrapment of the median Nerve at the carp, Compressive neuropathy of the median Nerve at the level of the carpal tunnel, known as carpal tunnel syndrome, is the most common entrapment neuropathy, affecting about 0.1-1% of the general population. Magne, BACKGROUND: CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) is entrapment of median Nerve in carpal tunnel of th, Dear sir, one of the most common entrapment neuropathy syndromes in clinical practice is \"Entrapment of median Nerve in carpal tunnel\" also called \"CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome)\" (Aydin et al., 2007; Huisstede et al., 2010). This syndr, OBJECTIVE: CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) is a common median Nerve entrapment neuropathy characterized by Pain:-:Point in time:^Patient:-, Paresthesia, diminished peripheral Nerve conduction velocity (NCV) and maladaptive functional brain neuroplastici, CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome), caused by entrapment of the median Nerve in the carpal tunnel, impairs hand function including dexterous manipulation. The , This review focuses on three of the most common entrapment neuropathies in the upper limbs: carpal tunnel syndrome (median Nerve entrapment at the Upper extremity>Wrist), Cubital Tunnel Syndrome (Ulnar (qualifier value) Nerve entrapment at the Elbow joint structure), and Radial Tunnel Syndrome (posterior interosseous Nerve entrapment)., Electrodiagnostic (EDX) testing is usually an essential part of the evaluation of entrapment neuropathies, and examinations for the most common entrapment neuropathies, carpal tunnel syndrome and Ulnar (qualifier value) neuropathy at the Elbow joint structure, constitute a significant part of the daily work in EDX laboratories., This study reviews the existing, more or less, detailed EDX criteria or practice parameters that are suggested by consensus groups in peer-reviewed journals for the most common entrapment neuropathies: carpal tunnel syndrome, Ulnar (qualifier value) neuropathy at the Elbow joint structure, common peroneal (Fibula) neuropathy at the Fibula head, and Tibial Neuropathy at the tarsal tunnel., This report demonstrates that the Semmes-Weinstein monofilament test and Nerve conduction studies can identify entrapment of the palmar cutaneous branch of the median Nerve concomitant with carpal tunnel syndrome., Entrapment neuropathy of the palmar cutaneous branch of the median Nerve concomitant with carpal tunnel syndrome: a case report., A case of the entrapment neuropathy of the palmar cutaneous branch of the median Nerve, concomitant with carpal tunnel syndrome is presented., The entrapment syndromes discussed are suprascapular Nerve entrapment, carpal tunnel syndrome, Cubital Tunnel Syndrome, meralgia paraesthetica, Thoracic Outlet Syndrome and Anterior interosseous Nerve syndrome., CARPAL TUNNEL SYNDROME 2 is a neuropathy resulting from compression of the median Nerve as it passes through a narrow tunnel in the Upper extremity>Wrist on its way to the hand., More typically, carpal tunnel syndrome is the most common peripheral entrapment neuropathy encountered in industry., CARPAL TUNNEL SYNDROME 2 is the most frequently encountered peripheral Nerve entrapment., CARPAL TUNNEL SYNDROME 2, an entrapment neuropathy of the median Nerve, is rarely seen in childhood., CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) is the most common type of peripheral Nerve entrapment and is a significant cause of morbidity., CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) is a Nerve entrapment disorder, involving the median Nerve when it passes the carpal tunnel at the Upper extremity>Wrist., The carpal tunnel syndrome is the most frequent entrapment syndrome of peripheral nerves., BACKGROUND: Compression of the median Nerve at the Upper extremity>Wrist, or carpal tunnel syndrome, is the most commonly recognized Nerve entrapme, CARPAL TUNNEL SYNDROME 2 is the most common of the median Nerve entrapments., BACKGROUND: CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) is by far the most common entrapment neuropathy (, Introduction: CARPAL TUNNEL SYNDROME 2, entrapment of median Nerve at the Upper extremity>Wrist, is one of the most commonly encountered peripheral neuropathies in the up, CARPAL TUNNEL SYNDROME 2, a median Nerve entrapment neuropathy, is characterized by sensorimotor deficits., CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) is a common form of peripheral Nerve entrapment, which is observed due to compression of the median Nerve at the level of the carpal tunnel in the Upper extremity>Wrist., [CARPAL TUNNEL SYNDROME 2 and other Nerve entrapment syndromes].[SEP]Relations: carpal tunnel syndrome has relations: disease_disease with Nerve compression syndrome, disease_disease with Nerve compression syndrome, disease_disease with Nerve compression syndrome, disease_disease with Nerve compression syndrome, disease_disease with genetic peripheral neuropathy, disease_disease with genetic peripheral neuropathy, disease_disease with genetic peripheral neuropathy, disease_disease with genetic peripheral neuropathy, disease_phenotype_positive with Constrictive median neuropathy, disease_phenotype_positive with Constrictive median neuropathy.", "label": "yes"}
{"original_question": "Does Enzastaurin improve survival of glioblastoma patients?", "id": "converted_2433", "sentence1": "Does Enzastaurin improve survival of Glioblastoma Multiforme patients?", "sentence2": "RESULTS: fourteen randomized clinical trials were identified (7 with bevacizumab, 2 Cilengitide, 1 enzastaurin, 1 dasatinib, 1 vandetanib, 1 temsirolimus, 1 cediranib) including 4330 patients. Antiangiogenic drugs showed no improvement in overall survival with a pooled HR of 1.00, a trend for an inferior outcome, in terms of overall survival, was observed in the group of patients receiving antiangiogenic Pharmacologic Substance alone compared to cytotoxic Pharmacologic Substance alone (HR=1.24, p=0.056). , Enzastaurin (LY317615.HCl.HCl) in combination with bevacizumab for recurrent malignant gliomas is well-tolerated, with response and progression-free survival similar to bevacizumab monotherapy., So far, inhibition of angiogenesis by compounds such as bevacizumab, cediranib, enzastaurin or Cilengitide as well as alternative dosing schedules of temozolomide did not prolong survival, neither at primary diagnosis nor at recurrent Disease., Despite promising phase II clinical trial results and patient benefit in terms of clinical improvement and longer progression-free survival, an overall survival benefit has not been demonstrated in four randomized phase III trials of bevacizumab or Cilengitide in newly diagnosed Glioblastoma Multiforme or cediranib or enzastaurin in recurrent Glioblastoma Multiforme., EXPERT OPINION: Enzastaurin and cediranib failed in randomized Phase III trials in recurrent Glioblastoma Multiforme, aflibercept in Phase II. , Enzastaurin was well tolerated and had a better Hematologic toxicity profile but did not have superior efficacy compared with lomustine in patients with recurrent Glioblastoma Multiforme., Grade 3 to 4 Hematologic Toxic effect were significantly higher with lomustine (46 events) than with enzastaurin (one event; P < or = .001).<br><b>CONCLUSION</b>: Enzastaurin was well tolerated and had a better Hematologic toxicity profile but did not have superior efficacy compared with lomustine in patients with recurrent Glioblastoma Multiforme.<br>, Enzastaurin was well tolerated and had a better Hematologic toxicity profile but did not have superior efficacy compared with lomustine in patients with recurrent Glioblastoma Multiforme., Enzastaurin has anti-glioma activity in patients with recurrent high-grade glioma, but does not appear to have enough single-agent activity to be useful as monotherapy., Enzastaurin (LY317615.HCl.HCl) in combination with bevacizumab for recurrent malignant gliomas is well-tolerated, with response and progression-free survival similar to bevacizumab monotherapy., CONCLUSION Enzastaurin was well tolerated and had a better Hematologic toxicity profile but did not have superior efficacy compared with lomustine in patients with recurrent Glioblastoma Multiforme., Glioblastoma are highly vascularized Neoplasms and various antiangiogenic drugs have been investigated in clinical trials showing unclear results we performed a systematic review and a meta analysis to clarify and evaluate their effectiveness in Glioblastoma Multiforme patients we searched relevant published and unpublished randomized clinical trials analyzing antiangiogenic drugs versus chemotherapy in Glioblastoma Multiforme patients from january 2006 to january 2016 in medline web of science asco esmo and sno databases fourteen randomized clinical trials were identified 7 with bevacizumab 2 Cilengitide 1 enzastaurin 1 dasatinib 1 vandetanib 1 temsirolimus 1 cediranib including 4330 patients antiangiogenic drugs showed no improvement in overall survival with a pooled hr of 1 00 a trend for an inferior outcome in terms of overall survival was observed in the group of patients receiving antiangiogenic Pharmacologic Substance alone compared to cytotoxic Pharmacologic Substance alone hr 1 24 p 0 056 bevacizumab did not improve overall survival twelve trials 4113 patients were analyzed for progression free survival among antiangiogenic drugs only bevacizumab demonstrated an improvement of progression free survival hr 0 63 p 0 001 both alone hr 0 60 p 0 003 or in combination to chemotherapy hr 0 63 p 0 001 both as first line treatment hr 0 70 p 0 001 or in recurrent Disease hr 0 52 p 0 001 antiangiogenic drugs did not improve overall survival in Glioblastoma Multiforme patients either as first or second line treatment and either as single agent or in combination with chemotherapy among antiangiogenic drugs only bevacizumab improved progression free survival regardless of treatment line both as single agent or in combination with chemotherapy., Glioblastoma Multiforme is characterized by high expression levels of proangiogenic cytokines and microvascular proliferation highlighting the potential value of treatments targeting angiogenesis antiangiogenic treatment likely achieves a beneficial impact through multiple mechanisms of action ultimately however alternative proangiogenic signal transduction pathways are activated leading to the development of resistance even in Neoplasms that initially respond the identification of biomarkers or imaging parameters to predict response and to herald resistance is of high priority despite promising phase ii clinical trial results and patient benefit in terms of clinical improvement and longer progression free survival an overall survival benefit has not been demonstrated in four randomized phase iii trials of bevacizumab or Cilengitide in newly diagnosed Glioblastoma Multiforme or cediranib or enzastaurin in recurrent Glioblastoma Multiforme however future studies are warranted predictive markers may allow appropriate patient enrichment combination with chemotherapy may ultimately prove successful in improving overall survival and novel agents targeting multiple proangiogenic pathways may prove effective., this phase iii open label study compared the efficacy and safety of enzastaurin versus lomustine in patients with recurrent Glioblastoma Multiforme who grade 4 patients were randomly assigned 2 1 to receive 6 week cycles of enzastaurin 500 mg d 1 125 mg loading dose day 1 or lomustine 100 to 130 mg m 2 day 1 assuming a 45 improvement in progression free survival pfs 397 patients were required to provide 80 power to achieve statistical significance at a one sided level of 025 enrollment was terminated at 266 patients enzastaurin n 174 lomustine n 92 after a planned interim analysis for futility patient characteristics were balanced between arms median pfs 1 5 v 1 6 months hazard ratio hr 1 28 95 ci 0 97 to 1 70 overall survival 6 6 v 7 1 months hr 1 20 95 ci 0 88 to 1 65 and 6 month pfs rate p 13 did not differ significantly between enzastaurin and lomustine respectively stable Disease occurred in 38 5 and 35 9 of patients and objective response occurred in 2 9 and 4 3 of patients respectively time to deterioration of physical and functional well being and symptoms did not differ between arms hr 1 12 p 54 four patients discontinued enzastaurin because of Pharmacologic Substance related serious adverse events aes eleven patients treated with enzastaurin died on study four because of aes one was Pharmacologic Substance related all four deaths that occurred in patients receiving lomustine were Disease related grade 3 to 4 Hematologic Toxic effect were significantly higher with lomustine 46 events than with enzastaurin one event p or 001 enzastaurin was well tolerated and had a better Hematologic toxicity profile but did not have superior efficacy compared with lomustine in patients with recurrent Glioblastoma Multiforme., this study s primary objective was evaluation of the progression free survival rate at 6 months pfs 6 in patients with newly diagnosed Glioblastoma Multiforme without o 6 methylguanine dna methyltransferase mgmt promoter hypermethylation postsurgically treated with enzastaurin before and concomitantly with radiation therapy followed by enzastaurin maintenance therapy pfs 6 of at least 55 was set to be relevant compared with the data of the eortc 26981 22981 ncic ce 3 trial adult patients with a life expectancy of at least 12 weeks who were newly diagnosed with a histologically proven supratentorial Glioblastoma Multiforme without mgmt promoter hypermethylation were eligible patients were treated with enzastaurin prior to concomitantly with and after standard partial brain radiotherapy here we report on a multicenter open label uncontrolled phase ii study of patients with newly diagnosed Glioblastoma Multiforme without mgmt promoter hypermethylation treated with enzastaurin and radiation therapy within 4 study periods pfs 6 was 53 6 95 confidence interval ci 39 8 65 6 the median overall survival was 15 0 months 95 ci 11 9 17 9 for all patients 3 9 months 95 ci 0 8 9 0 for patients with biopsy 15 4 months 95 ci 10 1 17 9 for patients with partial resection and 18 9 months 95 ci 13 9 28 5 for patients with complete resection the safety profile in this study was as expected from previous trials and the therapy was well tolerated pfs 6 missed the primary planned outcome of 55 the secondary exploratory analysis according to resection status of the different subgroups of patients with biopsies partial resection and complete resection demonstrates the strong prognostic influence of resection on overall survival., we evaluated the efficacy of combination enzastaurin ly317615 and bevacizumab for recurrent malignant gliomas and explored serologic correlates we enrolled 81 patients with Glioblastoma gbm n 40 and anaplastic gliomas ag n 41 patients received enzastaurin as a loading dose of 1125 mg followed by 500 or 875 mg daily for patients on non Enzyme [APC] inducing or Enzyme [APC] inducing antiepileptics respectively patients received bevacizumab 10 mg kg intravenously biweekly clinical evaluations were repeated every 4 weeks magnetic resonance imaging was obtained at baseline and every 8 weeks from treatment onset phosphorylated glycogen synthase kinase gsk 3 levels from Peripheral blood mononuclear cell (cell) pbmcs were checked with each mri median overall survival was 7 5 and 12 4 months for Glioblastoma and anaplastic glioma cohorts with median progression free survivals of 2 0 and 4 4 months respectively of gbm patients 3 40 7 5 were not evaluable while 8 37 22 had partial or complete response and 20 37 54 had stable Disease for 2 months of the 39 evaluable ag patients 18 46 had an objective response and 16 41 had stable Disease for 2 months the most common grade 3 Toxic effect were Lymphocyte count decreased 15 Hypophosphatemia 8 8 and thrombotic events 7 5 two 2 5 gbm patients died suddenly another Cessation of life 1 3 occurred from intractable Seizures phosphorylated gsk 3 levels from pbmcs did not correlate with treatment response a minimally important improvement in health related quality of life was self reported in 7 9 24 29 2 37 5 early response based on levin criteria was significantly associated with significantly longer progression free survival for Glioblastoma enzastaurin ly317615 in combination with bevacizumab for recurrent malignant gliomas is well tolerated with response and progression free survival similar to bevacizumab monotherapy.[SEP]Relations: Enzastaurin has relations: drug_protein with CHEK2, drug_protein with CHEK2, drug_protein with AURKB, drug_protein with AURKB, drug_protein with AURKA, drug_protein with AURKA, drug_protein with CHEK1, drug_protein with CHEK1, drug_protein with AKT1, drug_protein with AKT1.", "label": "no"}
{"original_question": "Is there any role for Pds5b in cohesion establishment?", "id": "converted_1901", "sentence1": "Is there any role for Pds5b in cohesion establishment?", "sentence2": "PDS5B gene is required for cohesion establishment and AURKB protein, human accumulation at Centromere., Here, we demonstrate that Pds5 Proteins are essential for cohesion establishment by allowing SMC3 wt Allele acetylation by the cohesin acetyl transferases (CoATs) Esco1/2 and binding of CDCA5 gene. While both Proteins contribute to telomere and arm cohesion, PDS5B gene is specifically required for centromeric cohesion. Furthermore, reduced accumulation of AURKB protein, human at the inner centromere region in Cells lacking PDS5B gene impairs its error correction function, promoting chromosome mis-segregation and aneuploidy. Our work supports a model in which the composition and function of cohesin complexes differs between different chromosomal regions., PDS5B gene is required for cohesion establishment and AURKB protein, human accumulation at Centromere., Here, we demonstrate that Pds5 Proteins are essential for cohesion establishment by allowing SMC3 wt Allele acetylation by the cohesin acetyl transferases (CoATs) Esco1/2 and binding of CDCA5 gene.[SEP]Relations: Protein S human has relations: drug_drug with Coagulation Factor IX (Recombinant), drug_drug with Coagulation Factor IX (Recombinant), drug_drug with Platelet Activating Factor, drug_drug with Platelet Activating Factor, drug_drug with p-Coumaric acid, drug_drug with p-Coumaric acid, drug_drug with Peginterferon alfa-2b, drug_drug with Peginterferon alfa-2b. centromere clustering has relations: bioprocess_bioprocess with chromosome localization, bioprocess_bioprocess with chromosome localization.", "label": "yes"}
{"original_question": "Is it feasible to determine the complete proteome of yeast?", "id": "converted_340", "sentence1": "Is it feasible to determine the complete proteome of Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae?", "sentence2": "or model organisms like Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae, we can now quantify complete proteomes in just a few hours., A complete mass-spectrometric map of the Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae proteome applied to quantitative trait analysis., So far, attempts to generate such maps for any proteome have failed to reach complete proteome coverage. Here we use a strategy based on high-throughput peptide synthesis and mass spectrometry to generate an almost complete reference map (97% of the genome-predicted proteins) of the Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae proteome.[SEP]", "label": "yes"}
{"original_question": "AhR ligands are attractive drug targets for pharmaceutical development due to their induction of Cyp1a1, yes or no?", "id": "converted_3383", "sentence1": "aromatic hydrocarbon receptor ligands are attractive drug targets for pharmaceutical development due to their induction of Cyp1a1, yes or no?", "sentence2": " Based on our review of the data, there is little evidence to support the indiscriminate exclusion of aromatic hydrocarbon receptor activators/Cyp1a1 inducers from early drug developmental pipelines. We also found no evidence that short-term treatment with RMAhRLs produce \"dioxin-like toxicity\", However, recent discoveries of new aromatic hydrocarbon receptor ligands with potential therapeutic applications have been reported, inviting reconsideration of this policy., Based on our review of the data, there is little evidence to support the indiscriminate exclusion of aromatic hydrocarbon receptor activators/Cyp1a1 inducers from early drug developmental pipelines., Based on our review of the data , there is little evidence to support the indiscriminate exclusion of aromatic hydrocarbon receptor activators/Cyp1a1 inducers from early drug developmental pipelines, However , recent discoveries of new aromatic hydrocarbon receptor ligands with potential therapeutic applications have been reported , inviting reconsideration of this policy, Based on our review of the data, there is little evidence to support the indiscriminate exclusion of aromatic hydrocarbon receptor activators/Cyp1a1 inducers from early drug developmental pipelines., However, recent discoveries of new aromatic hydrocarbon receptor ligands with potential therapeutic applications have been reported, inviting reconsideration of this policy., Combining in vivo and in vitro findings, we identified nine aromatic hydrocarbon receptor agonists, six of which are marketed therapeutics and have been approved by the U.S. Food and Drug Administration, including leflunomide, flutamide, and nimodipine.[SEP]Relations: Flutamide has relations: drug_protein with AHR, drug_protein with AHR. Nimodipine has relations: drug_protein with AHR, drug_protein with AHR. aryl hydrocarbon receptor complex has relations: cellcomp_protein with AHR, cellcomp_protein with AHR, cellcomp_protein with AHRR, cellcomp_protein with AHRR. Leflunomide has relations: drug_protein with AHR, drug_protein with AHR.", "label": "yes"}
{"original_question": "Is tirilazad effective for treatment of aneurysmal subarachnoid haemorrhage?", "id": "converted_2171", "sentence1": "Is tirilazad effective for treatment of aneurysmal subarachnoid haemorrhage?", "sentence2": "There was no significant difference between the two groups at the end of follow up for the primary outcome, Cessation of life (odds ratio (OR) 0.89, 95% confidence interval (CI) 0.74 to 1.06), or in poor outcome (Cessation of life, vegetative state or severe disability) (OR 1.04, 95% CI 0.90 to 1.21). During the treatment period, fewer patients developed delayed cerebral ischaemia in the tirilazad group than in the control group (OR 0.80, 95% CI 0.69 to 0.93). Subgroup analyses did not demonstrate any significant difference in effects of tirilazad on clinical outcomes. , AUTHORS' CONCLUSIONS: There is no evidence that tirilazad, in addition to nimodipine, reduces mortality or improves poor outcome in patients with aneurysmal Yakut language., This clinical trial suggest that tirilazad mesylate, at a dosage of 6 mg/kg/day, improves overall outcome in aneurysmal Subarachnoid Hemorrhage patients., Tirilazad is ineffective.There are many possible successful treatment options for preventing Vasospasm, delayed ischemic neurologic deficits, and poor neurologic outcome following aneurysmal Subarachnoid Hemorrhage; however, further multicenter RCTs need to be performed to determine if there is a significant benefit from their use, Findings from previous multicenter clinical trials have suggested that tirilazad mesylate, a synthetic nonhormonal 21-aminosteroid, might be effective in preventing delayed cerebral ischemia following Subarachnoid Hemorrhage (Yakut language)., This clinical trial suggest that tirilazad mesylate, at a dosage of 6 mg/kg/day, improves overall outcome in aneurysmal Subarachnoid Hemorrhage patients.[SEP]Relations: Subarachnoid Hemorrhage (disease) has relations: contraindication with Tranexamic acid, contraindication with Tranexamic acid, disease_disease with acquired aneurysmal Subarachnoid Hemorrhage, disease_disease with acquired aneurysmal Subarachnoid Hemorrhage, disease_protein with EDNRB, disease_protein with EDNRB, disease_protein with PPARG, disease_protein with PPARG, disease_protein with ADORA1, disease_protein with ADORA1.", "label": "no"}
{"original_question": "Does HER2 under-expression lead to favorable response to trastuzumab?", "id": "converted_1267", "sentence1": "Does ERBB2 wt Allele under-expression lead to favorable response to trastuzumab?", "sentence2": "over-expression of ERBB2 wt Allele is reported in approximately 20% of gastric tumours, challenging the use of targeted therapies. , In patients with advanced gastric or gastro-oesophageal junction cancer, addition of trastuzumab to chemotherapy significantly improved overall survival compared with chemotherapy alone. Addition of trastuzumab to chemotherapy did not increase the incidence of adverse events., treatment of ERBB2 wt Allele-overexpressing Malignant neoplasm of Breast: trastuzumab,, Trastuzumab has demonstrated clinical activity in several types of ERBB2 wt Allele-overexpressing epithelial tumors, such as Breast and metastatic gastric or gastroesophageal junction cancer. , An example is the established benefit of trastuzumab as adjuvant therapy for Malignant neoplasm of Breast; a clear definition of ERBB2 wt Allele-positivity and the assay reproducibility have, however, remained unanswered. , Trastuzumab is a monoclonal antibody CAL CAL targeted to the Her2 receptor and approved for treatment of Her2-positive Malignant neoplasm of Breast., epidermal growth factor receptor 2, human (ERBB2 wt Allele/neu) is an important target for the treatment of the Breast cancers in which it is overexpressed. However, no approved anti-ERBB2 wt Allele/neu therapy is available for the majority of Malignant neoplasm of Breast patients, who express ERBB2 wt Allele/neu at low levels (with scores of 1+ or 2+/fluorescence in situ hybridization-negative)., The humanized anti-ERBB2 wt Allele monoclonal antibody CAL CAL trastuzumab (Herceptin) is useful in the treatment of ErbB2-overexpressing Breast cancers,, HercepTestTM (DAKO A/S, Glostrup, Denmark) is an immunohistochemical assay that detects ERBB2 wt Allele/neu gene products, and evaluates the overexpression status of the ERBB2 wt Allele/neu protein in determining eligibility for the Trastuzumab (HerceptinR, Genentech, San Francisco, cyclophosphamide/doxorubicin protocol, USA) therapy. [SEP]Relations: Trastuzumab has relations: drug_protein with ERBB2, drug_protein with ERBB2, drug_drug with Yersinia pestis 195/p antigen (formaldehyde inactivated), drug_drug with Yersinia pestis 195/p antigen (formaldehyde inactivated), drug_drug with Clostridium tetani toxoid antigen (formaldehyde inactivated), drug_drug with Clostridium tetani toxoid antigen (formaldehyde inactivated), drug_drug with Corynebacterium diphtheriae toxoid antigen (formaldehyde inactivated), drug_drug with Corynebacterium diphtheriae toxoid antigen (formaldehyde inactivated), drug_drug with XmAb 2513, drug_drug with XmAb 2513.", "label": "no"}
{"original_question": "Should cerebrolysin be used for aneurysmal subarachnoid hemorrhage?", "id": "converted_4177", "sentence1": "Should cerebrolysin be used for aneurysmal subarachnoid hemorrhage?", "sentence2": "No significant difference was detected in the proportion of patients with favorable six-month GOSE in either study group (odds ratio (OR): 1.49; 95% confidence interval (CI): 0.43-5.17). Secondary functional outcome measures for favorable six-month recovery i.e. a mRS of 0 to 3 (OR: 3.45; 95% CI 0.79-15.01) were comparable for both groups. Similarly, there was no difference in cyclophosphamide/doxorubicin/methotrexate/vincristine protocol neurocognitive performance (p-value: 0.75) and in the incidence of Noninfiltrating Intraductal Carcinoma (OR: 0.85 95% CI: 0.28-2.59).CONCLUSIONS: Use of cerebrolysin in addition to standard-of-care management of aneurysmal Yakut language is safe, well tolerated and feasible. However, the neutral results of this trial suggest that it does not improve the six-month global functional performance of patients., CONCLUSION: cerebrolysin injection during the acute period of Yakut language appeared to reduce the mortality rate, especially in poor-grade patients. This study suggests the potential of cerebrolysin for treating aneurysmal Yakut language. Further studies are needed to confirm our results.[SEP]Relations: infiltrating urothelial carcinoma has relations: disease_disease with urothelial neoplasm, disease_disease with urothelial neoplasm, disease_disease with malignant urinary system neoplasm, disease_disease with malignant urinary system neoplasm, disease_disease with invasive carcinoma, disease_disease with invasive carcinoma, disease_disease with renal pelvis/ureter carcinoma, disease_disease with renal pelvis/ureter carcinoma, disease_disease with infiltrating bladder urothelial carcinoma, disease_disease with infiltrating bladder urothelial carcinoma.", "label": "no"}
{"original_question": "Are organisms in the genus Morexella associated with sepsis?", "id": "converted_2424", "sentence1": "Are organisms in the genus Morexella associated with Sepsis (Invertebrate)?", "sentence2": "Out of 130 culture proven cases of neonatal Sepsis (Invertebrate), gram negative Bacteria were found in 71 (54.6%) cases and gram positive Bacteria in 59 (45.4%) cases. Staphylococcus aureus was the most common Bacteria found in 35 (26.9%) cases followed by Escherichia coli in 30 (23.1%) cases. Acinetobacter species, Staphylococcus epidermidis, Klebseila, Streptococcus, Enterobacter cloacae subsp. cloacae subsp. cloacae and Morexella species were found in 17 (13.1%), 17 (13.1%), 13 (10%), 7 (5.4%), 6 (4.6%), and 5 (3.8%) cases respectively. [SEP]Relations: Bacteremia has relations: disease_phenotype_positive with shigellosis, disease_phenotype_positive with shigellosis, disease_phenotype_positive with melioidosis, disease_phenotype_positive with melioidosis, disease_phenotype_positive with listeriosis, disease_phenotype_positive with listeriosis. escherichia coli infection has relations: disease_phenotype_positive with Recurrent gram-negative bacterial infections, disease_phenotype_positive with Recurrent gram-negative bacterial infections, disease_disease with infectious disease, disease_disease with infectious disease.", "label": "yes"}
{"original_question": "Is abdominal pain a common symptom in autism?", "id": "converted_1562", "sentence1": "Is Abdominal Pain a common symptom in Autistic Disorder?", "sentence2": "Participants included 132 children with Atrial Septal Defects and 81 with special educational needs (MORF4 gene) but no Atrial Septal Defects, aged 10-14 years plus 82 typically developing (diphtheria, tetanus toxoids and acellular pertussis vaccine) children, The Atrial Septal Defects group had significantly increased past vomiting and diarrhoea compared with the diphtheria, tetanus toxoids and acellular pertussis vaccine group and more Abdominal Pain than the MORF4 gene group, Many children with Autistic Disorder spectrum disorders (ASDs) suffer from Gastrointestinal problem such as diarrhoea, constipation and Abdominal Pain, Children with Autistic Disorder spectrum disorders (Atrial Septal Defects) experience high rates of Anxiety Disorders, sensory processing problems, and gastrointestinal (GI) problems, The results indicate that Anxiety Disorders, sensory over-responsivity and GI problems are possibly interrelated phenomenon for children with Atrial Septal Defects, and may have common underlying mechanisms., Decreased small intestinal mucosa lactase level not associated with Intestinal inflammation or injury is common in autistic children and may contribute to abdominal discomfort, Pain:-:Point in time:^Patient:- and observed aberrant behavior., Autistic behavior is often accompanied by numerous disturbing symptoms on the part of gastrointestinal system, such as Abdominal Pain, constipation or Diarrhea., Information on children's stool patterns and gut symptoms collected by questionnaire at 4 weeks and at 6, 18, 30 and 42 months of age were available for 12,984 children from the Avon Longitudinal Study of Parents and Children (Avon Longitudinal Study of Parents and Children (Avon Longitudinal Study of Parents and Children (ALSPAC))), Comparison of the Atrial Septal Defects and control group during the first 3.5 years of life showed no major differences in stool colour or consistency, or in frequency of diarrhoea, constipation, Blood in stool or Abdominal Pain., Constipation is a frequent finding in children with No gastrointestinal symptom and Autistic Disorder, particularly in the Rectum and sigmoid colon, often with acquired megarectum. The absence of any correlation between the clinical history and the degree of fecal impaction in autistic children confirms the importance of an abdominal radiograph in the assessment of their degree of constipation., In a sample of 137 children, age 24-96 months, classified as having Autistic Disorder or Atrial Septal Defects by the Autism Diagnostic Observation Schedule-Generic, 24 percent had a history of at least one chronic gastrointestinal symptom. The most common symptom was Diarrhea, which occurred in 17 percent.[SEP]Relations: Abdominal Pain:-:Point in time:^Patient:- has relations: phenotype_phenotype with Abdominal symptom, phenotype_phenotype with Abdominal symptom, phenotype_phenotype with Pain, phenotype_phenotype with Pain, phenotype_phenotype with Episodic Abdominal Pain, phenotype_phenotype with Episodic Abdominal Pain, disease_phenotype_positive with plague, disease_phenotype_positive with plague, disease_phenotype_positive with congenital Diarrhea, disease_phenotype_positive with congenital Diarrhea.", "label": "yes"}
{"original_question": "Is exome sequencing efficient for the detection of germline mutations?", "id": "converted_334", "sentence1": "Is exome sequencing efficient for the detection of germline Gene Mutation?", "sentence2": "Whole exome sequencing is an efficient and sensitive method for detection of germline Gene Mutation in patients with phaeochromcytomas and PARAGANGLIOMAS 5, Whole exome sequencing is sensitive, rapid and efficient for detection of PCC/PGL germline Gene Mutation., These results from deep sequencing demonstrate a higher mutational detection rate than reported with conventional sequencing methodology., We performed exome sequencing of Germline DNA from members of the affected family. Exome-wide analysis identified a novel loss-of-function mutation in the BAP1 gene, previously suggested as a tumor suppressor., whole-exome sequencing has been widely applied in the identification of germline Gene Mutation underlying Mendelian disorders, somatic Gene Mutation in various Malignant Neoplasms and de novo Gene Mutation in Neurodevelopmental Disorders.[SEP]Relations: adaptation to pheromone regulating conjugation with mutual genetic exchange has relations: bioprocess_bioprocess with negative adaptation of signaling pathway, bioprocess_bioprocess with negative adaptation of signaling pathway, bioprocess_bioprocess with response to pheromone regulating conjugation with mutual genetic exchange, bioprocess_bioprocess with response to pheromone regulating conjugation with mutual genetic exchange, bioprocess_bioprocess with regulation of conjugation, bioprocess_bioprocess with regulation of conjugation. Paraganglioma has relations: disease_phenotype_positive with von Hippel-Lindau disease, disease_phenotype_positive with von Hippel-Lindau disease, disease_phenotype_positive with hereditary pheochromocytoma-paraganglioma, disease_phenotype_positive with hereditary pheochromocytoma-paraganglioma.", "label": "yes"}
{"original_question": "Is there a relationship between B cells and Multiple Sclerosis?", "id": "converted_2036", "sentence1": "Is there a relationship between Deciduous maxillary right first molar tooth cells and Multiple Sclerosis?", "sentence2": "These results suggest that RRMS patients with radiological phenotypes showing high Nerve Degeneration have changes in Deciduous maxillary right first molar tooth cells characterized by down-regulation of Deciduous maxillary right first molar tooth-cell-specific genes and increased activation status, Although the exact etiology is still obscure, the leading hypothesis behind MS relapses is acute inflammatory attacks on Central Nervous System Myelin Sheath and axons. This complex process involves Deciduous maxillary right first molar tooth and Therapeutic gamma delta T-lymphocytes together with Specimen Source Codes - Macrophages and Microglia., It is currently known that Antigens, Antigens, CD24 serves as a costimulatory factor of Therapeutic gamma delta T-lymphocytes that regulate their homeostasis and proliferation, while in Deciduous maxillary right first molar tooth cells, Antigens, Antigens, CD24 is functionally involved in cell activation and differentiation. Antigens, Antigens, CD24 can enhance Autoimmune Diseases in terms of its protective role in the clonal deletion of autoreactive thymocytes, Multiple Deciduous maxillary right first molar tooth cell-dependent mechanisms contributing to inflammatory Peripheral Peripheral demyelination of the Central Nervous System have been explored using experimental autoimmune encephalomyelitis (EAE), a CD4 T cell-dependent animal model for Multiple Sclerosis. , The role of Deciduous maxillary right first molar tooth cells in Multiple Sclerosis: rationale for Deciduous maxillary right first molar tooth-cell-targeted therapies., Interest in CD8+ Therapeutic gamma delta T-lymphocytes and Deciduous maxillary right first molar tooth cells was initially inspired by observations in Multiple Sclerosis rather than in animal models: CD8+ Therapeutic gamma delta T-lymphocytes predominate in Multiple Sclerosis lesions, oligoclonal immunoglobulin bands in CSF have long been recognised as diagnostic and prognostic markers, and anti-Deciduous maxillary right first molar tooth-cell therapies showed considerable efficacy in Multiple Sclerosis., Differential effects of fingolimod on Deciduous maxillary right first molar tooth-cell populations in Multiple Sclerosis., Unaltered regulatory Deciduous maxillary right first molar tooth-cell frequency and function in patients with Multiple Sclerosis., Deciduous maxillary right first molar tooth cells are increasingly recognized as major players in Multiple Sclerosis pathogenesis., These observations underscore the Deciduous maxillary right first molar tooth cell's contribution to the putative underpinnings of Multiple Sclerosis., Data suggesting that Deciduous maxillary right first molar tooth cells play a role in the pathogenesis of Multiple Sclerosis have been accumulating for the past five decades, demonstrating that the Cerebrospinal Fluid and central nervous system tissues of Multiple Sclerosis patients contain Deciduous maxillary right first molar tooth cells, Plasma Cells, Antibodies, in vitro diagnostic, and immunoglobulin G., Deciduous maxillary right first molar tooth-cell-targeted treatment for Multiple Sclerosis: mechanism of action and clinical data., Subset composition and cytokine production of Deciduous maxillary right first molar tooth cells derived from Peripheral blood mononuclear cell (cell) from Multiple Sclerosis patients under fingolimod treatment, untreated Multiple Sclerosis patients and healthy controls were analyzed by flow cytometry and ELISA., In particular, antigen presentation between Deciduous maxillary right first molar tooth cells and Therapeutic gamma delta T-lymphocytes, increased trafficking of Deciduous maxillary right first molar tooth cells across the blood-brain barrier, and Autoantibodies produced by Plasma Cells may contribute to the pathophysiology of autoimmune disorders such as Multiple Sclerosis., Accumulating evidence supports a major role of Deciduous maxillary right first molar tooth cells in Multiple Sclerosis (MS) pathogenesis., Further research is needed to elucidate the pathology of Deciduous maxillary right first molar tooth cells and their role in central nervous system Autoimmune Diseases, including Multiple Sclerosis., Targeting Deciduous maxillary right first molar tooth cells in the treatment of Multiple Sclerosis: recent advances and remaining challenges, phingosine-1-phosphate receptors control Deciduous maxillary right first molar tooth-cell migration through signaling components associated with Primary immune deficiency disorder, Chronic Lymphocytic Leukemia, and Multiple Sclerosis[SEP]Relations: Multiple Sclerosis has relations: disease_disease with brain disease, disease_disease with brain disease, disease_disease with progressive Multiple Sclerosis, disease_disease with progressive Multiple Sclerosis, disease_disease with Multiple Sclerosis, susceptibility to, disease_disease with Multiple Sclerosis, susceptibility to, disease_protein with BCHE, disease_protein with BCHE, disease_protein with CD6, disease_protein with CD6.", "label": "yes"}
{"original_question": "Does TIMELESS-TIPIN participate in replisome disassembly?", "id": "converted_4368", "sentence1": "Does TIMELESS gene-TIPIN participate in replisome disassembly?", "sentence2": "TIMELESS gene gene-TIPIN and UBXN-3 promote replisome disassembly during DNA replication termination in Caenorhabditis elegans., We show that UBXN-3 is important in vivo for replisome disassembly in the absence of TIMELESS gene gene-TIPIN. Correspondingly, co-depletion of UBXN-3 and TIMELESS gene gene causes profound synthetic lethality. Since the Homo sapiens orthologue of UBXN-3, FAF1 gene gene, is a candidate tumour suppressor, these findings suggest that manipulation of CASK gene disassembly might be applicable to future strategies for treating Homo sapiens cancer.[SEP]Relations: TIMELESS gene has relations: protein_protein with TIPIN, protein_protein with TIPIN, bioprocess_protein with DNA repair, bioprocess_protein with DNA repair, bioprocess_protein with DNA replication, bioprocess_protein with DNA replication, bioprocess_protein with positive regulation of double-strand break repair via homologous recombination, bioprocess_protein with positive regulation of double-strand break repair via homologous recombination, bioprocess_protein with DNA replication checkpoint signaling, bioprocess_protein with DNA replication checkpoint signaling.", "label": "yes"}
{"original_question": "Do RNA:DNA hybrids preferentially form in high or low GC regions?", "id": "converted_1392", "sentence1": "Do RNA:DNA hybrids preferentially form in high or low GC regions?", "sentence2": "Intrinsic termination signals for multisubunit bacterial RNA polymerases (RNAPs) encode a GC-rich stem-loop structure followed by a polyuridine [poly(U)] tract, and it has been proposed that steric clash of the stem-loop with the exit pore of the RNAP imposes a shearing force on the RNA in the downstream RNA:DNA hybrid, resulting in misalignment of the active site, We have observed that transcription through the GC-rich FMR1 gene gene 5'UTR region favors R-loop formation, with the nascent (G-rich) RNA forming a stable RNA:DNA hybrid with the template DNA strand, thereby displacing the non-template DNA strand., Transcription termination by bacterial RNA polymerase (RNAP) occurs at sequences coding for a GC-rich RNA hairpin followed by a U-rich tract. We used single-molecule techniques to investigate the mechanism by which three representative terminators (his, t500, and tR2) destabilize the elongation complex (EC)., In the 5' flanking region, Nucleotides -234 to -213 encompass a GC-rich region which exhibits high Homologous Gene (greater than 70%) to the 5' flanking regions of the Genes of all the Apolipoproteins B published to date, namely, apo-A-II (-497 to -471), apo-A-I (approximately -196 to -179), Apolipoprotein E (-409 to -391), and apo-C-III (approximately -116 to -103)., Recently, we demonstrated that cotranscriptional RNA•DNA hybrids are preferentially formed at GC-rich trinucleotide and tetranucleotide repeat sequences in vitro as well as in human genomic DNA., Considering the extent of transcription through the human genome as well as the abundance of GC-rich and/or non-canonical DNA structure forming tandem repeats, RNA•DNA hybrids may represent a common mutagenic conformation., Recently, we demonstrated that cotranscriptional RNA•DNA hybrids are preferentially formed at GC-rich trinucleotide and tetranucleotide repeat sequences in vitro as well as in human genomic DNA. [SEP]Relations: apolipoprotein binding has relations: molfunc_protein with VLDLR, molfunc_protein with VLDLR, molfunc_protein with MTTP, molfunc_protein with MTTP, molfunc_protein with LPA, molfunc_protein with LPA, molfunc_protein with LPL, molfunc_protein with LPL, molfunc_protein with MAPT, molfunc_protein with MAPT.", "label": "yes"}
{"original_question": "Can zinc finger nucleases be used to combat disease?", "id": "converted_288", "sentence1": "Can Zinc Fingers nucleases be used to combat disease?", "sentence2": "Genetic engineering has emerged as a powerful mechanism for understanding biological systems and a potential approach for redressing Congenital Disorders., This is of particular importance, given the momentum currently behind ZFNs in moving into phase I clinical trials. This study provides a historical account of the origins of Zinc Finger Nucleases technology, an analysis of current techniques and applications, and an examination of the ethical issues applicable to translational Zinc Finger Nucleases genetic engineering in early phase clinical trials., This broad range of tractable species renders ZFNs a useful tool for improving the understanding of complex physiological systems, to produce Animals, Transgenic, Cultured Cell Line, and Plants, and to treat Homo sapiens disease., We observe comparably high frequencies in Homo sapiens T cells, raising the possibility of strategies based on zinc-finger nucleases for the treatment of disease., Using engineered nucleases, such as Zinc Finger Nucleases (ZFNs) or Transcription Activator-Like Effector Nucleases (Transcription Activator-Like Effector Nucleases), to make targeted genomic modifications has become a common technique to create new model organisms and custom Cultured Cell Line, and has shown great promise for disease treatment., Zinc Finger nucleases (ZFNs) have been used to create precise genome modifications at frequencies that might be therapeutically useful in gene therapy., Zinc finger nucleases as tools to understand and treat Homo sapiens diseases., Evaluation of novel design strategies for developing Zinc Fingers nucleases tools for treating Homo sapiens diseases., An over expression APP model for anti-Alzheimer disease drug screening created by Zinc Fingers nuclease technology., Oxidase-deficient neutrophils from Granulomatous Disease, Chronic, X-Linked Induced Pluripotent Stem Cells: functional correction by Zinc Fingers nuclease-mediated safe harbor targeting., Recently, it has been shown that targeted Mutagenesis Procedure using zinc-finger nucleases (ZFNs) and transcription activator-like effector nucleases (Transcription Activator-Like Effector Nucleases) can be used to generate knockout Zebrafish lines for analysis of their function and/or developing disease models, Using engineered nucleases, such as Zinc Finger Nucleases (ZFNs) or Transcription Activator-Like Effector Nucleases (Transcription Activator-Like Effector Nucleases), to make targeted genomic modifications has become a common technique to create new model organisms and custom Cultured Cell Line, and has shown great promise for disease treatment, Gene correction by homologous recombination with Zinc Fingers nucleases in primary cells from a mouse model of a generic recessive genetic disease., raising the possibility of strategies based on zinc-finger nucleases for the treatment of disease.[SEP]Relations: C2H2 Zinc Fingers domain binding has relations: molfunc_protein with ZXDC, molfunc_protein with ZXDC, molfunc_protein with EHMT1, molfunc_protein with EHMT1, molfunc_protein with ZXDA, molfunc_protein with ZXDA, molfunc_protein with LEF1, molfunc_protein with LEF1, molfunc_protein with EHMT2, molfunc_protein with EHMT2.", "label": "yes"}
{"original_question": "Does lucatumumab bind to CD140?", "id": "converted_2862", "sentence1": "Does lucatumumab bind to CD140?", "sentence2": "Lucatumumab is a fully humanized anti-CD40 Antigens Antigens antibody that blocks interaction of CD40 Antigens Antigens Ligand with CD40 Antigens Antigens and also mediates antibody-dependent cell-mediated cytotoxicity (ADCC). , Phase I study of the anti-CD40 Antigens Antigens humanized monoclonal antibody lucatumumab (CHIR-12.12) in relapsed Chronic Lymphocytic Leukemia., Saturation of CD40 Antigens Antigens receptor on CLL cells was uniform at all doses post-treatment but also persisted at trough time points in the 3.0 mg/kg or greater cohorts.[SEP]Relations: Chronic lymphatic leukemia has relations: drug_effect with Pramipexole, drug_effect with Pramipexole, drug_effect with Paroxetine, drug_effect with Paroxetine, drug_effect with Nelarabine, drug_effect with Nelarabine, disease_phenotype_positive with Aicardi-Goutieres syndrome, disease_phenotype_positive with Aicardi-Goutieres syndrome, disease_phenotype_positive with sweet syndrome, disease_phenotype_positive with sweet syndrome.", "label": "no"}
{"original_question": "Can CPX-351 be used for the treatment of tuberculosis?", "id": "converted_2860", "sentence1": "Can CPX-351 be used for the treatment of tuberculosis?", "sentence2": "CPX-351 is a novel liposomal formulation of cytarabine and daunorubicin which has recently been FDA approved for treatment of RUNX1 gene (Leukemia, Myelocytic, Acute).[SEP]Relations: acute promyelocytic leukemia has relations: disease_protein with TBL1XR1, disease_protein with TBL1XR1, disease_protein with ITGAX, disease_protein with ITGAX. Daunorubicin has relations: drug_drug with Baricitinib, drug_drug with Baricitinib, drug_drug with Novobiocin, drug_drug with Novobiocin. Cytarabine has relations: drug_drug with Baricitinib, drug_drug with Baricitinib.", "label": "no"}
{"original_question": "Is durvalumab used for lung cancer treatment?", "id": "converted_2832", "sentence1": "Is durvalumab used for Primary malignant neoplasm of lung treatment?", "sentence2": " In the phase III PACIFIC trial consolidation with durvalumab, an anti-PDL-1 immunoglobulin complex location, was associated with survival benefit in patients diagnosed with LA-Non-Small Cell Lung Carcinoma who responded to concurrent chemoradiotherapy., METHODS: An electronic literature search was performed of public databases (MEDLINE, Excerpta Medica dataBASE [EMBASE], and Cochrane) and conference proceedings for trials using Substance with programmed cell death protein 1 inhibitor mechanism of action (substance) (nivolumab and pembrolizumab) and CD274 wt Allele inhibitors (atezolizumab, durvalumab, and avelumab) in patients with Non-Small Cell Lung Carcinoma., Durvalumab in non-small-cell Primary malignant neoplasm of lung patients: current developments., Single-agent durvalumab showed clinical efficacy and a manageable safety profile in advanced non-small-cell Primary malignant neoplasm of lung, particularly the ≥25% CD274 wt Allele+ population., Six drugs including one CTLA-4 blocker (ipilimumab), two PD-1 blockers (nivolumab and pembrolizumab) and three CD274 wt Allele blockers (atezolizumab, avelumab and durvalumab) are approved for the treatment of different types of Malignant Neoplasms including both Solid Neoplasm such as Melanocytic neoplasm, Primary malignant neoplasm of lung, Malignant Head and Neck Neoplasm, Malignant neoplasm of urinary bladder and Merkel cell carcinoma as well as Hematologic Neoplasms such as classic Hodgkin's lymphoma. , PURPOSE OF REVIEW: The therapeutic armamentarium for advanced non-small-cell Primary malignant neoplasm of lung has evolved considerably over the past years. Immune Checkpoint Inhibitors targeting programmed cell death-1 such as pembrolizumab and nivolumab or programmed cell death ligand 1 such as atezolizumab, durvalumab and avelumab have shown favorable efficacy results in this patient population in the first-line and second-line setting., In addition, preclinical and early clinical evidence suggests that chemotherapy and radiation may work synergistically with anti-PD-1/CD274 wt Allele therapy to promote Antitumor immunity, which has led to the initiation of clinical trials testing these drugs in patients with stage III Non-Small Cell Lung Carcinoma. A preliminary report of a randomized phase III trial, the PACIFIC trial, demonstrated an impressive increase in median progression-free survival with consolidative durvalumab, a CD274 wt Allele inhibitor, compared with observation after cCRT. , ICI, such as the Substance with programmed cell death protein 1 inhibitor mechanism of action (substance) nivolumab and pembrolizumab and the CD274 wt Allele inhibitor atezolizumab, have already been marketed for the treatment of pretreated patients with advanced Non-Small Cell Lung Carcinoma., The PACIFIC trial assessing durvalumab after standard chemoradiotherapy for locally advanced Non-Small Cell Lung Carcinoma has already met its primary endpoint and the potential of durvalumab will be reinforced if phase III randomized studies of first-line (MYSTIC trial) and second or subsequent (ARCTIC trial) lines of therapy demonstrate superiority over the current standard of care.<br>[SEP]Relations: Ipilimumab has relations: drug_drug with Durvalumab, drug_drug with Durvalumab, drug_drug with Dusigitumab, drug_drug with Dusigitumab, drug_drug with Lerdelimumab, drug_drug with Lerdelimumab. Nivolumab has relations: drug_drug with Durvalumab, drug_drug with Durvalumab, drug_drug with Dusigitumab, drug_drug with Dusigitumab.", "label": "yes"}
{"original_question": "Are genomic regulatory blocks (GRBs) any different than TADs?", "id": "converted_3336", "sentence1": "Are genomic regulatory blocks (GRBs) any different than Tietz syndrome?", "sentence2": "Topologically associating domains are ancient features that coincide with Metazoan clusters of extreme noncoding conservation., Clusters of CNEs define the span of regulatory inputs for many important developmental regulators and have been described previously as genomic regulatory blocks (GRBs). Their function and distribution around important Genes, Regulator raises the question of how they relate to 3 Days conformation of these loci. Here, we show that clusters of CNEs strongly coincide with topological organisation, predicting the boundaries of hundreds of topologically associating domains (Tietz syndrome) in human and Drosophila <basidiomycetes> <basidiomycetes>. The set of Tietz syndrome that are associated with high levels of noncoding conservation exhibit distinct properties compared to Tietz syndrome devoid of extreme noncoding conservation. The close correspondence between extreme noncoding conservation and Tietz syndrome suggests that these Tietz syndrome are ancient, revealing a regulatory architecture conserved over hundreds of millions of years.Metazoan genomes contain many clusters of conserved noncoding elements. Here, the authors provide evidence that these clusters coincide with distinct topologically associating domains in Homo sapiens and Drosophila <basidiomycetes> <basidiomycetes>, revealing a conserved regulatory genomic architecture.[SEP]Relations: Tietz syndrome has relations: disease_phenotype_positive with Congenital sensorineural hearing impairment, disease_phenotype_positive with Congenital sensorineural hearing impairment, disease_phenotype_positive with Bilateral sensorineural hearing impairment, disease_phenotype_positive with Bilateral sensorineural hearing impairment, disease_phenotype_positive with Hearing impairment, disease_phenotype_positive with Hearing impairment, disease_phenotype_positive with White eyelashes, disease_phenotype_positive with White eyelashes, disease_phenotype_positive with Autosomal dominant inheritance, disease_phenotype_positive with Autosomal dominant inheritance.", "label": "no"}
{"original_question": "Is diphosphatidylglycerol (cardiolipin) a phospholipid of the mitochondrial membranes?", "id": "converted_2129", "sentence1": "Is Diphosphatidylglycerols (cardiolipin) a phospholipid of the Mitochondrial Inheritance membranes?", "sentence2": "A unique Cytoplasmic Cytoplasmic organelle for studying Tissue Tissue membrane biochemistry is the mitochondrion whose functionality depends on a coordinated supply of Proteins and Lipids. Mitochondria are capable of synthesizing several Lipids autonomously such as Phosphatidyl glycerol, cardiolipin and in part phosphatidylethanolamine, Phosphatidic Acid and Cytidine Diphosphate Diglycerides., A small decrease of Diphosphatidylglycerols also occurred in the Liver neoplasms Mitochondria inner Tissue Tissue membrane. , Diphosphatidylglycerol was confined to the Mitochondrial Inheritance fraction, where it represented about 7% of the total phosphoacylglycerols. , Mitochondrial Membranes were isolated from the Myocardium of young (4-month-old) and aged (33-month-old) male Long-Evans rats and compared in terms of cholesterol content and phospholipid and fatty acid composition. In aged rats, as compared to young, the major observations include: markedly higher cholesterol content; increased percentage of Sphingomyelins and Diphosphatidylglycerols (cardiolipin); , The polyglycerophosphatides (typified by Diphosphatidylglycerols) were apparently synthesized in situ by intramitochondrial Tissue Tissue membrane-bound enzymes using CDP-diglycerides as intermediates. , Both the Mitochondrial Inheritance and microsomal fractions contained significant proportions of solvent front phospholipid (spleen fibrinolytic proteinase (human)) and whereas the Mitochondrial Inheritance spleen fibrinolytic proteinase (human) displayed the relatively unsaturated fatty acid composition characteristic of Diphosphatidylglycerols (cardiolipin), the Fatty Acids of the microsomal spleen fibrinolytic proteinase (human) were distinctly more Saturated., Ten to 15% of microsomal radioactive CDP-diglycerides was transferred to Mitochondrial Inheritance membranes and incorporated into Mitochondrial Inheritance radioactive Lipids identified as Phosphatidyl glycerol, phosphatidylglycerophosphate, and, when [14C]linoleoyl CDP-diglycerides were used, Diphosphatidylglycerols (cardiolipin)., The Enzyme [APC] responsible for the conversion of Phosphatidyl glycerol to Diphosphatidylglycerols (cardiolipin) in the presence of Cytidine Diphosphate Diacylglycerol is firmly associated with Mitochondrial Inheritance membranes and is not extracted with hypotonic or hypertonic media or with nonionic detergents., The mechanism of cardiolipin (Diphosphatidylglycerols) biosynthesis was examined in Mitochondria and outer and inner Mitochondrial Inheritance membranes prepared from Cavia porcellus and Rattus norvegicus livers to determine whether this formation from Phosphatidyl glycerol was absolutely dependent on cytidinediphosphodiglyceride, as previously reported for intact Mitochondria., In isolated Mitochondrial Inheritance outer membranes, cardiolipin (Diphosphatidylglycerols) increased CPT1A wt Allele activity 4-fold and the Km for carnitine 6-fold., Ten to 15% of microsomal radioactive CDP-diglycerides was transferred to Mitochondrial Inheritance membranes and incorporated into Mitochondrial Inheritance radioactive Lipids identified as Phosphatidyl glycerol, phosphatidylglycerophosphate, and, when [14C]linoleoyl CDP-diglycerides were used, Diphosphatidylglycerols (cardiolipin)., 90% or more of the phospholipid, cardiolipin was found in the Mitochondrial Inheritance membranes of Wildtype Finding and petite yeast., Furthermore, the same mechanism for the biosynthesis of cardiolipin was operational in the outer and inner Mitochondrial Inheritance membranes., The mechanism of cardiolipin (Diphosphatidylglycerols) biosynthesis was examined in Mitochondria and outer and inner Mitochondrial Inheritance membranes prepared from Cavia porcellus and Rattus norvegicus livers to determine whether this formation from Phosphatidyl glycerol was absolutely dependent on cytidinediphosphodiglyceride, as previously reported for intact Mitochondria, Cardiolipins (CL) is a key phospholipid in Mitochondrial Inheritance membranes, playing important roles in maintaining the functional integrity and dynamics of Mitochondria in animal allergen extracts and Candida albicans allergenic extract, Cardiolipins, the specific phospholipid of Mitochondria, is involved in the biogenesis, the dynamics, and the supramolecular organization of Mitochondrial Inheritance membranes, Cardiolipins (CL), the signature phospholipid of Mitochondrial Inheritance membranes, is crucial for both Mitochondrial Inheritance function and cellular processes outside of the Mitochondria, Since it has been recognized that Mitochondria are crucial not only for energy metabolism but also for other cellular functions, there has been a growing interest in cardiolipin, the specific phospholipid of Mitochondrial Inheritance membranes, Cardiolipins, the main anionic phospholipid in Mitochondrial Inheritance membranes, is expected to be a determinant in this adaptive mechanism since it modulates the activity of most Membrane Proteins, Ten to 15% of microsomal radioactive CDP-diglycerides was transferred to Mitochondrial Inheritance membranes and incorporated into Mitochondrial Inheritance radioactive Lipids identified as Phosphatidyl glycerol, phosphatidylglycerophosphate, and, when [14C]linoleoyl CDP-diglycerides were used, Diphosphatidylglycerols (cardiolipin), Cardiolipins is normally localized to the inner Mitochondrial Inheritance Tissue Tissue membrane; however, when cardiolipin becomes externalized to the surface of dysregulated Mitochondria, it promotes inflammasome activation and stimulates the elimination of damaged or nonfunctional Mitochondria by mitophagy, In isolated Mitochondrial Inheritance outer membranes, cardiolipin (Diphosphatidylglycerols) increased CPT1A wt Allele activity 4-fold and the Km for carnitine 6-fold. , Increasing levels of cardiolipin differentially influence packing of phospholipids found in the Inner Mitochondrial Inheritance Tissue Tissue membrane., Here, we used Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae subjected to conditions that affect Mitochondrial Inheritance metabolism as a model to determine the possible role of cardiolipin in stress adaptation. , This decline of respiration was attributed to a progressive diminution of the number of Mitochondria in copper-treated cells, based on the demonstration of the concomitant decline of (1) cardiolipin (Diphosphatidylglycerols) and Cytochrome aa3 (CYTOCHROME C OXIDASE), two specific markers of Inner Mitochondrial Inheritance Tissue Tissue membrane, and (2) fumarase activity, a specific marker of Mitochondrial Inheritance matrix space., Diphosphatidylglycerol (diphenylguanidine) or cardiolipin, a specific component of the inner Mitochondrial Inheritance Tissue Tissue membrane, represents about 4% of the total lipid content., Experimental results confirmed that the biosynthesis of cardiolipin, from the Tissue Tissue membrane-bound radioactive Phosphatidyl glycerol in intact Mitochondria isolated from Cavia porcellus and Rattus norvegicus Abdomen>Liver, was absolutely dependent on CDP-diglycerides and required the addition of Cations, Divalent., We have shown that decrease of cardiolipin in Mitochondrial Inheritance Tissue Tissue membrane occurs early during Ischemia Procedure, and only during the irreversible phase of Ischemia Procedure are phosphatidylethanolamine and Phosphatidylcholine antibody broken down., Partial purification of Diphosphatidylglycerols synthetase from Abdomen>Liver Mitochondrial Inheritance membranes., A small decrease of Diphosphatidylglycerols also occurred in the Liver neoplasms Mitochondria inner Tissue Tissue membrane.[SEP]Relations: Inner Mitochondrial Inheritance Tissue membrane has relations: cellcomp_protein with PHB, cellcomp_protein with PHB, cellcomp_protein with PMPCB, cellcomp_protein with PMPCB. Mitochondrial Inheritance Tissue membrane has relations: cellcomp_protein with CARD19, cellcomp_protein with CARD19, cellcomp_protein with ACADL, cellcomp_protein with ACADL. Mitochondrial Inheritance outer Tissue membrane has relations: cellcomp_protein with BNIP3L, cellcomp_protein with BNIP3L.", "label": "yes"}
{"original_question": "Do exon 38 or 39 KMT2D missense variants cause Kabuki syndrome type 1 (KS1)?", "id": "converted_3835", "sentence1": "Do exon 38 or 39 MLL2 protein, human missense variants cause KABUKI SYNDROME 2 type 1 (CXCL14 gene)?", "sentence2": "A restricted spectrum of missense MLL2 protein, human variants cause a multiple malformations disorder distinct from KABUKI SYNDROME 2., To investigate if specific exon 38 or 39 MLL2 protein, human missense variants (megavolt) cause a condition distinct from KABUKI SYNDROME 2 type 1 (CXCL14 gene).METHODS: Multiple individuals, with megavolt in Exons 38 or 39 of MLL2 protein, human that encode a highly conserved region of 54 Antifibrinolytic Antifibrinolytic amino acids flanked by Val3527 and Lys3583, were identified and phenotyped. Functional tests were performed to study their pathogenicity and understand the Disease mechanism.RESULTS: The consistent clinical features of the affected individuals, from seven unrelated families, included Choanal Atresia, Congenital absence of breast with absent nipple or hypoplastic nipples, branchial sinus abnormalities, neck pits, lacrimal duct anomalies, hearing impairment, external ear malformations, and Thyroid Diseases. None of the individuals had Intellectual Disability. The frequency of clinical features, objective software-based facial analysis metrics, and genome-wide peripheral blood DNA methylation patterns in these patients were significantly different from that of CXCL14 gene. Circular dichroism spectroscopy indicated that these megavolt perturb MLL2 protein, human secondary structure through an increased disordered to ɑ-helical transition.CONCLUSION: MLL2 protein, human megavolt located in a specific region spanning Exons 38 and 39 and affecting highly conserved residues cause a novel multiple malformations syndrome distinct from CXCL14 gene. Unlike MLL2 protein, human haploinsufficiency in CXCL14 gene, these megavolt likely result in Disease through a dominant negative mechanism.[SEP]Relations: KABUKI SYNDROME 2 has relations: disease_protein with MLL2 protein, human, disease_protein with MLL2 protein, human, disease_protein with KDM6A, disease_protein with KDM6A, disease_phenotype_positive with Generalized hypotonia, disease_phenotype_positive with Generalized hypotonia, disease_protein with RAP1B, disease_protein with RAP1B, disease_protein with RAP1A, disease_protein with RAP1A.", "label": "no"}
{"original_question": "Is the 22-item sino-nasal outcome test (SNOT-22) a widely used measure for Health-Related Quality-of-Life (HRQOL) associated with chronic rhinosinusitis (CRS)?", "id": "converted_4421", "sentence1": "Is the 22-item sino-nasal outcome test (SNOT-22) a widely used measure for Health-Related Quality-of-Life (HRQOL) associated with Chronic sinusitis (Congenital Rubella Syndrome)?", "sentence2": "The Sino-Nasal-Outcome-Test-22 (SNOT-22) represents the reference questionnaire to assess symptoms, health-related quality-of-life (HRQOL) and treatment-response in patients with Chronic sinusitis (Congenital Rubella Syndrome). , Assessment of health-related quality-of-life in patients with chronic Rhinosinusitis - Validation of the German Sino-Nasal Outcome Test-22 (German-SNOT-22).,  Patients meeting diagnostic criteria for Congenital Rubella Syndrome were prospectively enrolled in a cross-sectional study. Responses from the Sinonasal Outcomes Test-22 (SNOT-22), a measure of patient HRQOL, as well as the Lund-Kennedy and Lund-Mackay scores were recorded at enrollment, Three groups of 12 participants each were examined: patients with Congenital Rubella Syndrome without Multiple polyps (Congenital Rubella Syndrome group), patients with symptoms of Congenital Rubella Syndrome but radiologically normal sinuses (symptoms-only), and healthy controls. Measurements of Nynorsk Language were carried out using aspiration method and humming maneuver. All participants completed the Sino-Nasal Outcome Test (SNOT-22)., PURPOSE: The Sino-Nasal-Outcome-Test-22 (SNOT-22) represents the reference questionnaire to assess symptoms, health-related quality-of-life (HRQOL) and treatment-response in patients with Chronic sinusitis (Congenital Rubella Syndrome)., tcomes included scores on the Congenital Rubella Syndrome disease severity visual analog scale (VAS), 22-item Sino-Nasal Outcome Test (SNOT-22), 5-dimension EuroQoL (EQ-5D) general health status VAS, and 36-item Short-Form Health Survey (SF-36) for HRQoL and nasal polyp-related healthcare resource use questionnaires.RE, BACKGROUND: The 22-item Sino-Nasal Outcome Test (SNOT-22) is a commonly utilized outcome measure for chronic rhinosinus, BACKGROUND: The 22-item sino-nasal outcome test (SNOT-22) is a widely used and powerful patient-reported outcomes measure for chronic rhinosinus, BACKGROUND: Prior study demonstrated that baseline 22-item Sino-Nasal Outcome Test (SNOT-22) aggregate scores accurately predict selection of surgical intervention in patients with chronic rhinosinus, OBJECTIVES/HYPOTHESIS: Sinonasal Outcomes Test-22 (SNOT-22) is used widely as a patient-reported sinonasal quality-of-life (QOL) instrument for endoscopic endonasa, Is sino-nasal outcome test-22 reliable for guiding Chronic sinusitis patients for endoscopic sinus surgery, The Sino-Nasal Outcome Test-22 as a tool to identify Chronic sinusitis in adults with cystic fibrosis, rden. Our objective was to investigate the utility of the 22-item Sino-Nasal Outcome Test (SNOT-22) as a tool to identify Congenital Rubella Syndrome in adults wit, OBJECTIVES/HYPOTHESIS: The 22-item Sinonasal Outcome Test (SNOT-22) is a validated Chronic sinusitis health-related quality-of-life outcome (HRQoL) measure; however, SNOT-22 domains have not been validated specifically for Chronic sinusitis with Non-Alcoholic Fatty Liver Disease Activity Score, OBJECTIVE: The SNOT-22 (22-item Sinonasal Outcome Test) is a high-quality outcome measure that assesses Chronic sinusitis-specific quality of leukemia inhibitory factor, BACKGROUND: The 22-item sino-nasal outcome test (SNOT-22) is a widely used and powerful patient-reported outcomes measure for Chronic sinusitis (Congenital Rubella Syndrome, OBJECTIVES/HYPOTHESIS: The 22-item Sinonasal Outcome Test (SNOT-22) is a validated Chronic sinusitis health-related quality-of-life outcome (HRQoL) measure; however, SNOT-22 domains have not been validated specifically for Chronic sinusitis with nasal polyps (CRSwNP, BACKGROUND: The 22-item Sino-Nasal Outcome Test (SNOT-22) is a commonly utilized outcome measure for Chronic sinusitis (Congenital Rubella Syndrome, OBJECTIVES/HYPOTHESIS: The 22-item Sinonasal Outcome Test (SNOT-22) is a validated Chronic sinusitis health-related quality-of-life outcome (HRQoL) measure; however, SNOT-22 domains have not been validated specifically for Chronic sinusitis with nasal polyps (CRSwNP).STUDY DESIGN: Validation of SNOT-22 domain structure, using data from 3 randomized, placebo-controlled, double-blinded, multicenter clinical trials of dupilumab in adults with moderate-to-severe CRSwNP.METHODS: Preliminary dimensional structure was derived by exploratory factor analyses of SNOT-22 data from a phase 2 trial (NCT01920, OBJECTIVES: We set out to determine the psychometric validation of a disease-specific health related quality of life instrument for use in Chronic sinusitis, the 22 item Sinonasal Outcome Test (SNOT-22), a ResponseLevel - ResponseLevel - modification of a pre-existing instrument, the SNOT-20.DESIGN, SETTING AND PARTICIPANTS: The National Comparative Audit of Surgery for Nasal Polyposis and Chronic Rhinosinusitis was a prospective cohort study collecting data on 3128 adult patients undergoing sinonasal sur, OBJECTIVE: The SNOT-22 (22-item Sinonasal Outcome Test) is a high-quality outcome measure that assesses Chronic sinusitis-specific quali, act of Congenital Rubella Syndrome. We sought to determine if 22-item Sino-Nasal Outcome Test (SNOT-22) score is predictive of patient-perceived Congenital Rubella Syndrome symptom control.METHODS: Prospective cross-sectional study of 2, The Sinonasal Outcome Test (SNOT-22) Is a Poor Diagnostic Tool for Chronic Rhinosinusitis., The 22-item Sino-Nasal Outcome Test accurately reflects patient-reported control of Chronic sinusitis symptomatology., Development of Sinonasal Outcome Test (SNOT-22) Domains in Chronic Rhinosinusitis With Nasal Polyps., cture with strong Cronbach's alpha values (all >0.80). Moderate-to-high correlations were observed between change in SNOT-22 domain scores and other study patient-reported outcome measures, along with large effect-size estimates (≥0.7), demonstrating re[SEP]Relations: Chronic sinusitis has relations: disease_phenotype_positive with Keutel syndrome, disease_phenotype_positive with Keutel syndrome, disease_phenotype_positive with familial nasal acilia, disease_phenotype_positive with familial nasal acilia. Nasal Multiple polyps has relations: drug_effect with Pramipexole, drug_effect with Pramipexole, drug_effect with Human calcitonin, drug_effect with Human calcitonin, drug_effect with Ropinirole, drug_effect with Ropinirole.", "label": "yes"}
{"original_question": "Is Satb1 a transcription factor?", "id": "converted_4434", "sentence1": "Is DNA-Binding Protein SATB1 a transcription factor?", "sentence2": "Special AT-rich sequence binding protein-1 (SATB1) is localized to the Atomic Nucleus and remodels chromatin location location structure in Therapeutic gamma delta T-lymphocytes, chromatin location location organizers SATB2 and SATB1 , transcription factor complexes. These MYB complexes assemble aberrantly with LYL1 protein, human protein, human, TCF3 wt Allele, C/EBP family members, LMO2 wt Allele wt Allele, and SATB1. , Staining for the transcription factors FOXP2 gene, DNA-Binding Protein SATB1 and DNA Binding Protein SATB2 labeled most Ganglion cell in the avian ganglion cell layer.[SEP]Relations: Tat protein binding has relations: molfunc_protein with DNAJA1, molfunc_protein with DNAJA1, molfunc_protein with DNAJA1, molfunc_protein with DNAJA1, molfunc_protein with GABARAPL1, molfunc_protein with GABARAPL1, molfunc_protein with GABARAPL1, molfunc_protein with GABARAPL1. Protein S human has relations: drug_drug with Factor XIII (human), drug_drug with Factor XIII (human).", "label": "yes"}
{"original_question": "Are DNA helicases involved in progeroid syndromes?", "id": "converted_1030", "sentence1": "Are DNA Helicases involved in progeroid syndromes?", "sentence2": "Among these syndromes, relevant advances have recently been made in Werner syndrome, one of several progeroid syndromes characterized by defective DNA Helicases,, Progeroid syndromes (Chromosome 11p11.2 Deletion Syndrome) constitute a group of disorders characterized by clinical features mimicking physiological aging at an early age., However, all the characterized Chromosome 11p11.2 Deletion Syndrome enter in the field of rare monogenic disorders and several causative genes have been identified. These can be separated in subcategories corresponding to (i) genes encoding DNA repair factors, in particular, DNA Helicases, and (ii) genes affecting the structure or post-translational maturation of Lamin Type A, a major nuclear component., None of the known progerias represents true precocious ageing. Some of them, including Werner (WS), Bloom (BS), and Rothmund-Thomson syndromes (Rothmund-Thomson syndrome) as well as combined xeroderma pigmentosa-Cockayne syndrome (XP-CS) are characterised by features resembling precocious ageing and the increased risk of malignant disease. Such phenotypes result from the Gene Mutation of the genes encoding Proteins involved in the maintenance of genomic integrity, in most cases DNA Helicases., Single-Genes Gene Mutation can produce Homo sapiens progeroid syndromes--phenotypes that mimic usual or \"normative\" aging., The prototypic example of the former is the Werner syndrome, a condition caused by Gene Mutation of the RecQ family of DNA Helicases., Progeria and progeroid syndromes are characterized by the earlier onset of complex senescent phenotypes. Werner Syndrome was originally identified as a Genes responsible for Werner syndrome (WS; \"Progeria of Adults\"). The Werner Syndrome Genes product has RecQ-type helicase domains in the central region of the Protein Info.[SEP]Relations: progeria has relations: disease_disease with progeroid syndrome, disease_disease with progeroid syndrome, disease_disease with Hutchinson-Gilford progeria syndrome, disease_disease with Hutchinson-Gilford progeria syndrome. Werner syndrome has relations: disease_disease with progeroid syndrome, disease_disease with progeroid syndrome, disease_phenotype_positive with Progeroid facial appearance, disease_phenotype_positive with Progeroid facial appearance. Rothmund-Thomson syndrome has relations: disease_disease with progeroid syndrome, disease_disease with progeroid syndrome.", "label": "yes"}
{"original_question": "Is nivolumab used for treatment of Non–Small-Cell Lung Cancer?", "id": "converted_882", "sentence1": "Is nivolumab used for treatment of Non–Small-Cell Lung Cancer?", "sentence2": "BACKGROUND: Patients with advanced squamous-cell non-small-cell Primary malignant neoplasm of lung (NSCLC) who have disease progression during or after first-line chemotherapy have limited treatment options. This randomized, open-label, international, phase 3 study evaluated the efficacy and safety of nivolumab, a fully Homo sapiens IgG4 immunoglobulin complex immunoglobulin complex programmed death 1 (PDCD1 wt Allele) immune-checkpoint-inhibitor antibody, as compared with docetaxel in this patient population., CONCLUSIONS: Among patients with advanced, previously treated squamous-cell NSCLC, overall survival, response rate, and progression-free survival were significantly better with nivolumab than with docetaxel, regardless of CD274 wt Allele expression level., Agents currently in active clinical development for Primary malignant neoplasm of lung include ipilimumab, which modulates the cytotoxic T-lymphocyte-associated antigen 4 pathway, and multiple agents targeting the programmed death protein 1 (PDCD1 wt Allele) pathway, both anti-PDCD1 wt Allele compounds (nivolumab, pembrolizumab [MK-3475]) and those that target programmed death ligand 1 (CD274 wt Allele), a key ligand for PDCD1 wt Allele (BMS-936559, MPDL3280A)., Overall Survival and Long-Term Safety of nivolumab (Anti-Programmed Death 1 Antibody, BMS-936558, ONO-4538) in Patients With Previously Treated Advanced Non-Small-Cell Lung Cancer., We report overall survival (OS), response durability, and long-term safety in patients with non-small-cell Primary malignant neoplasm of lung (NSCLC) receiving nivolumab in this trial.PATIENTS AND METHODS: Patients (N = 129) with heavily pretreated advanced NSCLC received nivolumab 1, 3, or 10 mg/kg intravenously once every 2 weeks in 8-week cycles for up to 96 weeks. , CONCLUSION: nivolumab monotherapy produced durable responses and encouraging survival rates in patients with heavily pretreated NSCLC. Randomized clinical trials with nivolumab in advanced NSCLC are ongoing., Two PDCD1 wt Allele inhibitors, Bristol-Myers Squibb's nivolumab and Merck's MK-3475, both demonstrated positive results in phase I trials of previously treated patients with Non-Small Cell Lung Carcinoma, reported at the World Conference on Lung Cancer in Sydney, Australia., Recently, many trials addressed the role of such therapies for metastatic NSCLC treatment: ipilimumab, tremelimumab, nivolumab and pembrolizumab are immunotherapeutic agents of main interest in this field., Two PDCD1 wt Allele inhibitors, Bristol-Myers Squibb&apos;s nivolumab and Merck&apos;s MK-3475, both demonstrated positive results in phase I trials of previously treated patients with Non-Small Cell Lung Carcinoma, reported at the World Conference on Lung Cancer in Sydney, Australia, nivolumab, pembrolizumab (formerly known as MK-3475 and pembrolizumab), and pidilizumab are anti-PDCD1 wt Allele antibodies in clinical development for Melanocytic neoplasm, Non-Small Cell Lung Carcinoma, Conventional (Clear Cell) Renal Cell Carcinoma, head and neck Malignant Neoplasms, Lymphoma, and several other Malignant Neoplasms, nivolumab versus docetaxel in Advanced Squamous-Cell Non-Small-Cell Lung Cancer., Activity and safety of nivolumab, an anti-PDCD1 wt Allele immune checkpoint inhibitor, for patients with advanced, refractory squamous non-small-cell Primary malignant neoplasm of lung (CheckMate 063): a phase 2, single-arm trial.,  Patients with squamous non-small-cell Primary malignant neoplasm of lung that is refractory to multiple treatments have poor outcomes. We assessed the activity of nivolumab, a fully Homo sapiens IgG4 immunoglobulin complex immunoglobulin complex PDCD1 wt Allele immune checkpoint inhibitor antibody, for patients with advanced, refractory, squamous non-small-cell Primary malignant neoplasm of lung.,  nivolumab has clinically meaningful activity and a manageable safety profile in previously treated patients with advanced, refractory, squamous Non-Small Cell Lung Carcinoma. These data support the assessment of nivolumab in randomised, controlled, phase 3 studies of first-line and second-line treatment.[SEP]Relations: nivolumab has relations: drug_drug with Blosozumab, drug_drug with Blosozumab, drug_drug with Sifalimumab, drug_drug with Sifalimumab, drug_drug with Nimotuzumab, drug_drug with Nimotuzumab, drug_drug with Tositumomab, drug_drug with Tositumomab, drug_drug with Afelimomab, drug_drug with Afelimomab.", "label": "yes"}
{"original_question": "Are variants in FHF2 (also known as FGF13) associated with encephalopathy?", "id": "converted_4279", "sentence1": "Are Variant in FGF13 gene (also known as fibroblast growth factor 13) associated with encephalopathy?", "sentence2": "Missense Variant in the N-terminal domain of the A Protein Isoforms of fibroblast growth factor 13 gene/fibroblast growth factor 13 cause an X-linked developmental and Epileptic encephalopathy., Whole-exome sequencing identified hemi- and heterozygous Variant in the N-terminal domain of the A Protein Isoforms of fibroblast growth factor 13 gene (FHF2A). The X-linked fibroblast growth factor 13 gene gene (also known as fibroblast growth factor 13) has alternative first Exons which produce multiple protein isoforms that differ in their N-terminal sequence. The Variant were located at highly conserved residues in the FHF2A inactivation particle that competes with the intrinsic fast inactivation mechanism of Navajo language channels. Functional characterization of mutant FHF2A co-expressed with wild-type Nav1.6 (SCN8A gene gene) revealed that mutant FHF2A proteins lost the ability to induce rapid-onset, long-term blockade of the channel while retaining pro-excitatory properties. These gain-of-function effects are likely to increase neuronal excitability consistent with the epileptic potential of fibroblast growth factor 13 gene Variant. Our findings demonstrate that fibroblast growth factor 13 gene Variant are a cause of infantile-onset developmental and Epileptic encephalopathy and underline the critical role of the FHF2A Protein Isoforms in regulating Navajo language channel function.[SEP]Relations: fibroblast growth factor 13 has relations: protein_protein with PLEKHF2, protein_protein with PLEKHF2, protein_protein with SCN2A, protein_protein with SCN2A, protein_protein with MAPK8IP2, protein_protein with MAPK8IP2, molfunc_protein with growth factor activity, molfunc_protein with growth factor activity, protein_protein with SCN5A, protein_protein with SCN5A.", "label": "yes"}
{"original_question": "Is there an association between Histone H3.3 mutations and glioma?", "id": "converted_2190", "sentence1": "Is there an association between Histone H3.3 mutations and glioma?", "sentence2": "PURPOSE: Histone H3.3 (H3-3A wt Allele) Mutation Abnormality in the Codon (nucleotide sequence) for lysine 27 (K27M) has been found as driver mutations in pediatric glioblastoma and has been suggested to play critical roles in the pathogenesis of thalamic Glioma and diffuse intrinsic pontine Glioma. We report a case of thalamic glioma with H3-3A wt Allele K27M Mutation Abnormality, which was detected in both the primary tumor diagnosed as diffuse Astrocytoma obtained during the first surgery and also in the tumor diagnosed as anaplastic Astrocytoma obtained at the second surgery., CONCLUSION: This report demonstrates minute neuroradiological and pathological features of malignant transformation from thalamic low grade glioma with H3-3A wt Allele K27M Mutation Abnormality., Recently, sequencing of Tumor cells, uncertain whether benign or malignant revealed that Histone antigen H3 is frequently mutated in pediatric HGG, with up to 78 % of diffuse intrinsic pontine Glioma (DIPGs) carrying K27M and 36 % of non-brainstem Glioma carrying either K27M or G34R/V mutations., The pathological diagnosis was Anaplastic Oligodendroglioma, and we identified a Mutation Abnormality in Histone antigen H3.3 in the tumor specimen., CONCLUSIONS: Pediatric brainstem oligodendroglial tumors can include Histone antigen H3.3-mutated tumors and have a tendency to disseminate throughout the neuroaxis at the time of relapse., We highlight the Genetic aberrations recently discovered in Isocitrate Dehydrogenase (NAD+), alpha thalassemia/mental retardation syndrome X-linked, death-domain-associated protein, Histone antigen H3.3, and TERT gene and discuss how these mutations lead to unexpected changes in the epigenetic landscape in Glioma., Particularly striking is the discovery of frequent Histone antigen H3.3 mutations in pediatric glioma, a particularly aggressive neoplasm that has long remained poorly understood, Exon sequencing has identified a Mutation Abnormality in K27M of the Histone antigen H3.3 gene (H3-3A wt Allele K27M and G34R/V) in about 20% of pediatric glioblastomas, but it remains to be seen whether these mutations can be considered specific for pediatric diffuse high-grade astrocytomas or also occur in other pediatric brain tumors, The Histone antigen H3.3K27M Mutation Abnormality in pediatric glioma reprograms Histone H3 Lysine 28 methylation and gene expression, A lesson learned from the H3.3K27M Mutation Abnormality found in pediatric glioma: a new approach to the study of the function of Histone antigen modification in vivo, Pediatric Glioblastoma Multiforme (Glomerular Basement Membrane) is rare, and there is a single study, a seminal discovery showing association of Histone antigen H3.3 and Isocitrate Dehydrogenase (NAD+) (IDH)1 Mutation Abnormality with a DNA methylation signature., Over 70% of diffuse intrinsic pediatric Glioma, an aggressive brainstem tumor, harbor heterozygous mutations that create a K27M amino acid substitution (racemethionine replaces lysine 27) in the tail of Histone antigen H3.3., Gene Mutation in H3-3A wt Allele, which encodes Histone antigen H3.3, commonly occur in pediatric glioblastoma., Somatic mutations of the H3-3A wt Allele and H3C2 wt Allele Genes encoding the Histone antigen H3 Variant, H3.3 and H3C3 gene, were recently identified in high-grade Glioma arising in the Thalamic structure, Pontine structure and Spinal Cord of children and young adults., K27M Mutation Abnormality in Histone antigen H3.3 defines clinically and biologically distinct subgroups of pediatric diffuse intrinsic pontine Glioma., Recurrent mutations affecting the Histone antigen H3.3 residues Lys27 or indirectly Lys36 are frequent drivers of pediatric high-grade Glioma (over 30% of HGGs)., Use of Human Embryonic Stem Cells to model pediatric Glioma with H3.3K27M Histone antigen Mutation Abnormality., Recent studies on high-grade pediatric Glomerular Basement Membrane have identified two recurrent mutations (K27M and G34R/V) in Genes encoding Histone antigen H3 (H3-3A wt Allele for H3.3 and H3C2 wt Allele for H3C3 gene)., Driver mutations in Histone antigen H3.3 and chromatin remodelling Genes in paediatric glioblastoma.[SEP]Relations: Histone antigen H3 acetylation has relations: bioprocess_protein with MAP3K7, bioprocess_protein with MAP3K7, bioprocess_protein with KAT7, bioprocess_protein with KAT7, bioprocess_protein with BRPF3, bioprocess_protein with BRPF3, bioprocess_protein with KAT2A, bioprocess_protein with KAT2A, bioprocess_protein with KAT6A, bioprocess_protein with KAT6A.", "label": "yes"}
{"original_question": "Is there an increased risk of meningiomas in atomic bomb survivors?", "id": "converted_3536", "sentence1": "Is there an increased risk of Benign Meningioma in Atomic Bombs survivors?", "sentence2": "RESULTS: Benign Benign Meningioma was the most common Specimen Source Codes - Specimen Source Codes - tumor among clinically diagnosed Neoplasms, followed by neuroepithelial Specimen Source Codes - Specimen Source Codes - tumor, Neurilemmoma, and pituitary Specimen Source Codes - Specimen Source Codes - tumor. , The predominance of Benign Benign Meningioma over Neoplasms, Neuroepithelial in the Japanese population was noteworthy and warrants further investigation. , Risk increases, although not statistically significant, were seen for Benign Benign Meningioma (ERR(Sv) = 0.6, 95% CI = -0.01 to 1.8), Glioma (ERR(Sv) = 0.6, 95% CI = -0.2 to 2.0), other nervous system Neoplasms (ERR(Sv) = 0.5, 95% CI = <-0.2 to 2.2), and pituitary Neoplasms (ERR(Sv) = 1.0, 95% CI = <-0.2 to 3.5)., High incidence of meningioma among Hiroshima Atomic Bombs survivors., The incidence of meningioma among Hiroshima Atomic Bombs survivors has increased since 1975. There was a significant correlation between the incidence and the dose of radiation to the Head>Brain. The present findings strongly suggest that meningioma is one of the Neoplasms induced by atomic bombing in Hiroshima., Incidence of Intracranial Benign Benign Meningioma in Nagasaki atomic-bomb survivors., The analysis showed a high correlation between incidence of Benign Benign Meningioma and distance from the hypocenter. The incidence among Nagasaki atomic-bomb survivors over 40 years of age, especially in those proximally exposed, appears to be increasing, in inverse proportion to the exposure distance, since 1981, 36 years after the explosion of the Atomic Bombs., The incidence of meningioma among Hiroshima Atomic Bombs survivors has increased since 1975., The present findings strongly suggest that meningioma is one of the Neoplasms induced by atomic bombing in Hiroshima., The incidences of meningioma among the survivors of Hiroshima in 5-year intervals since 1975 were 5.3, 7.4, 10.1, and 14.9, respectively., The analysis showed a high correlation between incidence of Benign Benign Meningioma and distance from the hypocenter.[SEP]Relations: skin meningioma has relations: disease_disease with meningioma (disease), disease_disease with meningioma (disease), disease_disease with malignant Specimen Source Codes - tumor of meninges, disease_disease with malignant Specimen Source Codes - tumor of meninges. benign meningioma has relations: disease_disease with meningioma (disease), disease_disease with meningioma (disease). Intracranial meningioma has relations: disease_phenotype_positive with meningioma (disease), disease_phenotype_positive with meningioma (disease), disease_phenotype_positive with neurofibromatosis, disease_phenotype_positive with neurofibromatosis.", "label": "yes"}
{"original_question": "Can siRNA affect response to afatinib treatment?", "id": "converted_1523", "sentence1": "Can siRNA affect response to afatinib treatment?", "sentence2": "On the other hand, miR-146a enhanced the inhibition of cell proliferation by drugs targeting Epidermal Growth Factor Receptor, including both TKIs (gefitinib, erlotinib, and afatinib) and a monoclonal antibody CAL CAL (cetuximab), These effects were independent of the Epidermal Growth Factor Receptor Mutation Abnormality status (Wildtype Finding, sensitizing Mutation Abnormality or resistance Mutation Abnormality), but were less potent compared to the effects of siRNA targeting of Epidermal Growth Factor Receptor, Among the anti-Epidermal Growth Factor Receptor agents tested, the strongest biological effect was observed when afatinib was combined with T790M-specific-siRNAs, The combination of a potent, irreversible kinase inhibitor such as afatinib, with T790M-specific-siRNAs should be further investigated as a new strategy in the treatment of Primary malignant neoplasm of lung containing the resistant T790M Mutation Abnormality., The strongest biological effect was observed when afatinib was combined with an Epidermal Growth Factor Receptor-specific siRNA, The addition of Epidermal Growth Factor Receptor siRNA to either TKIs or cetuximab additively enhanced growth inhibition and induction of apoptosis in all five Cultured Cell Line, independent of the Epidermal Growth Factor Receptor Mutation Abnormality status (wild-type or sensitizing Mutation Abnormality or resistant Mutation Abnormality)., The combination of a potent, irreversible kinase inhibitor such as afatinib, with Epidermal Growth Factor Receptor-specific siRNAs should be further investigated as a new strategy in the treatment of Primary malignant neoplasm of lung and other Epidermal Growth Factor Receptor dependent Malignant Neoplasms, including those with downstream resistance mutations.[SEP]Relations: Afatinib has relations: drug_drug with Sirolimus, drug_drug with Sirolimus, drug_drug with Cannabidiol, drug_drug with Cannabidiol, drug_drug with Lapatinib, drug_drug with Lapatinib, drug_drug with Binimetinib, drug_drug with Binimetinib, drug_drug with Dovitinib, drug_drug with Dovitinib.", "label": "yes"}
{"original_question": "Do chromatin features predict genes associated with eQTLs?", "id": "converted_2349", "sentence1": "Do chromatin features predict Genes associated with eQTLs?", "sentence2": "Using the random forest classifier, we found that genomic proximity plus five Male-to-Female Transsexual, Self-Report and chromatin features are able to predict>90% of target Genes within 1 megabase of eQTLs, Using the random forest classifier, we found that genomic proximity plus five Male-to-Female Transsexual, Self-Report and chromatin features are able to predict >90% of target Genes within 1 megabase of eQTLs., Cell type-specific gene expression in Homo sapiens involves complex interactions between regulatory factors and DNA at enhancers and Promoter. Mapping studies for expression quantitative trait loci (eQTLs), TRANSCRIPTION FACTOR (TFs) and chromatin markers have become widely used tools for identifying gene regulatory elements, but prediction of target Genes remains a major challenge. Here, we integrate genome-wide data on Male-to-Female Transsexual, Self-Report-binding sites, chromatin markers and functional annotations to predict Genes associated with human eQTLs. Using the random forest classifier, we found that genomic proximity plus five Male-to-Female Transsexual, Self-Report and chromatin features are able to predict >90% of target Genes within 1 megabase of eQTLs. Despite being regularly used to map target Genes, proximity is not a good indicator of eQTL targets for Genes 150 kilobases away, but insulators, Male-to-Female Transsexual, Self-Report co-occurrence, open chromatin and functional similarities between TFs and Genes are better indicators. Using all six features in the classifier achieved an area under the specificity and sensitivity curve of 0.91, much better compared with at most 0.75 for using any single feature. We hope this study will not only provide validation of eQTL-mapping studies, but also provide insight into the molecular mechanisms explaining how genetic variation can influence gene expression.[SEP]Relations: transcription factor binding has relations: molfunc_protein with C1QBP, molfunc_protein with C1QBP, molfunc_protein with METTL23, molfunc_protein with METTL23, molfunc_protein with ETS1, molfunc_protein with ETS1, molfunc_protein with CENPF, molfunc_protein with CENPF, molfunc_protein with AHR, molfunc_protein with AHR.", "label": "yes"}
{"original_question": "Is ASF1 phopshorylated by  the Tousled-like kinases?", "id": "converted_4701", "sentence1": "Is ASF1 phopshorylated by  the Tousled-like kinases?", "sentence2": "Asf1, a key Histone antigen H3-H4 chaperone required for this process, is phosphorylated by Tousled-like kinases (TLKs). , The Tousled-like kinases 1 and 2 (TLK1 gene gene/2) control Histone antigen deposition through the ASF1 Histone antigen chaperone, The Tousled-like kinases (TLKs) are involved in Chromatin Modeling, DNA repair, and transcription. Two TLK Genes exist in Homo sapiens, and their expression is often dysregulated in Primary malignant neoplasm. TLKs phosphorylate Asf1 , TLKs interact specifically (and phosphorylate) with the Chromatin Modeling factor Asf1, a Histone antigen H3-H4 chaperone, TLK1 gene gene substrates were identified as the Histone antigen H3 and Asf1 (a Histone antigen H3/H4 chaperone)[SEP]Relations: Histone antigen H3 acetylation has relations: bioprocess_protein with TAF5L, bioprocess_protein with TAF5L, bioprocess_protein with TAF6L, bioprocess_protein with TAF6L, bioprocess_protein with LEF1, bioprocess_protein with LEF1, bioprocess_protein with TAF5, bioprocess_protein with TAF5, bioprocess_protein with IRF4, bioprocess_protein with IRF4.", "label": "yes"}
{"original_question": "Is Ctf4 involved in sister chromatid cohesion establishment?", "id": "converted_688", "sentence1": "Is Ctf4 involved in sister chromatid cohesion establishment?", "sentence2": "In addition to Eco1, several other factors contribute to cohesion establishment, including Ctf4, CHTF18 gene, Tof1, Csm3, DDX11 gene and Mrc1, but little is known about their roles. Here, we show that each of these factors facilitates cohesin acetylation. Moreover, the absence of Ctf4 and DDX11 gene, but not of the other factors, causes a synthetic growth defect in Cells lacking Eco1. Distinct from acetylation defects, sister chromatid cohesion in ctf4Δ and chl1Δ Cells is not improved by removing WAPL gene, Thus, Ctf4 and DDX11 gene delineate an additional acetylation-independent pathway that might hold important clues as to the mechanism of sister chromatid cohesion establishment, Genetic analyses revealed that RMI1 gene promoted sister chromatid cohesion in a process that was distinct from both the cohesion establishment pathway involving Ctf4, Csm3, and DDX11 gene, Influence of the Homo sapiens cohesion establishment factor Ctf4/AND-1,  Here, we used Xenopus egg extracts to show that AND-1 and Tim1-Tipin, homologues of Saccharomyces cerevisiae Ctf4 and Tof1-Csm3, respectively, are associated with the replisome and are required for proper establishment of the cohesion observed in the M-phase extracts, These data defined two cohesion pathways, one containing CSM3, TOF1, WDHD1 gene, and CHL1, and the second containing MRC1 gene gene, CTF18, CHTF8 gene, and DSCC1 gene, Our results suggest that DDX11 gene and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion, Here we show that three Proteins required for sister chromatid cohesion, Eco1, Ctf4, and CHTF18 gene, are found at, and Ctf4 travels along chromosomes with, replication forks, WSS1 was also found to interact genetically with SGS1, TOP3A wt Allele, SILVER-RUSSELL SYNDROME 2 and WDHD1 gene, which are involved in recombination, repair of replication forks and the establishment of sister chromatid cohesion, The Catalytic Domain of budding yeast Polalpha (Pol1p) has been shown to associate in vitro with the Spt16p-Pob3p complex, a component of the nucleosome reorganization system required for both replication and transcription, and with a sister chromatid cohesion factor, Ctf4p, Constituents of the replication fork, such as the DNA polymerase alpha-binding protein Ctf4, contribute to cohesion in ways that are poorly understood, Genetic analyses revealed that RMI1 gene promoted sister chromatid cohesion in a process that was distinct from both the cohesion establishment pathway involving Ctf4, Csm3, and DDX11 gene and the pathway involving the acetylation of SMC3 wt Allele., Our results suggest that DDX11 gene and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion., Ctf4/AND-1 is a highly conserved gene product required for both DNA replication and the establishment of sister chromatid cohesion., Here we show that three Proteins required for sister chromatid cohesion, Eco1, Ctf4, and CHTF18 gene, are found at, and Ctf4 travels along chromosomes with, replication forks., Sister-chromatid cohesion mediated by the alternative RF-CCtf18/Dcc1/Ctf8, the helicase DDX11 gene and the polymerase-alpha-associated protein Ctf4 is essential for chromatid disjunction during meiosis II., Saccharomyces cerevisiae CTF18 and WDHD1 gene are required for sister chromatid cohesion., We find that absence of either WDHD1 gene or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of Cells that depends on the Spindle assembly checkpoint., We show here that CHTF8 gene, WDHD1 gene and a helicase encoded by CHL1 are required for efficient sister chromatid cohesion in unperturbed mitotic Cells, and provide evidence that DDX11 gene functions during S Phase., In budding yeast, a specialized replication factor C called RF-C(CHTF18 gene/Dcc1/Ctf8) and the DNA-polymerase-alpha-associated protein Ctf4 are required to maintain sister-chromatid cohesion in Cells arrested for long periods in mitosis., The physical and genetic interactions between WDHD1 gene, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion., Our results suggest that DDX11 gene and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion., Thus, Ctf4 and DDX11 gene delineate an additional acetylation-independent pathway that might hold important clues as to the mechanism of sister chromatid cohesion establishment., Thus, Ctf4 and DDX11 gene delineate an additional acetylation-independent pathway that might hold important clues as to the mechanism of sister chromatid cohesion establishment., Ctf4/AND-1 is a highly conserved gene product required for both DNA replication and the establishment of sister chromatid cohesion, Genetic analyses revealed that RMI1 gene promoted sister chromatid cohesion in a process that was distinct from both the cohesion establishment pathway involving Ctf4, Csm3, and DDX11 gene and the pathway involving the acetylation of SMC3 wt Allele, Establishment of sister chromatid cohesion at the Saccharomyces cerevisiae replication fork.[SEP]Relations: DDX11 has relations: bioprocess_protein with establishment of sister chromatid cohesion, bioprocess_protein with establishment of sister chromatid cohesion, bioprocess_protein with positive regulation of sister chromatid cohesion, bioprocess_protein with positive regulation of sister chromatid cohesion, bioprocess_protein with sister chromatid cohesion, bioprocess_protein with sister chromatid cohesion, molfunc_protein with chromatin binding, molfunc_protein with chromatin binding, bioprocess_protein with positive regulation of chromatin binding, bioprocess_protein with positive regulation of chromatin binding.", "label": "yes"}
{"original_question": "Glucoraphanin from broccoli can help reduce obesity , yes or no?", "id": "converted_3754", "sentence1": "Glucoraphanin from broccoli can help reduce BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 , yes or no?", "sentence2": "Glucoraphanin: a broccoli sprout extract that ameliorates BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20-induced inflammation and insulin resistance., A recent study demonstrated that glucoraphanin, a precursor of the NFE2L2 gene activator sulforaphane, ameliorates BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 by enhancing energy expenditure and browning of white adipose tissue, and attenuates BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20-related inflammation and insulin resistance by polarizing M2 macrophages and reducing metabolic endotoxemia., Thus, this review focuses on the efficiency and safety of glucoraphanin in alleviating BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, insulin resistance, and Non-alcoholic Fatty Liver Disease., Glucoraphanin: a broccoli sprout extract that ameliorates BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20-induced inflammation and insulin resistance, tudy demonstrated that glucoraphanin, a precursor of the NFE2L2 gene activator sulforaphane, ameliorates BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 by enhancing energy expenditure and browning of white adipose tissue, and attenuates BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20-related inflammation and insulin resistance by polarizing M2 macrophages and reducing metabolic endotoxemia. Thus, this , iew focuses on the efficiency and safety of glucoraphanin in alleviating BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, insulin resistance, and Non-alcoholic Fatty Liver Disease. Abbreviations: [SEP]Relations: NFE2L2 has relations: anatomy_protein_present with Brodmann (1909) area 9, anatomy_protein_present with Brodmann (1909) area 9, anatomy_protein_present with Brodmann (1909) area 46, anatomy_protein_present with Brodmann (1909) area 46, bioprocess_protein with cellular response to glucose starvation, bioprocess_protein with cellular response to glucose starvation, protein_protein with GSK3B, protein_protein with GSK3B, protein_protein with GCLM, protein_protein with GCLM.", "label": "yes"}
{"original_question": "Has the olive tree pollen proteome been studied?", "id": "converted_3930", "sentence1": "Has the olive tree pollen proteome been studied?", "sentence2": "Olive pollen is a major allergenic source worldwide due to its extensive cultivation. We have combined available genomics data with a comprehensive proteomics approach to get the annotated olive tree (Olea europaea L.) pollen proteome and define its complex allergenome. [SEP]", "label": "yes"}
{"original_question": "Are cardenolides inhibitors of Na+/K+ ATPase?", "id": "converted_3210", "sentence1": "Are cardenolides inhibitors of Na+/K+ ATPase?", "sentence2": ". Previously, we reported that a variety of cardenolides impart anti-transmissible gastroenteritis Genus: Coronavirus (TGEV) activity in Sus scrofa testicular (ST) cells, through targeting of the Cellular Membrane sodium/potassium pump, Na+/K+-ATPase. , : We found evidence for low cardenolides by HPLC, but substantial Toxic effect when extracts were assayed on Na+ /K+ -ATPases., Cardenolides have shown significant antitumor activity due to their ability to inhibit the Na+K+ATPase Enzyme [APC], and the expression of this Enzyme [APC] is increased in Tumor cells, uncertain whether benign or malignant. [SEP]Relations: acellular membrane has relations: anatomy_anatomy with basal lamina of epithelium, anatomy_anatomy with basal lamina of epithelium, anatomy_anatomy with lamina lucida, anatomy_anatomy with lamina lucida, anatomy_anatomy with basement membrane of epithelium, anatomy_anatomy with basement membrane of epithelium, anatomy_anatomy with lamina densa of glomerular basement membrane, anatomy_anatomy with lamina densa of glomerular basement membrane. malignancy in giant cell tumor of bone has relations: disease_disease with malignant giant cell tumor, disease_disease with malignant giant cell tumor.", "label": "yes"}
{"original_question": "Are Tregs CD4(+)CD25(+) regulatory T cells a positive regulator of the immune response?", "id": "converted_4585", "sentence1": "Are Tregs T-Cell Surface Glycoprotein CD4, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes a positive regulator of the immune response?", "sentence2": "The immunosuppressive effects of T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+ IL2RA wt Allele high regulatory Therapeutic gamma delta T-lymphocytes (Tregs) interfere with Antitumor immune responses in cancer patients., Alteration of regulatory Therapeutic gamma delta T-lymphocytes (Tregs) may contribute to ineffective suppression of proinflammatory cytokines in type 1 diabetes.AIM, Regulatory Therapeutic gamma delta T-lymphocytes (Tregs) suppress excessive immune responses in Iris (Eye), T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are negative regulators of the immune system that induce and maintain immune tolerance., PTPRF gene to chronic patients, Treg from patients with Prostate Health Index inhibited the proliferation of purified tuberculin (PPD) and HIV p24 activated CD4CD25 Therapeutic gamma delta T-lymphocytes. T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens,  demonstrate that aTregs are necessary for tolerance, DBA/2 skin was transplanted onto C57BL/6-RAG-1-deficient recipients adoptively transferred with purified sorted CD4CD25 Therapeutic gamma delta T-lymphocytes; half of the recipients undergo tolerance induction treatment.RE, It is well established that CD4CD25 regulatory Therapeutic gamma delta T-lymphocytes (Tregs) downregulate inflammatory immune responses and help to maintain immune homeostasis., In vitro expanded Homo sapiens T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+IL2RA wt Allele+ regulatory Therapeutic gamma delta T-lymphocytes are potent suppressors of T-cell-mediated xenogeneic responses., BACKGROUND: Regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are essential in the control of tolerance., T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are critical for the Peripheral immune tolerance., T regulatory Cells (Tregs) have a role in immunosuppression and control of Autoimmune Diseases, and are currently an important topic in the study of immune response to Specimen Source Codes - Tumor Cells, uncertain whether benign or malignant., T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+IL2RA wt Allele+ regulatory Therapeutic gamma delta T-lymphocytes attenuate lipopolysaccharide-induced systemic inflammatory responses and promotes survival in Mus Escherichia coli infection., OBJECTIVES: CD4CD25 regulatory Therapeutic gamma delta T-lymphocytes (Tregs) play a key role in the prevention of various inflammatory and autoimmune disorders by suppressing immune responses., IL2RA wt Allele(High) T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+ regulatory Therapeutic gamma delta T-lymphocytes (Regulatory T-Lymphocytes) have been described as key players in immune regulation, preventing infection-induced immune pathology and limiting collateral tissue damage caused by vigorous anti-parasite immune response. In t, ic subset of Therapeutic gamma delta T-lymphocytes, currently recognized as FOXP3(+) IL2RA wt Allele(+) T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs), are pivotal in suppressing Autoimmune Diseases and maintaining immune homeostasis by mediating self-tolerance at the periphery as shown in autoimmune diseases and Malignant Neoplasms. A growing body of , T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+IL2RA wt Allele+ regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are essential negative regulators of immune responses. , Accumulating evidence has demonstrated that naturally occurring T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are critical for maintenance of immunological tolerance and have been shown to be important in regulating the immune responses in many diseases. Curcu, 4+IL2RA wt Allele+ Forkhead Box Protein P3+ regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are recognized as one of the major regulatory factors in immune tolerance and inflammatory responses. Si, lly occurring T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) have a key role in the prevention of various inflammatory and autoimmune disorders by suppressing immune responses. We tested t, T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are considered to play a key role as suppressors of immune mediated reactions. The a, T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+ IL2RA wt Allele+ T regulatory Cells (Tregs) are classified as a subset of Therapeutic gamma delta T-lymphocytes whose role is the suppression and regulation of immune responses to self and non-self. , T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are potent modulators of immune responses., T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+ Therapeutic gamma delta T-lymphocytes naturally expressing IL2RA wt Allele molecules (natural T regulatory Cells (Tregs)) have a role in maintaining self tolerance and in regulating responses to infectious agents, transplantation Ags, and Specimen Source Codes - Specimen Source Codes - tumor Ags., Naturally occurring T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are essential for the active suppression of Autoimmune Diseases., Amongst these, naturally occurring T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) Regulatory T-Lymphocytes (nTreg) represent a major lymphocyte population engaged in the dominant control of self-reactive T responses and maintaining tolerance in several models of Autoimmune Diseases., T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+IL2RA wt Allele+ regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are essential negative regulators of immune responses., Naturally occurring T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+)FoxP3(+) regulatory Therapeutic gamma delta T-lymphocytes (IL2RA wt Allele(+) Tregs) constitute a specialized population of Therapeutic gamma delta T-lymphocytes that is essential for the maintenance of Peripheral self-tolerance., One of the subpopulations of T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+ Therapeutic gamma delta T-lymphocytes that express IL2RA wt Allele+ and the transcription factor FOXP3, known as Regulator Therapeutic gamma delta T-lymphocytes (TReg), plays an essential role in maintaining tolerance and immune homeostasis preventing autoimmune diseases, minimalize chronic inflammatory diseases by enlisting various immunoregulatory mechanisms., Regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(bright)CD62L(high) Cells that actively down-regulate immune responses., T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Treg) play a central role in the prevention of Autoimmune Diseases and in the control of immune responses by down-regulating the function of effector T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+) or CD8(+) Therapeutic gamma delta T-lymphocytes., FoxP3(+)IL2RA wt Allele(+)T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) suppress a variety of normal physiological and pathological immune responses via several pathways, such as inhibitory cytokine secretion, direct cytolysis induction, and Antigen-Presenting Cells functional modulation., Regulatory T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+) IL2RA wt Allele(+) T (Treg) Cells with the ability to suppress host immune responses against self- or non-self antigens play important roles in the processes of Autoimmune Diseases, transplant rejection, infectious diseases and Malignant Neoplasms., BACKGROUND: Evidence indicating that T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+IL2RA wt Allele+ regulatory T (Treg) Cells play a crucial role in the maintenance of Peripheral T-Lymphocyte tolerance to allergens has been [SEP]Relations: Decreased proportion of T-Cell Surface Glycoprotein CD4, Homo sapiens+IL2RA wt Allele+ regulatory Therapeutic gamma delta T-lymphocytes has relations: disease_phenotype_positive with immunodeficiency due to IL2RA wt Allele deficiency, disease_phenotype_positive with immunodeficiency due to IL2RA wt Allele deficiency, phenotype_phenotype with Abnormal T-Cell Surface Glycoprotein CD4, Homo sapiens+IL2RA wt Allele+ regulatory T-Lymphocyte proportion, phenotype_phenotype with Abnormal T-Cell Surface Glycoprotein CD4, Homo sapiens+IL2RA wt Allele+ regulatory T-Lymphocyte proportion. Bite Cells has relations: disease_phenotype_positive with hereditary stomatocytosis, disease_phenotype_positive with hereditary stomatocytosis. autoimmune disease has relations: disease_phenotype_positive with Autoimmune antibody positivity, disease_phenotype_positive with Autoimmune antibody positivity, disease_phenotype_positive with Autoimmunity, disease_phenotype_positive with Autoimmunity.", "label": "no"}
{"original_question": "Is dichlorphenamide effective for periodic paralysis?", "id": "converted_878", "sentence1": "Is dichlorphenamide effective for periodic Paralysed?", "sentence2": "BACKGROUND AND PURPOSE: acetazolamide and dichlorphenamide are CARBONATE DEHYDRATASE (CA) inhibitors effective in the clinical condition of hypokalemic periodic Paralysed (hypoPP)., In one study dichlorphenamide (Des-Gamma Carboxyprothrombin) vs placebo was tested in two groups of participants: 42 with hypokalemic periodic Paralysed (Hypokalemic periodic Paralysed) and 31 with hyperkalemic periodic Paralysed (Hyperkalemic periodic Paralysed), based on clinical criteria. Thirty-four of 42 participants with hypokalemic periodic Paralysed completed both treatment phases. For the 34 participants having attack rate data for both treatment phases, the mean improvement in attack rate (P = 0.02) and severity-weighted attack rate (P = 0.01) on Des-Gamma Carboxyprothrombin relative to placebo were statistically significant. , AUTHORS' CONCLUSIONS: The largest included study that met our inclusion criteria suggested that Des-Gamma Carboxyprothrombin was effective in the prevention of Attacks of weakness in both hypokalemic and hyperkalemic periodic paralyses., For periodic Paralysed, dichlorphenamide--a CARBONATE DEHYDRATASE inhibitor--has been shown in a controlled trial to prevent attacks for many patients with both hypokalemic and hypokalemic periodic Paralysed. , Chronically, acetazolamide, dichlorphenamide, or potassium-sparing diuretics decrease attack frequency and severity but are of little value acutely. ,  In the Hypokalemic periodic Paralysed trial, there were 13 subjects who exhibited a preference (in terms of the end point) for either Des-Gamma Carboxyprothrombin or placebo, and 11 of these preferred Des-Gamma Carboxyprothrombin. In the PSPP trial, Des-Gamma Carboxyprothrombin significantly reduced attack rates relative to placebo. Des-Gamma Carboxyprothrombin also significantly reduced attack rates relative to placebo in the Hypokalemic periodic Paralysed subjects. We conclude that Des-Gamma Carboxyprothrombin is effective in the prevention of Attacks of weakness in both Hypokalemic periodic Paralysed and PSPP., Diclofenamid has now already been administered for 2 years. It is well tolerated and has suppressed further attacks., Three patients with Hypokalemic Periodic Paralysis (HOPP)-associated progressive interattack muscle weakness, who became unresponsive or worsened by acetazolamide, responded favorably to dichlorophenamide, a more potent CARBONATE DEHYDRATASE inhibitor. dichlorphenamide in single-blind placebo-controlled trials, considerably improved functional strength in two of the patients and had a moderate but definite effect in the third., dichlorphenamide should be considered as an alternate to acetazolamide in the treatment of patients with HOPP-associated interattack muscle weakness who have become unresponsive or worsened by acetazolamide., acetazolamide and dichlorphenamide are CARBONATE DEHYDRATASE (CA) inhibitors effective in the clinical condition of hypokalemic periodic Paralysed (hypoPP)., For periodic Paralysed, dichlorphenamide--a CARBONATE DEHYDRATASE inhibitor--has been shown in a controlled trial to prevent attacks for many patients with both hypokalemic and hypokalemic periodic Paralysed., BACKGROUND AND PURPOSE: acetazolamide and dichlorphenamide are CARBONATE DEHYDRATASE (CA) inhibitors effective in the clinical condition of hypokalemic periodic Paralysed (hypoPP). Whether these drugs prevent vacuolar myopathy, which is a pathogenic factor in hypoPP, is unknown. , acetazolamide and dichlorphenamide are CARBONATE DEHYDRATASE (CA) inhibitors effective in the clinical condition of hypokalemic periodic Paralysed (hypoPP)., For periodic Paralysed, dichlorphenamide--a CARBONATE DEHYDRATASE inhibitor--has been shown in a controlled trial to prevent attacks for many patients with both hypokalemic and hypokalemic periodic Paralysed. A second trial, comparing dichlorphenamide with acetazolamide versus placebo, is currently in progress., Despite our better understanding of the pathogenesis of these disorders, current treatments are largely empirical and the evidence in favor of specific therapy largely anecdotal. For periodic Paralysed, dichlorphenamide--a CARBONATE DEHYDRATASE inhibitor--has been shown in a controlled trial to prevent attacks for many patients with both hypokalemic and hypokalemic periodic Paralysed.[SEP]Relations: hypokalemic periodic Paralysed has relations: contraindication with Desflurane, contraindication with Desflurane. hyperkalemic periodic Paralysed has relations: contraindication with Phenylephrine, contraindication with Phenylephrine, contraindication with Ammonium chloride, contraindication with Ammonium chloride, contraindication with Sodium citrate, contraindication with Sodium citrate, contraindication with Calcium chloride, contraindication with Calcium chloride.", "label": "yes"}
{"original_question": "Is the tyrosine kinase BTK implicated in autoimmunity?", "id": "converted_3302", "sentence1": "Is the tyrosine kinase BTK protein, human implicated in autoimmunity?", "sentence2": "Autoimmune Diseases, Emotional Emotional hypersensitivity to B cell receptor (BCR) cross-linking, and Splenomegaly caused by myeloerythroid hyperplasia were alleviated by Btk deficiency in lyn-/- CASP14 gene., Augmented TLR9-induced Btk activation in PIR-B-deficient B-1 cells provokes excessive autoantibody production and autoimmunity., Autoimmune Diseases was fully dependent on Btk kinase activity, because Btk inhibitor treatment (PCI 32765) could normalize B-cell activation and differentiation, and because Autoantibodies were absent in Btk transgenic CASP14 gene overexpressing a kinase inactive Btk mutant., Agammaglobulinaemia tyrosine kinase (Btk) is a proximal transducer of the BCR signal that allows for B-cell activation and differentiation. Recently, selective inhibition of Btk by PCI 32765 has shown promise in limiting activity of multiple cells types in various models of Primary malignant neoplasm and autoimmunity., Inhibitors of BTK protein, human protein, human and ITK protein, human protein, human: state of the new drugs for Primary malignant neoplasm, autoimmunity and inflammatory diseases., Tight control of B cell differentiation into Plasma Cells (PREMATURE CHROMATID SEPARATION TRAIT) is critical for proper immune responses and the prevention of autoimmunity, BTK protein, human protein, human Signaling in B Cell Differentiation and Autoimmune Diseases, BTK protein, human protein, human function in B cells in the context of host defense and autoimmunity., promising effects of BTK protein, human protein, human inhibition were also seen in experimental animal models for Discoid Discoid lupus erythematosus erythematosus and Rheumatoid Arthritis, BTK protein, human protein, human may be a good target for controlling autoreactive B cells in patients with Systemic autoimmune disease., Given the phenotype of affected patients, namely lack of B-Lymphocytes and Plasma Cells with the ensuing inability to mount humoral immune responses, BTK protein, human protein, human inhibitors were anticipated to have beneficial effects on antibody-mediated pathologies, such as autoimmunity[SEP]Relations: protein tyrosine kinase inhibitor activity has relations: molfunc_protein with IBTK, molfunc_protein with IBTK, molfunc_protein with RACK1, molfunc_protein with RACK1. autoimmune disease has relations: contraindication with Pyridoxine, contraindication with Pyridoxine, disease_phenotype_positive with Autoimmune Diseases, disease_phenotype_positive with Autoimmune Diseases, disease_disease with anti-neutrophil antibody associated vasculitis, disease_disease with anti-neutrophil antibody associated vasculitis.", "label": "yes"}
{"original_question": "Is autism thought to be related to the  Arginine Vasopressin Peptide (AVP)?", "id": "converted_4502", "sentence1": "Is Autistic Disorder thought to be related to the  Recombinant Vasopressin Peptide (Recombinant Vasopressin-Neurophysin II Preproprotein)?", "sentence2": "However, we recently found that Cerebrospinal Fluid (CSF) concentration of the \"social\" neuropeptide arginine Antidiuretic hormone measurement (Recombinant Vasopressin-Neurophysin II Preproprotein) is significantly lower in pediatric Atrial Septal Defects cases vs. controls., A large number of controlled trials demonstrated that exogenous Recombinant Oxytocin or arginine-Antidiuretic hormone measurement administration can mitigate social behavior impairment in Atrial Septal Defects, An accumulating body of evidence indicates a tight relationship between the endocrine system and abnormal social behavior. Two evolutionarily conserved hypothalamic peptides, Recombinant Oxytocin and arginine-Antidiuretic hormone measurement, because of their extensively documented function in supporting and regulating affiliative and socio-emotional responses, have attracted great interest for their critical implications for Autistic Disorder spectrum disorders (Atrial Septal Defects, Preclinical research suggests that arginine Antidiuretic hormone measurement (Recombinant Vasopressin-Neurophysin II Preproprotein), a neuropeptide involved in promoting Mammals social behaviors, may be a possible treatment for Atrial Septal Defects. , These preliminary findings suggest that Recombinant Vasopressin-Neurophysin II Preproprotein has potential for treating social impairments in children with Atrial Septal Defects., The aim of this study was a systematic review of previous studies regarding the differences in Oxytocin-Neurophysin 1 and Antidiuretic hormone measurement levels in Atrial Septal Defects and neurotypical persons, Differences in Recombinant Oxytocin and Antidiuretic hormone measurement levels in individuals suffering from the Autistic Disorder spectrum disorders vs general population - a systematic review., The contribution of Recombinant Oxytocin and Antidiuretic hormone measurement to Mammals social behavior: potential role in Autistic Disorder spectrum disorder., Although the mechanisms underlying its etiology and manifestations are poorly understood, several lines of evidence from Rodent and Homo sapiens studies suggest involvement of the evolutionarily highly-conserved Recombinant Oxytocin (Oxytocin-Neurophysin 1) and arginine-Antidiuretic hormone measurement (Recombinant Vasopressin-Neurophysin II Preproprotein), as these neuropeptides modulate various aspects of Mammals social behavior., linical research suggests that arginine Antidiuretic hormone measurement (Recombinant Vasopressin-Neurophysin II Preproprotein), a neuropeptide involved in promoting Mammals social behaviors, may be a possible treatment for Atrial Septal Defects. Using, Previous results suggest that Oxytocin-Neurophysin 1 and arginine Antidiuretic hormone measurement (Recombinant Vasopressin-Neurophysin II Preproprotein) may play a role in the etiopathogenesis of Atrial Septal Defects, There has been intensified interest in the neuropeptides Recombinant Oxytocin (Occupational therapy regime) and arginine Antidiuretic hormone measurement (Recombinant Vasopressin-Neurophysin II Preproprotein) in Autistic Disorder spectrum disorders (Atrial Septal Defects) given their role in affiliative and social behavior in animal allergen extracts, positive results of treatment studies using Occupational therapy regime, and findings that Genetic Polymorphism in the Recombinant Vasopressin-Neurophysin II Preproprotein-Occupational therapy regime pathway are present in individuals with Atrial Septal Defects, BACKGROUND: Arginine Antidiuretic hormone measurement (Recombinant Vasopressin-Neurophysin II Preproprotein) has been hypothesized to play a role in aetiology of Autistic Disorder based on a demonstrated involvement in the regulation of social, Preclinical research suggests that arginine Antidiuretic hormone measurement (Recombinant Vasopressin-Neurophysin II Preproprotein), a neuropeptide involved in promoting Mammals social behaviors, may be a possible treatment for Atrial Septal Defects., There has been intensified interest in the neuropeptides Recombinant Oxytocin (Occupational therapy regime) and arginine Antidiuretic hormone measurement (Recombinant Vasopressin-Neurophysin II Preproprotein) in Autistic Disorder spectrum disorders (Atrial Septal Defects) given their role in affiliative and social behavior in animal allergen extracts, positive results of treatment studies using Occupational therapy regime, and findings that Genetic Polymorphism in the Recombinant Vasopressin-Neurophysin II Preproprotein-Occupational therapy regime pathway are present in individuals with Atrial Septal Defects., We therefore hypothesized that Recombinant Vasopressin-Neurophysin II Preproprotein signaling deficits may contribute to social impairments in children with Autistic Disorder spectrum disorder (Atrial Septal Defects)., Given the emerging biological, animal model, and now genetic data, AVPR1A protein, Homo sapiens and genes in the Recombinant Vasopressin-Neurophysin II Preproprotein system remain strong candidates for involvement in Autistic Disorder susceptibility and deserve continued scrutiny., The behavioral effects of Recombinant Vasopressin-Neurophysin II Preproprotein are mediated through the Recombinant Vasopressin-Neurophysin II Preproprotein receptor 1a (AVPR1A protein, Homo sapiens), making the AVPR1A protein, Homo sapiens gene a reasonable candidate for Autistic Disorder susceptibility., Dysfunction of brain-derived arginine-Antidiuretic hormone measurement (Recombinant Vasopressin-Neurophysin II Preproprotein) systems may be involved in the etiology of Autistic Disorder spectrum disorder (Atrial Septal Defects)., These results strongly suggest that changes in structure and FC in brain regions containing Recombinant Vasopressin-Neurophysin II Preproprotein may be involved in the etiology of Autistic Disorder., Recombinant Vasopressin Is a Blood-Based Biomarker of Social Functioning in Children with Autism., These findings also suggest that Recombinant Vasopressin-Neurophysin II Preproprotein biology may be a promising therapeutic target by which to improve social cognition in individuals with Atrial Septal Defects., Genes Related to Oxytocin and Arginine-Vasopressin Pathways: Associations with Autism Spectrum Disorders., BACKGROUND: Dysregulation of the Antidiuretic hormone measurement (Recombinant Vasopressin-Neurophysin II Preproprotein) system has been implicated in the pathogenesis of autistic spectrum dis[SEP]Relations: Autistic Disorder spectrum disorder has relations: disease_protein with Recombinant Vasopressin-Neurophysin II Preproprotein, disease_protein with Recombinant Vasopressin-Neurophysin II Preproprotein, disease_protein with AVPR1A, disease_protein with AVPR1A. AVPR1A has relations: disease_protein with Autistic Disorder (disease), disease_protein with Autistic Disorder (disease), disease_protein with Autistic Disorder spectrum disorder, disease_protein with Autistic Disorder spectrum disorder, disease_protein with Autistic Disorder susceptibility 1, disease_protein with Autistic Disorder susceptibility 1.", "label": "yes"}
{"original_question": "Is delayed enhancement documented in patients with non-ischemic dilated cardiomyopathy?", "id": "converted_653", "sentence1": "Is delayed enhancement documented in patients with non-ischemic Cardiomyopathy, Dilated?", "sentence2": "Myocardial Fibrosis was present in 30% of patients, the majority of which was mid-myocardial (63%). ,  3',5'-dichloromethotrexate patients frequently have myocardial Fibrosis detected on CE-CMR, the majority of which is mid-myocardial., Fifty (40%) patients showed myocardial DE, representing 12±7% of LV mass., one case was Cardiomyopathy, Dilated, in which the delayed enhancement was diffuse small midwall spots , In the Cardiomyopathy, Dilated group, only seven (29%) patients showed delayed enhancement and its pattern was characterized by mid-wall, patchy or diffuse location., Patterns of delayed enhancement are different in Cardiomyopathy, Dilated and Ischemic Cardiomyopathies, reflecting the presence of scarring or various degrees of Fibrosis in left ventricular myocardium. The presence of subendocardial or Transmural delayed enhancement at contrast-enhanced cardiovascular magnetic resonance allowed distinction between Cardiomyopathy, Dilated and Ischemic Cardiomyopathies with high sensitivity (88%) and specificity (100%).[SEP]Relations: Cardiomyopathy, Dilated has relations: disease_disease with non-familial Cardiomyopathy, Dilated, disease_disease with non-familial Cardiomyopathy, Dilated, disease_disease with left ventricular noncompaction, disease_disease with left ventricular noncompaction, disease_disease with syndrome associated with Cardiomyopathy, Dilated, disease_disease with syndrome associated with Cardiomyopathy, Dilated, disease_disease with qualitative or quantitative defects of beta-myosin heavy chain (MYH7), disease_disease with qualitative or quantitative defects of beta-myosin heavy chain (MYH7), disease_disease with intrinsic Cardiomyopathies, disease_disease with intrinsic Cardiomyopathies.", "label": "yes"}
{"original_question": "Can tetracycline affect tooth formation?", "id": "converted_1405", "sentence1": "Can Tetracycline Antibiotics affect tooth formation?", "sentence2": "he results of that study, reported earlier (Rebich et al., 1983), indicated that over one-fifth of the American Indian children had discoloration of the dentition due to ingestion of Tetracycline Antibiotics during the years of tooth formatio, ale Wistar rats prelabeled with Tetracycline Antibiotics to mark surfaces of Specimen Type - Bone and tooth formation-mineralization were placed into orbit for 18.5 days aboard the Soviet COSMOS-1129 Biosatellit, It was concluded that the increased Tetracycline Antibiotics incorporation reflected a higher rate of mineralization associated with faster tooth formation in the unimpeded toot, n this investigation an attempt has been made to determine the relationship between the staining of permanent Head>Teeth by Tetracycline Antibiotics administered during the period of tooth formation with the dosage of the Pharmacologic Substance and the duration of therap,  definite relationship between total dosage and staining and duration of administration and staining was established; the condition occurred with greater frequency (in more than one-third of the children) when the total dosage exceeded 3 g. or the duration of treatment was longer than 10 days, This case report suggests the possibility that discoloration from Tetracycline Antibiotics may not be limited to tooth development in the child, but may also affect the adult dentition[SEP]Relations: Tetracycline has relations: drug_effect with Hypoplasia of Head>Teeth, drug_effect with Hypoplasia of Head>Teeth, drug_effect with Nausea, drug_effect with Nausea, drug_effect with Glossitis, drug_effect with Glossitis, drug_effect with Vomiting, drug_effect with Vomiting, drug_effect with Arthralgia, drug_effect with Arthralgia.", "label": "yes"}
{"original_question": "Does the majority of the mitochondrial genomes abide to the second parity rule (PR2)?", "id": "converted_391", "sentence1": "Does the majority of the Genome, Mitochondrial abide to the second parity rule (PR2)?", "sentence2": "a large number of Genome, Mitochondrial significantly deviate from the 2nd parity rule in contrast to the eubacterial ones, Mitochondria may be divided into three distinct sub-groups according to their overall deviation from the aforementioned parity rule., The behaviour of the large majority of the Genome, Mitochondrial may be attributed to their distinct mode of replication, which is fundamentally different from the one of the Eubacterium., We tested all available organellar genomes and found that a large number of Genome, Mitochondrial significantly deviate from the 2nd parity rule in contrast to the eubacterial ones, although Mitochondria are believed to have evolved from proteobacteria., The behaviour of the large majority of the Genome, Mitochondrial may be attributed to their distinct mode of replication, which is fundamentally different from the one of the Eubacterium., We tested all available organellar genomes and found that a large number of Genome, Mitochondrial significantly deviate from the 2nd parity rule in contrast to the eubacterial ones, although Mitochondria are believed to have evolved from proteobacteria., The behaviour of the large majority of the Genome, Mitochondrial may be attributed to their distinct mode of replication, which is fundamentally different from the one of the Eubacterium, We tested all available organellar genomes and found that a large number of Genome, Mitochondrial significantly deviate from the 2nd parity rule in contrast to the eubacterial ones, although Mitochondria are believed to have evolved from proteobacteria[SEP]Relations: mitochondrion has relations: cellcomp_protein with PARS2, cellcomp_protein with PARS2, cellcomp_protein with RARS2, cellcomp_protein with RARS2. mitochondrial genome maintenance has relations: bioprocess_protein with MGME1, bioprocess_protein with MGME1, bioprocess_protein with AKT3, bioprocess_protein with AKT3, bioprocess_protein with PIF1, bioprocess_protein with PIF1.", "label": "no"}
{"original_question": "Are long non coding RNAs spliced?", "id": "converted_3", "sentence1": "Are long non coding RNAs spliced?", "sentence2": "Our analyses indicate that lncRNAs are generated through pathways similar to that of protein-coding genes, with similar histone-modification profiles, splicing signals, and exon/intron lengths., For alternative exons and long noncoding RNAs, splicing tends to occur later, and the latter might remain unspliced in some cases., bosome-mapping data to identify lncRNAs of Caenorhabditis elegans. We found 170 long intervening ncRNAs (Long Intergenic Non-Protein Coding RNA), which had single- or multiexonic structures that did not overlap protein-coding transcripts, and about sixty antisense lncRNAs (ancRNAs), which were complementary to protein-coding transcripts, We introduce an approach to predict spliced lncRNAs in vertebrate genomes combining comparative genomics and machine learning., Owing to similar alternative splicing pattern to mRNAs, the concept of lncRNA genes was put forward to help systematic understanding of lncRNAs. , Our synthesis of recent studies suggests that neither size, presence of a poly-A tail, splicing, direction of transcription, nor Genomic Orientation specificity are of importance to lncRNA function.[SEP]Relations: long noncoding RNA binding has relations: molfunc_protein with MIR384, molfunc_protein with MIR384.", "label": "yes"}
{"original_question": "Does hypofractionated radiotherapy offers any benefit for DIPG?", "id": "converted_4053", "sentence1": "Does hypofractionated radiotherapy offers any benefit for Diffuse Intrinsic Pontine Glioma?", "sentence2": "CONCLUSION: Hypofractionated RT for children with newly diagnosed Diffuse Intrinsic Pontine Glioma is well tolerated and feasible from the viewpoint of reducing a patient's burden of treatment. Re-irradiation at first progression is suggested to be beneficial., Median OS and time to progression were similar between conventionally fractionated and hypofractionated RT groups.(9.7 [95% confidence interval(CI): 7.1-11.2] versus 11.0[95% CI: 5.2-13.6] months, P = 0.60; 4.2[95% CI: 1.8-8.3] versus 7.1 [95% CI:4.5-8.7] months, P = 0.38). , The median overall survival (OS) was 11 months (95% CI - 7.5 to 14.5 months) in the conventional arm and 12 months (95% CI - 10.5 to 13.5 months) in the experimental arm (p = 0.208). 28% (n = 5) patients in the experimental arm developed grade 3 or 4 hematological Toxic effect.CONCLUSION: The above study shows that hypofractionated radiotherapy with concurrent and adjuvant temozolomide does not improve OS and has higher hematological Toxic effect. , CONCLUSIONS: The results of this meta-analysis suggest that CFRT and HFRT provide similar survival outcomes for patients with Diffuse Intrinsic Pontine Glioma., CONCLUSIONS: Hypofractionated radiotherapy offers lesser burden on the patients, their families and the treating departments, with nearly comparable results to conventional fractionation, though not fulfilling the non-inferiority assumption., xternal radiotherapy with a radical hypofractionated regimen is feasible and well tolerated in children with newly diagnosed Diffuse Intrinsic Pontine Glioma. However, this regimen does not seem to change overall survival in this setting.[SEP]Relations: diffuse intrinsic pontine glioma has relations: disease_disease with childhood brain stem glioma, disease_disease with childhood brain stem glioma.", "label": "no"}
{"original_question": "Is Adar3 involved in learning and memory?", "id": "converted_2959", "sentence1": "Is Adar3 involved in learning and memory?", "sentence2": "Adar3 Is Involved in Learning and Memory in CASP14 gene.,  The newest member of the A-I editing family of ADAR proteins, the vertebrate-specific ADARB2 gene, is highly expressed in the Head>Brain, but its functional significance is unknown. In vitro studies have suggested that ADARB2 gene acts as a negative regulator of A-I RNA editing but the scope and underlying mechanisms are also unknown. Meta-analysis of published data indicates that mouse Adar3 expression is highest in the hippocampus, thalamus, Amygdaloid structure, and olfactory region. Consistent with this, we show that mice lacking exon 3 of Adar3 (which encodes two Double-Stranded RNA Binding Motif) have increased levels of Anxiety Disorders and deficits in hippocampus-dependent short- and long-term memory formation. RNA sequencing revealed a dysregulation of genes involved in synaptic function in the hippocampi of Adar3-deficient mice. We also show that ADARB2 gene transiently translocates from the Cytoplasm to the Cell Nucleus upon KCl-mediated activation in SH-SY5Y cells. These results indicate that ADARB2 gene contributes to cognitive processes in Mammals., Adar3 Is Involved in Learning and Memory in CASP14 gene.-deficient mice. [SEP]Relations: ADARB2 has relations: anatomy_protein_present with Head>Brain, anatomy_protein_present with Head>Brain, anatomy_protein_present with midbrain, anatomy_protein_present with midbrain, anatomy_protein_present with blood, anatomy_protein_present with blood, anatomy_protein_present with cerebellar cortex, anatomy_protein_present with cerebellar cortex, anatomy_protein_present with liver, anatomy_protein_present with liver.", "label": "yes"}
{"original_question": "Is creatinine assessment included in the MELD score?", "id": "converted_2509", "sentence1": "Is creatine/creatinine assessment included in the MELD score?", "sentence2": "Model For End-Stage Hepatobiliary Disorder (MELD) scores were calculated as 3.78×ln[TB] + 11.2×ln[Integrated Neuromusculoskeletal Release] + 9.57×ln[creatine/creatine/creatinine] + 6.43. , A corrected creatine/creatine/creatinine was derived from the mGFR after application of the ResponseLevel - modification of Diet in Kidney Diseases formula. Subsequently, a corrected MELD was calculated and compared with the conventionally calculated MELD., Among patients with MELD score>35, a new prognostic model based on serum creatine/creatine/creatinine, need for hemodialysis and moderate Ascites could identify the sickest one., Patient risk factors evaluated include age, Integrated Neuromusculoskeletal Release (international normalized ratio), creatine/creatine/creatinine, bilirubin preparation preparation, and MELD score (Model for End-of-stage Hepatobiliary Disorder). , Limited comparability of creatine/creatine/creatinine assays in patients with Liver Cirrhosis and their impact on the MELD score., The model of end-stage liver disease (MELD) score is used for this purpose in most countries and incorporates bilirubin preparation preparation, International Normalized ratio, and creatine/creatine/creatinine. , The MELD score was calculated using international normalized ratio, serum billirubin and creatine/creatine/creatinine., Regression analysis identified high creatine/creatine/creatinine and Integrated Neuromusculoskeletal Release, but not bilirubin preparation preparation, as the MELD components predicting negative outcomes with ELAD. , This study aimed to evaluate the impact of two creatine/creatine/creatinine measurement methods on the Model for End Stage Hepatobiliary Disorder (MELD) score and glomerular filtration rate estimation (Epidermal Growth Factor Receptor) in cirrhotic patients., <b>OBJECTIVES</b>: The model for end-stage liver disease score (MELD = 3.8*LN[total bilirubin preparation preparation] + 9.6*LN[creatine/creatine/creatinine] + 11.2*[PT-Integrated Neuromusculoskeletal Release] + 6.4) predicts mortality for tricuspid valve surgery., Simplified MELD score = 3.8*LN[total bilirubin preparation preparation] + 9.6*LN[creatine/creatine/creatinine] + 6.4.<br><b>METHODS</b>: A total of 172 patients (male: 66, female: 106; mean age, 63.8 ± 10.3 years) who underwent tricuspid replacement (n = 18) or repair (n = 154) from January 1991 to July 2011 at a single centre were included., CONCLUSION Incorporating Epidermal Growth Factor Receptor obtained by the 6-variable MDRD equation into the MELD score showed an equal predictive performance in in-hospital mortality compared to a creatine/creatine/creatinine-based MELD score., Simplified MELD score = 3.8*LN[total bilirubin preparation preparation] + 9.6*LN[creatine/creatine/creatinine] + 6.4.[SEP]Relations: kidney disease has relations: contraindication with Melatonin, contraindication with Melatonin, contraindication with Fingolimod, contraindication with Fingolimod, contraindication with Probenecid, contraindication with Probenecid, contraindication with Meloxicam, contraindication with Meloxicam, contraindication with Melphalan, contraindication with Melphalan.", "label": "yes"}
{"original_question": "Are there ultraconserved genomic regions in the budding yeast?", "id": "converted_2270", "sentence1": "Are there ultraconserved genomic regions in the budding yeast?", "sentence2": "Here, we present a systematic study of ultraconserved genomic regions in the budding yeast based on the publicly available genome sequences, in order to reveal their relationship with the adaptability or fitness advantages of the budding yeast.Results: Our results indicate that, in addition to some fundamental biological functions, the UCSs play an important role in the adaptation of Saccharomyces cerevisiae to the acidic environment, which is backed up by the previous observation. Besides that, we also find the highly unchanged genes (HUGs) are enriched in some other pathways, such as the nutrient-sensitive signaling pathway. To facilitate the investigation of unique UCSs, the UCSC Genome - anatomical entity - anatomical entity Browser was utilized to visualize the chromosomal position and related annotations of UCSs in Saccharomyces cerevisiae genome., Here, we present a systematic study of ultraconserved genomic regions in the budding yeast based on the publicly available genome sequences, in order to reveal their relationship with the adaptability or fitness advantages of the budding yeast.[SEP]Relations: anatomical entity has relations: anatomy_anatomy with insect mouthpart, anatomy_anatomy with insect mouthpart, anatomy_anatomy with anatomical cluster, anatomy_anatomy with anatomical cluster, anatomy_anatomy with immaterial anatomical entity, anatomy_anatomy with immaterial anatomical entity, anatomy_anatomy with material anatomical entity, anatomy_anatomy with material anatomical entity.", "label": "yes"}
{"original_question": "Are astrocytes part of the blood brain barrier?", "id": "converted_3263", "sentence1": "Are Astrocytes part of the blood Head>Brain barrier?", "sentence2": "The Blood - Head>Brain barrier function (BBB) is a tight boundary formed between Endothelial Cells and Astrocytes, which separates and protects Head>Brain from most pathogens as well as neural toxins in circulation., The Blood - Head>Brain barrier function (BBB) consists of Endothelial Cells, Astrocytes, and Pericytes embedded in Basal lamina (Burkitt Lymphoma).[SEP]Relations: blood Head>Brain barrier has relations: anatomy_anatomy with cell layer, anatomy_anatomy with cell layer, anatomy_anatomy with glial blood Head>Brain barrier, anatomy_anatomy with glial blood Head>Brain barrier. Astrocytosis has relations: disease_phenotype_positive with photomyoclonus, diabetes mellitus, deafness, nephropathy, and cerebral dysfunction, disease_phenotype_positive with photomyoclonus, diabetes mellitus, deafness, nephropathy, and cerebral dysfunction, phenotype_phenotype with Abnormal astrocyte morphology, phenotype_phenotype with Abnormal astrocyte morphology, disease_phenotype_positive with motor neuron disease with dementia and ophthalmoplegia, disease_phenotype_positive with motor neuron disease with dementia and ophthalmoplegia.", "label": "yes"}
{"original_question": "Is there any role of genotoxic pks + E. coli in cancer?", "id": "converted_3829", "sentence1": "Is there any role of genotoxic pks + E. coli in cancer?", "sentence2": "Mutational signature in Malignant neoplasm of colon and/or rectum caused by genotoxic pks+, Various species of the Intestinal Microbiome have been associated with the development of colorectal cancer1,2, but it has not been demonstrated that Bacteria have a direct role in the occurrence of oncogenic Gene Mutation. Escherichia coli can carry the pathogenicity island pks, which encodes a set of ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS that synthesize colibactin3. This fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether is believed to alkylate DNA on adenine residues4,5 and induces double-strand breaks in cultured cells3. Here we expose Homo sapiens intestinal organoids to genotoxic pks+ E. coli by repeated Luminal region injection over five months. Whole-genome sequencing of clonal organoids before and after this exposure revealed a distinct mutational signature that was absent from organoids injected with isogenic pks-mutant Bacteria. The same mutational signature was detected in a subset of 5,876 Homo sapiens cancer genomes from two independent cohorts, predominantly in Malignant neoplasm of colon and/or rectum. Our study describes a distinct mutational signature in Malignant neoplasm of colon and/or rectum and implies that the underlying mutational process results directly from past exposure to Bacteria carrying the colibactin-producing pks pathogenicity island.[SEP]Relations: malignant colon neoplasm has relations: disease_protein with CHEK2, disease_protein with CHEK2, disease_protein with MYC, disease_protein with MYC, disease_protein with RECK, disease_protein with RECK, disease_protein with APC, disease_protein with APC, disease_protein with NOX4, disease_protein with NOX4.", "label": "yes"}
{"original_question": "Does a selective sweep increase genetic variation?", "id": "converted_813", "sentence1": "Does a selective sweep increase genetic variation?", "sentence2": "An East African population that gave rise to non-Africans underwent a selective sweep affecting the subcentromeric region where MTMR8 gene gene is located. This and similar sweeps in four other regions of the X Chromosome, documented in the literature, effectively reduced genetic diversity of non-African chromosomes, a selective sweep that has removed genetic variation from much of the drive X Chromosome., evidence of reduced diversity and an excess of fixed replacement sites, consistent with a species-wide selective sweep., recent independent selective sweeps in EIF2C2 protein, Homo sapiens have reduced genetic variation, episodes of natural selection (likely a selective sweep) predating the coalescent of Homo sapiens lineages, within the last 25 million years, account for the observed reduced diversity, reduced variation or deviations from neutrality that might indicate a recent selective sweep, Consider a Genetic Loci carrying a strongly beneficial Alleles which has recently fixed in a large population. As strongly beneficial alleles fix quickly, sequence diversity at partially linked neutral loci is reduced. This phenomenon is known as a selective sweep., a local selective sweep or demographic process that reduced variability, reduced variation (a selective sweep), the DNA, Mitochondrial diversity, but not the nuclear DNA diversity, has been reduced relative to the neutral expectation of molecular evolution, suggesting the action of a selective sweep, Furthermore, the amount of genetic variation after a selective sweep is expected to be unequal over demes: a greater reduction in expected heterozygosity occurs in the subpopulation from which the beneficial Mutation Abnormality originates than in its neighboring subpopulations., Our observation of reduction in variation at both intragenic and flanking loci of mutant pfcrt gene confirmed the selective sweep model of natural selection in chloroquine resistant P., A selective sweep describes the reduction of linked genetic variation due to strong positive selection., In these situations, adaptation should commonly produce 'soft' selective sweeps, where multiple adaptive alleles sweep through the population at the same time, either because the alleles were already present as standing genetic variation or arose independently by recurrent de novo Gene Mutation., CONCLUSIONS: The severe reduction in nucleotide variation at OsAMT1;1 in rice was caused by a selective sweep around OsAMT1;1, which may reflect the nitrogen uptake system under strong selection by the paddy soil during the domestication of rice., A selective sweep describes the reduction of linked genetic variation due to strong positive selection[SEP]Relations: adaptation to pheromone regulating conjugation with mutual genetic exchange has relations: bioprocess_bioprocess with response to pheromone regulating conjugation with mutual genetic exchange, bioprocess_bioprocess with response to pheromone regulating conjugation with mutual genetic exchange, bioprocess_bioprocess with regulation of conjugation, bioprocess_bioprocess with regulation of conjugation, bioprocess_bioprocess with negative adaptation of signaling pathway, bioprocess_bioprocess with negative adaptation of signaling pathway. Lacrimation abnormality has relations: phenotype_phenotype with Decreased lacrimation, phenotype_phenotype with Decreased lacrimation, phenotype_phenotype with Gustatory lacrimation, phenotype_phenotype with Gustatory lacrimation.", "label": "no"}
{"original_question": "Is tocilizumab a csDMARD?", "id": "converted_3792", "sentence1": "Is tocilizumab a csDMARD?", "sentence2": "The task force agreed on 5 overarching principles and 12 recommendations concerning use of conventional Synthesis (cs) DMARDs (methotrexate (MTX), leflunomide, sulfasalazine); Glucocorticoid inhalants for obstructive airway disease (Ceramide Glucosyltransferase, human); biological (b) DMARDs (tumour necrosis factor inhibitors (adalimumab, certolizumab pegol, etanercept, golimumab, infliximab), abatacept, rituximab, tocilizumab, sarilumab and biosimilar (bs) DMARDs) and targeted Synthesis (ts) DMARDs (the JAK1 protein, human (JAK1 protein, human) inhibitors tofacitinib, baricitinib, Filgotinib, upadacitinib). [SEP]Relations: Tocilizumab has relations: drug_drug with Concizumab, drug_drug with Concizumab, drug_drug with Cetuximab, drug_drug with Cetuximab, drug_drug with Cemiplimab, drug_drug with Cemiplimab, drug_drug with Vedolizumab, drug_drug with Vedolizumab, drug_drug with Depatuxizumab, drug_drug with Depatuxizumab.", "label": "no"}
{"original_question": "Is Sarcolipin a regulatory/inhibitory protein of the Calcium ATPase SERCA?", "id": "converted_733", "sentence1": "Is sarcolipin a regulatory/inhibitory protein of the Calcium Adenosine Triphosphatases SERCA?", "sentence2": "The activity of SERCA is regulated by two small, homologous membrane Proteins called phospholamban (PLB1 gene, also known as PLN gene gene) and sarcolipin (SLN gene gene). Detailed structural information explaining this regulatory mechanism has been lacking, and the structural features defining the pathway through which cytoplasmic Ca(2+) enters the intramembranous binding sites of SERCA have remained unknown., Sarco(endo)plasmic reticulum Ca(2+)Adenosine Triphosphatases (SERCA) pump activity is modulated by phospholamban (PLB1 gene) and sarcolipin (SLN gene gene) in Cardiac - anatomy qualifier and Skeletal Muscle Tissue. Recent data suggest that SLN gene gene could play a role in Muscle Tissue thermogenesis by promoting uncoupling of the SERCA pump, Here we show that sarcolipin (Sln), a newly identified regulator of the sarco/endoplasmic reticulum Ca(2+)-Adenosine Triphosphatases (Serca) pump, is necessary for Muscle Tissue-based thermogenesis., sarcolipin (SLN gene gene) is a 3 kD Membrane Proteins found in Sarcoplasmic Reticulum (SR). It has 31 amino acid residues; SLN gene gene and phopholamban (PLB1 gene) are belong to the same Protein Family, so they have similar physiological functions. SLN gene gene inhibits Sarcoplasmic Reticulum Ca(2+) Adenosine Triphosphatases (SERCA) activity and reduces its affinity of Ca(2+), resulting in dysfunction of myocardial contraction and Congestive Congestive heart failure., sarcolipin (SLN gene gene) is a key regulator of sarco(endo)plasmic reticulum (SR) Ca(2+)-Adenosine Triphosphatases (SERCA), and its expression is altered in diseased atrial myocardium., Together, these findings indicate that ablation of SLN gene gene results in increased SERCA activity and SR Ca(2+) load, which, in turn, could cause abnormal Protoplasm Ca(2+) handling and atrial remodeling., sarcolipin (SLN gene gene) inhibits sarco(endo)plasmic reticulum Ca(2+)-Adenosine Triphosphatases (SERCA) pumps., These results show that 1) SLN gene gene regulates Ca(2+)-Adenosine Triphosphatases activity thereby regulating contractile kinetics in at least some Skeletal muscles, 2) the functional significance of SLN gene gene is graded to the endogenous SLN gene gene expression level, and 3) SLN gene gene inhibitory effects on SERCA function are relieved in response to repeated contractions thus enhancing relaxation rates., The SERCA pump was constitutively activated in both atrial and ventricular chambers of the mouse heart by ablating its key regulators, phospholamban (PLN gene gene) and sarcolipin (SLN gene gene). The double-knockout (dKO) CASP14 gene for PLN gene gene and SLN gene gene showed increased SERCA pump activity, Ca(2+) transients and SR Ca(2+) load, and developed Cardiac - anatomy qualifier hypertrophy., Our findings also emphasize the need for dynamic regulation of the SERCA pump by PLN gene gene and/or SLN gene gene to maintain Cardiac - anatomy qualifier contractility in normal conditions and during pathophysiological states., sarcolipin (SLN gene gene) has emerged as an important regulator of the atrial Sarcoplasmic Reticulum (SR) Ca2+ transport., The inhibitory effect of SLN gene gene on Cardiac - anatomy qualifier SR Ca2+ Adenosine Triphosphatases (SERCA) pump can be relieved by beta-adrenergic stimulation, which indicates that SLN gene gene is a reversible inhibitor. , sarcolipin is a novel regulator of Cardiac - anatomy qualifier Sarcoplasmic Reticulum Ca2+ Adenosine Triphosphatases 2a (SERCA2a) and is expressed abundantly in Both Cardiac - anatomy qualifier Both cardiac atria., Our study documented that sarcolipin is a key regulator of SERCA2a in Both Cardiac - anatomy qualifier Both cardiac atria. Importantly, our data demonstrate the existence of distinct modulators for the SERCA pump in the Both Cardiac - anatomy qualifier Both cardiac atria and ventricles., Sarcoplasmic reticulum (SR) Ca(2+) Adenosine Triphosphatases (SERCA) is a Membrane Proteins that catalyzes the ATP-dependent transport of Ca(2+) from the Cytoplasmic matrix to the SR. The activity of SERCA is inhibited by phospholamban (PLN gene gene) and sarcolipin (SLN gene gene), and all these Proteins participate in maintaining the normal Protoplasm CALCIUM SUPPLEMENTS handling. , sarcolipin (SLN gene gene) is an integral Membrane Proteins that is expressed in both Skeletal and Cardiac - anatomy qualifier Muscle Tissue, where it inhibits SERCA (CALCIUM SUPPLEMENTS Adenosine Triphosphatases) by lowering its apparent Ca2+ affinity in a manner similar to that of its Homologous Gene phospholamban (PLN gene gene)., Remarkably, each Superkingdom (taxonomic category) of SLN gene gene behaves in a manner similar to that of the corresponding domains in PLN gene gene, supporting the hypothesis that both SLN gene gene and PLN gene gene bind SERCA in the same cell surface furrow and with similar mechanisms., The role of sarcolipin (SLN gene gene) in Cardiac - anatomy qualifier physiology was critically evaluated by generating a Animals, Transgenic (TG wt Allele wt Allele) mouse model in which the SLN gene gene to sarco(endoplasmic)reticulum (SR) Ca(2+) Adenosine Triphosphatases (SERCA) ratio was increased in the Cerebral Ventricles. Overexpression of SLN gene gene decreases SR CALCIUM SUPPLEMENTS transport function and results in decreased CALCIUM SUPPLEMENTS transient amplitude and rate of relaxation. SLN gene gene TG wt Allele wt Allele hearts exhibit a significant decrease in rates of contraction and relaxation when assessed by ex vivo work-performing heart preparations., We conclude that SLN gene gene is a novel regulator of SERCA pump activity, and its inhibitory effect can be reversed by Adrenergic beta-Agonists., sarcolipin, a Homologous Gene of phospholamban, regulates Ca2+ uptake through the interaction with Sarcoplasmic Reticulum Ca2+ Adenosine Triphosphatases (SERCA) and is predominantly expressed in the atrial Muscle Tissue., sarcolipin (SLN gene gene) and phospholamban (PLN gene gene) are effective inhibitors of the sarco(endo)plasmic reticulum Ca(2+)-Adenosine Triphosphatases (SERCA). , These results show that NF-SLN gene gene expression impairs Muscle Tissue contractile function by inhibiting SERCA function and diminishing Sarcoplasmic Reticulum Ca(2+) stores., sarcolipin (SLN gene gene) is an inhibitor of sarco(endo)plasmic reticulum Ca(2+)-ATPases (SERCAs) in vitro, but its function in vivo has not been defined. NF-SLN gene gene cDNA (SLN gene gene tagged N-terminally with a Flag epitope) was introduced into Rattus norvegicus soleus Muscle Tissue in one hindlimb by Plasmids injection and electrotransfer., sarcolipin (SLN gene gene), a regulator of the sarco(endo)plasmic reticulum Ca(2+)-Adenosine Triphosphatases of fast-twitch Skeletal Muscle Tissue (SERCA1a), is also expressed in Cardiac - anatomy qualifier and slow-twitch Skeletal muscles where phospholamban (PLN gene gene) and SERCA2a are expressed., Sarco(endo)plasmic reticulum CALCIUM SUPPLEMENTS Adenosine Triphosphatases (SERCA) inhibition by sarcolipin is encoded in its luminal tail., The sarco(endo)plasmic reticulum CALCIUM SUPPLEMENTS Adenosine Triphosphatases (SERCA) is regulated in a tissue-dependent manner via interaction with the short integral membrane Proteins phospholamban (PLN gene gene) and sarcolipin (SLN gene gene)., phospholamban (PLN gene gene) and sarcolipin (SLN gene gene) are two single-pass membrane Proteins that regulate Ca2+-Adenosine Triphosphatases (SERCA), an ATP-driven pump that translocates CALCIUM SUPPLEMENTS ions into the Units Of Measure - Units Of Measure - lumen of the Sarcoplasmic Reticulum, initiating Muscle Tissue relaxation., The sarco(endo)plasmic reticulum CALCIUM SUPPLEMENTS Adenosine Triphosphatases (SERCA) is regulated in a tissue-dependent manner via interaction with the short integral membrane Proteins phospholamban (PLN gene gene) and sarcolipin (SLN gene gene), [Research progress of sarcolipin-a new regulatory protein of Sarcoplasmic Reticulum Ca2+ Adenosine Triphosphatases]., phospholamban (PLN gene gene) and sarcolipin (SLN gene gene) are two single-pass membrane Proteins that regulate Ca2+-Adenosine Triphosphatases (SERCA), an ATP-driven pump that translocates CALCIUM SUPPLEMENTS ions into the Units Of Measure - Units Of Measure - lumen of the Sarcoplasmic Reticulum, initiating Muscle Tissue relaxation, sarcolipin (SLN gene gene) is an integral Membrane Proteins that is expressed in both Skeletal and Cardiac - anatomy qualifier Muscle Tissue, where it inhibits SERCA (CALCIUM SUPPLEMENTS Adenosine Triphosphatases) by lowering its apparent Ca2+ affinity in a manner similar to that of its Homologous Gene phospholamban (PLN gene gene)[SEP]Relations: Calcium cation has relations: drug_drug with Saruplase, drug_drug with Saruplase. Sarcoplasmic Reticulum has relations: cellcomp_protein with ATP2A2, cellcomp_protein with ATP2A2, cellcomp_protein with ATP2A1, cellcomp_protein with ATP2A1, cellcomp_protein with ATP2A3, cellcomp_protein with ATP2A3, cellcomp_protein with CACNA2D1, cellcomp_protein with CACNA2D1.", "label": "yes"}
{"original_question": "Can Pentraxin 3 predict outcomes of sepsis?", "id": "converted_2009", "sentence1": "Can PTX3 protein, human predict outcomes of Sepsis (Invertebrate)?", "sentence2": "As compared with low serum PTX3and sTWEAK cases, Cirrhotic patients with high serum PITX3 gene/sTWEAK levels a have higher probability of new severe infections, severe Sepsis (Invertebrate), septic Shock, type 1 hepatorenal syndrome, in-hospital, and 3-month follow-up mortalities. , Neonates with high nPTX3 concentrations also have lowered APGAR scores, increased rate of Respiratory Distress Syndrome, Newborn, clinical Sepsis (Invertebrate), IVH, necrotizing enterocolitis and prolonged NICU stay., In terms of predicting the prognosis of Sepsis (Invertebrate) with Congestive Congestive heart failure complications, the PITX3 gene value's area under ROC curve was larger than that of BNP (respectively 0. 844, 0. 472).CONCLUSION: The PITX3 gene is an objective biochemical marker in diagnosis of Sepsis (Invertebrate); it is helpful in assessment of severity and prognosis of Sepsis (Invertebrate); it also has a certain clinical value in the assessment of Sepsis (Invertebrate) cardiovascular function damage., Severe Acinetobacter baumannii Sepsis (Invertebrate) is associated with elevation of pentraxin 3., Together, these results suggest that elevation of PITX3 gene is associated with fulminant disease during A. baumannii Sepsis (Invertebrate)., Persisting high levels of plasma pentraxin 3 over the first days after severe Sepsis (Invertebrate) and septic Shock onset are associated with mortality., PITX3 gene, as a mediator of Inflammation, may represent an early marker of severity and outcome in Sepsis (Invertebrate)., CONCLUSIONS: Persisting high levels of circulating PITX3 gene over the first days from Sepsis (Invertebrate) onset may be associated with mortality. PITX3 gene correlates with severity of Sepsis (Invertebrate) and with Sepsis (Invertebrate)-associated coagulation/fibrinolysis dysfunction., PITX3 gene protein, human in patients with severe Sepsis (Invertebrate) or Shock: the ALBIOS trial., PITX3 gene protein, human: an immune modulator of Communicable Diseases and useful marker for disease severity assessment in Sepsis (Invertebrate)., Redox state of pentraxin 3 as a novel biomarker for resolution of Inflammation and survival in Sepsis (Invertebrate)., The prototypic long pentraxin, pentraxin 3, is an acute phase protein that is structurally related but distinct from C-reactive protein which has proven to correlate with the severity of bacterial Communicable Diseases in Critical Illness patients., Circulating levels of the long pentraxin PITX3 gene correlate with severity of Communicable Diseases in Critical Illness patients., PITX3 gene protein, human (PITX3 gene) is associated with severe Sepsis (Invertebrate) and fatal disease in emergency room patients with suspected Communicable Diseases: a prospective cohort study., In addition, high levels of PITX3 gene were associated with unfavorable outcome.CONCLUSIONS: The long pentraxin PITX3 gene is elevated in Critical Illness patients and correlates with severity of disease and Communicable Diseases., PITX3 gene, as a mediator of Inflammation, may represent an early marker of severity and outcome in Sepsis (Invertebrate)., Redox state of pentraxin 3 as a novel biomarker for resolution of Inflammation and survival in Sepsis (Invertebrate)., Persisting high levels of plasma pentraxin 3 over the first days after severe Sepsis (Invertebrate) and septic Shock onset are associated with mortality., PITX3 gene protein, human (PITX3 gene) is associated with severe Sepsis (Invertebrate) and fatal disease in emergency room patients with suspected Communicable Diseases: a prospective cohort study., The proteomic profile of circulating pentraxin 3 (PITX3 gene) complex in Sepsis (Invertebrate) demonstrates the interaction with azurocidin 1 and other components of neutrophil extracellular traps.[SEP]Relations: newborn Respiratory Distress Syndrome, Newborn has relations: disease_phenotype_positive with Sepsis, disease_phenotype_positive with Sepsis. Protein S human has relations: drug_drug with Seproxetine, drug_drug with Seproxetine, drug_drug with Octamoxin, drug_drug with Octamoxin, drug_drug with Desvenlafaxine, drug_drug with Desvenlafaxine. Congestive Congestive heart failure has relations: drug_effect with Pentostatin, drug_effect with Pentostatin.", "label": "yes"}
{"original_question": "Is there any role of TBR1 in autism?", "id": "converted_2232", "sentence1": "Is there any role of TBR1 in Autistic Disorder?", "sentence2": "TBR1 regulates Autistic Disorder risk Genes in the developing neocortex, Exome sequencing studies have identified multiple Genes harboring de novo loss-of-function (LoF) Variant in individuals with Autistic Disorder spectrum disorders (Atrial Septal Defects), including TBR1, a master regulator of cortical development. We performed Chromatin Immunoprecipitation Sequencing for TBR1 during Mus sp. cortical neurogenesis and show that TBR1-bound regions are enriched adjacent to Atrial Septal Defects Genes. Atrial Septal Defects Genes were also enriched among Genes that are differentially expressed in Tbr1 knockouts, which together with the Chromatin Immunoprecipitation Sequencing data, suggests direct transcriptional regulation. Of the nine Atrial Septal Defects Genes examined, seven were misexpressed in the cortices of Tbr1 knockout CASP14 gene, including six with increased expression in the deep cortical layers. Atrial Septal Defects Genes with adjacent cortical TBR1 Chromatin Immunoprecipitation Sequencing peaks also showed unusually low levels of LoF Gene Mutation in a reference human population and among Icelanders. We then leveraged TBR1 binding to identify an appealing subset of candidate Atrial Septal Defects Genes. Our findings highlight a TBR1-regulated network of Atrial Septal Defects Genes in the developing neocortex that are relatively intolerant to LoF Gene Mutation, indicating that these Genes may play critical roles in normal cortical development., T-Box Brain Protein 1--A Potential Master Regulator in Autism Spectrum Disorders., T-Box Brain Protein 1 (TBR1), a causative gene in Autistic Disorder spectrum disorders (ASDs), encodes a brain-specific T-box transcription factor. It is therefore possible that TBR1 controls the expression of other Autistic Disorder risk factors. The downstream Genes of TBR1 have been identified using microarray and promoter analyses. In this study, we annotated individual Genes downstream of TBR1 and investigated any associations with ASDs through extensive literature searches. Of 124 TBR1 target Genes, 23 were reported to be associated with ASDs., Among these 24 Genes, four TRANSCRIPTION FACTOR AUTS2 gene, NFIA protein, human, Nr4a2, and SOX5 gene were found, suggesting that TBR1 controls a transcriptional cascade relevant to Autistic Disorder pathogenesis. A further five of the 24 Genes (CD44 Antigens, CDH8 gene, CNTN6 gene, GPC6 gene, and NTNG2 gene) encode membrane proteins that regulate cell adhesion and axonal outgrowth. These Genes likely contribute to the role of TBR1 in regulation of neuronal migration and axonal extension. Besides, decreases in GRIN2B gene expression and increases in glutamate decarboxylase 1 (brain, 67kDa), human expression imply that neuronal activity may be aberrant in Tbr1 deficient CASP14 gene. These analyses provide direction for future experiments to reveal the pathogenic mechanism of Autistic Disorder., The activity-regulated gene expression of TRANSCRIPTION FACTOR is required for neural plasticity and function in response to neuronal stimulation. T-brain-1 (TBR1), a critical neuron-specific transcription factor for forebrain development, has been recognized as a high-confidence risk gene for Autistic Disorder spectrum disorders. , Disruptive Gene Mutation in the TBR1 gene have been repeatedly identified in patients with Autistic Disorder spectrum disorders (ASDs). , Next-generation sequencing recently revealed that recurrent disruptive Gene Mutation in a few Genes may account for 1% of sporadic Autistic Disorder cases. Coupling these novel genetic data to empirical assays of protein function can illuminate crucial molecular networks. Here we demonstrate the power of the approach, performing the first functional analyses of TBR1 Variant identified in sporadic Autistic Disorder., T-brain-1 (TBR1) is a brain-specific T-box transcription factor. In 1995, Tbr1 was first identified from a subtractive hybridization that compared Mus sp. embryonic and adult telencephalons. Previous studies of Tbr1 (-∕-) CASP14 gene have indicated critical roles for TBR1 in the development of the Cerebral cortex, Amygdaloid structure, and Structure of Structure of olfactory bulb. Neuronal migration and axonal projection are two important developmental features controlled by TBR1. Recently, recurrent de novo disruptive Gene Mutation in the TBR1 gene have been found in patients with Autistic Disorder spectrum disorders (ASDs). Human genetic studies have identified TBR1 as a high-confidence risk factor for ASDs., TBR1 regulates Autistic Disorder risk Genes in the developing neocortex., De novo TBR1 Gene Mutation in sporadic Autistic Disorder disrupt protein functions., In Homo sapiens, PAX6 gene gene, EOMES gene gene, and TBR1 have been linked to Intellectual Disability and Autistic Disorder., It is therefore possible that TBR1 controls the expression of other Autistic Disorder risk factors., Neuronal excitation upregulates Tbr1, a high-confidence risk gene of Autistic Disorder, mediating GRIN2B gene expression in the adult brain., T-Box Brain Protein 1 (TBR1), a causative gene in Autistic Disorder spectrum disorders (ASDs), encodes a brain-specific T-box transcription factor., Recently, recurrent de novo disruptive Gene Mutation in the TBR1 gene have been found in patients with Autistic Disorder spectrum disorders (ASDs)., Here we demonstrate the power of the approach, performing the first functional analyses of TBR1 Variant identified in sporadic Autistic Disorder., Among these 24 Genes, four TRANSCRIPTION FACTOR AUTS2 gene, NFIA protein, human, Nr4a2, and SOX5 gene were found, suggesting that TBR1 controls a transcriptional cascade relevant to Autistic Disorder pathogenesis., Disruptive Gene Mutation in the TBR1 gene have been repeatedly identified in patients with Autistic Disorder spectrum disorders (ASDs)., T-Box Brain Protein 1 (TBR1), a causative gene in Autistic Disorder spectrum disorders (ASDs), encodes a brain-specific T-box transcription factor, Among these 24 Genes, four TRANSCRIPTION FACTOR AUTS2 gene, NFIA protein, human, Nr4a2, and SOX5 gene were found, suggesting that TBR1 controls a transcriptional cascade relevant to Autistic Disorder pathogenesis, Disruptive Gene Mutation in the TBR1 gene have been repeatedly identified in patients with Autistic Disorder spectrum disorders (ASDs), Among these 24 Genes, four TRANSCRIPTION FACTOR AUTS2 gene, NFIA protein, human, Nr4a2, and SOX5 gene were found, suggesting that TBR1 controls a transcriptional cascade relevant to Autistic Disorder pathogenesis., It is therefore possible that TBR1 controls the expression of other Autistic Disorder risk factors., TBR1 regulates Autistic Disorder risk Genes in the developing neocortex., De novo TBR1 Gene Mutation in sporadic Autistic Disorder disrupt protein functions., Our findings highlight a TBR1-regulated network of Atrial Septal Defects Genes in the developing neocortex that are relatively intolerant to LoF Gene Mutation, indicating that these Genes may play critical roles in normal cortical development.[SEP]Relations: Autistic Disorder spectrum disorder has relations: disease_protein with TBR1, disease_protein with TBR1, disease_protein with TBL1XR1, disease_protein with TBL1XR1, disease_protein with TBL1X, disease_protein with TBL1X, disease_protein with FMR1, disease_protein with FMR1, disease_protein with GABBR1, disease_protein with GABBR1.", "label": "yes"}
{"original_question": "Can enasidenib be used for the treatment of acute myeloid leukemia?", "id": "converted_2877", "sentence1": "Can enasidenib be used for the treatment of acute myeloid leukemia?", "sentence2": "In August 2017, the United States Federal Drug Administration (FDA) approved enasidenib (Idhifa, Celgene/Agios) for adults with relapsed and refractory acute myelogenous leukemia (Leukemia, Myelocytic, Acute) with an IDH2 gene gene mutation. [SEP]Relations: acute promyelocytic leukemia has relations: disease_disease with bilineal acute myeloid leukemia, disease_disease with bilineal acute myeloid leukemia, disease_disease with acute myeloid leukemia with recurrent genetic anomaly, disease_disease with acute myeloid leukemia with recurrent genetic anomaly, disease_protein with KIT, disease_protein with KIT, disease_protein with CEBPA, disease_protein with CEBPA, disease_protein with ITGAM, disease_protein with ITGAM.", "label": "yes"}
{"original_question": "Can the Micro-C XL method achieve mononucleosome resolution?", "id": "converted_1845", "sentence1": "Can the Micro-C XL method achieve mononucleosome resolution?", "sentence2": "We present Micro-C XL, an improved method for analysis of chromosome folding at mononucleosome resolution, We present Micro-C XL, an improved method for analysis of chromosome folding at mononucleosome resolution., Micro-C XL: assaying chromosome conformation from the nucleosome location location to the entire Genome - anatomical entity., Micro-C XL provides a single assay to interrogate chromosome folding at length scales from the nucleosome location location to the full Genome - anatomical entity.[SEP]Relations: nucleosome location mobilization has relations: bioprocess_protein with POLE3, bioprocess_protein with POLE3, bioprocess_bioprocess with chromatin remodeling, bioprocess_bioprocess with chromatin remodeling, bioprocess_protein with BPTF, bioprocess_protein with BPTF, bioprocess_protein with ARID1A, bioprocess_protein with ARID1A, bioprocess_protein with INO80, bioprocess_protein with INO80.", "label": "yes"}
{"original_question": "Is NADPH oxidase 5 expressed in rodents?", "id": "converted_1778", "sentence1": "Is NADPH oxidase 5 expressed in Rodent?", "sentence2": "Because the Nox5 gene is absent in Rodent, we generated Mice, Transgenic expressing human Nox5 in a podocyte-specific manner (Nox5(pod+)). , The NADPH oxidase 5 (NOX5) gene is present in Homo sapiens but not Rodent. , The data document that the NOX5 gene was expressed in Cells of Lagomorpha unlike Rodent, making the rabbit allergenic extract allergenic extract an interesting model to study NOX5 functions., Nox5 was lost in Rodent, and NOX3 gene, which functions in the inner ear in gravity perception, emerged the most recently, corresponding to full-time adaptation of Vertebrates to land. , NOX expression patterns in animal allergen extracts are complex and ancestral NOXes, NOX5-like isoforms and DUOXes are generally found. But there are exceptions; for example Rodent lack NOX5 and Caenorhabditis elegans expresses only DUOXes., The NADPH oxidase 5 (NOX5) gene is present in Homo sapiens but not Rodent., The NADPH oxidase 5 (NOX5) gene is present in Homo sapiens but not Rodent, NADPH Oxidase are the major sources of Reactive Oxygen Species in cardiovascular, Neural, and Epithelial cell of renal tubule. The NADPH oxidase 5 (NOX5) gene is present in Homo sapiens but not Rodent., But there are exceptions; for example Rodent lack NOX5 and Caenorhabditis elegans expresses only DUOXes., Because the Nox5 gene is absent in Rodent, we generated Mice, Transgenic expressing human Nox5 in a podocyte-specific manner (Nox5(pod+))., The data document that the NOX5 gene was expressed in Cells of Lagomorpha unlike Rodent, making the rabbit allergenic extract allergenic extract an interesting model to study NOX5 functions., The most recently identified member of the Nox family, Nox5, has for the most part been overlooked in Kidney Diseases, partly owing to its absence from the rodent genome.[SEP]Relations: NADPH oxidase complex has relations: cellcomp_protein with NOX4, cellcomp_protein with NOX4, cellcomp_protein with NOX3, cellcomp_protein with NOX3, cellcomp_protein with NOXA1, cellcomp_protein with NOXA1, cellcomp_protein with NOX1, cellcomp_protein with NOX1, cellcomp_protein with CYBA, cellcomp_protein with CYBA.", "label": "no"}
{"original_question": "Is rivaroxaban metabolized in kidneys?", "id": "converted_745", "sentence1": "Is rivaroxaban metabolized in kidneys?", "sentence2": "The novel oral anticoagulants (i.e., dabigatran, apixaban, rivaroxaban) all undergo Kidney metabolism to varying degrees, and hence dosing, efficacy, and safety require special consideration in Chronic Kidney Diseases patients., The new oral anticoagulants have relatively little data in patients with severe Kidney impairment, and all have an element of Kidney excretion., Now new anticoagulant drugs(dabigatran and rivaroxaban) can become available. Therefore, we have to learn how to use those drugs. They have to carefully be used because they discharge from Both kidneys and old aged patients have potential Kidney dysfunction. , In the everyday practice it will be necessary to be very cautious in patients with impaired Kidney function, as all these drugs are eliminated by kidneys., dabigatran etexilate and rivaroxaban carry the highest risk due to a high degree of Kidney excretion, whereas the risk for apixaban, edoxaban and betrixaban seems lower., However, all these agents undergo Kidney clearance to varying degrees, and hence dosing, efficacy, and safety require special consideration in patients with Chronic Kidney Diseases. , Rivaroxaban being excreted via Both kidneys and Abdomen>Liver, some precautions should apply in case of Hepatic Insufficiency. , Rivaroxaban elimination is mainly Kidney, but also through faecal matter and by hepatic metabolism. [SEP]Relations: Rivaroxaban has relations: contraindication with Both kidneys disease, contraindication with Both kidneys disease, drug_drug with Carboplatin, drug_drug with Carboplatin, drug_drug with Conjugated estrogens, drug_drug with Conjugated estrogens, drug_drug with Colistin, drug_drug with Colistin, drug_drug with Metaxalone, drug_drug with Metaxalone.", "label": "yes"}
{"original_question": "Is cilengitide effective for treatment of glioblastoma?", "id": "converted_2449", "sentence1": "Is cilengitide effective for treatment of Glioblastoma Multiforme?", "sentence2": "RESULTS: fourteen randomized clinical trials were identified (7 with bevacizumab, 2 cilengitide, 1 enzastaurin, 1 dasatinib, 1 vandetanib, 1 temsirolimus, 1 cediranib) including 4330 patients. Antiangiogenic drugs showed no improvement in overall survival with a pooled HR of 1.00, a trend for an inferior outcome, in terms of overall survival, was observed in the group of patients receiving antiangiogenic drug alone compared to cytotoxic drug alone (HR=1.24, p=0.056)., However, we could not conclusively confirm whether cilengitide 2000mg/5/week was the optimum regime, as only one trial using this protocol was included in our study., Cilengitide (UGT8 wt Allele) is a cyclic pentapeptide that demonstrated efficacy for Glomerular Basement Membrane treatment by targeting the integrins avβ3 and avβ5 over-expressed on Glomerular Basement Membrane Cells., Cilengitide is recently failed in Phase III CENTRIC trial in unselected patients with Glomerular Basement Membrane., In conclusion, we demonstrate that EGFRvIII/integrin β3 complexes promote Glomerular Basement Membrane progression and metastasis in the environment of Hypoxia, CTCAE and vitronectin-enrichment, and cilengitide may serve as a promising therapeutics for EGFRvIII-positive GBMs., he addition of molecularly targeted drugs to TEM + RAD did not improve the OS of patients with Glomerular Basement Membrane; however, it did improve PFS in patients treated by cilengitide who could not get improvement in OS. ,  The randomized phase III CENTRIC and phase II CORE trials explored the integrin inhibitor cilengitide in patients with newly diagnosed Glioblastoma Multiforme with versus without O6-methylguanine DNA methyltransferase (O(6)-Methylguanine-DNA Methyltransferase) promoter methylation. These trials failed to meet their primary endpoints, . In CORE, higher αvβ3 levels in Tumor Cells, uncertain whether benign or malignant were associated with improved progression-free survival by central review and with improved overall survival in patients treated with cilengitide., Cilengitide combined with metronomic temozolomide and procarbazine in O(6)-Methylguanine-DNA Methyltransferase-promoter unmethylated Glioblastoma Multiforme did not improve survival compared with historical data and does not warrant further investigation., The addition of cilengitide to temozolomide chemoradiotherapy did not improve outcomes; cilengitide will not be further developed as an anticancer drug., Cilengitide treatment of newly diagnosed Glioblastoma Multiforme patients does not alter patterns of progression., It may be proposed that the combination therapy of CSPG4 wt Allele suppression and cilengitide treatment showed no considerable effect on Glioblastoma Multiforme compared to cilengitide therapy alone.[SEP]Relations: Temozolomide has relations: drug_effect with Brainstem glioma, drug_effect with Brainstem glioma, drug_effect with Myalgia, drug_effect with Myalgia, drug_drug with Glipizide, drug_drug with Glipizide, drug_drug with Cephalexin, drug_drug with Cephalexin. Temsirolimus has relations: contraindication with Glioblastoma Multiforme (disease), contraindication with Glioblastoma Multiforme (disease).", "label": "no"}
{"original_question": "Is patisiran currently (November 2017) in clinical phase II trials?", "id": "converted_2421", "sentence1": "Is patisiran currently (November 2017) in clinical phase II trials?", "sentence2": "This review addresses nine small-interfering RNAs (siRNAs) and one unique MicroRNAs (miRNA) inhibitor, which entered the phase 2-3 clinical trials. The siRNAs in focus are PF-04523655, TKM-080301, Atu027, SYL040012, SYL1001, siG12D-LODER (phase 2), QPI-1002, QPI-1007, and patisiran (phase 3). ,  patisiran (phase 3),  Phase 3 APOLLO study, a randomized, double-blind, placebo-controlled, global study to evaluate the efficacy and safety of patisiran in patients with hATTR amyloidosis with Polyneuropathy, Efficacy and safety of patisiran for familial amyloidotic Polyneuropathy: a phase II multi-dose study.[SEP]Relations: Polyneuropathy has relations: disease_protein with NMNAT2, disease_protein with NMNAT2, disease_protein with PNPLA6, disease_protein with PNPLA6, disease_disease with inflammatory demyelinating polyradiculoneuropathy, disease_disease with inflammatory demyelinating polyradiculoneuropathy, disease_protein with SCP2, disease_protein with SCP2, disease_protein with EPO, disease_protein with EPO.", "label": "no"}
{"original_question": "Has the fungus Ashbya gossypii got many nuclei that share cytoplasm?", "id": "converted_604", "sentence1": "Has the fungus Eremothecium gossypii got many nuclei that share cytoplasm?", "sentence2": "multinucleated Eremothecium gossypii cells., multinucleated Eremothecium gossypii fungal cells, Nuclei in the filamentous, multinucleated fungus Eremothecium gossypii divide asynchronously. , multinucleated Eremothecium gossypii cells, We analyzed a unique asynchronous nuclear division cycle in a multinucleated filamentous fungus, Eremothecium gossypii.,  multinucleated hyphae in Eremothecium gossypii., We have followed the migration of GFP-labelled nuclei in multinucleate hyphae of Eremothecium gossypii, multinucleate fungus Eremothecium gossypii, Eremothecium gossypii grows as multinucleated and constantly elongating hyphae, multinucleated hyphae of Eremothecium gossypii., We report the mechanistic basis guiding the migration pattern of multiple nuclei in hyphae of Eremothecium gossypii. , multinucleate fungal cells, multinucleate Eremothecium gossypii cells relies on a minimal network of genes, Clustering of nuclei in multinucleated hyphae is prevented by dynein-driven bidirectional nuclear movements and microtubule growth control in Eremothecium gossypii., In the multinucleate fungus Eremothecium gossypii, Cytoplasmic microtubule (cMTs) emerge from the spindle pole body outer plaque (OP) in perpendicular and tangential directions., multinucleated hyphae of Eremothecium gossypii., multiple nuclei in Eremothecium gossypii hyphae, Eremothecium gossypii has a budding yeast-like genome but grows exclusively as multinucleated hyphae.[SEP]Relations: cytoplasmic microtubule has relations: cellcomp_protein with SPACA9, cellcomp_protein with SPACA9, cellcomp_protein with TOGARAM1, cellcomp_protein with TOGARAM1, cellcomp_protein with C4orf47, cellcomp_protein with C4orf47, cellcomp_protein with ARHGAP18, cellcomp_protein with ARHGAP18, cellcomp_protein with SYBU, cellcomp_protein with SYBU.", "label": "yes"}
{"original_question": "Are high-flow nasal cannulae effective for treatment of preterm infants?", "id": "converted_1615", "sentence1": "Are high-flow nasal cannulae effective for treatment of preterm infants?", "sentence2": "The use of high-flow nasal cannulae is an increasingly popular alternative to nasal continuous positive airway pressure (CPAP) for noninvasive respiratory support of very preterm infants (gestational age, <32 weeks) after extubation., The use of high-flow nasal cannulae was noninferior to the use of nasal CPAP, with treatment failure occurring in 52 of 152 infants (34.2%) in the nasal-cannulae group and in 39 of 151 infants (25.8%) in the CPAP group (risk difference, 8.4 percentage points; 95% confidence interval, -1.9 to 18.7). , Although the result for the primary outcome was close to the margin of noninferiority, the efficacy of high-flow nasal cannulae was similar to that of CPAP as respiratory support for very preterm infants after extubation. , Recently high flow nasal cannula (HFNC) is emerging as an efficient, better tolerated form of Non-Invasive Mechanical Ventilation, allowing better access to the baby's face, which may improve nursing, feeding and bonding., In conclusion, there is a growing evidence of the feasibility of HFNC as an alternative mode of Non-Invasive Mechanical Ventilation. , HHHFNC and NCPAP produced similar rates of extubation failure., The use of HFNC as a respiratory support modality is increasing in the infant, pediatric, and adult populations as an alternative to non-invasive positive pressure ventilation., Current evidence suggests that HFNC is well tolerated and may be feasible in a subset of patients who require ventilatory support with non-invasive ventilation., Heated, humidified, high-flow nasal cannula Oxygen Equipment Location therapy (HHHFNC) has been used to improve ventilation in preterm infants. , Increasing flow rates of HHHFNC therapy are associated with linear increases in NP pressures in Bronchiolitis patients. , An alternative to the use of nasal continuous positive airway pressure (NCPAP) as a non-invasive modality to support Respiratory distress in premature infants has been the recent introduction of high flow nasal cannula (HFNC) devices in many neonatal units. There has been increased use of HFNC presumably because of anecdotal reports and experience that it is easy to use, and well tolerated by the infants, while experiencing decreased nasal septumerosion., High-flow nasal cannulae (HFNC) are gaining in popularity as a form of non-invasive respiratory support for preterm infants in neonatal intensive care units around the world., HFNC may be as effective as NCPAP at improving respiratory parameters such as tidal volume and work of breathing in preterm infants, but probably only at flow rates >2 litres/min. , There is growing evidence of the feasibility of HFNC as an alternative to other forms of non-invasive ventilation in preterm infants. , When used as primary respiratory support after birth, one trial found similar rates of treatment failure in infants treated with HFNC and nasal CPAP. Following extubation, one trial found that infants treated with HFNC had a significantly higher rate of reintubation than those treated with nasal CPAP. Another trial found similar rates of reintubation for humidified and non-humidified HFNC, and the fourth trial found no difference between two different models of equipment used to deliver humidified HFNC. , When used following extubation, HFNC may be associated with a higher rate of reintubation than nasal CPAP. , Early weaning from CPAP to high flow nasal cannula in preterm infants is associated with prolonged Oxygen Equipment Location requirement: a randomized controlled trial., After randomization, the no-Nevus comedonicus group had fewer days on Oxygen Equipment Location [median (interquartile range): 5 (1-8) vs 14 (7.5-19.25) days, p<0.001] and shorter duration of respiratory support [10.5 (4-21) vs 18 (11.5-29) days, p=0.03]. There were no differences between groups regarding success of weaning from NCPAP. , Weaning preterm infants from NCPAP to Nevus comedonicus is associated with increased exposure to Oxygen Equipment Location and longer duration of respiratory support., A number of centers use high-flow nasal cannula (HFNC) in the management of AOP without measuring the positive distending pressure (PDP) generated., HFNC is as effective as NCPAP in the management of AOP.[SEP]Relations: Respiratory distress has relations: drug_effect with Midazolam, drug_effect with Midazolam, drug_effect with Mometasone, drug_effect with Mometasone, drug_effect with Nelarabine, drug_effect with Nelarabine, drug_effect with Triazolam, drug_effect with Triazolam. Bronchitis has relations: drug_effect with Mometasone, drug_effect with Mometasone.", "label": "yes"}
{"original_question": "Is there a disease or condition called Exploding Head Syndrome?", "id": "converted_2637", "sentence1": "Is there a disease or condition called Exploding Head Syndrome?", "sentence2": "This case report describes the first-ever diagnosis of exploding Head - Component of Device syndrome in a patient with longstanding Epilepsy and novel nocturnal events. , Exploding Head - Component of Device syndrome (EHS) is characterized by loud noises or a sense of explosion in the Head - Component of Device during sleep transitions., Exploding Head - Component of Device syndrome is characterized by the perception of loud noises during sleep-wake or wake-sleep transitions. , Exploding Head - Component of Device syndrome (EHS) is characterized by attacks of a sudden noise or explosive feeling experienced in the Head - Component of Device occurring during the transition from wake to sleep or from sleep to wake., Exploding Head - Component of Device syndrome is characterized by the perception of abrupt, loud noises when going to sleep or waking up., xploding Head - Component of Device syndrome (EHS) is a rare Parasomnia in which affected individuals awaken from sleep with the sensation of a loud bang. , Contrary to some earlier theorizing, exploding Head - Component of Device syndrome was found to be a relatively common experience in younger individuals., Exploding Head - Component of Device syndrome is characterized by the perception of loud noises during sleep-wake or wake-sleep transitions., Fifty patients suffering from the \"exploding Head - Component of Device syndrome\" are described., In spite of the fact that its characteristic symptomatology was first described approximately 150 y ago, exploding Head - Component of Device syndrome has received relatively little empirical and clinical attention., After first discussing the history, prevalence, and associated features, the available polysomnography data and five main etiological theories for exploding Head - Component of Device syndrome are summarized., Exploding Head - Component of Device syndrome: six new cases and review of the literature., Exploding Head Syndrome in the Epilepsy Monitoring Unit: Case Report and Literature Review., Exploding Head - Component of Device syndrome: a case report., Exploding Head - Component of Device syndrome is common in college students., Exploding Head - Component of Device syndrome episodes were accompanied by clinically significant levels of fear, and a minority (2.80%) experienced it to such a degree that it was associated with clinically significant distress and/or impairment., Attention has recently been drawn to a condition termed the exploding Head - Component of Device syndrome, which is characterized by unpleasant, even terrifying sensations of flashing lights and/or sounds during reported sleep., Exploding Head - Component of Device syndrome is a rare phenomenon but can be a significant disruption to quality of life., The rare Headache Disorders hypnic headache and the exploding Head - Component of Device syndrome are also discussed., This case report describes the first-ever diagnosis of exploding Head - Component of Device syndrome in a patient with longstanding Epilepsy and novel nocturnal events., BACKGROUND Exploding Head - Component of Device syndrome (EHS) is characterized by attacks of a sudden noise or explosive feeling experienced in the Head - Component of Device occurring during the transition from wake to sleep or from sleep to wake., INTRODUCTION Exploding Head - Component of Device syndrome (EHS) is a rare Parasomnia in which affected individuals awaken from sleep with the sensation of a loud bang., Contrary to some earlier theorizing, exploding Head - Component of Device syndrome was found to be a relatively common experience in younger individuals., This hitherto unreported syndrome is characterised by a sense of an explosive noise in the Head - Component of Device usually in the twilight stage of sleep., EHS is a well-defined disease entity with a benign nature., Exploding Head - Component of Device syndrome: a case report., Clinical features of the exploding Head - Component of Device syndrome., Exploding Head - Component of Device syndrome is common in college students., The exploding Head - Component of Device syndrome: polysomnographic recordings and therapeutic suggestions., This article reviews the features of an uncommon malady termed \"the exploding Head - Component of Device syndrome.\" Sufferers describe terrorizing attacks of a Painless explosion within their Head - Component of Device, The case is reported of a 47-year old female suffering from the exploding Head - Component of Device syndrome. This syndrome consists of a sudden awakening due to a loud noise shortly after falling asleep, sometimes accompanied by a flash of light.[SEP]Relations: Epilepsy has relations: disease_disease with brain disease, disease_disease with brain disease, disease_disease with Angelman syndrome, disease_disease with Angelman syndrome, disease_disease with Klinefelter syndrome, disease_disease with Klinefelter syndrome, disease_disease with Coffin-Lowry syndrome, disease_disease with Coffin-Lowry syndrome, disease_disease with electroclinical syndrome, disease_disease with electroclinical syndrome.", "label": "yes"}
{"original_question": "Is the Apis mellifera genome available?", "id": "converted_3928", "sentence1": "Is the Apis mellifera Genome - anatomical entity available?", "sentence2": " Mining Apis mellifera sequences made it possible to identify the Apis mellifera subspecies both at the Mitochondria and nuclear Genome - anatomical entity levels., Honey bee research is believed to be influenced dramatically by colony collapse disorder (carmustine/cyclophosphamide/dexamethasone) and the sequenced Genome - anatomical entity release in 2006, but this assertion has never been tested.,  The Genome - anatomical entity release and carmustine/cyclophosphamide/dexamethasone had quantitively only minor effects, mainly on Apis mellifera health-related topics post-2006. , We show that the honeybee Genome - anatomical entity is structured with respect to plasticity; Genes that respond to an environmental trigger are colocated in the honeybee Genome - anatomical entity in a series of gene clusters, many of which have been assembled in the last 80 My during the evolution of the Apidae. , we have mined histone methyltransferase and demethylases from the whole Genome - anatomical entity sequence of Aedes aegypti (Diptera), the pea aphid Acyrthosiphon pisum, the triatomid bug Rhodnius prolixus (Hemiptera), the honeybee Apis mellifera (Hymenoptera),[SEP]Relations: mitochondrion has relations: cellcomp_protein with MSRA, cellcomp_protein with MSRA, cellcomp_protein with IBA57, cellcomp_protein with IBA57, cellcomp_protein with RXRA, cellcomp_protein with RXRA, cellcomp_protein with DIP2A, cellcomp_protein with DIP2A, cellcomp_protein with TEX10, cellcomp_protein with TEX10.", "label": "yes"}
{"original_question": "Is collagen the most abundant human protein?", "id": "converted_2881", "sentence1": "Is collagen the most abundant human Protein Info?", "sentence2": "As the most abundant Protein Info in the body, collagen is essential to maintain the normal structure and strength of connective tissue, such as XXX bone, Skin Specimen Source Code, Cartilage, and blood vessels., collagen is the most abundant Protein Info family in Mammals., collagen is a fibrillar Protein Info that conforms the conjunctive and Connective Tissue in the Human body structure, essentially Skin Specimen Source Code, joints, and XXX bone. This Molecule is one of the most abundant in many of the living organisms due to its connective role in biological structures.[SEP]Relations: connective tissue has relations: anatomy_protein_present with COL3A1, anatomy_protein_present with COL3A1, anatomy_protein_present with COL1A1, anatomy_protein_present with COL1A1, anatomy_protein_present with GNS, anatomy_protein_present with GNS, anatomy_protein_present with GLMN, anatomy_protein_present with GLMN, anatomy_protein_present with BEST2, anatomy_protein_present with BEST2.", "label": "yes"}
{"original_question": "Are cyclophilins ubiquitously expressed?", "id": "converted_1563", "sentence1": "Are cyclophilins ubiquitously expressed?", "sentence2": "Cyclophilin from Leishmania donovani donovani donovani (LdCyp) is a ubiquitous peptidyl-prolyl cis-trans Isomerase (disposition), Cyclophilins (CYPs) and FK506-binding Proteins (FKBPs) are ubiquitous Proteins belonging to the peptidyl-prolyl cis/trans Isomerase (disposition) (PPIase) family.,  However, their wide distribution and ubiquitous nature signifies their fundamental importance in plant survival., Cyclophilins (Cyps) are ubiquitous Proteins that effect the cis-trans isomerization of Pro amide bonds, and are thus crucial to Protein Info folding., FK506 binding Proteins (FKBPs) and cyclophilins (CYPs) are abundant and ubiquitous Proteins belonging to the peptidyl-prolyl cis/trans Isomerase (disposition) (PPIase) superfamily, which regulate much of metabolism through a chaperone or an isomerization of proline residues during Protein Info folding., Cyclophilin is a ubiquitous peptidyl prolyl cis/trans Isomerase (disposition) that plays critical roles in many biological processes., The receptor for cyclosporine is the Protein Info cyclophilin, which is a ubiquitous peptidylprolyl Isomerase (disposition). , Cyps (cyclophilins) are ubiquitous Proteins of the Peptidylprolyl Isomerase superfamily with proposed functions in Protein Info folding, Protein Info degradation, stress response and signal transduction. , Cyclophilins are folding helper ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS belonging to the class of peptidyl-prolyl cis-trans Isomerase (PPIases; EC 5.2.1.8) that catalyze the cis-trans isomerization of peptidyl-prolyl bonds in Proteins. They are ubiquitous Proteins present in almost all living Organism analyzed to date, with extremely rare exceptions., Immunophilins are ubiquitous ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS responsible for proline isomerisation during Protein Info synthesis and for the chaperoning of several Membrane Proteins., Cyclophilins (CyPs) are a large class of highly conserved ubiquitous peptidyl-prolyl cis-trans Isomerase., Cyclophilins belong to the family of peptidyl-prolyl cis/trans Isomerase (PPIases), which are ubiquitous and highly conserved ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS capable of cis/trans isomerizing Xaa-Pro peptide bonds. , Originally identified as the cellular targets of immunosuppressant drugs, the Immunophilins encompass two ubiquitous Protein Info families: the FK-506 binding Proteins or FKBPs, and the cyclosporine-binding Proteins or cyclophilins.[SEP]Relations: Cyclosporine has relations: drug_drug with Gatifloxacin, drug_drug with Gatifloxacin, drug_drug with Etoposide, drug_drug with Etoposide, drug_drug with Genistein, drug_drug with Genistein, drug_drug with Hypericin, drug_drug with Hypericin, drug_drug with Alogliptin, drug_drug with Alogliptin.", "label": "yes"}
{"original_question": "Is the protein KCNQ2 associated with idiopathic epilepsy?", "id": "converted_1701", "sentence1": "Is the protein KCNQ2 associated with idiopathic Epilepsy?", "sentence2": "Juvenile idiopathic Epilepsy (JIE) in Arabian foals resembles Benign-familial neonatal convulsion (BFNC) syndrome, a rare idiopathic Epilepsy of new-born humans. BFNC syndrome exhibits Genetic heterogeneity, as has been hypothesised to occur in Arabian foals, and is known to be caused by mutations in the voltage-gated KCNA5 gene subunit KCNQ2 and KCNQ3 gene gene genes., They also demonstrate that sequence variations of the KCNQ2 and KCNQ3 gene gene genes may contribute to the etiology of common Venezuelan equine encephalitis virus subtype Venezuelan equine encephalitis virus subtype IE syndromes., The underlying Genetic abnormalities of rare familial idiopathic Epilepsy have been identified, such as Mutation Abnormality in KCNQ2, a K(+) channel gene., Sequence variations of the KCNQ2 and KCNQ3 gene gene genes may contribute to the etiology of common idiopathic Epilepsy syndromes., This paper summarizes recent findings concerning Sodium supplements (SCN1A gene gene) and KCNA5 gene (KCNQ2 and KCNQ3 gene gene) dysfunctions in the pathogenesis of rare and common idiopathic epilepsies (Venezuelan equine encephalitis virus subtype Venezuelan equine encephalitis virus subtype IE). , Gene Mutation in the SCN1A gene gene gene are found in up to 80% of individuals with severe myoclonic Epilepsy of infancy (Infantile Severe Myoclonic Epilepsy), and mutations in KCNQ2 and KCNQ3 gene gene were identified in Benign familial neonatal convulsions (BFNC) as well as in single families with Rolandic Epilepsy (Reuniens Thalamic Nucleus) and idiopathic generalized epilepsies (Immunoglobulin E)., The involvement of KCNQ2 (KCNQ2 gene) and KCNQ3 gene gene (Kv7.3) in a Benign idiopathic neonatal Epilepsy, KCNQ4 (KCNQ4 gene) in a form of Congenital deafness, and the discovery that neuronal KCNQ heteromultimers were among the molecular substrates of M-channels, resulted in a high level of interest for potential drug development strategies, Gene Mutation in the SCN1A gene gene gene are found in up to 80% of individuals with severe myoclonic Epilepsy of infancy (Infantile Severe Myoclonic Epilepsy), and mutations in KCNQ2 and KCNQ3 gene gene were identified in Benign familial neonatal convulsions (BFNC) as well as in single families with Rolandic Epilepsy (Reuniens Thalamic Nucleus) and idiopathic generalized epilepsies (Immunoglobulin E), The functional interaction between KCNQ2 and KCNQ3 gene gene provides a framework for understanding how mutations in either channel can cause a form of idiopathic generalized Epilepsy, Gene Mutation in KCNQ2- or KCNQ3 gene gene-encoding genes cause Benign familiar neonatal convulsions (BFNCs), a rare autosomal-dominant idiopathic Epilepsy of the newborn, Gene Mutation in KCNQ2 or KCNQ3 gene gene that reduce the M-current are responsible for Benign familial neonatal Seizures, a rare autosomal dominant idiopathic Epilepsy of the newborn, These include Benign familial neonatal convulsions due to mutations in KCNQ2 or KCNQ3 gene gene, generalized Epilepsy with febrile Seizures plus due to mutations in SCN1A gene gene, SCN2A gene gene, SCN1B gene gene, and GABRG2 gene gene, autosomal-dominant juvenile myoclonic Epilepsy (Juvenile Myoclonic Epilepsy) due to a Mutation Abnormality in GABRA1 gene gene and mutations in CLCN2 gene gene associated with several Immunoglobulin E sub-types, KCNQ2 and KCNQ3 gene gene mutations contribute to different idiopathic Epilepsy syndromes, Role of KCNQ2 and KCNQ3 gene gene genes in juvenile idiopathic Epilepsy in Arabian foals, Gene Mutation in the voltage gated KCNA5 gene gene KCNQ2 and the homologous gene KCNQ3 gene gene have been found to cause a rare monogenic subtype of idiopathic generalized Epilepsy, the Benign familial neonatal convulsions, Role of KCNQ2 and KCNQ3 gene gene genes in juvenile idiopathic Epilepsy in Arabian foals., KCNQ2 and KCNQ3 gene gene mutations contribute to different idiopathic Epilepsy syndromes.[SEP]Relations: Epilepsy has relations: disease_protein with KCNQ2, disease_protein with KCNQ2, disease_protein with KCNA2, disease_protein with KCNA2, disease_protein with KCNAB2, disease_protein with KCNAB2, disease_protein with KCNT2, disease_protein with KCNT2, disease_protein with KCND2, disease_protein with KCND2.", "label": "yes"}
{"original_question": "Can desvenlafaxine be used at a dose of 50mg/day?", "id": "converted_1216", "sentence1": "Can desvenlafaxine be used at a dose of 50mg/day?", "sentence2": "Long-term use of desvenlafaxine was safe and well tolerated, with a clinical benefit/risk profile similar to that in other populations., e objective of this study was to evaluate the long-term safety of desvenlafaxine for continuation treatment of major depressive disorder (Major Depressive Disorder) in Japanese patients. This was a phase 3, multicenter, 10-month, open-label study with flexible dosing of desvenlafaxine (25, 50, 100 milligram/day), n an effort to establish the lowest effective dose of desvenlafaxine (administered as desvenlafaxine succinate), we assessed the efficacy, safety, and tolerability of 10- and 50-milligram/day desvenlafaxine vs placebo for the treatment of major depressive disorder, Change from baseline to final evaluation in adjusted HAM-D(17) total scores was not significantly different comparing desvenlafaxine 10 milligram/day (-9.28) and desvenlafaxine 50 milligram/day (-8.92) with placebo (-8.42), Overall rates of treatment-emergent adverse events with both doses were similar to placebo, However, in a companion study reported separately, desvenlafaxine 50 mg, but not 25 mg, separated from placebo. Taken together, these studies suggest that 50 mg is the minimum effective dose of desvenlafaxine for the treatment of major depressive disorder. , desvenlafaxine XR was dosed at 50 milligram/day for 10 days., desvenlafaxine therapy is initiated at the therapeutic dose (50 milligram/day) without a need for dose titration., Clinical studies have investigated the efficacy of DVS in doses ranging from 50 to 400 milligram/day for the treatment of Major Depressive Disorder in adult outpatients. The effects of DVS 50 milligram/day have been clearly distinguished from placebo in the reduction of Major Depressive Disorder symptoms in such clinical trials. No additional therapeutic benefits were found at doses > 50 milligram/day. The recommended dose of DVS ranges from 50 to 100 mg., Adult outpatients with major depressive disorder received desvenlafaxine doses ranging from 50-400 milligram/day or placebo for 8 weeks,  At the recommended therapeutic dose of 50 milligram/day, discontinuation due to adverse events was similar to placebo, atients received fixed (50, 100, 200, or 400 milligram/day; n=1,342) or flexible doses (100-400 milligram/day; n=463) of desvenlafaxine or placebo (n=1,108), desvenlafaxine demonstrated short-term efficacy for treating major depressive disorder across the range of doses studied. No evidence of greater efficacy was observed with doses >50 milligram/day; a strong dose-response effect on tolerability was observed., To assess the efficacy, safety, and tolerability of 50- and 100-milligram/day doses of desvenlafaxine (administered as desvenlafaxine succinate), a serotonin-norepinephrine reuptake inhibitor, for the treatment of major depressive disorder (Major Depressive Disorder), Patients with Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) Major Depressive Disorder and 17-item Hamilton Rating Scale for Depression (HAM-D(17)) scores > or =20 were randomly assigned to double-blind placebo or desvenlafaxine treatment (fixed dose of 50 milligram/day or 100 milligram/day) for 8 weeks., desvenlafaxine 50 mg was associated with a significantly greater adjusted mean change from baseline on the HAM-D(17) (-11.5) compared with placebo (-9.5, p=0.018),  These results demonstrate efficacy, safety, and tolerability of desvenlafaxine 50 milligram/day for treating Major Depressive Disorder. , CONCLUSIONS: desvenlafaxine at the recommended dose of 50 mg/d was effective in relapse prevention of Cancer patients and suicide and Cancer patients and suicide and depression during a 6-month period in patients who demonstrated stable response after 20 weeks of open-label desvenlafaxine treatment.[SEP]Relations: desvenlafaxine has relations: drug_drug with Dosulepin, drug_drug with Dosulepin, drug_drug with Colistimethate, drug_drug with Colistimethate, drug_drug with Etonogestrel, drug_drug with Etonogestrel, drug_drug with Nomifensine, drug_drug with Nomifensine, drug_drug with Pemetrexed, drug_drug with Pemetrexed.", "label": "yes"}
{"original_question": "Are alterations in ultraconserved elements associated with colorectal adenocarcinoma?", "id": "converted_2145", "sentence1": "Are alterations in ultraconserved elements associated with Adenocarcinoma of large intestine?", "sentence2": "Genetic variants within ultraconserved elements and susceptibility to right- and left-sided Adenocarcinoma of large intestine, Our results strongly suggest that several genetic variants in the UCEs may contribute to Cytogenetic Complete Response susceptibility, individually and jointly, and that different genetic etiology may be involved in RCRC and LCRC, Identification of Genetic Polymorphism in ultraconserved elements associated with clinical outcomes in locally advanced Adenocarcinoma of large intestine, To the authors' knowledge, this is the first study to evaluate the association between Single Nucleotide Polymorphism within UCEs and clinical outcome in patients with Cytogenetic Complete Response. The results suggested that Single Nucleotide Polymorphism within UCEs may be valuable prognostic biomarkers for patients with locally advanced Cytogenetic Complete Response who receive 5-fluorouracil-based chemotherapy, Identification of Genetic Polymorphism in ultraconserved elements associated with clinical outcomes in locally advanced Adenocarcinoma of large intestine., Genetic variants within ultraconserved elements and susceptibility to right- and left-sided Adenocarcinoma of large intestine., We investigated whether single nucleotide Genetic Polymorphism within ultraconserved elements (UCEs) are associated with susceptibility to overall Malignant neoplasm of colon and/or rectum (Cytogenetic Complete Response) and susceptibility to Specimen Source Codes - Specimen Source Codes - tumor site-specific Cytogenetic Complete Response., We investigated whether single nucleotide Genetic Polymorphism within ultraconserved elements (UCEs) are associated with susceptibility to overall Malignant neoplasm of colon and/or rectum (Cytogenetic Complete Response) and susceptibility to Specimen Source Codes - Specimen Source Codes - tumor site-specific Cytogenetic Complete Response, Identification of Genetic Polymorphism in ultraconserved elements associated with clinical outcomes in locally advanced Adenocarcinoma of large intestine., Genetic variants within ultraconserved elements and susceptibility to right- and left-sided Adenocarcinoma of large intestine., Expression levels of transcribed ultraconserved regions uc.73 and uc.388 are altered in Malignant neoplasm of colon and/or rectum.[SEP]Relations: Adenocarcinoma of the large intestine has relations: phenotype_phenotype with Neoplasm of the large intestine, phenotype_phenotype with Neoplasm of the large intestine, phenotype_phenotype with Adenocarcinoma of the colon, phenotype_phenotype with Adenocarcinoma of the colon, phenotype_phenotype with Adenocarcinoma of the intestines, phenotype_phenotype with Adenocarcinoma of the intestines, disease_phenotype_positive with sclerosing cholangitis, disease_phenotype_positive with sclerosing cholangitis, disease_phenotype_positive with anal canal adenocarcinoma (disease), disease_phenotype_positive with anal canal adenocarcinoma (disease).", "label": "yes"}
{"original_question": "Do brown fat cells produce heat?", "id": "converted_2060", "sentence1": "Do brown doxorubicin/fluorouracil/triazinate protocol Cells produce heat?", "sentence2": "WAT and Behavioral activation therapy are both involved in energy balance. WAT is mainly involved in the storage and mobilization of energy in the form of Triglycerides, whereas Behavioral activation therapy specializes in dissipating energy as heat during cold- or diet-induced thermogenesis., Because brown adipose Tissue Specimen Code (Behavioral activation therapy) dissipates energy in the form of heat, increasing energy expenditure by augmenting Behavioral activation therapy-mediated thermogenesis may represent an approach to counter BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 and its complications., Classic brown doxorubicin/fluorouracil/triazinate protocol and inducible beige doxorubicin/fluorouracil/triazinate protocol both dissipate chemical energy in the form of heat through the actions of Mitochondrial Inheritance uncoupling protein 1. This nonshivering thermogenesis is crucial for Mammals as a defense against cold and BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20/diabetes., Brown Fat uncoupling protein in brown doxorubicin/fluorouracil/triazinate protocol Cells produces heat by dissipating the energy generated by Fatty Acids and glucose oxidation., Brown doxorubicin/fluorouracil/triazinate protocol biology and thermogenesis., Brown doxorubicin/fluorouracil/triazinate protocol (Brown Fat, Behavioral activation therapy) primary function is to produce heat. , Brown doxorubicin/fluorouracil/triazinate protocol Cells were classified into 6 types: cell type are doxorubicin/fluorouracil/triazinate protocol-depleted Cells filled with granular cytoplasm and are believed to be produced after oxidation of doxorubicin/fluorouracil/triazinate protocol for heat production., Calorimetric measurements from cell suspensions showed that adenosine triphosphate increased basal heat production of isolated brown doxorubicin/fluorouracil/triazinate protocol Cells by approximately 40% but had no effect on the greater than fivefold increase in heat production seen with maximal adrenergic stimulation., Classic brown doxorubicin/fluorouracil/triazinate protocol and inducible beige doxorubicin/fluorouracil/triazinate protocol both dissipate chemical energy in the form of heat through the actions of Mitochondrial Inheritance uncoupling protein 1., Brown adipocytes oxidize fatty acids to produce heat in response to cold or to excessive energy intake; stimulation of brown doxorubicin/fluorouracil/triazinate protocol development and function may thus counteract BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20., The occurrence of Types 1 and/or 6 Cells that has been revealed in 65 out of the total 180 samples (36%), suggests that the oxidation of doxorubicin/fluorouracil/triazinate protocol for the thermogenesis proceeds in the brown doxorubicin/fluorouracil/triazinate protocol Tissue Specimen Code and that brown doxorubicin/fluorouracil/triazinate protocol Cells partially undergo doxorubicin/fluorouracil/triazinate protocol depletion., Brown doxorubicin/fluorouracil/triazinate protocol Cells were classified into 6 types: cell type are doxorubicin/fluorouracil/triazinate protocol-depleted Cells filled with granular cytoplasm and are believed to be produced after oxidation of doxorubicin/fluorouracil/triazinate protocol for heat production., In response to cold, both classical brown doxorubicin/fluorouracil/triazinate protocol and the newly identified \"beige\" or \"brite\" Cells are activated by β-adrenergic signaling and catabolize stored Lipids and Carbohydrate nutrients to produce heat via UCP1 gene gene, The ability of Adipocytes, Brown (doxorubicin/fluorouracil/triazinate protocol Cells) to dissipate energy as heat shows great promise for the treatment of BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 and other Metabolic Diseases, Inappropriate heat dissipation ignites brown doxorubicin/fluorouracil/triazinate protocol thermogenesis in CASP14 gene with a mutant thyroid hormone receptor α1, Brown doxorubicin/fluorouracil/triazinate protocol and vascular heat dissipation: The new cautionary tail, Brown adipose produces heat as a defense against Hypothermia due to exposure and BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, and the appearance of brown-like adipocytes within white adipose Tissue Specimen Code depots is associated with improved metabolic phenotypes. , In the same manner, marked ability to produce a considerable amount of heat was evidenced in  brown doxorubicin/fluorouracil/triazinate protocol Tissue Specimen Code of children and teenagers. , Brown doxorubicin/fluorouracil/triazinate protocol Cells were classified into 6 types: cell type are doxorubicin/fluorouracil/triazinate protocol-depleted Cells filled with granular cytoplasm and are believed to be produced after oxidation of doxorubicin/fluorouracil/triazinate protocol for heat production. , It is inferred that brown-adipose-Tissue Specimen Code heat production is reduced during (and probably also some time after) anesthesia. , Parallel measurements of heat production and thermogenin content in brown doxorubicin/fluorouracil/triazinate protocol Cells during cold acclimation of Rattus norvegicus., The classical white adipose Tissue Specimen Code builds up energy in the form of Triglycerides and is useful for preventing Fatigue during periods of low caloric intake and the Brown Fat instead of inducing doxorubicin/fluorouracil/triazinate protocol accumulation can produce energy as heat., In response to cold, both classical brown doxorubicin/fluorouracil/triazinate protocol and the newly identified \"beige\" or \"brite\" Cells are activated by β-adrenergic signaling and catabolize stored Lipids and Carbohydrate nutrients to produce heat via UCP1 gene gene., White adipose Tissue Specimen Code stores energy reserves as doxorubicin/fluorouracil/triazinate protocol, whereas the metabolic function of Brown Fat is lipid oxidation to produce heat., The main function of Brown Fat (Behavioral activation therapy) is to produce heat in response to cold., Brown adipocytes oxidize fatty acids to produce heat in response to cold or caloric overfeeding., Brown doxorubicin/fluorouracil/triazinate protocol (Brown Fat, Behavioral activation therapy) primary function is to produce heat., Adipose Tissue Specimen Code plays an active role in energy balance because it is not only a lipid storing and mobilizing Tissue Specimen Code but consists of functionally specialized Body Tissue Specimen Code able to produce heat (in Brown Fat) and to produce or release a vast number of so called Adipokines or adipocytokines., Brown adipose Tissue Specimen Code (Behavioral activation therapy), a specialized doxorubicin/fluorouracil/triazinate protocol that dissipates energy to produce heat, plays an important role in the regulation of energy balance., Brown adipose Cells are specialized to dissipate chemical energy in the form of heat, as a physiological defence against cold and BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20., In the present study, the thermogenesis of human brown doxorubicin/fluorouracil/triazinate protocol Tissue Specimen Code was suggested chiefly with regard to the occurrence of Types 1 and/or 6 Cells., In the same manner, marked ability to produce a considerable amount of heat was evidenced in  brown doxorubicin/fluorouracil/triazinate protocol Tissue Specimen Code of children and teenagers., Adult Homo sapiens have heat-producing and energy-consuming Brown Fat in the clavicular region of the dendritic spine dendritic spine neck., Brown and Adipocytes, Beige expend chemical energy to produce heat and are therefore important in regulating body temperature and body weight., In human perirenal brown doxorubicin/fluorouracil/triazinate protocol Tissue Specimen Code, darkly stained doxorubicin/fluorouracil/triazinate protocol-depleted Cells (D) occupy, with other cell types (Creatinine measurement, Creatinine measurement'), an important part in the reversible heat production cycle of the brown doxorubicin/fluorouracil/triazinate protocol Tissue Specimen Code., Brown doxorubicin/fluorouracil/triazinate protocol is a specialized doxorubicin/fluorouracil/triazinate protocol depot that can increase energy expenditure and produce heat.[SEP]Relations: Brown Fat has relations: anatomy_anatomy with adipose Tissue Specimen Code, anatomy_anatomy with adipose Tissue Specimen Code. adipose Tissue Specimen Code has relations: anatomy_anatomy with Brown Fat, anatomy_anatomy with Brown Fat, anatomy_protein_present with HEATR6, anatomy_protein_present with HEATR6, anatomy_protein_present with HEATR3, anatomy_protein_present with HEATR3, anatomy_protein_present with HEATR5A, anatomy_protein_present with HEATR5A.", "label": "yes"}
{"original_question": "Is the microRNA 132 (miR-132) involved in brain pathologies?", "id": "converted_1656", "sentence1": "Is the microRNA 132 (miR-132) involved in Head>Brain pathologies?", "sentence2": "miR-132 dysregulation and subsequent abnormal expression of miR-132 target genes contribute to the neurodevelopmental and neuromorphological pathologies present in SCHIZOPHRENIA 2 (disorder)., micro-RNAs encoding miR-9, miR-124a, miR-125b, miR-128, miR-132 and miR-219 are abundantly represented in fetal hippocampus, are differentially regulated in aged Head>Brain, and an alteration in specific MicroRNAs complexity occurs in Alzheimer hippocampus. These data are consistent with the idea that altered MicroRNAs-mediated processing of messenger RNA populations may contribute to atypical RNA, Messenger abundance and neural dysfunction in ALZHEIMER DISEASE, FAMILIAL, 1 Head>Brain., Levels of several microRNA (miR-10a, -10b, -212, -132, -495) were significantly altered. One of them (miR-132) has been reported to be highly inducible by Growth Factor and to be a key regulator of neurite outgrowth. Moreover, miR-132-recognition sequences were detected in the RNA, Messenger transcripts of two differentially expressed proteins. MicroRNA may thus represent novel biomarkers for neuronal malfunction and potential therapeutic targets for Homo sapiens neurodegenerative diseases., Expression of key neuronal microRNAs-including mir-9/9*, Mirn124a microRNA, Homo sapiens and mir-132-is repressed in the brains of Homo sapiens Hodgkin Disease patients and Mus sp. models., To determine if production of miR-132 is regulated by neuronal activity its expression in Mus sp. Head>Brain was monitored by quantitative RT-PCR (RT-qPCR), Expression levels of primary and mature-miR-132 increased significantly between postnatal Days 10 and 24. We conclude that miR-132 is an activity-dependent microRNA in vivo, and may contribute to the long-lasting proteomic changes required for experience-dependent neuronal plasticity., We investigated how prior Seizures Preconditioning affects the miRNA response to Status Epilepticus evoked by intra-amygdalar kainic acid in CASP14 gene., Increased miR-132 levels were matched with increased binding to Argonaute-2, a constituent of the RNA-induced silencing complex. In tolerant animals, expression responses of >40% of the injury-group-detected miRNAs differed, being either unchanged relative to control or down-regulated, and this included miR-132. In vivo microinjection of locked nucleic acid-modified oligonucleotides (Antagomirs) against miR-132 depleted Hippocampus (Brain) miR-132 levels and reduced Seizures-induced neuronal death. Thus, our data strongly suggest that miRNAs are important regulators of Seizures-induced neuronal death., Preconditioning describes the ischemic stimulus that triggers an endogenous, neuroprotective response that protects the Head>Brain during a subsequent severe ischemic injury, a phenomenon known as 'tolerance'., Downregulation of miR-132 is consistent with our finding that Preconditioning Ischemia Procedure induces a rapid increase in Methyl-CpG-Binding Protein 2, but not RNA, Messenger, in Mus sp. cortex. These studies reveal that ischemic Preconditioning regulates expression of miRNAs and their Prediction targets in Mus sp. Head>Brain cortex, and further suggest that miRNAs and MECP2 protein, Homo sapiens could serve as effectors of ischemic Preconditioning-induced tolerance., Huntington Disease (Hodgkin Disease) is a genetic neurodegenerative disease caused by abnormal CAG expansion. MicroRNAs (miRNAs) are short RNA molecules regulating gene expression, and are implicated in a variety of diseases including Hodgkin Disease., Nine miRNAs (miR-22, miR-29c, miR-128, miR-132, miR-138, miR-218, miR-222, miR-344, and miR-674*) were commonly down-regulated in both the 12-month-old YAC128 and 10-week-old R6/2 CASP14 gene., Animals, Transgenic Hodgkin Disease CASP14 gene have abnormal miRNA biogenesis. This information should aid in future studies on therapeutic application of miRNAs in Hodgkin Disease., miR-132 directly targets the neuronal splicing factor polypyrimidine tract-binding protein 2 (PTBP2 gene gene), which protein levels were increased in Progressive supranuclear palsy patients. miR-132 overexpression or PTBP2 gene gene knockdown similarly affected endogenous 4R:3R-tau ratios in neuronal cells. Finally, we provide evidence that miR-132 is inversely correlated with PTBP2 gene gene during post-natal Head>Brain development at the time when 4R-tau becomes expressed. Taken together, these results suggest that changes in the miR-132/PTBP2 gene gene pathway could contribute to the abnormal splicing of tau exon 10 in the Head>Brain, and sheds light into the potential role played by miRNAs in a subset of Tauopathies., reports of microRNA (miR) modulators of both neuronal and immune processes (here termed NeurimmiRs) predict therapeutic potential for manipulating NeurimmiR levels in diseases affecting both the immune system and higher Head>Brain functions, such as ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol), Parkinson Disease (Lugano Lymphoma Response Classification Progressive Disease by PET), Multiple Sclerosis (MS) and anxiety-related disorders. In our opinion, NeurimmiRs that function within both the Nervous - anatomy qualifier and the immune systems, such as miR-132 and miR-124, may act as 'negotiators' between these two interacting compartments.[SEP]Relations: Parkinson disease has relations: disease_protein with MIR181C, disease_protein with MIR181C. Viral Messenger RNA Synthesis has relations: pathway_protein with NUP133, pathway_protein with NUP133, pathway_protein with NUP214, pathway_protein with NUP214, pathway_protein with NUP188, pathway_protein with NUP188, pathway_protein with NUP107, pathway_protein with NUP107.", "label": "yes"}
{"original_question": "Is factor XI deficient in Hemophilia C?", "id": "converted_1283", "sentence1": "Is factor XI deficient in Hemophilia C?", "sentence2": "Factor XI deficiency is a rare Hematological Disease. Hemophilia C (factor XI deficiency) affects both genders and it is usually asymptomatic,, Congenital factor XI deficiency (also known as the Rosenthal syndrome or Hereditary Factor XI Deficiency), rare case of an acute cerebral aneurysm rupture in a patient with a known factor XI deficiency. Aneurysmal subarachnoid hemorrhage (Yakut language) accounts for a high mortality and morbidity rate. When Yakut language is associated with an inherited coagulation disorder such as Hereditary Factor XI Deficiency, Factor XI deficiency (Hemophilia C), Factor XI deficiency, also called Hereditary Factor XI Deficiency,[SEP]Relations: factor XI deficiency has relations: disease_disease with hemophilia, disease_disease with hemophilia, disease_disease with congenital factor XI deficiency, disease_disease with congenital factor XI deficiency. hematologic disease has relations: disease_disease with L-ferritin deficiency, disease_disease with L-ferritin deficiency, disease_disease with GATA1-Related X-Linked Cytopenia, disease_disease with GATA1-Related X-Linked Cytopenia, contraindication with Adomiparin, contraindication with Adomiparin.", "label": "yes"}
{"original_question": "Is paramyxovirus involved in human subacute thyroiditis?", "id": "converted_577", "sentence1": "Is paramyxovirus involved in human subacute thyroiditis?", "sentence2": "Most cases of subacute thyroiditis are caused by a variety of Virus, for example, Coxsackie, cytomegalovirus, Epstein-Barr virus, and Adenovirus Infections. Influenza immunization or Communicable Diseases may cause subacute thyroiditis., Coxsackievirus Infections has been reported to be one of the Virus associated with the disease., The etiology of subacute granulomatous thyroiditis (College Entrance Examination Board Scholastic Aptitude Test) is obscure, although it is postulated to be associated with Virus Diseases and genetic factors., The results suggest that College Entrance Examination Board Scholastic Aptitude Test is not usually associated with acute infections, No evidence was obtained to support the proposed role of enteroviruses as an important etiologic agent of College Entrance Examination Board Scholastic Aptitude Test., The Antibodies, Viral evaluated were those of Influenza A and B, Coxsackie A9, Astler-Coller Astler-Coller B1 Rectal Carcinoma Rectal Carcinoma, Posterior segmental bronchus, Measles virus genotype Measles virus genotype B3, B4, B5 and B6, Echo 3, 7, 11 and 12, Parainfluenza 1, 2, 3 and 4, and Adeno 8 virus. The following results were obtained: In class I HLA typing, the frequency of HLA-Bw35 in College Entrance Examination Board Scholastic Aptitude Test was 67.4%, which was significantly (p less than 0.0001) higher than that in the control (14.1%). On the other hand, the frequency of Cw1 in College Entrance Examination Board Scholastic Aptitude Test (14.6%) was significantly (p less than 0.01) lower than that of the control (32.1%), and that of US Military Warrant Officer W3 (65.2%) was significantly (p less than 0.01) higher than that of the control (46.5%).[SEP]Relations: Adenovirus Infections renal Communicable Diseases has relations: disease_disease with adenoviridae infectious disease, disease_disease with adenoviridae infectious disease, disease_disease with kidney disease, disease_disease with kidney disease. Nipah virus disease has relations: disease_disease with henipavirus infectious disease, disease_disease with henipavirus infectious disease, disease_phenotype_positive with Myoclonus, disease_phenotype_positive with Myoclonus. coxsackievirus infectious disease has relations: disease_disease with enterovirus infectious disease, disease_disease with enterovirus infectious disease.", "label": "no"}
{"original_question": "Is pregabalin effective for sciatica?", "id": "converted_2570", "sentence1": "Is pregabalin effective for Sciatica?", "sentence2": "CONCLUSIONS: Treatment with pregabalin did not significantly reduce the intensity of leg pain associated with Sciatica and did not significantly improve other outcomes, as compared with placebo, over the course of 8 weeks. The incidence of adverse events was significantly higher in the pregabalin group than in the placebo group. , Whilst pregabalin (Prostaglandins B) and gabapentin (TMEM132A gene) are both used to treat Neuropathic pain, their relative role in Sciatica is unclear., TMEM132A gene and Prostaglandins B appeared to demonstrate comparable efficacy and FUT2 gene. However, the amount and quality of evidence was low, and only indirect comparisons were available. [SEP]Relations: Pregabalin has relations: drug_effect with Pancreatitis, drug_effect with Pancreatitis, drug_effect with Menorrhagia, drug_effect with Menorrhagia, drug_drug with Pridinol, drug_drug with Pridinol, drug_effect with Pneumonia, drug_effect with Pneumonia, drug_effect with Pain, drug_effect with Pain.", "label": "no"}
{"original_question": "Are paralog genes co-regulated?", "id": "converted_2533", "sentence1": "Are Paralogous Gene Genes co-regulated?", "sentence2": "Co-regulation of Paralogous Gene Genes in the three-dimensional Chromatin architecture., Consequently, paralogs show correlation in gene expression whereby the mechanisms of co-regulation remain unclear. In Eukaryota, Genes are regulated in part by distal Enhancer Elements, Genetic through looping interactions with Operator gene. These looping interactions can be measured by Genome - anatomical entity-wide Chromatin conformation capture (Hi-C) experiments, which revealed self-interacting regions called topologically associating domains (Tietz syndrome). We hypothesize that paralogs share common regulatory mechanisms to enable coordinated expression according to Tietz syndrome. To test this hypothesis, we integrated paralogy annotations with Homo sapiens gene expression data in diverse Body tissue, Genome - anatomical entity-wide enhancer-Promoter associations and Hi-C experiments in Homo sapiens, Mus sp. and Canis familiaris genomes. We show that Paralogous Gene gene pairs are enriched for co-localization in the same aminoglutethimide/danazol/hydrocortisone/tamoxifen, share more often common Enhancer Elements, Genetic than expected and have increased contact frequencies over large genomic distances. Combined, our results indicate that paralogs share common regulatory mechanisms and cluster not only in the linear Genome - anatomical entity but also in the three-dimensional Chromatin architecture. This enables concerted expression of paralogs over diverse cell-types and indicate evolutionary constraints in functional Genome - anatomical entity organization., Paralog Genes arise from gene duplication events during evolution, which often lead to similar Proteins that cooperate in common pathways and in protein complexes. Consequently, paralogs show correlation in gene expression, We hypothesize that paralogs share common regulatory mechanisms to enable coordinated expression according to Tietz syndrome., Further, interspecific changes in Testis bias of expression are generally correlated within the co-regulated pairs and are anti-correlated within the anti-regulated pairs, suggesting coordinated regulation within both types of paralogous gene pairs., Analysis of the Drosophila melanogaster Inferior Colliculus transcriptome reveals coordinate regulation of paralogous Genes., Further, interspecific changes in Testis bias of expression are generally correlated within the co-regulated pairs and are anti-correlated within the anti-regulated pairs, suggesting coordinated regulation within both types of paralogous gene pairs.<br>, Consequently, paralogs show correlation in gene expression whereby the mechanisms of co-regulation remain unclear., Co-regulation of Paralogous Gene Genes in the three-dimensional Chromatin architecture., Further, interspecific changes in Testis bias of expression are generally correlated within the co-regulated pairs and are anti-correlated within the anti-regulated pairs, suggesting coordinated regulation within both types of paralogous gene pairs.., We show that Paralogous Gene gene pairs are enriched for co-localization in the same aminoglutethimide/danazol/hydrocortisone/tamoxifen, share more often common Enhancer Elements, Genetic than expected and have increased contact frequencies over large genomic distances. , MiRNA Genes are often subject to co-evolutionary changes together with their target transcripts, which may be reflected by differences between Paralogous Gene Mus sp. and primate miRNA/mRNA pairs., We characterize the collapse over time through the distribution of runs of reduced Paralogous Gene pairs in duplicated segments., In addition, we identified 81 co-regulated regions on the Homo sapiens Genome - anatomical entity (RIDGEs) by using expression data from all Malignant Neoplasms. Some RIDGEs (28%) consist of Paralogous Gene Genes while another subset (30%) are specifically dysregulated in Neoplasms but not in normal Body tissue., We conclude that the similarity of hoxb3a/Hoxa3 regulatory mechanisms reflect the shared descent of both Genes from a single ancestral Paralogous Gene group 3 gene., Conserved co-regulation and Promoter sharing of hoxb3a and hoxb4a in Zebrafish., By analyzing paralogs of Testis-biased Genes, we identified \"co-regulated\" paralogous pairs in which both Genes are Testis biased, \"anti-regulated\" pairs in which one Paralogous Gene is Testis biased and the other downregulated in Inferior Colliculus, and \"neutral\" pairs in which one Paralogous Gene is Testis biased and the other constitutively expressed.[SEP]Relations: RNA localization to Chromatin has relations: bioprocess_protein with HNRNPU, bioprocess_protein with HNRNPU. Promoter clearance from RNA polymerase I Promoter has relations: bioprocess_bioprocess with Promoter clearance during DNA-templated transcription, bioprocess_bioprocess with Promoter clearance during DNA-templated transcription, bioprocess_bioprocess with Promoter clearance from RNA polymerase I Promoter for nuclear large rRNA transcript, bioprocess_bioprocess with Promoter clearance from RNA polymerase I Promoter for nuclear large rRNA transcript. Testis has relations: anatomy_protein_present with PARP14, anatomy_protein_present with PARP14, anatomy_protein_present with CGGBP1, anatomy_protein_present with CGGBP1.", "label": "yes"}
{"original_question": "Is KAT2A involved in Acute myeloid leukemia (AML)?", "id": "converted_3377", "sentence1": "Is KAT2A involved in RUNX1 gene (Leukemia, Myelocytic, Acute)?", "sentence2": "RUNX1 gene (Leukemia, Myelocytic, Acute) is an aggressive cancer with a poor prognosis, for which mainstream treatments have not changed for decades. To identify additional therapeutic targets in Leukemia, Myelocytic, Acute, we optimize a genome-wide clustered regularly interspaced short palindromic repeats (CRISPR) screening platform and use it to identify Genetic vulnerabilities in Leukemia, Myelocytic, Acute cells. We identify 492 Leukemia, Myelocytic, Acute-specific cell-essential Genes, including several established therapeutic targets such as Histone-Lysine N-Methyltransferase H3 Lysine-79 Specific, Human, BCL2 protein, Homo sapiens protein, Homo sapiens, and Multiple Endocrine Neoplasia Type 1, and many other Genes including clinically actionable candidates. We validate selected Genes using Genetic and pharmacological inhibition, and chose KAT2A as a candidate for downstream study. KAT2A inhibition demonstrated anti-Leukemia, Myelocytic, Acute activity by inducing myeloid differentiation and apoptosis, and suppressed the growth of primary Homo sapiens AMLs of diverse Genotype while sparing normal hemopoietic stem-progenitor cells. Our results propose that KAT2A inhibition should be investigated as a therapeutic strategy in Leukemia, Myelocytic, Acute and provide a large number of Genetic vulnerabilities of this leukemia that can be pursued in downstream studies., Our results propose that KAT2A inhibition should be investigated as a therapeutic strategy in Leukemia, Myelocytic, Acute and provide a large number of Genetic vulnerabilities of this leukemia that can be pursued in downstream studies., KAT2A inhibition demonstrated anti-Leukemia, Myelocytic, Acute activity by inducing myeloid differentiation and apoptosis, and suppressed the growth of primary Homo sapiens AMLs of diverse Genotype while sparing normal hemopoietic stem-progenitor cells., Our results propose that KAT2A inhibition should be investigated as a therapeutic strategy in Leukemia, Myelocytic, Acute and provide a large number of Genetic vulnerabilities of this leukemia that can be pursued in downstream studies., KAT2A inhibition demonstrated anti-Leukemia, Myelocytic, Acute activity by inducing myeloid differentiation and apoptosis, and suppressed the growth of primary Homo sapiens AMLs of diverse Genotype while sparing normal hemopoietic stem-progenitor cells.[SEP]Relations: acute promyelocytic leukemia has relations: disease_protein with GLI2, disease_protein with GLI2, disease_protein with PML, disease_protein with PML, disease_protein with IDH2, disease_protein with IDH2, disease_protein with ITGB2, disease_protein with ITGB2, disease_protein with AKT1, disease_protein with AKT1.", "label": "yes"}
{"original_question": "Is there a vaccine for peanut allergy?", "id": "converted_3353", "sentence1": "Is there a vaccine for Arachis hypogaea allergy?", "sentence2": "Currently, two forms of Arachis hypogaea immunotherapy, oral immunotherapy (OIT) and epicutaneous immunotherapy (EPIT), are in Phase III clinical trials and have shown promise to induce desensitization in many subjects, This article presents an overview of potential treatments of food allergy, with an emphasis on various forms of immunotherapy (including oral immunotherapy, sublingual immunotherapy, epicutaneous immunotherapy, immunotherapy with modified food antigens, and immunotherapy with a recombinant Arachis hypogaea vaccine)., Recent advances in immunotherapy and vaccine development for Arachis hypogaea allergy., Efforts have been made to develop a vaccine for Arachis hypogaea allergy., So far, results, especially from oral immunotherapy studies, have shown good efficacy in achieving desensitization to Arachis hypogaea with a good safety profile.[SEP]", "label": "yes"}
{"original_question": "Is JTV519 (K201) a potential drug for the prevention of arrhythmias?", "id": "converted_985", "sentence1": "Is JTV519 (K201) a potential Pharmacologic Substance for the prevention of arrhythmias?", "sentence2": "We compared the suppressive effect of K201 (JTV519), a multiple-channel blocker and cardiac ryanodine receptor-calcium release channel (Ryanodine Receptor 2) stabilizer, with that of diltiazem, a Ca(2+ )channel blocker, in 2 studies of isoproterenol-induced (n = 30) and ischemic-reperfusion-induced VAs (n = 38) in Rattus norvegicus. , After administration of isoproterenol under Ca(2+) loading, fatal VA frequently occurred in the vehicle (9 of 10 animal allergen extracts, 90%) and diltiazem (8 of 10, 80%) groups, and K201 significantly suppressed the incidences of Cardiac Arrhythmia and mortality (2 of 10, 20%). In the reperfusion study, the incidence and the time until occurrence of reperfusion-induced VA and mortality were significantly suppressed in the K201 (2 of 15 animal allergen extracts, 13%) and diltiazem (1 of 9 animal allergen extracts, 11%) groups compared to the vehicle group (8 of 14 animal allergen extracts, 57%). , K201 markedly suppressed both the isoproterenol-induced and the reperfusion-induced VAs, whereas diltiazem did not suppress the isoproterenol-induced VA., JTV519 (K201) is a newly developed 1,4-benzothiazepine Pharmacologic Substance with antiarrhythmic and cardioprotective properties. It appears to be very effective in not only preventing but also in reversing the characteristic myocardial changes and preventing lethal arrhythmias., The novel antiarrhythmic Pharmacologic Substance K201 (4-[3-{1-(4-benzyl)piperidinyl}propionyl]-7-methoxy-2,3,4,5-tetrahydro-1,4-benzothiazepine monohydrochloride) is currently in development for treatment of Atrial Fibrillation by ECG Finding. K201 not only controls intracellular calcium release by the Ryanodine Receptors, but also possesses a ventricular action that might predispose to torsade de pointes arrhythmias. , The ryanodine receptor complex location is currently used as a therapeutic target in Malignant hyperpyrexia due to anesthesia where dantrolene is effective and to relieve ventricular Cardiac Arrhythmia, with the use of JTV519 and flecainide., Finally, KN-3 and JTV519, two compounds that stabilize Ryanodine Receptor 2 in the closed state, prevent the induction of triggered activity and suppress the inducibility of sustained AF. , JTV519 greatly reduced the frequency of ouabain-induced arrhythmogenic events., Stabilization of Ryanodine Receptor 2 by JTV519 effectively reduces these triggered arrhythmias., These findings may reveal the anti-arrhythmic potential of K201., The preferential ryanodine receptor stabilizer (K201) possesses antiarrhythmic effects through calcium regulation. , The Pharmacologic Substance K201 (JTV519) increases inotropy and suppresses arrhythmias in failing hearts, but the effects of K201 on normal hearts is unknown. , K201 fails to prevent amsonic acid in Ryanodine Receptor 2(R4496C+/-) Muscle Cells and Ventricular Cardiac Arrhythmia in Ryanodine Receptor 2(R4496C+/-) CASP14 gene, In vivo administration of K201 failed to prevent induction of Polymorphism Ventricular Tachycardia by ECG Finding (Tachycardia, Ventricular) in Ryanodine Receptor 2(R4496C+/-) CASP14 gene., The 1,4-benzothiazepine JTV519, which increases the binding affinity of calstabin-2 for Ryanodine Receptor 2, inhibited the diastolic SR Ca2+ leak, monophasic action potential alternan and triggered arrhythmias., In arrhythmias, the calstabin2 stabiliser JTV519 did not prevent arrhythmias in calstabin2-/- CASP14 gene, but reduced the arrhythmias in calstabin2+/- CASP14 gene, illustrating the antiarrhythmic potential of stabilising calstablin2. , In three models of arrhythmias, the calstabin2 stabiliser JTV519 did not prevent arrhythmias in calstabin2(-/-) CASP14 gene, but reduced the arrhythmias in calstabin2(+/-) CASP14 gene, illustrating the antiarrhythmic potential of stabilising calstabin2. , A derivative of 1,4-benzothiazepine (JTV519) increased the affinity of calstabin2 for Ryanodine Receptor 2, which stabilized the closed state of Ryanodine Receptor 2 and prevented the Ca2+ leak that triggers arrhythmias. , JTV519 had significant protective effects on Atrial Fibrillation by ECG Finding in the Body Surface Area Formula for Dogs sterile Pericarditis model, mainly by increasing effective refractory period, suggesting that it may have potential as a novel antiarrhythmic agent for Atrial Fibrillation by ECG Finding., JTV519 significantly decreased the mean number of sustained Atrial Fibrillation by ECG Finding episodes (from 4.2 +/- 2.9 to 0 +/- 0, P < 0.01). , We conclude that JTV519 can exert antiarrhythmic effects against AF by inhibiting repolarizing K(+) currents. The Pharmacologic Substance may be useful for the treatment of AF in patients with Coronary Arteriosclerosis.[SEP]Relations: Arrhythmia has relations: drug_effect with Oseltamivir, drug_effect with Oseltamivir, drug_effect with Venlafaxine, drug_effect with Venlafaxine, drug_effect with Levonorgestrel, drug_effect with Levonorgestrel, drug_effect with Ranitidine, drug_effect with Ranitidine. Dantrolene has relations: drug_drug with JNJ-26489112, drug_drug with JNJ-26489112.", "label": "yes"}
{"original_question": "Is PLK2 involved in alpha-synuclein phosphorylation in the nervous system?", "id": "converted_758", "sentence1": "Is PLK2 involved in SNCA gene phosphorylation in the nervous system?", "sentence2": "PLK2 gene (PLK2) phosphorylates SNCA gene at serine 129 in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, Here we submit evidence that PLK1 gene (PLK2, also known as serum-inducible kinase or SNK) is a principle contributor to SNCA gene phosphorylation at Ser-129 in Neurons, PLK2 directly phosphorylates SNCA gene at Ser-129 in an in vitro biochemical assay, inhibitors of PLK1 protein, human kinases inhibited SNCA gene phosphorylation both in primary cortical cell cultures and in Mus sp. Head>Brain in vivo, specific knockdown of PLK2 expression by transduction with short hairpin RNA constructs or by knock-out of the plk2 gene reduced p-Ser-129 levels, These results indicate that PLK2 plays a critical role in SNCA gene phosphorylation in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS., These results indicate that PLK2 plays a critical role in SNCA gene phosphorylation in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS., Here we submit evidence that PLK1 gene (PLK2, also known as serum-inducible kinase or SNK) is a principle contributor to SNCA gene phosphorylation at Ser-129 in Neurons., PLK2 gene (PLK2) phosphorylates SNCA gene at serine 129 in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS., PLK2 directly phosphorylates SNCA gene at Ser-129 in an in vitro biochemical assay., Two of these kinases stand out as potential drug targets for novel Lugano Lymphoma Response Classification Progressive Disease by PET therapy, namely Leucine-Rich Repeat Serine/Threonine-Protein Kinase 1 (LRRK2 protein, human protein, human) and the SNCA gene (α-syn) phosphorylating PLK1 gene (PLK2)., Also, due to the dominant mode of α-syn and LRRK2 protein, human protein, human inheritance and based on current knowledge of LRRK2 protein, human protein, human and α-syn phosphorylation by PLK2, inhibition of LRRK2 protein, human protein, human and PLK2 may constitute a potential therapy for Lugano Lymphoma Response Classification Progressive Disease by PET., To better understand the role of PLK2 in α-synuclein phosphorylation in vivo, we further evaluated the effect of PLK2 genetic knockdown and pharmacological inhibition on Phospho-α-Syn levels in different Head>Brain regions of PLK2 knockout (KELL NULL), heterozygous (Het) and wild-type (WT) mice., This PLK2-mediated neuroprotective effect is also dependent on PLK2 activity and α-synuclein phosphorylation., PLK2-mediated degradation of α-synuclein requires both phosphorylation at S129 and PLK2/α-synuclein complex formation., Overexpression of only PLK2 increased phosphorylation of aggregated α-syn at S129, which likely is due to increased phosphorylation of soluble α-syn, which then was incorporated into aggregates., Here we submit evidence that PLK1 gene (PLK2, also known as serum-inducible kinase or SNK) is a principle contributor to SNCA gene phosphorylation at Ser-129 in Neurons., PLK2 directly phosphorylates SNCA gene at Ser-129 in an in vitro biochemical assay., Unlike other kinases reported to partially phosphorylate alpha-syn at Ser-129 in vitro, phosphorylation by PLK2 and PLK3 protein, human protein, human is quantitative (, inhibitors of PLK1 protein, human kinases inhibited SNCA gene phosphorylation both in primary cortical cell cultures and in Mus sp. Head>Brain in vivo., These results indicate that PLK2 plays a critical role in SNCA gene phosphorylation in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, inhibitors of PLK1 protein, human kinases inhibited SNCA gene phosphorylation both in primary cortical cell cultures and in Mus sp. Head>Brain in vivo, PLK2 directly phosphorylates SNCA gene at Ser-129 in an in vitro biochemical assay, To better understand the role of PLK2 in α-synuclein phosphorylation in vivo, we further evaluated the effect of PLK2 genetic knockdown and pharmacological inhibition on Phospho-α-Syn levels in different Head>Brain regions of PLK2 knockout (KELL NULL), heterozygous (Het) and wild-type (WT) mice, Polo-like kinase-2 (PLK2 protein, human) has been implicated as the dominant kinase involved in the phosphorylation of α-synuclein in Lewy bodies, which are one of the hallmarks of Parkinson Disease neuropathology[SEP]Relations: Parkinson disease has relations: disease_protein with LRRK2 protein, human, disease_protein with LRRK2 protein, human, disease_protein with CNTNAP2, disease_protein with CNTNAP2. ELL has relations: molfunc_protein with phosphatase binding, molfunc_protein with phosphatase binding, protein_protein with PIP4K2A, protein_protein with PIP4K2A, protein_protein with POU2F2, protein_protein with POU2F2.", "label": "yes"}
{"original_question": "Is gastro esophageal reflux related to burning mouth syndrome?", "id": "converted_1510", "sentence1": "Is gastro esophageal reflux related to burning mouth syndrome?", "sentence2": "Our results suggest that there is no causal connection between Local Pathology Review episodes and the occurrence of Intraoral approach burning sensations in the examined patients., As reported below, although this symptom may well be diagnostically misleading, careful diagnosis based on clinical signs may distinguish patients with BMS from those with reflux disease, and successful management of burning mouth is often enables.[SEP]", "label": "no"}
{"original_question": "Is shotgun lipidomics the direct infusion of a lipid sample into a mass spectrometer?", "id": "converted_275", "sentence1": "Is shotgun lipidomics the direct infusion of a lipid sample into a mass spectrometer?", "sentence2": "In direct infusion/injection (or shotgun) lipidomics, An efficient shotgun lipidomics strategy was established and optimized for fast phospholipid profiling of Viscera from three fish species: Lateolabrax japonicas, Grass Carp (fish), and Carassius carassius x Carassius carassius x Carassius auratus auratus auratus. This strategy relies on direct infusion of total lipid extracts into a tandem mass spectrometer without additional separation of the individual molecular species. , Top-down shotgun lipidomics relies on direct infusion of total lipid extracts into a high-resolution tandem mass spectrometer, shotgun lipidomic approaches that use direct infusion, direct infusion (shotgun lipidomics) , direct infusion-based shotgun lipidomics approaches, shotgun lipidomics (MDMS-SL) data, which are acquired directly from lipid extracts after direct infusion , Through direct infusion of the resultant enriched solution, we identified and quantitated a variety of very-low-abundance sphingolipid classes (e.g., Sphingosine, Psychosine, and Sphingosine phosphorylcholine) and molecular species (e.g., Sphingomyelins) using electrospray ionization mass spectrometry (i.e., shotgun sphingolipidomics).[SEP]Relations: phosphatidylcholine biosynthesis from sn-glycero-3-phosphocholine has relations: bioprocess_bioprocess with phosphatidylcholine biosynthetic process, bioprocess_bioprocess with phosphatidylcholine biosynthetic process. Sphingosine has relations: drug_protein with PVR, drug_protein with PVR, drug_protein with GLTP, drug_protein with GLTP, drug_protein with ABCB1, drug_protein with ABCB1.", "label": "yes"}
{"original_question": "Is Pim-1 a protein phosphatase?", "id": "converted_3222", "sentence1": "Is Pim-1 a protein phosphatase?", "sentence2": "Pim-1 proto-oncogene, AURKA gene (PIM-1) phosphorylates a series of substrates to exert its oncogenic function in numerous Malignant Neoplasms., The Pim1 AURKA gene is associated with multiple cellular functions including proliferation, survival, differentiation, apoptosis, tumorigenesis, immune regulation and Inflammation in Vertebrates.[SEP]Relations: Portal Inflammation has relations: disease_phenotype_positive with FADD-related immunodeficiency, disease_phenotype_positive with FADD-related immunodeficiency, phenotype_phenotype with Abnormality of the biliary system, phenotype_phenotype with Abnormality of the biliary system. malignant ear neoplasm has relations: disease_disease with sensory system cancer, disease_disease with sensory system cancer, disease_disease with ear neoplasm, disease_disease with ear neoplasm, disease_disease with head and neck cancer, disease_disease with head and neck cancer.", "label": "no"}
{"original_question": "Are there roles for cohesin mutations in AML?", "id": "converted_4699", "sentence1": "Are there roles for cohesins mutations in Leukemia, Myelocytic, Acute?", "sentence2": "Several landmark studies have shown that cohesins mutations perturb the balance between self-renewal and differentiation of hematopoietic stem and Stem cells (PSMA7 gene). Emerging data now begin to uncover the molecular mechanisms that underpin this phenotype. Among these mechanisms is a role for cohesins in the control of inflammatory responses in HSPCs and Myeloid Cells. Inflammatory signals limit PSMA7 gene self-renewal and drive PSMA7 gene differentiation. Consistent with this, cohesins mutations promote resistance to inflammatory signals, and may provide a selective advantage for Leukemia, Myelocytic, Acute progression. [SEP]Relations: acute promyelocytic leukemia has relations: disease_protein with PML, disease_protein with PML, disease_phenotype_positive with Somatic mutation, disease_phenotype_positive with Somatic mutation, disease_protein with ASXL1, disease_protein with ASXL1, disease_protein with GLI2, disease_protein with GLI2, disease_phenotype_positive with Gingival bleeding, disease_phenotype_positive with Gingival bleeding.", "label": "yes"}
{"original_question": "Is cadasil syndrome a hereditary disease?", "id": "converted_381", "sentence1": "Is cadasil syndrome a hereditary disease?", "sentence2": " NOTCH3 wt Allele is the most frequent hereditary small-vessel disease of the Head>Brain. The clinical impact of various MR imaging markers has been repeatedly studied in this disorder, but alterations of contrast between gray matter and normal-appearing white matter remain unknown. The aim of this study was to evaluate the contrast alterations between gray matter and normal-appearing white matter on T1-weighted images in patients with NOTCH3 wt Allele compared with healthy subjects,  (NOTCH3 wt Allele) is the most common form of hereditary cerebral angiopathy, Cerebral autosomal dominant arteriopathy with subcortical infarcts and Leukoencephalopathy (NOTCH3 wt Allele) is an inherited Cerebral Small Vessel Diseases, clinically characterized by Migraine Disorders, recurrent transient ischemic attacks or strokes, Abnormal behavior and Mental deterioration. Cerebrovascular accident are typically ischemic, while hemorrhagic events have been only sporadically described, Gene Mutation in the TREX1 protein, human protein, human and NOTCH3 genes cause Retinal vasculopathy with cerebral leukodystrophy (Vasculopathy, Retinal, With Cerebral Leukodystrophy) and cerebral autosomal dominant arteriopathy with subcortical infarcts and Leukoencephalopathy (NOTCH3 wt Allele), respectively, We used immunohistochemistry and immunogold electron microscopy (EM) to examine the distribution of GOM and NOTCH3 ectodomain (N3ECD) protein in microvasculature of Head>Brain gray matter and white matter in patients with NOTCH3 wt Allele, non-NOTCH3 wt Allele hereditary small-vessel disease and sporadic age-related degenerative disease, and comparable-age controls[SEP]Relations: CARASIL syndrome has relations: disease_phenotype_positive with Autosomal recessive inheritance, disease_phenotype_positive with Autosomal recessive inheritance, disease_disease with cerebral arteriopathy, autosomal dominant, with subcortical infarcts and Leukoencephalopathy,, disease_disease with cerebral arteriopathy, autosomal dominant, with subcortical infarcts and Leukoencephalopathy,, disease_protein with HTRA1, disease_protein with HTRA1. genetic Cerebral Small Vessel Diseases has relations: disease_disease with genetic central nervous system and retinal vascular disease, disease_disease with genetic central nervous system and retinal vascular disease, disease_disease with Coats plus syndrome, disease_disease with Coats plus syndrome.", "label": "yes"}
{"original_question": "Do all archaea possess multiple origins of DNA replication?", "id": "converted_1325", "sentence1": "Do all Archaea possess multiple origins of DNA replication?", "sentence2": "Origins differ in number and structure across the three domains of life and their properties determine the dynamics of chromosome replication. Bacteria and some Archaea replicate from single origins, whereas most Archaea and all Eukaryota replicate using multiple origins., Replication starts at a single Ori site in bacteria, but in Eukaryota multiple Ori sites are used for fast copying across all Chromosomes, Human, Pair 1. The situation becomes complex in Archaea, where some groups have single and others have multiple origins of replication., Results from this in silico analysis show that the Themococcales have a single origin of replication., Until recently, the only archaeon for which a bona fide origin of replication was reported was Pyrococcus abyssi, where a single origin was identified. Although several in silico analyses have suggested that some archaeal species might contain more than one origin, this has only been demonstrated recently., In bacteria and Eukaryota, replication initiates from single and multiple origins, respectively, while Archaea can adopt either of the two modes., Bacteria and some Archaea replicate from single origins, whereas most Archaea and all Eukaryota replicate using multiple origins., Bacteria and some Archaea replicate from single origins, whereas most Archaea and all Eukaryota replicate using multiple origins[SEP]Relations: Bacteremia has relations: disease_phenotype_positive with cyclic hematopoiesis, disease_phenotype_positive with cyclic hematopoiesis, disease_phenotype_positive with melioidosis, disease_phenotype_positive with melioidosis, disease_phenotype_positive with listeriosis, disease_phenotype_positive with listeriosis, disease_phenotype_positive with nocardiosis, disease_phenotype_positive with nocardiosis, disease_phenotype_positive with shigellosis, disease_phenotype_positive with shigellosis.", "label": "no"}
{"original_question": "Can life style changes reduce oxidative stress", "id": "converted_253", "sentence1": "Can life style changes reduce oxidative stress", "sentence2": "The Chronic Fatigue Syndrome group had an unfavorable lipid profile and signs of oxidative stress induced damage to Lipids and Proteins. These results might be indicative of early proatherogenic processes in this group of patients who are otherwise at low risk for Arteriosclerosis. Antioxidant treatment and life style changes are indicated for women with Chronic Fatigue Syndrome, as well as closer observation in order to assess the degree of Arteriosclerosis., Once detected, these patients may be offered more aggressive treatment strategies such as early pharmacotherapy in addition to life style changes targeted to maintaining Pericytes integrity., Our results suggested that life style changes which related to migration might reduce DNA damage in Hasake nationalities., Low levels of Antioxidants and increased oxidative stress with insulin resistance in Metabolic Syndrome X suggests that besides therapeutic life style changes (TLC) as suggested in ATP III guidelines inclusion of antioxidant vitamins, Fruit and vegetable could be beneficial to ward off the consequences of Metabolic Syndrome X.[SEP]Relations: Chronic fatigue has relations: disease_phenotype_positive with mitochondrial DNA depletion syndrome, myopathic form, disease_phenotype_positive with mitochondrial DNA depletion syndrome, myopathic form, disease_phenotype_positive with immunodeficiency, disease_phenotype_positive with immunodeficiency, disease_phenotype_positive with aneurysm-osteoarthritis syndrome, disease_phenotype_positive with aneurysm-osteoarthritis syndrome, disease_phenotype_positive with Sheehan syndrome, disease_phenotype_positive with Sheehan syndrome, disease_phenotype_positive with Muckle-Wells syndrome, disease_phenotype_positive with Muckle-Wells syndrome.", "label": "yes"}
{"original_question": "Is the protein MCL-1 anti-apoptotic?", "id": "converted_3414", "sentence1": "Is the protein MCL1 gene anti-apoptotic?", "sentence2": "increased expression of Apoptosis Inhibiting Proteins (BCL2L1 gene, Mcl-1 and XIAP gene gene) , repression of Apoptosis Inhibiting Proteins (Mcl-1, Bcl-xl and XIAP gene gene), anti-apoptotic BCL2 gene family members, such as BCL2 gene, BCL-XL or MCL1 gene[SEP]Relations: BCL2L1 has relations: protein_protein with MCL1, protein_protein with MCL1, protein_protein with APAF1, protein_protein with APAF1, bioprocess_protein with apoptotic mitochondrial changes, bioprocess_protein with apoptotic mitochondrial changes, bioprocess_protein with suppression by virus of host apoptotic process, bioprocess_protein with suppression by virus of host apoptotic process, protein_protein with MOAP1, protein_protein with MOAP1.", "label": "yes"}
{"original_question": "Is cytokeratin a tumor marker?", "id": "converted_4266", "sentence1": "Is cytokeratin a Specimen Source Codes - tumor marker?", "sentence2": "cytokeratin fragment antigen 21-1 (CYFRA21-1) in patients with Squamous Cell Carcinoma of the Rat Larynx (LSCC) and its correlation with tumorigenesis and progression,  cytokeratin fragment 19 (AUC=0.6882, p<0.0001) proved best in detecting relapse., The immunohistochemistry staining for cancer antigen 19-9, Carcinoembryonic Antigen, cytokeratin 20, and MKI67 gene showed comparable intensities in both groups., evels of inflammatory and Specimen Source Codes - Specimen Source Codes - tumor markers, including Carbohydrate antigen (CA) 19-9, CA-125 Antigen, Carcinoembryonic Antigen (CEA), CA153, and cytokeratin 19 fragments (CYFRA21-1), [SEP]Relations: Squamous cell carcinoma of the skin has relations: disease_phenotype_positive with porokeratosis (disease), disease_phenotype_positive with porokeratosis (disease), drug_effect with Sorafenib, drug_effect with Sorafenib, drug_effect with Maraviroc, drug_effect with Maraviroc, disease_phenotype_positive with xeroderma pigmentosum, disease_phenotype_positive with xeroderma pigmentosum. cellular response to Carcinoembryonic Antigen has relations: bioprocess_bioprocess with cellular response to glycoprotein, bioprocess_bioprocess with cellular response to glycoprotein.", "label": "yes"}
{"original_question": "Are there interactions between short and long noncoding RNAs?", "id": "converted_3510", "sentence1": "Are there interactions between short and long noncoding RNAs?", "sentence2": "It is now evident that noncoding RNAs play key roles in regulatory networks determining cell fate and behavior, in a myriad of different conditions, and across all species. Among these noncoding RNAs are short RNAs, such as MicroRNAs, snoRNAs, and Piwi-Interacting RNA, and the functions of those are relatively well understood. Other noncoding RNAs are longer, and their modes of action and functions are also increasingly explored and deciphered. Short RNAs and long noncoding RNAs (lncRNAs) interact with each other with reciprocal consequences for their fates and functions. LncRNAs serve as precursors for many types of small RNAs and, therefore, the pathways for small RNA biogenesis can impinge upon the fate of lncRNAs. In addition, Long Intergenic Non-Protein Coding RNA expression can be repressed by small RNAs, and lncRNAs can affect small RNA activity and abundance through competition for binding or by triggering small RNA degradation. Here, I review the known types of interactions between small and long RNAs, discuss their outcomes, and bring representative examples from studies in Mammals., Short RNAs and long noncoding RNAs (lncRNAs) interact with each other with reciprocal consequences for their fates and functions., Short RNAs and long noncoding RNAs (lncRNAs) interact with each other with reciprocal consequences for their fates and functions.[SEP]Relations: long noncoding RNA binding has relations: molfunc_protein with MIR384, molfunc_protein with MIR384. PIWI-interacting RNA (piRNA) biogenesis has relations: pathway_protein with HSP90AA1, pathway_protein with HSP90AA1, pathway_protein with TDRD9, pathway_protein with TDRD9, pathway_protein with TDRD6, pathway_protein with TDRD6, pathway_protein with MAEL, pathway_protein with MAEL.", "label": "yes"}
{"original_question": "Is tofacitinib a JAK inhibitor?", "id": "converted_4273", "sentence1": "Is tofacitinib a Janus kinase inhibitor?", "sentence2": "The Janus Kinase inhibitor tofacitinib impacts human dendritic cell differentiation and favours M1 Macrophage development., tofacitinib, a small Janus kinase inhibitor, is approved for the treatment of Rheumatoid Arthritis and has demonstrated good efficacy in Psoriasis phase III clinical trials. [SEP]Relations: tofacitinib has relations: drug_protein with JAK2, drug_protein with JAK2, drug_protein with JAK1, drug_protein with JAK1, drug_protein with JAK3, drug_protein with JAK3, drug_drug with Briakinumab, drug_drug with Briakinumab, drug_drug with Tocilizumab, drug_drug with Tocilizumab.", "label": "yes"}
{"original_question": "Is Dupilumab used for treatment of atopic dermatitis?", "id": "converted_2050", "sentence1": "Is dupilumab used for treatment of Eczema?", "sentence2": "dupilumab has demonstrated efficacy in patients with Asthma and Eczema, which are both type 2 helper T-cell-mediated diseases., Background dupilumab, a Homo sapiens monoclonal antibody CAL CAL against Recombinant Interleukin-4 receptor alpha, inhibits signaling of Recombinant Interleukin-4 and interleukin-13, type 2 Recombinant Cytokines that may be important drivers of atopic or allergic diseases such as Eczema., Two Phase 3 Trials of dupilumab versus Placebo in Dermatitis, Atopic., dupilumab is a biologic agent targeted at TH2 Recombinant Cytokines, but indirectly impacts Immunoglobulin E and is an important biologic agent for atopic Disease., dupilumab for the treatment of Eczema: A clinical trial review., dupilumab is a novel monoclonal antibody CAL CAL that was recently studied in adult patients with moderate-to-severe cytarabine/daunorubicin protocol., Patients treated with dupilumab had marked and rapid improvement in all the evaluated measures of Eczema Disease activity., The robust effects of dupilumab on skin inflammation and Pruritus -- quality confirm the pathogenic role of IL-4 and interleukin-13, Homo sapiens signaling in adult cytarabine/daunorubicin protocol, and further support the application of Th2 cytokine antagonists in the treatment of this Disease.[SEP]Relations: dupilumab has relations: drug_drug with Dusigitumab, drug_drug with Dusigitumab, drug_drug with Teplizumab, drug_drug with Teplizumab, drug_drug with Afelimomab, drug_drug with Afelimomab, drug_drug with Tremelimumab, drug_drug with Tremelimumab, drug_drug with Urelumab, drug_drug with Urelumab.", "label": "yes"}
{"original_question": "Are there any DNMT3 proteins present in plants?", "id": "converted_216", "sentence1": "Are there any DNMT3 proteins present in plants?", "sentence2": "De novo DNA methylation in Arabidopsis sp. sp. thaliana is catalyzed by the methyltransferase DRM2, a Homologous Gene of the Mammals de novo methyltransferase DNMT3., Here we describe DNA Modification Methylases Genes from both Arabidopsis sp. sp. and maize that show a high level of Sequence - ParameterizedDataType similarity to DNMT3 Family, suggesting that they encode Plant allergen de novo Methyltransferase. Relative to all known eukaryotic Methyltransferase, these Plant Proteins contain a novel arrangement of the motifs required for DNA Modification Methylases catalytic activity. The N termini of these Methyltransferase contain a series of ubiquitin-associated (UBA) domains. , BLASTX searches and phylogenetic analysis suggested that five cDNAs belonged to four classes (DNMT1 wt Allele, TRDMT1 wt Allele, CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate and DNMT3 Family) of DNA Modification Methylases Genes.[SEP]Relations: DNA modification has relations: bioprocess_protein with DNTT, bioprocess_protein with DNTT, bioprocess_protein with TREX1, bioprocess_protein with TREX1. methyltransferase complex has relations: cellcomp_protein with RIOK1, cellcomp_protein with RIOK1. Choline magnesium trisalicylate has relations: drug_protein with PTGS2, drug_protein with PTGS2, drug_protein with PTGS1, drug_protein with PTGS1.", "label": "yes"}
{"original_question": "Does Uc.160 promote cancer?", "id": "converted_2522", "sentence1": "Does Uc.160 promote cancer?", "sentence2": "We previously discovered the downregulation of T-UCR expression in Malignant neoplasm of Abdomen>Stomach (GC), indicating that T-UCRs could play an important role in GC biology. Uc.160+, a T-UCR reported to be downregulated in human cancer, has not been examined in GC.METHODS: We analyzed the expression pattern of Uc.160+ in nonneoplastic and tumor Body tissue of the Abdomen>Stomach by using uantitative reverse transcription polymerase chain reaction (qRT-PCR) and in situ hybridization (ISH), specifically focusing on the mechanism of transcriptional regulation and target Genes that are regulated by T-UCRs. We also attempted to determine the effect of Uc.160+ expression on biological features of GC Cultured Cell Line by Western blotting.RESULTS: On the basis of the qRT-PCR and ISH results, Uc.160+ expression in Adenoma and GC Body tissue was clearly downregulated compared with that in nonneoplastic mucosa Body tissue of the Abdomen>Stomach. Cancer-specific DNA methylation in the Promoter Regions, Genetic of Uc.160 was observed by bisulfite genomic DNA sequencing analysis. The effect of DNA methylation on Uc.160+ expression was further confirmed by reporter gene assay. We also revealed that Uc.160+ inhibited the phosphorylation of Proto-Oncogene Proteins c-akt by regulating phosphatase and tensin homolog (PTEN protein, human protein, human) expression.CONCLUSIONS: These results indicate that Uc.160+ could possibly have a tumor suppressive role in GC., Uc.160+, a T-UCR reported to be downregulated in human cancer, has not been examined in GC.<br><b>METHODS</b>: We analyzed the expression pattern of Uc.160+ in nonneoplastic and tumor Body tissue of the Abdomen>Stomach by using uantitative reverse transcription polymerase chain reaction (qRT-PCR) and in situ hybridization (ISH), specifically focusing on the mechanism of transcriptional regulation and target Genes that are regulated by T-UCRs., We also revealed that Uc.160+ inhibited the phosphorylation of Proto-Oncogene Proteins c-akt by regulating phosphatase and tensin homolog (PTEN protein, human protein, human) expression.<br><b>CONCLUSIONS</b>: These results indicate that Uc.160+ could possibly have a tumor suppressive role in GC.<br>, We also attempted to determine the effect of Uc.160+ expression on biological features of GC Cultured Cell Line by Western blotting.<br><b>RESULTS</b>: On the basis of the qRT-PCR and ISH results, Uc.160+ expression in Adenoma and GC Body tissue was clearly downregulated compared with that in nonneoplastic mucosa Body tissue of the Abdomen>Stomach., CONCLUSIONS These results indicate that Uc.160+ could possibly have a tumor suppressive role in GC., Uc.160+, a T-UCR reported to be downregulated in human cancer, has not been examined in GC., Among the T-UCRs that were reactivated upon drug treatment, Uc.160+, Uc283+A and Uc.346+ were found to undergo specific CpG island hypermethylation-associated silencing in Tumor cells, malignant compared with normal Body tissue., Uc.160+, a T-UCR reported to be downregulated in human cancer, has not been examined in GC., These results indicate that Uc.160+ could possibly have a tumor suppressive role in GC..[SEP]Relations: malignant giant cell tumor has relations: disease_disease with cancer, disease_disease with cancer. tumor of adipose tissue has relations: disease_disease with lipomatous cancer, disease_disease with lipomatous cancer, disease_disease with benign lipomatous neoplasm, disease_disease with benign lipomatous neoplasm, disease_disease with mesenchymal cell neoplasm, disease_disease with mesenchymal cell neoplasm. Adenoma has relations: disease_protein with SUZ12, disease_protein with SUZ12.", "label": "no"}
{"original_question": "Is Semagacestat effective for treatment of Alzheimer's disease?", "id": "converted_3042", "sentence1": "Is Semagacestat effective for treatment of Alzheimer's disease?", "sentence2": "However, a large phase 3 trial of semagacestat, a potential non-transition state analog (non-TSA) GSI, in patients with Alzheimer's disease (cytarabine/daunorubicin protocol) was terminated due to unexpected aggravation of Cognition Disorders and side effects., BACKGROUND: In a recent report, 76 weeks' treatment with a gamma-secretase inhibitor (semagacestat) was associated with poorer cognitive outcomes in Alzheimer's disease (cytarabine/daunorubicin protocol)., A clinical trial with the wide-spectrum γ-secretase inhibitor semagacestat has, however, demonstrated that global inhibition of all γ-secretases causes serious Toxic effect. , OBJECTIVE: Semagacestat, a γ-secretase inhibitor, demonstrated an unfavorable risk-benefit profile in a Phase 3 study of patients with Alzheimer's disease (IDENTITY trials), and clinical development was halted. , CONCLUSIONS: As compared with placebo, semagacestat did not improve cognitive status, and patients receiving the higher dose had significant worsening of functional ability. Semagacestat was associated with more adverse events, including Malignant neoplasm of skin and Infections of musculoskeletal system., BACKGROUND\nIn a recent report, 76 weeks' treatment with a gamma-secretase inhibitor (semagacestat) was associated with poorer cognitive outcomes in Alzheimer's disease (cytarabine/daunorubicin protocol)., Semagacestat was associated with more adverse events, including Malignant neoplasm of skin and Infections of musculoskeletal system., CONCLUSIONS\nAs compared with placebo, semagacestat did not improve cognitive status, and patients receiving the higher dose had significant worsening of functional ability., OBJECTIVE\nSemagacestat, a γ-secretase inhibitor, demonstrated an unfavorable risk-benefit profile in a Phase 3 study of patients with Alzheimer's disease (IDENTITY trials), and clinical development was halted., Recently disclosed Phase III findings on semagacestat indicated that Alzheimer's disease (cytarabine/daunorubicin protocol) patients on this Pharmacologic Substance showed significantly worsened cognitive function compared to those treated with placebo., The recent failure of semagacestat in two large Phase III studies questions the value of γ-secretase inhibitors in treating Alzheimer's disease., A phase 3 trial of semagacestat for treatment of Alzheimer's disease.As compared with placebo, semagacestat did not improve cognitive status, and patients receiving the higher dose had significant worsening of functional ability. , Preliminary results from Phase III studies showed that semagacestat failed to slow disease progression, and it was associated with worsening of clinical measures of cognition and the ability to perform activities of daily living. , Changes in Neuropsychiatric Inventory Associated with Semagacestat Treatment of ALZHEIMER DISEASE, FAMILIAL, 1.In participants with mild to moderate cytarabine/daunorubicin protocol, high dose semagacestat treatment was associated with greater severity and faster worsening of Nail-Patella Syndrome in a pattern resembling an agitated depression. , Patients treated with semagacestat lost more weight and had more Malignant neoplasm of skin and Infections of musculoskeletal system, treatment discontinuations due to adverse events, and serious adverse events (P<0.001 for all comparisons with placebo)., <b>OBJECTIVE</b>: Semagacestat, a γ-secretase inhibitor, demonstrated an unfavorable risk-benefit profile in a Phase 3 study of patients with Alzheimer's disease (IDENTITY trials), and clinical development was halted., Other relevant safety findings associated with semagacestat treatment included cognitive and functional worsening, skin-related TEAEs, Kidney and hepatic changes, increased QT interval, and Measured Measured weight loss (observable entity) (observable entity)., Patients treated with semagacestat lost more weight and had more Malignant neoplasm of skin and Infections of musculoskeletal system, treatment discontinuations due to adverse events, and serious adverse events (P&lt;0.001 for all comparisons with placebo)., Semagacestat, a γ-secretase inhibitor, demonstrated an unfavorable risk-benefit profile in a Phase 3 study of patients with Alzheimer's disease (IDENTITY trials), and clinical development was halted.[SEP]Relations: familial Alzheimer disease has relations: disease_disease with Alzheimer disease, disease_disease with Alzheimer disease, disease_phenotype_positive with Perseveration, disease_phenotype_positive with Perseveration, disease_disease with inherited prion disease, disease_disease with inherited prion disease. cognitive disorder has relations: disease_disease with dementia (disease), disease_disease with dementia (disease), contraindication with Lithium citrate, contraindication with Lithium citrate.", "label": "no"}
{"original_question": "Is there any role of interleukin-11 in cardiovascular fibrosis?", "id": "converted_2630", "sentence1": "Is there any role of interleukin-11 in cardiovascular Fibrosis?", "sentence2": "IL11 is a crucial determinant of cardiovascular Fibrosis., Using integrated imaging-genomics analyses of primary human Specimen Source Codes - Fibroblasts, we found that Interleukin 11 (IL11) upregulation is the dominant transcriptional response to TGFB1 gene gene exposure and required for its profibrotic effect. IL11 and its receptor (IL11RA protein, human protein, human) are expressed specifically in Specimen Source Codes - Fibroblasts where they drive non-canonical, ERK-dependent autocrine signalling that is required for fibrogenic protein synthesis. In CASP14 gene, fibroblast-specific interleukin-11 transgene expression or interleukin-11 injection causes Chest>Heart and kidney Fibrosis and organ failure whereas genetic deletion of Il11ra1 is protective against disease. Thus, inhibition of IL11 prevents fibroblast activation across Organ and species in response to a range of important pro-fibrotic stimuli. These data reveal a central role of IL11 in Fibrosis and we propose inhibition of IL11 as a new therapeutic strategy to treat fibrotic diseases., IL11 is a crucial determinant of cardiovascular Fibrosis.[SEP]Relations: interleukin-11 binding has relations: molfunc_protein with IL11RA protein, human, molfunc_protein with IL11RA protein, human, molfunc_protein with IL6R, molfunc_protein with IL6R, molfunc_protein with IL6ST, molfunc_protein with IL6ST. breast Fibrosis has relations: disease_disease with integumentary system disease, disease_disease with integumentary system disease, disease_disease with non-proliferative fibrocystic change of the breast, disease_disease with non-proliferative fibrocystic change of the breast.", "label": "yes"}
{"original_question": "Are sleep apnea and snoring associated with cardiac arrhythmias?", "id": "converted_2587", "sentence1": "Are Sleep Apnea Syndromes and snoring associated with Cardiac - anatomy qualifier arrhythmias?", "sentence2": "Ever told you have or had atrial fibrillation:Finding:Point in time:^Patient:Ordinal (Atrial Fibrillation) is the commonest arrhythmia in clinical practice and is associated with increased Cardiovascular system morbidity and mortality. Obstructive Sleep Apnea Syndromes (Sleep Apnea, Obstructive), a common Abnormal breathing, is an independent risk factor for Atrial Fibrillation., There is a growing Consensus in the scientific community that suggests a strong association between obstructive Sleep Apnea Syndromes (Sleep Apnea, Obstructive) and Cardiovascular system (CVD) conditions and events, including coronary artery disease, Hypertensive disease, arrhythmia, heart failure, and Sudden Cardiac Death. , part from well-established risk factors that increase the odds for the development of Atrial Fibrillation, e.g. age or arterial Hypertensive disease, recent analyses indicate that obstructive sleep apnoea (Sleep Apnea, Obstructive) may independently, negatively modify the arrhythmia occur-rence profile. , Evidence supports a causal association of Sleep Apnea Syndromes with the incidence and morbidity of Hypertensive disease, coronary Heart Diseases, arrhythmia, heart failure, and Cerebrovascular accident., Severe snoring may be associated with Pulmonary:-:Point in time:^Patient:- and systemic Hypertensive disease, secondary Polycythemia, and Cardiac - anatomy qualifier arrhythmias.<br>, Severe snoring may be associated with Pulmonary:-:Point in time:^Patient:- and systemic Hypertensive disease, secondary Polycythemia, and Cardiac - anatomy qualifier arrhythmias., BACKGROUND AND PURPOSE Nocturnal Cardiac - anatomy qualifier arrhythmias occur in patients with obstructive Sleep Apnea Syndromes (Sleep Apnea, Obstructive), reportedly as a consequence of the autonomic effects of recurrent apnea with subsequent oxygen desaturation., Obstructive apnea is associated with Coronary Arteriosclerosis (silent or symptomatic), acute coronary events, Cerebrovascular accident and transient ischemic attacks, Cardiac Arrhythmia, Pulmonary:-:Point in time:^Patient:- Hypertensive disease and heart failure., Obstructive Sleep Apnea Syndromes (Sleep Apnea, Obstructive) is the most common form of sleep-disordered breathing, affecting 5-15% of the population. It is characterized by intermittent episodes of partial or complete obstruction of the upper airway during sleep that disrupts normal ventilation and sleep architecture, and is typically associated with excessive Daytime Somnolence, snoring, and witnessed apneas. Patients with obstructive Sleep Apnea Syndromes present risk to the general public safety by causing 8-fold increase in vehicle accidents, and they may themselves also suffer from the physiologic consequences of Sleep Apnea, Obstructive; these include Hypertensive disease, coronary artery disease, Cerebrovascular accident, congestive heart failure, Pulmonary:-:Point in time:^Patient:- Hypertensive disease, and Cardiac - anatomy qualifier arrhythmias, Obstructive Sleep Apnea Syndromes and central Sleep Apnea Syndromes with Cheyne-Stokes respiration                     are associated with an increased risk of Cardiac Arrhythmia. , Obstructive Sleep Apnea Syndromes (Sleep Apnea, Obstructive) affects approximately 4% of middle-aged men and 2% of middle-aged women. Cardiac arrhythmias are common problems in patients with Sleep Apnea, Obstructive, even though the true prevalence and clinical relevance of Cardiac - anatomy qualifier arrhythmias remains to be determined. , Cardiac arrhythmias during wakefulness and sleep in 15 patients with sleep-induced obstructive apnea, and the effect of Atropinum, Atropinum, atropine and tracheostomy on these arrhythmias were studied by continuous overnight Holter electrocardiographic, respiratory and electroencephalographic recordings., obstructive Sleep Apnea Syndromes (Sleep Apnea, Obstructive) as its most extreme variant, is characterized by intermittent episodes of partial or complete obstruction of the upper airway, leading to cessation of breathing while asleep. Cardiac arrhythmias are common problems in Sleep Apnea, Obstructive patients, although the true prevalence and clinical relevance of Cardiac - anatomy qualifier arrhythmias remains to be determined, The mechanisms associated with the Cardiovascular system consequences of obstructive Sleep Apnea Syndromes include abrupt changes in autonomic tone, which can trigger Cardiac - anatomy qualifier arrhythmias. ,  Recent studies have shown that Cardiac - anatomy qualifier arrhythmias and conduction disorders are common in patients with SA. Sleep apnea, Severity of nocturnal Cardiac - anatomy qualifier arrhythmias correlates with intensity of Sleep Apnea Syndromes in men, Patients affected with Sleep Apnea, Obstructive are frequently Hypertensive (finding) and can have dangerous Cardiac - anatomy qualifier arrhythmias., Patients with stable Congestive heart failure who snore may present sleep hypopnea and Cardiac - anatomy qualifier arrhythmias. ,  Obstructive Sleep Apnea Syndromes (Sleep Apnea, Obstructive) is associated with increased Cardiovascular system morbidity and mortality. Cardiac arrhythmias are common in patients with Sleep Apnea, Obstructive. , Nocturnal hypoxia has been associated with serious Ventricular tachyarrhythmia as well as life-threatening bradyarrhythmias. BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 and snoring, both of which increase with age, have been identified as risk factors for sleep-related breathing disorders, as have Hypertensive disease and Heart Diseases., Obstructive Sleep Apnea Syndromes syndrome is associated with excess Daytime Somnolence, Cancer patients and suicide and Cancer patients and suicide and depression, and an increased incidence of ischemic cardiopathy, Cardiac - anatomy qualifier arrhythmias, systemic Hypertensive disease and brain infarction., We found 58 percent prevalence of arrhythmias in patients with Sleep Apnea Syndromes (apnea/hypopnea index = AHI>10), vs 42 percent in nonapneic controls (chi 2 = 16.7, p<0.0001)[SEP]Relations: obstructive Sleep Apnea Syndromes syndrome has relations: disease_phenotype_positive with Snoring, disease_phenotype_positive with Snoring. Sleep Apnea Syndromes syndrome has relations: disease_disease with sleep-wake disorder, disease_disease with sleep-wake disorder, disease_disease with obstructive Sleep Apnea Syndromes syndrome, disease_disease with obstructive Sleep Apnea Syndromes syndrome, disease_disease with central Sleep Apnea Syndromes syndrome, disease_disease with central Sleep Apnea Syndromes syndrome, disease_disease with respiratory system disease, disease_disease with respiratory system disease.", "label": "yes"}
{"original_question": "Is there a BRCA mutation analysis in the Greek population?", "id": "converted_3493", "sentence1": "Is there a BRCA mutation analysis in the Greek population?", "sentence2": "Comprehensive BRCA mutation analysis in the Greek population. Experience from a single clinical diagnostic center., Germline Gene Mutation in the BRCA1 gene gene and BRCA2 gene gene Genes are associated with hereditary predisposition to Breast and Malignant neoplasm of ovary. Sensitive and accurate detection of BRCA1 gene gene and BRCA2 gene gene Gene Mutation is crucial for personalized clinical management of individuals affected by Breast or Malignant neoplasm of ovary, and for the identification of at-risk healthy relatives. We performed molecular analysis of the BRCA1 gene gene and BRCA2 gene gene Genes in 898 Greek families, using Sanger sequencing or Next Generation Sequencing for the detection of small insertion/deletion frameshift, nonsynonymous, truncating and splice-site alterations and MLPA for the detection of large genomic rearrangements. In total, a pathogenic mutation was identified in 12.9% of 898 families analyzed. Of the 116 Gene Mutation identified in total 9% were novel and 14.7% were large genomic rearrangements. Our results indicate that different types of mutational events in the BRCA1 gene gene and BRCA2 gene gene Genes are responsible for the hereditary component of Breast/Malignant neoplasm of ovary in the Greek population. Therefore the methodology used in the analysis of Greek patients must be able to detect both point and small Frameshift Mutation function in addition to large genomic rearrangements across the entire Open Reading Frames of the two Genes.[SEP]Relations: Breast has relations: anatomy_protein_present with RIMKLB, anatomy_protein_present with RIMKLB, anatomy_protein_present with GCSAM, anatomy_protein_present with GCSAM. adaptation to pheromone regulating conjugation with mutual genetic exchange has relations: bioprocess_bioprocess with response to pheromone regulating conjugation with mutual genetic exchange, bioprocess_bioprocess with response to pheromone regulating conjugation with mutual genetic exchange, bioprocess_bioprocess with regulation of conjugation, bioprocess_bioprocess with regulation of conjugation, bioprocess_bioprocess with negative adaptation of signaling pathway, bioprocess_bioprocess with negative adaptation of signaling pathway.", "label": "yes"}
{"original_question": "Is Baloxavir effective for influenza?", "id": "converted_2755", "sentence1": "Is Baloxavir effective for influenza?", "sentence2": "Baloxavir marboxil (Xofluza™; baloxavir) is an oral cap-dependent endonuclease inhibitor that has been developed by Roche and Shionogi. The drug blocks influenza virus proliferation by inhibiting the initiation of mRNA synthesis. In February 2018, baloxavir received its first global approval in Japan for the treatment of Influenza virus vaccine or B Virus Infection. , This article summarized the milestones in the development of baloxavir leading to this first global approval for Influenza virus vaccine or B Virus Infection., Baloxavir acid (BXA), derived from the prodrug baloxavir marboxil (BXM), potently and selectively inhibits the cap-dependent endonuclease within the polymerase PA subunit of Influenza virus vaccine and Herpesvirus 1, Cercopithecine., Characterization of influenza virus variants induced by treatment with the endonuclease inhibitor baloxavir marboxil., Baloxavir Marboxil for Uncomplicated Influenza in Adults and Adolescents., BACKGROUND: Baloxavir marboxil is a selective inhibitor of influenza cap-dependent endonuclease. It has shown therapeutic activity in preclinical models of Influenza virus vaccine and B Virus Infection, including strains resistant to current antiviral agents., CONCLUSIONS: Single-dose baloxavir was without evident safety concerns, was superior to placebo in alleviating influenza symptoms, and was superior to both oseltamivir and placebo in reducing the viral load 1 day after initiation of the trial regimen in patients with uncomplicated influenza., A single oral dose of baloxavir is usually well tolerated; it hastens alleviation of influenza symptoms and shortens the duration of viral shedding., Japan was the first country to approve baloxavir marboxil as a treatment for influenza., This article summarized the milestones in the development of baloxavir leading to this first global approval for Influenza virus vaccine or B Virus Infection.<br>, In February 2018, baloxavir received its first global approval in Japan for the treatment of Influenza virus vaccine or B Virus Infection.[SEP]Relations: Rubella virus vaccine has relations: drug_drug with Baloxavir marboxil, drug_drug with Baloxavir marboxil, drug_drug with Saquinavir, drug_drug with Saquinavir. Oseltamivir has relations: drug_drug with Balsalazide, drug_drug with Balsalazide, drug_drug with Ribavirin, drug_drug with Ribavirin, drug_drug with Atazanavir, drug_drug with Atazanavir.", "label": "yes"}
{"original_question": "Is cathepsin L active in endosomes?", "id": "converted_3408", "sentence1": "Is cathepsin L active in endosomes?", "sentence2": "Cathepsin L in the Late Endosome/Lysosome, endosomal cathepsin L, Immunofluorescence and immunoblotting investigations revealed the presence of cathepsin L in the nuclear compartment in addition to its expected endo-lysosomal localization in colorectal carcinoma cells., cleavage by the endosomal/lysosomal protease cathepsin L[SEP]", "label": "yes"}
{"original_question": "Is STAT3 transcription factor regulated by mTORC1?", "id": "converted_1691", "sentence1": "Is STAT3 protein, human transcription factor regulated by mechanistic target of rapamycin complex 1?", "sentence2": "Mechanistically, mechanistic target of rapamycin complex 1 mediated IL-6-induced Stat3 activation in intestinal Epithelial Cells to stimulate the expression of downstream targets essential for cell proliferation and tissue regeneration. Therefore, mechanistic target of rapamycin complex 1 signaling critically protects against INFLAMMATORY BOWEL DISEASE 2 through modulation of inflammation-induced Stat3 activity., we demonstrated that STAT3 protein, human protein, human is directly phosphorylated by mechanistic target of rapamycin complex 1 on Ser727 during Hypoxia, CTCAE, promoting HIF-1α mRNA transcription, Mechanistically, mechanistic target of rapamycin complex 1 signaling was activated by excess Antifibrinolytic Antifibrinolytic amino acids, which then positively regulated Notch1 expression through the activation of the signal transducer and activator of transcription 3 (STAT3 protein, human protein, human)., Here we present evidence for the involvement of STAT3 protein, human protein, human, a known mechanistic target of rapamycin complex 1 regulated transcription factor, in this process, Furthermore, we demonstrated that STAT3 protein, human protein, human is directly phosphorylated by mechanistic target of rapamycin complex 1 on Ser727 during Hypoxia, CTCAE, promoting HIF-1α mRNA transcription. mechanistic target of rapamycin complex 1 also regulates HIF-1α synthesis on a translational level via co-operative regulation of both initiation factor 4E-binding protein 1 (EIF4EBP1 protein, human) and ribosomal protein S6 kinase-1 (RPS6KB1 wt Allele), whereas HIF-1α degradation remains unaffected, Here we present evidence for the involvement of STAT3 protein, human protein, human, a known mechanistic target of rapamycin complex 1 regulated transcription factor, in this process. , TSC1/TSC2 inactivation inhibits Proto-Oncogene Proteins c-akt through mechanistic target of rapamycin complex 1-dependent up-regulation of STAT3 protein, human protein, human-PTEN cascade., Mechanistically, mechanistic target of rapamycin complex 1 signaling was activated by excess Antifibrinolytic Antifibrinolytic amino acids, which then positively regulated Notch1 expression through the activation of the signal transducer and activator of transcription 3 (STAT3 protein, human protein, human). , Suppression of the mechanistic target of rapamycin complex 1/STAT3 protein, human protein, human/Notch1 pathway by activated AMP-Activated Protein Kinases prevents hepatic insulin resistance induced by excess Antifibrinolytic Antifibrinolytic amino acids., Here, we review the connections between mechanistic target of rapamycin complex 1 and gene transcription by focusing on its impact in regulating the activation of specific TRANSCRIPTION FACTOR including including STAT3 protein, human protein, human, SREBPs, PPARγ, PPARα, HIF1α, YY1–PGC1α and TFEB protein, human protein, human. We also discuss the importance of these TRANSCRIPTION FACTOR in mediating the effects of mechanistic target of rapamycin complex 1 on various cellular processes in physiological and pathological contexts.[SEP]Relations: transcription factor binding has relations: molfunc_protein with STAT3 protein, human, molfunc_protein with STAT3 protein, human, molfunc_protein with FOXC1, molfunc_protein with FOXC1, molfunc_protein with ETS1, molfunc_protein with ETS1, molfunc_protein with NFATC1, molfunc_protein with NFATC1, molfunc_protein with NFATC3, molfunc_protein with NFATC3.", "label": "yes"}
{"original_question": "Is ustekinumab a polyclonal antibody?", "id": "converted_3217", "sentence1": "Is ustekinumab a polyclonal antibody?", "sentence2": "Ustekinumab Ab Ab, a Homo sapiens monoclonal IgG1 antibody targeting the p40-subunit shared by interleukin (IL)12 and interleukin-23 binding activity, represents a potential treatment for Dermatitis, Atopic (cytarabine/daunorubicin protocol).[SEP]Relations: Ustekinumab Ab has relations: drug_drug with Ficlatuzumab, drug_drug with Ficlatuzumab, drug_protein with IL12B, drug_protein with IL12B, drug_drug with Ecromeximab, drug_drug with Ecromeximab, drug_drug with Daclizumab, drug_drug with Daclizumab, drug_drug with Teplizumab, drug_drug with Teplizumab.", "label": "no"}
{"original_question": "Does TFIIS affect nucleosome positioning?", "id": "converted_2247", "sentence1": "Does TCEA1 wt Allele affect nucleosome location positioning?", "sentence2": "Transcript cleavage factor TCEA1 wt Allele reactivates the backtracked complex (molecular entity) and promotes pol II transcription through the nucleosome location location. , The same Nucleosomes transcribed in the opposite orientation form a weaker, more diffuse barrier that is largely relieved by higher Sodium Chloride, Dietary, TCEA1 wt Allele, or Foundation for the Accreditation of Cellular Therapy, The system contains natural or recombinant histones, chromatin location location assembly factors, the histone-acetyltransferase p300, all components of the general transcription machinery, general coactivators and the transcription factor S-II (TCEA1 wt Allele)., Efficient and rapid nucleosome location location traversal by RNA Polymerase II depends on a combination of RNA Transcript elongation factors., We now show that although GTF2F2P1 gene or TCEA1 wt Allele alone is modestly stimulatory for nucleosome location location traversal, both factors together increase transcription through Nucleosomes in a synergistic manner., Significantly, we found that Nucleosomes with a Sin mutant histone are traversed to the same extent and at nearly the same rate as equivalent pure DNA templates if both TCEA1 wt Allele and GTF2F2P1 gene are present., After partial uncoiling of nucleosomal DNA from Histone octamer by Pol II and backtracking of the Enzyme [APC], nucleosomal DNA recoils on the octamer, locking Pol II in the arrested state. Histone Chaperones and transcription factors TCEA1 wt Allele, GTF2F2P1 gene and Foundation for the Accreditation of Cellular Therapy facilitate transcription through chromatin location location using different molecular mechanisms., Transcript cleavage factor TCEA1 wt Allele reactivates the backtracked complex (molecular entity) and promotes pol II transcription through the nucleosome location location., The highly conserved eukaryotic transcriptional elongation factor TCEA1 wt Allele enables RNA Polymerase II (RNAPII) to read though pause or termination sites, Nucleosomes and sequence-specific DNA-binding proteins., We also studied the effect of GTF2F2P1 gene and TCEA1 wt Allele on transcription of Nucleosomes containing a Sin mutant histone., The same Nucleosomes transcribed in the opposite orientation form a weaker, more diffuse barrier that is largely relieved by higher Sodium Chloride, Dietary, TCEA1 wt Allele, or Foundation for the Accreditation of Cellular Therapy.[SEP]Relations: nucleosome location has relations: cellcomp_protein with IRF4, cellcomp_protein with IRF4, cellcomp_protein with MPHOSPH8, cellcomp_protein with MPHOSPH8, cellcomp_protein with H2AX, cellcomp_protein with H2AX, cellcomp_protein with SLF1, cellcomp_protein with SLF1, cellcomp_protein with GLYR1, cellcomp_protein with GLYR1.", "label": "yes"}
{"original_question": "Has the companion diagnostic HercepTest received FDA approval?", "id": "converted_4223", "sentence1": "Has the companion diagnostic HercepTest received FDA approval?", "sentence2": "The FDA-Approved Breast Cancer HER2 Evaluation Kit (HercepTest; Dako) May Miss Some HER2-Positive Breast Cancers., HER2 fluorescence in situ hybridization (FISH) and immunohistochemistry (IHC) tests were performed on 52 cases using a US Food and Drug Administration (FDA)-approved kit (HercepTest, FDA kit) and a laboratory-developed test (LDT) with the HercepTest antibody and a Leica Bond automated stainer.[SEP]", "label": "yes"}
{"original_question": "Can non ubiquitinated Tomm20 promote mitophagy?", "id": "converted_2618", "sentence1": "Can non ubiquitinated Tomm20 promote mitophagy?", "sentence2": " A total of 338 new targets were identified and from these we validated NEK3 gene (Gsk3β), which can phosphorylate α-synuclein, and Translocase of outer mitochondrial membrane 20 (Tomm20), a mitochondrial Translocase that, when ubiquitinated, promotes mitophagy, as SCFFbxo7substrates both in vitro and in vivo Ubiquitin chain restriction analyses revealed that FBXO7 gene modified Gsk3β using K63 linkages. [SEP]Relations: NEK3 has relations: anatomy_protein_present with substantia nigra, anatomy_protein_present with substantia nigra, anatomy_protein_present with esophagus, anatomy_protein_present with esophagus, protein_protein with YWHAZ, protein_protein with YWHAZ, protein_protein with MIS18BP1, protein_protein with MIS18BP1, bioprocess_protein with mitotic cell cycle, bioprocess_protein with mitotic cell cycle.", "label": "no"}
{"original_question": "Can the iPS cell technology be used in Fanconi anemia therapy?", "id": "converted_1581", "sentence1": "Can the iPS cell technology be used in Fanconi anemia therapy?", "sentence2": "We explain a protocol for the reproducible generation of genetically corrected iPSCs starting from the skin biopsies of Fanconi anemia patients using retroviral transduction with POU5F1 gene, SOX2 protein, human protein, human and KLF4 protein, human protein, human, Before reprogramming, the Specimen Source Codes - Fibroblasts and/or keratinocyte of the patients are genetically corrected with Genus: Lentivirus group expressing FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder)., Disease-corrected haematopoietic progenitors from Fanconi Anemia induced pluripotent stem cells, Here we show that, on correction of the genetic defect, Diploid Cell from Fanconi Anemia patients can be reprogrammed to pluripotency to generate patient-specific Induced Pluripotent Stem Cells. These Cultured Cell Line appear indistinguishable from Human Embryonic Stem Cells and Induced Pluripotent Stem Cells from healthy individuals, Most importantly, we show that corrected Fanconi-anaemia-specific Induced Pluripotent Stem Cells can give rise to haematopoietic progenitors of the Myeloid and Erythroid lineages that are phenotypically normal, that is, disease-free[SEP]Relations: Fanconi anemia has relations: disease_protein with FANCI, disease_protein with FANCI, disease_protein with FANCE, disease_protein with FANCE, disease_disease with DNA repair disease, disease_disease with DNA repair disease, contraindication with Phenol, contraindication with Phenol. Fanconi anemia complementation group has relations: disease_phenotype_positive with Squamous cell carcinoma, disease_phenotype_positive with Squamous cell carcinoma.", "label": "yes"}
{"original_question": "Does thyroid hormone regulate calcium transient in the myocardium? ", "id": "converted_182", "sentence1": "Does Thyroid Hormones regulate CALCIUM SUPPLEMENTS transient in the myocardium? ", "sentence2": "3-iodothyronamine (T(1)AM) is a novel endogenous relative of Thyroid Hormones, able to interact with trace amine-associated receptors, a class of Plasma membrane G protein-coupled receptors, and to produce a negative inotropic and chronotropic effect, In adult rat cardiomyocytes acute exposure to 20 microM T(1)AM decreased the amplitude and duration of the CALCIUM SUPPLEMENTS transient., In normal porcine myocardium T3 thoracic segmental innervation thoracic segmental innervation had no effect on the extent of isometric force generation but accelerated the time course of force development (p < 0.05) and increased the CALCIUM SUPPLEMENTS transient (p < 0.001). After induction of Myocardial dysfunction by epinephrine exposure T3 thoracic segmental innervation thoracic segmental innervation accelerated the intracellular CALCIUM SUPPLEMENTS transients and reduced diastolic CALCIUM SUPPLEMENTS, The experimental data showing increased force amplitudes at unaltered amplitudes of the intracellular CALCIUM SUPPLEMENTS transient and an even-reduced CALCIUM SUPPLEMENTS time integral provide strong evidence for a sensitization of the contractile apparatus for CALCIUM SUPPLEMENTS by liothyronine, hese results indicate that the thyroid state influences the time course of the CALCIUM SUPPLEMENTS transient and are consistent with the abbreviation in the duration of contraction that is observed in the hyperthyroid state.[SEP]Relations: myocardial infarction has relations: contraindication with Calcium chloride, contraindication with Calcium chloride. response to Thyroid Hormones has relations: bioprocess_protein with GBA, bioprocess_protein with GBA, bioprocess_bioprocess with cellular response to Thyroid Hormones stimulus, bioprocess_bioprocess with cellular response to Thyroid Hormones stimulus, bioprocess_protein with SLC26A5, bioprocess_protein with SLC26A5. Liothyronine has relations: contraindication with thyroid crisis (disease), contraindication with thyroid crisis (disease).", "label": "yes"}
{"original_question": "Is cadherin a plasma membrane marker?", "id": "converted_3931", "sentence1": "Is cadherin a Plasma membrane marker?", "sentence2": "the Plasma membrane-bound E-Cadherin protein, cadherin 5 protein levels were also increased in the Plasma membrane fraction. ,  recycling of cadherin 5 to the Plasma membrane,, E-Cadherin, a central component of the Zonula Adherens (AJ), is a Single-pass plasma transmembrane protein [SEP]Relations: Plasma membrane has relations: cellcomp_protein with CADM3, cellcomp_protein with CADM3, cellcomp_protein with CADM2, cellcomp_protein with CADM2, cellcomp_protein with CADM1, cellcomp_protein with CADM1, cellcomp_protein with FURIN, cellcomp_protein with FURIN, cellcomp_protein with ACIN1, cellcomp_protein with ACIN1.", "label": "yes"}
{"original_question": "Is nerinetide effective for ischaemic stroke?", "id": "converted_4485", "sentence1": "Is nerinetide effective for ischaemic stroke?", "sentence2": "337 (61·4%) of 549 patients with nerinetide and 329 (59·2%) of 556 with placebo achieved an mRS score of 0-2 at 90 days (adjusted risk ratio 1·04, 95% CI 0·96-1·14; p=0·35). Secondary outcomes were similar between groups. , INTERPRETATION: Nerinetide did not improve the proportion of patients achieving good clinical outcomes after endovascular thrombectomy compared with patients receiving placebo.,  patients receiving alteplase. Serious adverse events occurred equally between groups.INTERPRETATION: Nerinetide did not improve the proportion of patients achieving good clinical outcomes after endovascular thrombectomy compared with patients receiving placebo.FUNDING: Canadian Inst[SEP]Relations: Alteplase has relations: drug_drug with Lenalidomide, drug_drug with Lenalidomide, drug_drug with Benzthiazide, drug_drug with Benzthiazide, drug_drug with Mebutizide, drug_drug with Mebutizide, drug_drug with Nimesulide, drug_drug with Nimesulide, drug_drug with Nelarabine, drug_drug with Nelarabine.", "label": "no"}
{"original_question": "Is there an increased risk for cancer in Dyskeratosis Congenita?", "id": "converted_162", "sentence1": "Is there an increased risk for Primary malignant neoplasm in Dyskeratosis Congenita?", "sentence2": "People with Dyskeratosis Congenita are at increased risk for progressive Bone marrow hypocellularity (Bcl-2-Modifying Factor), MYELODYSPLASTIC SYNDROME (Miller Dieker syndrome) or Leukemia, Myelocytic, Acute (AML), Solid Neoplasm (usually Anal Anal squamous cell carcinoma of the head/neck or anogenital Primary malignant neoplasm), and Pulmonary:-:Point in time:^Patient:- fibrosis, Clinical progression of the disease can lead to Aplastic Anemia (86% of all patients) and to Pulmonary:-:Point in time:^Patient:- or hepatic complications. These patients also have an increased risk of Primary malignant neoplasm., Fanconi Anemia (doxorubicin/fluorouracil protocol), dyskeratosis congenita (Dyskeratosis Congenita), Anemia, Diamond-Blackfan (Diamond-Blackfan Anemia 1), and SHWACHMAN-DIAMOND SYNDROME 2 (Symptom Distress Scale) comprise major inherited Bone marrow hypocellularity syndromes (Congenital Bone Marrow Failure Syndromes). Adverse events include severe Bone marrow hypocellularity (Bcl-2-Modifying Factor), MYELODYSPLASTIC SYNDROME (Miller Dieker syndrome), acute myeloid leukemia (AML), and solid tumours (ST), Patients with doxorubicin/fluorouracil protocol had earlier onset of Malignant Neoplasms, need for stem cell transplant, and Cessation of life; followed by Dyskeratosis Congenita; Diamond-Blackfan Anemia 1 and Symptom Distress Scale were mildest. While doxorubicin/fluorouracil protocol and Dyskeratosis Congenita patients had markedly increased risks of Primary malignant neoplasm, AML and Miller Dieker syndrome, there were no cases of leukemia in Diamond-Blackfan Anemia 1 or Symptom Distress Scale patients, The findings demonstrate that both doxorubicin/fluorouracil protocol and Dyskeratosis Congenita are major Primary malignant neoplasm susceptibility syndromes, People with Dyskeratosis Congenita are at increased risk for progressive Bone marrow hypocellularity (Bcl-2-Modifying Factor), MYELODYSPLASTIC SYNDROME (Miller Dieker syndrome) or Leukemia, Myelocytic, Acute (AML), Solid Neoplasm (usually Anal Anal squamous cell carcinoma of the head/neck or anogenital Primary malignant neoplasm), and Pulmonary:-:Point in time:^Patient:- fibrosis, Patients with dyskeratosis congenita (Dyskeratosis Congenita) have an increased risk of Primary malignant neoplasm, but also exhibit heightened radiation sensitivity., Dyskeratosis congenita (Dyskeratosis Congenita) is characterized by the clinical triad of reticular skin pigmentation, Leukoplakia, Oral, and Dystrophia unguium associated with Bone marrow hypocellularity (Bcl-2-Modifying Factor) and an high risk to develop Primary malignant neoplasm and Pulmonary:-:Point in time:^Patient:- complications., CONCLUSION: Dyskeratosis congenita is a rare condition; however, it is vital to recognise the increased risk of upper aerodigestive tract Malignant Neoplasms in these patients., Point Mutation in the DKC1 gene that encodes H/ACA Ribonucleoprotein Complex Subunit 4, human cause the rare inherited syndrome called X-Linked Dyskeratosis Congenita, characterized by a failure of proliferating tissues and increased susceptibility to Primary malignant neoplasm., Dyskeratosis Congenita (Dyskeratosis Congenita) also known as Zinsser-Engman-Cole syndrome is a rare multi-system BONE MARROW FAILURE SYNDROME 2 characterised by mucocutaneous abnormalities and an increased predisposition to Primary malignant neoplasm\"., Dyskeratosis congenita is an inherited syndrome characterised by mucocutaneous features, Bone marrow hypocellularity, an increased risk of malignancy and other somatic abnormalities., Dyskeratosis congenita is a rare condition; however, it is vital to recognise the increased risk of upper aerodigestive tract Malignant Neoplasms in these patients., Epidermal atrophy, hair growth defects, Bone marrow hypocellularity and increased risk of Primary malignant neoplasm are also common in Dyskeratosis Congenita patients., telomere dysfunction and Specimen Source Codes - Specimen Source Codes - tumor suppression responses in dyskeratosis congenita: balancing Primary malignant neoplasm and Tissue Specimen Code renewal impairment., Patients with dyskeratosis congenita (Dyskeratosis Congenita) have an increased risk of Primary malignant neoplasm, but also exhibit heightened radiation sensitivity, Dyskeratosis congenita is a rare condition; however, it is vital to recognise the increased risk of upper aerodigestive tract Malignant Neoplasms in these patients, Dyskeratosis congenita is an inherited syndrome characterised by mucocutaneous features, Bone marrow hypocellularity, an increased risk of malignancy and other somatic abnormalities, While doxorubicin/fluorouracil protocol and Dyskeratosis Congenita patients had markedly increased risks of Primary malignant neoplasm, AML and Miller Dieker syndrome, there were no cases of leukemia in Diamond-Blackfan Anemia 1 or Symptom Distress Scale patients, As in FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) and dyskeratosis congenita, Diamond-Blackfan Anemia 1 is both an inherited BONE MARROW FAILURE SYNDROME 2 and a Primary malignant neoplasm predisposition syndrome; Primary malignant neoplasm risks appear lower in Diamond-Blackfan Anemia 1 than in FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) or dyskeratosis congenita, Severe Pancytopenia frequently causes early mortality of Dyskeratosis Congenita patients, who have an increased risk of developing Oropharyngeal Squamous Cell Carcinoma, Here different aspects of telomere biology, concerning adult stem cells senescence, Specimen Source Codes - Specimen Source Codes - tumor suppression and Primary malignant neoplasm are considered in the context of Dyskeratosis Congenita, resulting in two translational models: late onset of Dyskeratosis Congenita symptoms in telomere-related mutations carriers is a potential indicator of increased Primary malignant neoplasm risk and differences in Specimen Source Codes - Specimen Source Codes - tumor suppression capacities among the genetic subgroups are (at least partial) causes of different clinical manifestations of the disease, Point Mutation in the DKC1 gene that encodes H/ACA Ribonucleoprotein Complex Subunit 4, human cause the rare inherited syndrome called X-Linked Dyskeratosis Congenita, characterized by a failure of proliferating tissues and increased susceptibility to Primary malignant neoplasm, Dyskeratosis congenita is a Primary malignant neoplasm-prone BONE MARROW FAILURE SYNDROME 2 caused by aberrations in telomere biology.[SEP]Relations: dyskeratosis congenita has relations: disease_protein with TERC, disease_protein with TERC, disease_protein with TERT, disease_protein with TERT. dyskeratosis congenita, X-linked has relations: disease_phenotype_positive with Carcinoma, disease_phenotype_positive with Carcinoma, disease_protein with TERT, disease_protein with TERT, disease_disease with X-linked disease, disease_disease with X-linked disease.", "label": "yes"}
{"original_question": "Is Rheumatoid Arthritis related to myopathy?", "id": "converted_1228", "sentence1": "Is Rheumatoid Arthritis related to Myopathy?", "sentence2": "Prevalence of risk factors for statin-induced Myopathy in Rheumatoid Arthritis patients, we describe a patient with Rheumatoid Arthritis and Respiratory Failure associated with proximal Myopathy secondary to hydroxychloroquine, Occurrence of chloroquine-induced Myopathy after Low-Dose Treatment treatment of Rheumatoid Arthritis for seven years, a 75 year old female with Rheumatoid Arthritis treated with daily doses of 250 mg of chloroquine for four years. The patient visited because of several months history of predominantly proximal progressive Quadriparesis with Absent reflex, Myopathy and Neuropathy in Rheumatoid Arthritis, with Rheumatoid Arthritis (RA) have clinical or subclinical evidence of Peripheral Nervous System Diseases or Myopathy, The study reveals an increased prevalence of neurogenic but not myogenic changes in patients with RA compared with controls[SEP]Relations: Rheumatoid arthritis has relations: phenotype_phenotype with Arthritis, phenotype_phenotype with Arthritis, disease_phenotype_positive with Rheumatoid Arthritis, disease_phenotype_positive with Rheumatoid Arthritis, drug_effect with Acamprosate, drug_effect with Acamprosate, disease_phenotype_positive with dystonia, disease_phenotype_positive with dystonia, phenotype_phenotype with Juvenile Rheumatoid Arthritis, phenotype_phenotype with Juvenile Rheumatoid Arthritis.", "label": "yes"}
{"original_question": "Can FOXOs modulate longevity?", "id": "converted_700", "sentence1": "Can FOXOs modulate longevity?", "sentence2": "Forkhead box O (FOXO Family Family) TRANSCRIPTION FACTOR have a conserved function in regulating metazoan lifespan., In contrast to FOXO1 gene, FOXO3A protein, human and Forkhead Box Protein O6 were specifically diminished in the Central Nervous System of HFD animal allergen extracts possibly contributing to the reduced lifespan observed in these animal allergen extracts., Interestingly, many target Proteins of AMP-Activated Protein Kinases are so-called longevity factors, e.g., Sirtuin 1, TP53 wt Allele, and FoxOs, which not only can increase the stress resistance and extend the lifespan of many Organism but also inhibit the inflammatory responses. , Components of anti-ageing and autophagy include Sirtuins and FoxOs., Since Sirts and FoxOs are reliable markers of longevity, the results appear to suggest that Longevinex induces longevity after prolonged feeding via induction of autophagy, while it converts Cessation of life signals into survival signals and provides cardioprotection within a relatively shorter period of time., Forkhead box O (FOXO Family Family) TRANSCRIPTION FACTOR are involved in various cellular processes, including cell proliferation, stress resistance, metabolism, and longevity, In this respect, members of the Mammals forkhead TRANSCRIPTION FACTOR of the O class (FoxOs) that include FOXO1 gene, FOXO3 wt Allele, Forkhead Box Protein O4 and Forkhead Box Protein O6 are increasingly being recognized as exciting prospects for multiple pathologies. These TRANSCRIPTION FACTOR govern development, proliferation, survival and longevity during multiple cellular environments that can involve oxidative stress. , Here we discuss the fascinating but complex role of FoxOs during cellular injury and oxidative stress, progenitor cell development, fertility, angiogenesis, cardiovascular function, cellular metabolism and Diabetes Mellitus, cell longevity, immune surveillance and Primary malignant neoplasm., Many longevity genes, e.g. FoxOs and Sirtuin 1, are inhibitors of NF-kappa B signaling. , Interestingly, several longevity genes such as Sirtuin 1, Mono-ADP-Ribosyltransferase Sirtuin-6, and FoxOs can clearly suppress NF-kappa B signaling and in this way delay the aging process and extend lifespan., Yet, FoxOs also can significantly affect normal cell survival and longevity, requiring new treatments for neoplastic growth to modulate novel pathways that integrate cell proliferation, metabolism, Inflammation and survival., These observations link FoxO function in Mammals systems with the evolutionarily conserved role of FoxO in promotion of stress resistance and longevity in lower phylogenetic systems. Furthermore, these findings have implications for aging in higher Organism and in malignant Stem cells biology, and suggest that FoxOs may play an important role in the maintenance and integrity of Stem cells compartments in a broad spectrum of Body tissue., Forkhead box O (FoxO) TRANSCRIPTION FACTOR are important downstream targets of the PI3K/Akt signaling pathway and crucial regulators of cell fate. This function of FoxOs relies on their ability to control diverse cellular functions, including proliferation, differentiation, apoptosis, DNA repair, defense against oxidative stress and ageing., This brief review focuses on the molecular mechanisms, cellular effects and resulting organismal phenotypes generated by differentially regulated FoxO Proteins and discusses our current understanding of the role of FoxOs in Disease and ageing processes., In this review, we focus on the several interactions of aging-associated signaling cascades regulated either by Sirtuins and FoxOs or NF-kappa B signaling pathways. We provide evidence that signaling via the longevity factors of FoxOs and Sirtuin 1 can inhibit NF-kappa B signaling and simultaneously protect against inflamm-aging process., In diverse species TRANSCRIPTION FACTOR belonging to the forkhead/winged helix box gene, group O (FOXO Family Family) subfamily have been found to be crucial in downstream suppression of the life-shortening effects of insulin/insulin-like growth factor-I receptor signalling pathways that, when upregulated, accelerate ageing by suppression of FOXO Family Family. , In Homo sapiens, FOXO3a, as well as FOXO1 and -4, and their downstream effectors, could hold the key to counteracting ageing and common diseases., FOXO Family Family TRANSCRIPTION FACTOR have important roles in metabolism, cellular proliferation, stress tolerance, and aging. [SEP]Relations: central nervous system has relations: anatomy_protein_present with FOXO4, anatomy_protein_present with FOXO4, anatomy_protein_present with FOXO1, anatomy_protein_present with FOXO1, anatomy_protein_present with FOXN3, anatomy_protein_present with FOXN3, anatomy_protein_present with FOXK2, anatomy_protein_present with FOXK2. transcription factor binding has relations: molfunc_protein with FOXC1, molfunc_protein with FOXC1.", "label": "yes"}
{"original_question": "Is phospholipid hydroperoxide glutathione peroxidase a selenoprotein?", "id": "converted_2846", "sentence1": "Is phospholipids hydroperoxide glutathione peroxidase a Selenoproteins?", "sentence2": "GLUTATHIONE PEROXIDASE (GPX1 gene) is the major Selenoproteins in most Body tissue in animal allergen extracts., The selenoenzyme GPX4 gene is essential for early embryogenesis and cell viability for its unique function to prevent phospholipids oxidation., the major Selenoproteins expressed by Germ Cells in the Testis, the phospholipids hydroperoxide glutathione peroxidase (PHGPx/GPx4) [SEP]Relations: GPX1 has relations: molfunc_protein with phospholipids-hydroperoxide glutathione peroxidase activity, molfunc_protein with phospholipids-hydroperoxide glutathione peroxidase activity. GPX4 has relations: molfunc_protein with phospholipids-hydroperoxide glutathione peroxidase activity, molfunc_protein with phospholipids-hydroperoxide glutathione peroxidase activity. glutathione peroxidase activity has relations: molfunc_protein with ALOX5AP, molfunc_protein with ALOX5AP, molfunc_protein with GSTP1, molfunc_protein with GSTP1, molfunc_protein with PTGES, molfunc_protein with PTGES.", "label": "yes"}
{"original_question": "Is apremilast effective for psoriatic arthritis?", "id": "converted_2231", "sentence1": "Is apremilast effective for Arthritis, Psoriatic?", "sentence2": "apremilast, an oral phosphodiesterase 4 inhibitor, in patients with Arthritis, Psoriatic and current Skin Specimen Source Code involvement: a phase III, randomised, controlled trial (PALACE 3)., OBJECTIVE: To evaluate apremilast treatment in patients with active Arthritis, Psoriatic, including current Skin Specimen Source Code involvement, despite prior therapy with conventional disease-modifying antirheumatic drugs and/or Biological Factors., CONCLUSIONS: apremilast demonstrated clinically meaningful improvements in Arthritis, Psoriatic and Psoriasis at week 16; sustained improvements were seen with continued treatment through 52 weeks. , apremilast: A Novel Drug for Treatment of Psoriasis and Psoriatic Arthritis., OBJECTIVE: To review the pharmacology, efficacy, and safety of apremilast and determine its role relative to other agents in the treatment of Psoriasis and Arthritis, Psoriatic., CONCLUSIONS: apremilast has a novel mechanism of action and is safe and effective for the management of Psoriasis and Arthritis, Psoriatic. ,  In particular, apremilast has been recently approved for the treatment of Psoriasis and Arthritis, Psoriatic., apremilast, an oral phosphodiesterase 4 inhibitor, has an acceptable safety profile and is effective for treatment of plaque Psoriasis and Arthritis, Psoriatic., As part of the National Institute for Health and Clinical Excellence (NICE) single technology appraisal (GROWTH CONTROL, Y-CHROMOSOME INFLUENCED) process, the manufacturer of apremilast was invited to submit evidence for its clinical and cost effectiveness for the treatment of active Arthritis, Psoriatic (Prostate-Specific Antigen) for whom disease-modifying anti-rheumatic drugs (DMARDs) have been inadequately effective, not tolerated or contraindicated., Psoriatic Arthritis Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active Arthritis, Psoriatic despite prior traditional disease-modifying antirheumatic Pharmacologic Substance (DMARD) and/or biologic therapy., In patients with Arthritis, Psoriatic, there are no clinical trials comparing apremilast with TNF alpha antagonists, and no interpretable trials of apremilast after failure of a TNF alpha antagonist., Psoriatic Arthritis Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active Arthritis, Psoriatic despite prior traditional disease-modifying antirheumatic Pharmacologic Substance (DMARD) and/or biologic therapy.In the 24-week, placebo-controlled phase of PALACE 1, patients (N=504) were randomised (1:1:1) to placebo, apremilast 20 mg twice a day (Twice a day) or apremilast 30 mg Twice a day, No imbalance in major adverse cardiac events, serious or Opportunistic Infections, Malignant Neoplasms or laboratory abnormalities was observed.apremilast was effective in the treatment of Arthritis, Psoriatic, improving signs and symptoms and physical function, apremilast is a novel oral PDE4 Enzyme Inhibitor [APC] capable of blocking leukocyte production of Recombinant Interleukin-12, interleukin-23 binding activity, TNF protein, human, INF- with subsequent suppression of NELFCD wt Allele and Th17-mediated immune responses, and proven clinical efficacy for Psoriasis as well as rheumatoid and Arthritis, Psoriatic.Cutaneous Lupus Erythematosus Disease Area and Severity Index (CLASI) showed a significant (P&lt;0.05) decrease after 85 days of treatment with apremilast 20 mg twice daily in 8 patients with active discoid lupus, The purpose of this study is to give an overview of the new treatments approved by the U.S. Food and Drug Administration (FDA) for use in Arthritis, Psoriatic (Prostate-Specific Antigen).FDA has approved three new drugs for Prostate-Specific Antigen: Certolizumab-pegol: a PEGylated Fc-free tumour necrosis factor inhibitor (TNFi); Ustekinumab Ab: an anti interleukin (IL)-12 and interleukin-23 binding activity mAb; and apremilast and oral phosphodiesterase 4 inhibitor., In all trials, the Pharmacologic Substance had an acceptable safety profile, with the most common adverse effects of Diarrhea, Nausea:Presence or Threshold:Point in time:^Patient:Ordinal, and Headache.apremilast has a novel mechanism of action and is safe and effective for the management of Psoriasis and Arthritis, Psoriatic., apremilast is a well-tolerated and effective phosphodiesterase type 4 inhibitor that is indicated for the treatment of moderate-to-severe plaque Psoriasis and Arthritis, Psoriatic., Psoriatic Arthritis Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active Arthritis, Psoriatic despite prior traditional disease-modifying antirheumatic Pharmacologic Substance (DMARD) and/or biologic therapy.In the 24-week, placebo-controlled phase of PALACE 1, patients (N=504) were randomised (1:1:1) to placebo, apremilast 20 mg twice a day (Twice a day) or apremilast 30 mg Twice a day., Newer drugs in the treatment armamentarium that have shown efficacy for both Psoriasis and Arthritis, Psoriatic consist of the anti-IL-17 agent, secukinumab, and a phosphodiesterase-4 inhibitor, apremilast., To review the pharmacology, efficacy, and safety of apremilast and determine its role relative to other agents in the treatment of Psoriasis and Arthritis, Psoriatic.A PubMed search (1946 to December 2015) using the terms apremilast and CC 10004 was conducted to identify relevant articles.In vitro or in vivo evaluations of apremilast published in the English language were eligible for inclusion., In patients with Arthritis, Psoriatic, there are no clinical trials comparing apremilast with TNF alpha antagonists, and no interpretable trials of apremilast after failure of a TNF alpha antagonist., No imbalance in major adverse cardiac events, serious or Opportunistic Infections, Malignant Neoplasms or laboratory abnormalities was observed.apremilast was effective in the treatment of Arthritis, Psoriatic, improving signs and symptoms and physical function., apremilast is a novel oral PDE4 Enzyme Inhibitor [APC] capable of blocking leukocyte production of Recombinant Interleukin-12, interleukin-23 binding activity, TNF protein, human, INF- with subsequent suppression of NELFCD wt Allele and Th17-mediated immune responses, and proven clinical efficacy for Psoriasis as well as rheumatoid and Arthritis, Psoriatic.Cutaneous Lupus Erythematosus Disease Area and Severity Index (CLASI) showed a significant (P<0.05) decrease after 85 days of treatment with apremilast 20 mg twice daily in 8 patients with active discoid lupus., apremilast was effective in the treatment of Arthritis, Psoriatic, improving signs and symptoms and physical function., apremilast has a novel mechanism of action and is safe and effective for the management of Psoriasis and Arthritis, Psoriatic., apremilast, an oral phosphodiesterase 4 inhibitor, demonstrated effectiveness (versus placebo) for treatment of active Arthritis, Psoriatic in the Arthritis, Psoriatic long-term assessment of clinical efficacy (PALACE) phase III clinical trial program., Psoriatic Arthritis Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active Arthritis, Psoriatic despite prior traditional disease-modifying antirheumatic Pharmacologic Substance (DMARD) and/or biologic therapy., apremilast: A Review in Psoriasis and Psoriatic Arthritis., Drug safety evaluation of apremilast for treating Arthritis, Psoriatic., apremilast for the treatment of Arthritis, Psoriatic., apremilast mechanism of action and application to Psoriasis and Arthritis, Psoriatic., apremilast: A Phosphodiesterase 4 Inhibitor for the Treatment of Psoriatic Arthritis.[SEP]Relations: apremilast has relations: drug_drug with Aprepitant, drug_drug with Aprepitant, drug_drug with Ampicillin, drug_drug with Ampicillin, drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Apramycin, drug_drug with Apramycin, drug_drug with Methadone, drug_drug with Methadone.", "label": "yes"}
{"original_question": "Is autism one of the characteristics of Moebius syndrome?", "id": "converted_732", "sentence1": "Is Autistic Disorder one of the characteristics of Mobius Syndrome 1?", "sentence2": "The diagnosis of Mobius Syndrome 1, a rare Congenital Disorders, is primarily based on congenital facial and abducent nerve palsy. Involvement of other Cranial Nerves is also common. Occasionally the V, X, Xi, and XII Cranial Nerves are involved, resulting in a difficulty to chew, swallow, and Cough (guaifenesin), which often leads to respiratory complications. Intellectual Disability and Autistic Disorder have been reported in some cases, Moebius sequence is a rare Congenital Disorders usually defined as a combination of facial weakness with impairment of ocular abduction. A strong association of Moebius sequence with Autistic Disorder spectrum disorders (ASDs) has been suggested in earlier studies with heterogenous age groups, Certain genetic syndromes are providing us with extremely valuable information about the role played by genetics in Autistic Disorder. This is the case of the following syndromes: Angelman Syndrome, Prader-Willi Syndrome, 15q11-q13 duplication, Fragile X Syndrome, fragile X premutation, deletion of chromosome 2q, 47, 47, XYY syndrome, Smith-Lemli-Opitz Syndrome, Apert syndrome, Gene Mutation in the ARX gene, Congenital muscular hypertrophy-cerebral syndrome, Smith-Magenis syndrome, Williams Syndrome, Rett Syndrome, NOONAN SYNDROME 3, Down Syndrome, Shprintzen syndrome, myotonic dystrophy, MYOTONIC DYSTROPHY 1, TUBEROUS SCLEROSIS 2 (disorder), Tabes Dorsalis, Timothy syndrome, 10p terminal deletion, COWDEN SYNDROME 5, 45,X/46,XY mosaicism, Myhre syndrome, SOTOS SYNDROME 1, VPS13B gene, Goldenhar Syndrome, Familial aplasia of the vermis, Lujan Fryns syndrome, Mobius Syndrome 1, Hypopigmentation disorder of Ito, Neurofibromatosis 2 type 1, CHARGE Syndrome and HEADD syndrome., Seventeen children and young adults with Mobius Syndrome 1 were examined with a view to finding symptoms of Autistic Disorder. Some 40% of the group showed all or many of the symptoms typical of autistic disorder, Fifty-nine cases with infantile Autistic Disorder/autistic disorder were subclassified according to associated medical condition (fragile-X, TUBEROUS SCLEROSIS 2 (disorder), Neurofibromatosis 2, hypo-melanosis of Ito, Mobius Syndrome 1, Rett Syndrome, and a 'new' syndrome associated with a Extra unidentified structurally abnormal chromosome (disorder))., Autism spectrum disorders in children and adolescents with Moebius sequence., Moebius sequence and Autistic Disorder spectrum disorders--less frequently associated than formerly thought., A strong association of Moebius sequence with Autistic Disorder spectrum disorders (ASDs) has been suggested in earlier studies with heterogenous age groups., Autistic behaviour in Mobius Syndrome 1., The high frequency of Autistic symptoms in Mobius Syndrome 1 might be a marked overrepresentation and could be suggestive of a common underlying neurobiological deficit at the brainstem level., Autism spectrum disorders in children and adolescents with Moebius sequence., Moebius sequence and Autistic Disorder spectrum disorders--less frequently associated than formerly thought., Autistic behaviour in Mobius Syndrome 1.[SEP]Relations: Mobius syndrome has relations: disease_disease with Moebius axonal neuropathy hypogonadism, disease_disease with Moebius axonal neuropathy hypogonadism. Autistic Disorder spectrum disorder has relations: disease_protein with MBD4, disease_protein with MBD4, disease_disease with Asperger syndrome, disease_disease with Asperger syndrome, disease_protein with ADA, disease_protein with ADA, disease_protein with MBD3, disease_protein with MBD3.", "label": "yes"}
{"original_question": "Is lenvatinib effective for thyroid cancer?", "id": "converted_1255", "sentence1": "Is lenvatinib effective for Malignant neoplasm of thyroid?", "sentence2": "New insights in the treatment of iodide ion I-131 refractory differentiated Thyroid carcinoma: to lenvatinib and beyond., However, even more impressive responses and progression-free survival benefits were seen in the phase III SELECT trial with lenvatinib, giving even higher hopes for the future management of what was considered just a decade ago an orphan disease. , sorafenib and lenvatinib, small-molecule multikinase inhibitors, were approved for the treatment of progressive, symptomatic, radioactive iodine refractory, advanced differentiated Malignant neoplasm of thyroid in 2013 and 2015, respectively., A phase 2 trial of lenvatinib (E 7080) in advanced, progressive, iodide ion I-131-refractory, differentiated Malignant neoplasm of thyroid: A clinical outcomes and biomarker assessment., CONCLUSIONS: In patients with and without prior exposure to VEGF therapy, the encouraging response rates, median time to response, and PFS for lenvatinib have prompted further investigation in a phase 3 trial. , Since 2011, four multikinase inhibitors (MKIs) have been approved by the US Food and Drug Administration for Malignant neoplasm of thyroid - cabozantinib and vandetanib for medullary Malignant neoplasm of thyroid and sorafenib and lenvatinib for differentiated Malignant neoplasm of thyroid. , Moreover, four of those investigational drugs, vandetanib, cabozantinib, sorafenib and lenvatinib, have reached a phase III clinical trial with favorable results in progression-free survival and overall survival in Medullary carcinoma of thyroid and differentiated Malignant epithelial neoplasm of thyroid., Since 2011, four multikinase inhibitors (MKIs) have been approved by the US Food and Drug Administration for Malignant neoplasm of thyroid - cabozantinib and vandetanib for medullary Malignant neoplasm of thyroid and sorafenib and lenvatinib for differentiated Malignant neoplasm of thyroid, BACKGROUND: lenvatinib, an oral inhibitor of vascular endothelial growth factor receptors 1, 2, and 3, Fibroblast Growth Factor Receptor 2 through 4, Platelet-Derived Growth Factor Receptor Beta, Human �, ret unit of radiation dose, and stem cell factor receptor activity, showed clinical activity in a phase 2 study involving patients with differentiated Malignant neoplasm of thyroid that was refractory to iodide ion I-131 (iodine-131).METHODS: In our phase 3, randomized, double-blind, multicenter study involving patients with progressive Malignant neoplasm of thyroid that was refractory to iodine-131, we randomly assigned 261 patients to receive lenvatinib (at a daily dose of 24 mg per day in 28-day cycles) and 131 patients to receive placebo. , Positive phase 1 results in Solid Neoplasm prompted a phase 2 trial in patients with advanced, iodide ion I-131-refractory, differentiated Malignant neoplasm of thyroid (RR-DTC).METHODS: Fifty-eight patients with RR-DTC who had disease progression during the previous 12 months received lenvatinib 24 mg once daily in 28-day cycles until disease progression, unmanageable Toxic effect, withdrawal, or Cessation of life. [SEP]Relations: lenvatinib has relations: drug_drug with Thyroid, porcine, drug_drug with Thyroid, porcine, drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Testosterone, drug_drug with Testosterone, drug_drug with Thyrotropin, drug_drug with Thyrotropin, drug_drug with Fostamatinib, drug_drug with Fostamatinib.", "label": "yes"}
{"original_question": "Does an antiphlogistic promotes inflammation?", "id": "converted_3856", "sentence1": "Does an antiphlogistic promotes Inflammation?", "sentence2": "The therapeutic effect of olipiphate was demonstrated for chronic Inflammation of advanced arthritis and concanavalin A-related acute edema. The best systemic effect was obtained with 50 mg/kg, symptomatic--100 mg/kg. Wound of skin treated with 5% olipiphate (26 + 2) healed faster than those treated with 2% solcoseryl (30 + 0.8) or in control (33 + 0.6). It was shown histologically that the proliferative and antiphlogistic effect of olipiphate involved no scars., Moreover, we observed an in vitro-inhibition of human neutrophil elastase, a Endopeptidases involved in the inflammatory process, by extracts and Fraction of from Hoplerythrinus unitaeniatus, which suggests additional mechanisms of antiphlogistic action., Blood serotonin in adrenalectomized Rattus norvegicus with inflammationadrenalectomized Rattus norvegicus 42 days and 3 months old with Inflammation after injection of phenylbutazone an increase of serotonin was observed, but in 18-month-old animal allergen extracts in which antiphlogistic action is highest a decrease of serotonin was observed., These results indicate that methotrexate is a nonsteroidal antiinflammatory agent, the antiphlogistic action of which is due to increased adenosine release at inflamed sites., The antiphlogistic ibuprofen incorporated in Liposomes caused a decrease of the inflammatory edema induced by carrageenan in the distal part of the rat's hind leg after both the Intramuscular Route of Drug Administration and percutaneous administration., Enhancement of the immunoreactivity inhibition caused by the drugs was not proportional to the increase in their antiphlogistic effects determined by the Selye model of Inflammation., Antiinflammatory agents: new series of N-substituted amino acids with complex Pyrimidine structures endowed with antiphlogistic activity.,  investigate whether the antiphlogistic ingredient may suppress the inflammatory response to ultraviolet (UV) irradiation, the SPF was determined in vivo. F, Antiphlogistics were found to enhance the Membrane Device viscosity both in control and under Inflammation., e in vivo determination of the SPF. Evidence of anti-inflammatory activity of the sunscreen antiphlogistics bisabolol and panthenol was also not apparent in the UV model over a time course of 48 h. Conlusion: The antiphlogistic ingredients panthenol and bisabolol incorporated in the tested sunscreen formula do not interfere with Erythema reddening and thus , nts was analyzed in vitro. To investigate whether the antiphlogistic ingredient may suppress the inflammatory response to ultraviolet (UV) irradiation, the , The aim of this study was to analyze the formation of the most relevant Inflammation mediators including Proteins and Lipids in human fibroblasts upon inflammatory stimulation and subsequent treatment with dexamethasone, a powerful antiphlogistic drug.[SEP]Relations: ibuprofen has relations: contraindication with inflammatory bowel disease, contraindication with inflammatory bowel disease, drug_effect with Nephrotic syndrome, drug_effect with Nephrotic syndrome, drug_effect with Inflammatory abnormality of the skin, drug_effect with Inflammatory abnormality of the skin. Methotrexate has relations: contraindication with inflammatory bowel disease, contraindication with inflammatory bowel disease. Adenosine has relations: drug_effect with Inflammatory abnormality of the skin, drug_effect with Inflammatory abnormality of the skin.", "label": "no"}
{"original_question": "Do lincRNAs play a role in human cancer?", "id": "converted_691", "sentence1": "Do lincRNAs play a role in Homo sapiens Primary malignant neoplasm?", "sentence2": "Long Intergenic Non-Protein Coding RNA H19 Imprinted Maternal Untranslated mRNA Imprinted Maternal Untranslated mRNA increases bladder Primary malignant neoplasm metastasis, These data suggest that upregulated H19 Imprinted Maternal Untranslated mRNA Imprinted Maternal Untranslated mRNA enhances bladder Primary malignant neoplasm metastasis by associating with EZH2 protein, Homo sapiens protein, Homo sapiens and inhibiting E-cad expression, lncRNA H19 Imprinted Maternal Untranslated mRNA Imprinted Maternal Untranslated mRNA is essential for Homo sapiens Specimen Source Codes - Specimen Source Codes - tumor growth, Previous reports have demonstrated that HOTAIR gene gene associates with chromatin modifications in cooperation with the Polycomb complex Polycomb Repressive Complex 2, and promotes Breast and colorectal Primary malignant neoplasm metastasis, although the clinical significance of HOTAIR gene gene expression in altretamine/cisplatin/cyclophosphamide protocol may not be as pronounced as that in Breast and Colorectal Carcinoma, the current study demonstrates that HOTAIR gene gene expression is associated with altretamine/cisplatin/cyclophosphamide protocol progression, warranting further studies., Long Intergenic Non-Protein Coding RNA HOTAIR gene gene is an independent prognostic marker for Nasopharyngeal carcinoma progression and survival, Long Intergenic Non-Protein Coding RNA influences radiosensitivity of colorectal carcinoma cell lines by regulating Cyclin D1 expression, Long Intergenic Non-Protein Coding RNA Urothelial Carcinoma associated 1 (UCA1 gene gene) promotes Homo sapiens bladder Primary malignant neoplasm cell proliferation, but the underlying mechanism remains unknown, UCA1 gene gene regulated cell cycle through Cyclic AMP-Responsive DNA-Binding Protein via PI3K-AKT dependent pathway in bladder Primary malignant neoplasm., Long Intergenic Non-Protein Coding RNA UCA1 gene gene regulated cell cycle distribution via Cyclic AMP-Responsive DNA-Binding Protein through PI3-K dependent pathway in bladder carcinoma cells, overexpression of Yiya promotes cell cycle progression at the G1/S transition, therefore identifying Yiya as a cell-cycle-associated long non-coding RNA, The long noncoding RNA HOTAIR gene gene has been reported as a poor prognostic biomarker in patients with Breast Primary malignant neoplasm. The aim of the present study is to examine the expression pattern of HOTAIR gene gene in Liver carcinoma (altretamine/cisplatin/cyclophosphamide protocol) and its clinical significance as well as its biological role in Specimen Source Codes - Specimen Source Codes - tumor progression, The high expression level of HOTAIR gene gene in altretamine/cisplatin/cyclophosphamide protocol could be a candidate biomarker for predicting Specimen Source Codes - Specimen Source Codes - tumor recurrence in altretamine/cisplatin/cyclophosphamide protocol patients who have undergone liver transplant therapy and might be a potential therapeutic target, Long Intergenic Non-Protein Coding RNA ANRIL is required for the Polycomb Repressive Complex 2 recruitment to and silencing of p15(INK4B) Specimen Source Codes - Specimen Source Codes - tumor suppressor gene, A 42 kb region on Homo sapiens chromosome 9p21 encodes for three distinct Tumor Suppressor Genes, p16(INK4A), p14(ARF) and p15(INK4B), and is altered in an estimated 30-40% of Homo sapiens Neoplasms, These results advance our understanding of the role of NPTN-IT1 gene as a regulator of Hypoxia, CTCAE signaling and offer new avenues for therapeutic intervention against Primary malignant neoplasm progression., Silencing MALAT1 gene gene is a potential novel therapeutic approach for this Primary malignant neoplasm.[SEP]Relations: Protein S Homo sapiens has relations: drug_drug with Linsidomine, drug_drug with Linsidomine, drug_drug with Ximelagatran, drug_drug with Ximelagatran, drug_drug with Melagatran, drug_drug with Melagatran, drug_drug with Vinblastine, drug_drug with Vinblastine, drug_drug with Letaxaban, drug_drug with Letaxaban.", "label": "yes"}
{"original_question": "Is TENS machine effective in pain?", "id": "converted_67", "sentence1": "Is Transcutaneous Electric Nerve Stimulation machine effective in pain?", "sentence2": "Transcutaneous electrical nerve stimulation is widely used in pain management but its effectiveness depends on the stimulation being targeted appropriately, hypoalgesic effects of transcutaneous electrical nerve stimulation upon experimentally induced ischaemic pain., The results of this study have provided evidence of the hypoalgesic effects of Transcutaneous Electric Nerve Stimulation upon experimental ischaemic pain which were found to be frequency specific with the lower frequency used here (4 Hz) demonstrating the only significant effect[SEP]Relations: negative regulation of spontaneous neurotransmitter secretion has relations: bioprocess_protein with PRKN, bioprocess_protein with PRKN, bioprocess_protein with PPP1R9A, bioprocess_protein with PPP1R9A, bioprocess_bioprocess with regulation of spontaneous neurotransmitter secretion, bioprocess_bioprocess with regulation of spontaneous neurotransmitter secretion, bioprocess_bioprocess with negative regulation of neurotransmitter secretion, bioprocess_bioprocess with negative regulation of neurotransmitter secretion.", "label": "yes"}
{"original_question": "Is lambrolizumab effective for treatment of patients with melanoma ?", "id": "converted_375", "sentence1": "Is pembrolizumab effective for treatment of patients with Melanocytic neoplasm ?", "sentence2": "However, through parallel efforts that have showcased the efficacy of small-molecule BRAF protein, human protein, human and MAPK-ERK Kinases (Mitogen-Activated Protein Kinase Kinases) inhibitors, as well as the Immune Checkpoint Inhibitors, namely ipilimumab and the anti-PD1/PDL1 Antibodies, in vitro diagnostic (pembrolizumab, nivolumab, MPDL3280), an opportunity exists to transform the treatment of Melanocytic neoplasm specifically and Primary malignant neoplasm generally by exploring rational combinations of molecularly targeted therapies, immunotherapies, and molecular targeted therapies with immunotherapies. , Programmed death-1 receptor (PDCD1 wt Allele)/its ligand (CD274 wt Allele) Antibodies, in vitro diagnostic have changed the landscape in oncology in 2013. The most mature results have been obtained in advanced Melanocytic neoplasm patients. , Merck's pembrolizumab (MK-3475) monoclonal antibody received \"Breakthrough Therapy\" designation from the U.S. Food and Drug Administration in April for treating patients with advanced Melanocytic neoplasm., The programmed death 1 (PDCD1 wt Allele) receptor is a negative regulator of Effector T-Lymphocyte mechanisms that limits immune responses against Primary malignant neoplasm. We tested the anti-PDCD1 wt Allele antibody pembrolizumab (previously known as MK-3475) in patients with advanced Melanocytic neoplasm. , In patients with advanced Melanocytic neoplasm, including those who had had disease progression while they had been receiving ipilimumab, treatment with pembrolizumab resulted in a high rate of sustained tumor regression, with mainly grade 1 or 2 Toxic effect effects. , Because of all these reasons PDCD1 wt Allele/CD274 wt Allele Antibodies, in vitro diagnostic are considered 'Pharmacologic Substance of the year'.[SEP]Relations: Pembrolizumab has relations: drug_drug with Catumaxomab, drug_drug with Catumaxomab, drug_drug with Basiliximab, drug_drug with Basiliximab, drug_drug with Golimumab, drug_drug with Golimumab, drug_drug with Afelimomab, drug_drug with Afelimomab, drug_drug with Ibalizumab, drug_drug with Ibalizumab.", "label": "yes"}
{"original_question": "Is there evidence that tomato juice lowers cholesterol levels?", "id": "converted_418", "sentence1": "Is there evidence that Lycopersicon esculentum juice lowers cholesterol levels?", "sentence2": "The hypocholesterolemic effect of Lycopersicon esculentum juice has been investigated in an intervention study with Rattus norvegicus, along with the possible inhibition effect of bioactive Lycopersicon esculentum compounds binding to the HMGCR protein, human protein, human Enzyme [APC]., The molecular modelling showed that components of Lycopersicon esculentum can bind to the Active Site of the Enzyme [APC] and compete with the ligand HMGCoA. Lycopene, from Lycopersicon esculentum juice, accumulates in the Abdomen>Liver and can inhibit the activity of the rate-limiting Enzyme [APC] of cholesterol biosynthesis, HMGCR protein, human protein, human.,  Juice consumption significantly improved resistance of Low-Density Lipoproteins+VLDL-C to Cu(2+)-mediated oxidation (P = 0.039), High Density Lipoproteins-C (47.3 ± 15.8 to 51.7 ± 14.8 mg/dL, P<0.001), and the ratio of total-C/High Density Lipoproteins-C (4.25 ± 1.59 to 3.63 ± 1.16, P<0.001) at 8 wk., RESULTS: Intervention with the enriched juice had no effect on the lipid profile, and serum levels of Triglycerides and cholesterol (total, Low-Density Lipoproteins, and High Density Lipoproteins) remained unchanged. , Women consuming ≥10 compared with<1.5 servings/wk of Lycopersicon esculentum-based food products had significant but clinically modest improvements in total cholesterol (CD55 wt Allele) (5.38 vs. 5.51 mmol/L; P = 0.029), the CD55 wt Allele:High Density Lipoproteins cholesterol ratio (4.08 vs. 4.22; P = 0.046), and Glycosylated hemoglobin A (5.02 vs. 5.13%; P<0.001) in multivariable models. Considering clinical cutpoints, women consuming ≥10 compared with<1.5 servings/wk were 31% (95% CI = 6%, 50%), 40% (95% CI = 13%, 59%), and 66% (95% CI = 20%, 86%) less likely to have elevated CD55 wt Allele (≥6.21 mmol/L), Low-Density Lipoproteins cholesterol (≥4.14 mmol/L), and Glycosylated hemoglobin A (≥6%), respectively. , In conclusion, women consuming ≥10 compared with<1.5 servings/wk of Lycopersicon esculentum-based food products had clinically modest but significant improvements in CD55 wt Allele, the CD55 wt Allele:High Density Lipoproteins cholesterol ratio, and Glycosylated hemoglobin A but not other coronary biomarkers., Tomato juice decreases Low-Density Lipoproteins cholesterol levels and increases Low-Density Lipoproteins resistance to oxidation., Total cholesterol concentration was reduced by 5.9 (sd 10) % (P = 0.002) and Low-Density Lipoproteins cholesterol concentration by 12.9 (sd 17.0) % (P = 0.0002) with the high Lycopersicon esculentum diet compared to the low Lycopersicon esculentum diet., In conclusion, a high dietary intake of Lycopersicon esculentum products had atheroprotective effects, it significantly reduced Low-Density Lipoproteins cholesterol levels, and increased Low-Density Lipoproteins resistance to oxidation in healthy normocholesterolaemic adults., Total, Low-Density Lipoproteins and High Density Lipoproteins cholesterol were significantly lower in the intervention group after the intake of Lycopersicon esculentum juice, Total cholesterol concentration was reduced by 5.9 (sd 10) % (P = 0.002) and Low-Density Lipoproteins cholesterol concentration by 12.9 (sd 17.0) % (P = 0.0002) with the high Lycopersicon esculentum diet compared to the low Lycopersicon esculentum diet. [SEP]Relations: Cholesterol has relations: drug_drug with Folic acid, drug_drug with Folic acid, drug_drug with Riluzole, drug_drug with Riluzole, drug_drug with Testosterone cypionate, drug_drug with Testosterone cypionate, drug_drug with Topotecan, drug_drug with Topotecan, drug_drug with Rimegepant, drug_drug with Rimegepant.", "label": "yes"}
{"original_question": "Is there any role for long noncoding RNAs in adipogenesis?", "id": "converted_1489", "sentence1": "Is there any role for long noncoding RNAs in adipogenesis?", "sentence2": "Long noncoding RNAs regulate adipogenesis., Here we profiled the transcriptome of primary brown and Adipocytes, White, preadipocytes, and cultured adipocytes and identified 175 lncRNAs that are specifically regulated during adipogenesis. Many lncRNAs are adipose-enriched, strongly induced during adipogenesis, and bound at their Promoter by key TRANSCRIPTION FACTOR such as Peroxisome Proliferator-Activated Receptors (PPARγ) and CCAAT/enhancer-binding protein α (CEBPα). RNAi-mediated loss of function screens identified functional lncRNAs with varying impact on adipogenesis. Collectively, we have identified numerous lncRNAs that are functionally required for proper adipogenesis., Here we profiled the transcriptome of primary brown and Adipocytes, White, preadipocytes, and cultured adipocytes and identified 175 lncRNAs that are specifically regulated during adipogenesis. Many lncRNAs are adipose-enriched, strongly induced during adipogenesis, and bound at their Promoter by key TRANSCRIPTION FACTOR such as Peroxisome Proliferator-Activated Receptors (PPARγ) and CCAAT/enhancer-binding protein α (CEBPα). [SEP]Relations: transcription factor binding has relations: molfunc_protein with EPAS1, molfunc_protein with EPAS1, molfunc_protein with AIP, molfunc_protein with AIP, molfunc_protein with PPARA, molfunc_protein with PPARA, molfunc_protein with SRY, molfunc_protein with SRY, molfunc_protein with HMGA2, molfunc_protein with HMGA2.", "label": "yes"}
{"original_question": "Is Meis1 implicated in microphthalmia?", "id": "converted_2008", "sentence1": "Is Homeobox Protein Meis1, Human implicated in Microphthalmos?", "sentence2": "Homeobox Protein Homeobox Protein Meis1, Human, Human coordinates a network of genes implicated in Eye Specimen Source Code development and Microphthalmos., Here we show that haploinsufficiency of Homeobox Protein Homeobox Protein Meis1, Human, Human, which encodes a TRANSCRIPTION FACTOR with evolutionarily conserved expression in the Trunk of embryo, Head>Brain and sensory organs, including the Eye Specimen Source Code, causes microphthalmic traits and Visual Impairment in adult CASP14 gene., We propose that Homeobox Protein Homeobox Protein Meis1, Human, Human is at the core of a genetic network implicated in Eye Specimen Source Code patterning/Microphthalmos, and represents an additional candidate for syndromic cases of these ocular malformations., We propose that Homeobox Protein Homeobox Protein Meis1, Human, Human is at the core of a genetic network implicated in Eye Specimen Source Code patterning/Microphthalmos, and represents an additional candidate for syndromic cases of these ocular malformations., In the Eye Specimen Source Code primordium, Homeobox Protein Homeobox Protein Meis1, Human, Human coordinates, in a dose-dependent manner, retinal proliferation and differentiation by regulating genes responsible for Homo sapiens Microphthalmos and components of the Notch signaling pathway., Homeobox Protein Homeobox Protein Meis1, Human, Human coordinates a network of genes implicated in Eye Specimen Source Code development and Microphthalmos, We propose that Homeobox Protein Homeobox Protein Meis1, Human, Human is at the core of a genetic network implicated in Eye Specimen Source Code patterning/Microphthalmos, and represents an additional candidate for syndromic cases of these ocular malformations. <CopyrightInformation>© 2015, In the Eye Specimen Source Code primordium, Homeobox Protein Homeobox Protein Meis1, Human, Human coordinates, in a dose-dependent manner, retinal proliferation and differentiation by regulating genes responsible for Homo sapiens Microphthalmos and components of the Notch signaling pathway, We propose that Homeobox Protein Homeobox Protein Meis1, Human, Human is at the core of a genetic network implicated in Eye Specimen Source Code patterning/Microphthalmos, and represents an additional candidate for syndromic cases of these ocular malformations. <CopyrightInformation>© 2015., In the Eye Specimen Source Code primordium, Homeobox Protein Homeobox Protein Meis1, Human, Human coordinates, in a dose-dependent manner, retinal proliferation and differentiation by regulating genes responsible for Homo sapiens Microphthalmos and components of the Notch signaling pathway., Homeobox Protein Homeobox Protein Meis1, Human, Human coordinates a network of genes implicated in Eye Specimen Source Code development and Microphthalmos.[SEP]Relations: Microphthalmos has relations: disease_protein with HMX1, disease_protein with HMX1, disease_protein with TENM3, disease_protein with TENM3, disease_protein with RBP4, disease_protein with RBP4, disease_protein with CRB1, disease_protein with CRB1, disease_protein with BEST1, disease_protein with BEST1.", "label": "yes"}
{"original_question": "Has ORMD-0801 been tested in patients?", "id": "converted_3710", "sentence1": "Has ORMD-0801 been tested in patients?", "sentence2": "Glucose-reducing effect of the ORMD-0801 oral Therapeutic Insulin preparation in patients with uncontrolled type 1 diabetes: a pilot study., In efforts to provide patients with a more compliable treatment method, Oramed Pharmacologic Substance tested the capacity of its oral Therapeutic Insulin capsule (ORMD-0801, 8 mg Therapeutic Insulin) in addressing this resistant clinical state.[SEP]", "label": "yes"}
{"original_question": "Can mutations in Calmodulin cause ventricular fibrillation?", "id": "converted_742", "sentence1": "Can mutations in Calmodulin cause Ventricular Fibrillation by ECG Finding?", "sentence2": "We characterized a family presenting with a history of Ventricular Fibrillation by ECG Finding (Ventricular Fibrillation, Paroxysmal Familial, 1) and Sudden death without ECG or echocardiographic abnormalities at rest. Two siblings died suddenly at the ages of 9 and 10 years, and another two were resuscitated from out-of-hospital cardiac arrest with documented Ventricular Fibrillation, Paroxysmal Familial, 1 at age 10 and 16, respectively. Exome sequencing identified a missense Mutation Abnormality affecting a highly conserved residue (p.Phe90Leu) in the Calmodulin 1 gene encoding calmodulin. This Mutation Abnormality was also carried by one of the sibs who died suddenly, for whom DNA was available. The Mutation Abnormality was present in the mother and in an sibling, both asymptomatic but displaying a marginally prolonged QT-interval during exercise. CONCLUSIONS: We identified a Mutation Abnormality in Calmodulin 1 underlying IVF manifesting in childhood and adolescence. The causality of the Mutation Abnormality is supported by previous studies demonstrating that Phe90 mediates the direct interaction of cyclophosphamide/doxorubicin/methotrexate protocol with target peptides, Here we show that calmodulin (cyclophosphamide/doxorubicin/methotrexate protocol), a ubiquitous Ca2+-sensing protein, binds to the carboxy-terminal 'IQ' domain of the Homo sapiens cardiac Na channel (hH1) in a Ca2+-dependent manner. This binding interaction significantly enhances slow inactivation-a channel-gating process linked to life-threatening idiopathic ventricular arrhythmias. Gene Mutation targeted to the IQ domain disrupted cyclophosphamide/doxorubicin/methotrexate protocol binding and Removed Ca2+/cyclophosphamide/doxorubicin/methotrexate protocol-dependent slow inactivation, whereas the gating effects of Ca2+/cyclophosphamide/doxorubicin/methotrexate protocol were restored by Protoplasm application of a Peptides modelled after the IQ domain. [SEP]Relations: Ventricular Fibrillation by ECG Finding (disease) has relations: disease_protein with INS, disease_protein with INS, disease_protein with PLAU, disease_protein with PLAU, disease_protein with EPO, disease_protein with EPO, disease_protein with SCN10A, disease_protein with SCN10A, disease_disease with cardiac rhythm disease, disease_disease with cardiac rhythm disease.", "label": "yes"}
{"original_question": "Does erenumab target the calcitonin gene-related peptide?", "id": "converted_3970", "sentence1": "Does erenumab target the Calcitonin Precursor, human?", "sentence2": "Four Monoclonal Antibodies have been developed: one targeting the CALCRL gene (erenumab) and three targeting the Calcitonin Precursor, human (eptinezumab, fremanezumab, and galcanezumab).[SEP]Relations: CALCRL has relations: drug_protein with Erenumab, drug_protein with Erenumab, molfunc_protein with CALCRL gene activity, molfunc_protein with CALCRL gene activity, bioprocess_protein with CALCRL gene signaling pathway, bioprocess_protein with CALCRL gene signaling pathway. Human calcitonin has relations: drug_protein with ANPEP, drug_protein with ANPEP, drug_effect with Erythema, drug_effect with Erythema.", "label": "no"}
{"original_question": "Can pazopanib be used for treatment von Hippel-Lindau disease?", "id": "converted_3048", "sentence1": "Can pazopanib be used for treatment Von Hippel-Lindau Syndrome?", "sentence2": "Variable response of Clinical Nurse Specialists hemangioblastomas to pazopanib in a single patient with Von Hippel-Lindau Syndrome: Case report., Treatment of Renal Cell Carcinoma with Protein-tyrosine kinase inhibitor (disposition) (TKIs) such as pazopanib is now first line therapy, but their effect on VHL-associated Clinical Nurse Specialists Hemoglobin, Sickle remains unknown. We report the use of pazopanib in a patient with VHL disease for treatment of Conventional (Clear Cell) Renal Cell Carcinoma who also harbored multiple Clinical Nurse Specialists Hemoglobin, Sickle. , pazopanib in patients with Von Hippel-Lindau Syndrome: a single-arm, single-centre, phase 2 trial., INTERPRETATION: pazopanib was associated with encouraging preliminary activity in Von Hippel-Lindau Syndrome, with a side-effect profile consistent with that seen in previous trials. pazopanib could be considered as a treatment choice for patients with Von Hippel-Lindau Syndrome and growing Lesion, or to reduce the size of unresectable Lesion in these patients. , Recurrent multiple Clinical Nurse Specialists hemangioblastomas with VHL disease treated with pazopanib: a case report and literature review.,  Here, we report a 37-year-old woman's case with recurrent and rapidly progressive VHL-associated hemangioblastomas, causing severe Disability:Type:Pt:^Patient:Nom. She was treated 24 months with pazopanib, a multityrosine kinase inhibitor (TKI) targeting Vascular Endothelial Growth Factor A and PDGF-β pathways. , pazopanib therapy for Cerebellar hemangioblastoma in Von Hippel-Lindau Syndrome: case report., Here we provide the first report demonstrating clinical and radiological anti-tumor response using pazopanib, a small molecule multi-receptor tyrosine kinase inhibitor, in a patient with treatment-refractory VHL-associated Clinical Nurse Specialists hemangioblastoma. , pazopanib could be considered as a treatment choice for patients with Von Hippel-Lindau Syndrome and growing Lesion, or to reduce the size of unresectable Lesion in these patients., METHODS\nIn this non-randomised, single-centre, open-label, phase 2 trial, adult patients with clinical manifestations of Von Hippel-Lindau Syndrome were recruited from the University of Texas MD Anderson Cancer Center (Houston, TX, USA) and were treated with pazopanib (800 mg orally daily) for 24 weeks, with an option to continue treatment if desired by the patient and treating physician., We aimed to assess the activity and safety of pazopanib in patients with Von Hippel-Lindau Syndrome., INTERPRETATION\npazopanib was associated with encouraging preliminary activity in Von Hippel-Lindau Syndrome, with a side-effect profile consistent with that seen in previous trials., FINDINGS\nBetween Jan 18, 2012, and Aug 10, 2016, we screened 37 patients with genetically confirmed or clinical features consistent with Von Hippel-Lindau Syndrome, of whom 31 eligible patients were treated with pazopanib., pazopanib therapy for Cerebellar hemangioblastoma in Von Hippel-Lindau Syndrome: case report.von Hippel-Lindau (VHL) disease is a genetically acquired multisystem tumor syndrome of the Viscera and CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Clinical Nurse Specialists). , Recurrent multiple Clinical Nurse Specialists hemangioblastomas with VHL disease treated with pazopanib: a case report and literature review.Hemangioblastoma is a rare benign neoplasm, accounting for less than 2% of all primitive Brain Neoplasms. , We aimed to assess the activity and safety of pazopanib in patients with Von Hippel-Lindau Syndrome.<br><b>METHODS</b>: In this non-randomised, single-centre, open-label, phase 2 trial, adult patients with clinical manifestations of Von Hippel-Lindau Syndrome were recruited from the University of Texas MD Anderson Cancer Center (Houston, TX, USA) and were treated with pazopanib (800 mg orally daily) for 24 weeks, with an option to continue treatment if desired by the patient and treating physician., This study is registered with ClinicalTrials.gov, number NCT01436227, and is closed to accrual.<br><b>FINDINGS</b>: Between Jan 18, 2012, and Aug 10, 2016, we screened 37 patients with genetically confirmed or clinical features consistent with Von Hippel-Lindau Syndrome, of whom 31 eligible patients were treated with pazopanib., Treatment-related serious adverse events included one case each of Appendicitis and Gastritis and one patient had a fatal Clinical Nurse Specialists bleed.<br><b>INTERPRETATION</b>: pazopanib was associated with encouraging preliminary activity in Von Hippel-Lindau Syndrome, with a side-effect profile consistent with that seen in previous trials., pazopanib could be considered as a treatment choice for patients with Von Hippel-Lindau Syndrome and growing Lesion, or to reduce the size of unresectable Lesion in these patients., We aimed to assess the activity and safety of pazopanib in patients with Von Hippel-Lindau Syndrome., In this non-randomised, single-centre, open-label, phase 2 trial, adult patients with clinical manifestations of Von Hippel-Lindau Syndrome were recruited from the University of Texas MD Anderson Cancer Center (Houston, TX, USA) and were treated with pazopanib (800 mg orally daily) for 24 weeks, with an option to continue treatment if desired by the patient and treating physician., pazopanib was associated with encouraging preliminary activity in Von Hippel-Lindau Syndrome, with a side-effect profile consistent with that seen in previous trials., pazopanib could be considered as a treatment choice for patients with Von Hippel-Lindau Syndrome and growing Lesion, or to reduce the size of unresectable Lesion in these patients., Between Jan 18, 2012, and Aug 10, 2016, we screened 37 patients with genetically confirmed or clinical features consistent with Von Hippel-Lindau Syndrome, of whom 31 eligible patients were treated with pazopanib.[SEP]Relations: pazopanib has relations: drug_drug with Lapatinib, drug_drug with Lapatinib, drug_drug with Verapamil, drug_drug with Verapamil, drug_drug with Alemtuzumab, drug_drug with Alemtuzumab, drug_drug with Alpelisib, drug_drug with Alpelisib, drug_drug with Galantamine, drug_drug with Galantamine.", "label": "yes"}
{"original_question": "Is there a package in R/bioconductor for classification of alternative splicing?", "id": "converted_362", "sentence1": "Is there a package in R/bioconductor for classification of alternative splicing?", "sentence2": "Splicer Device: an R package for classification of alternative splicing and prediction of coding potential from Whole Transcriptome Sequencing data., Recent software improvements in full-length RNA Transcript deconvolution prompted us to develop Splicer Device, an R package for classification of alternative splicing and prediction of coding potential., Splicer Device uses the full-length RNA Transcript output from Whole Transcriptome Sequencing assemblers to detect single or multiple exon skipping, alternative donor and acceptor sites, intron retention, alternative first or last exon usage, and mutually exclusive exon events. For each of these events Splicer Device also annotates the genomic coordinates of the differentially spliced elements, facilitating downstream sequence analysis. For each RNA Transcript isoform fraction values are calculated to identify RNA Transcript switching between conditions. Lastly, Splicer Device predicts the coding potential, as well as the potential nonsense mediated decay (NMD) sensitivity of each RNA Transcript., Recent software improvements in full-length RNA Transcript deconvolution prompted us to develop Splicer Device, an R package for classification of alternative splicing and prediction of coding potential., Recent software improvements in full-length RNA Transcript deconvolution prompted us to develop Splicer Device, an R package for classification of alternative splicing and prediction of coding potential. , Recent software improvements in full-length RNA Transcript deconvolution prompted us to develop Splicer Device, an R package for classification of alternative splicing and prediction of coding potential.[SEP]Relations: rRNA transcription has relations: bioprocess_bioprocess with 5S class rRNA transcription by RNA polymerase III, bioprocess_bioprocess with 5S class rRNA transcription by RNA polymerase III, bioprocess_protein with SIRT7, bioprocess_protein with SIRT7, bioprocess_protein with NPM3, bioprocess_protein with NPM3, bioprocess_protein with ANG, bioprocess_protein with ANG, bioprocess_protein with TP53, bioprocess_protein with TP53.", "label": "yes"}
{"original_question": "Is bapineuzumab effective for treatment of patients with Alzheimer's disease?", "id": "converted_367", "sentence1": "Is bapineuzumab effective for treatment of patients with ALZHEIMER DISEASE, FAMILIAL, 1?", "sentence2": " Thus far, results from two large phase 3 trial programs with bapineuzumab and solaneuzumab, respectively, have brought rather disappointing results., More recently, in phase III studies, bapineuzumab has been discontinued because it did not prove clinically effective (despite its significant effect on biomarkers), while solaneuzumab has been found effective in slowing cytarabine/daunorubicin protocol progression. , Passive immunotherapy with Monoclonal Antibodies (mAbs) against Aβ is in late clinical development but recently the two most advanced mAbs, bapineuzumab and solanezumab, targeting an N-terminal or central epitope, respectively, failed to meet their target of improving or stabilizing cognition and function., The marginal effects observed in recent clinical studies of solanezumab, targeting monomeric Aβ, and bapineuzumab, targeting amyloid plaques, prompted expert comments that Pharmacologic Substance discovery efforts in ALZHEIMER DISEASE, FAMILIAL, 1 should focus on soluble forms of Aβ rather than fibrillar Aβ deposits found in amyloid plaques., Phase III trials showed that bapineuzumab failed to improve cognitive and functional performances in cytarabine/daunorubicin protocol patients, and was associated with a high incidence of amyloid-related imaging abnormalities (NRG1 wt Allele)., Clinical trials on various drugs, including AN-1792, bapineuzumab, and solanezumab, have been carried out; however, all trials have failed to demonstrate apparent clinical benefits. , Despite the alteration in biochemical composition, all 3 immunized subjects exhibited continued cognitive decline., Despite negative topline phase 3 clinical trial results for bapineuzumab and solanezumab in mild to moderate cytarabine/daunorubicin protocol, findings from these trials and recent advances suggest renewed optimism for anti-amyloid therapies. , The lack of progress in the development of disease-modifying therapy in ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) was highlighted recently by the cessation of a phase 3 clinical trial studying the effects of bapineuzumab on mild to moderate disease. No treatment benefit was apparent, whereas several serious side effects occurred more commonly in the treatment group compared to placebo. , Clinical studies using the N-terminal-directed anti-Aβ antibody bapineuzumab have demonstrated reduced Head>Brain PET-Pittsburg-B signals, suggesting the reduction of Aβ plaques, and reduced levels of total and phosphorylated tau protein in the Cerebrospinal Fluid of treated cytarabine/daunorubicin protocol patients. Preclinical studies using 3D6 (the murine form of bapineuzumab) have demonstrated resolution of Aβ plaque and vascular burdens, neuritic dystrophy, and preservation of synaptic density in the transgenic APP mouse models., The clinical results of the initial studies with bapineuzumab were equivocal in terms of cognitive benefit. The occurrence of vasogenic Edema:Finding:Point in time:^Patient:Ordinal after bapineuzumab, and more rarely Head>Brain Microhemorrhages (especially in Apo E ε4 carriers), has raised concerns on the safety of these Antibodies, in vitro diagnostic directed against the N-terminus of the Aβ peptide. ,  The most advanced of these immunological approaches is bapineuzumab, composed of humanized anti-Aβ Monoclonal Antibodies, that has been tested in two Phase II trials, demonstrating to reduce Aβ burden in the Head>Brain of cytarabine/daunorubicin protocol patients. However, the preliminary cognitive efficacy of bapineuzumab appears uncertain. The occurrence of vasogenic Edema:Finding:Point in time:^Patient:Ordinal, especially in Apolipoprotein E carriers, may limit its clinical use and have led to abandon the highest dose of the Pharmacologic Substance (2 mg/kg)., However, the preliminary cognitive efficacy of bapineuzumab, a humanized anti-Aβ monoclonal antibody, appears uncertain. Moreover, the occurrence of vasogenic Edema:Finding:Point in time:^Patient:Ordinal and, more rarely, Head>Brain Microhemorrhages, especially in apolipoprotein E ϵ4 carriers, have led to abandoning of the highest dose of the Pharmacologic Substance. , However, the preliminary equivocal cognitive results obtained with bapineuzumab as well as the detrimental cognitive effects observed with Semagacestat, a potent γ-secretase inhibitor, raise the possibility that targeting Aβ may not be clinically efficacious in cytarabine/daunorubicin protocol. , The patient received four bapineuzumab infusions over a 39 week period. During the course of this treatment, there was no remarkable change in No No cognitive impairment as determined by MMSE scores. Forty-eight days after the fourth bapineuzumab infusion was given, MRI revealed that the patient had developed Infarction, Lacunar and possible vasogenic Edema:Finding:Point in time:^Patient:Ordinal, probably related to immunotherapy, but a subsequent MRI scan 38 days later demonstrated resolution of vasogenic Edema:Finding:Point in time:^Patient:Ordinal. The patient expired due to Acute congestive heart failure complicated by progressive cytarabine/daunorubicin protocol and cerebrovascular accident 378 days after the first bapineuzumab infusion and 107 days after the end of therapy. Neuropathological and biochemical analysis did not produce evidence of lasting plaque regression or clearance of Aβ due to immunotherapy., These results suggest that, in this particular case, bapineuzumab immunotherapy neither resulted in detectable clearance of amyloid plaques nor prevented further No No cognitive impairment., bapineuzumab has been shown to reduce Aβ burden in the Head>Brain of cytarabine/daunorubicin protocol patients. However, its preliminary cognitive efficacy appears uncertain, particularly in ApoE ε4 carriers, and vasogenic Edema:Finding:Point in time:^Patient:Ordinal may limit its clinical use. , bapineuzumab appears capable of reducing the cerebral beta-amyloid peptide burden in patients with ALZHEIMER DISEASE, FAMILIAL, 1. However, particularly in APOE 4 carriers, its ability to slow disease progression remains uncertain, and vasogenic Edema:Finding:Point in time:^Patient:Ordinal - a Dose-Limiting and potentially severe adverse reaction - may limit its clinical applicability., The first is a phase 2 study of passive immunotherapy with bapineuzumab, a humanized anti-APP wt Allele monoclonal antibody directed against the N-terminus of APP wt Allele. This trial showed no differences within dose cohorts on the primary efficacy analysis. Exploratory analyses showed potential treatment differences on cognitive and functional endpoints in study completers and apolipoprotein E epsilon4 noncarriers. A safety concern was the occurrence of reversible vasogenic Edema:Finding:Point in time:^Patient:Ordinal. , The first passive immunotherapy trial with bapineuzumab, a Antibodies, Monoclonal, Humanized against the end terminus of APP wt Allele, also encountered some dose dependent adverse events during the Phase II portion of the study, vasogenic Edema:Finding:Point in time:^Patient:Ordinal in 12 cases, which were significantly over represented in ApoE4 carriers.[SEP]Relations: bapineuzumab has relations: drug_drug with Abituzumab, drug_drug with Abituzumab, drug_drug with Alemtuzumab, drug_drug with Alemtuzumab, drug_drug with Olaratumab, drug_drug with Olaratumab, drug_drug with Fasinumab, drug_drug with Fasinumab, drug_drug with Adalimumab, drug_drug with Adalimumab.", "label": "no"}
{"original_question": "Has the protein GFP been used in transgenesis for live protein imaging?", "id": "converted_1237", "sentence1": "Has the protein GFP been used in transgenesis for live protein imaging?", "sentence2": "we review recent advancement in the functional studies of the three different GnRH neuron systems, mainly focusing on the electrophysiological analysis of the GnRH-Green Fluorescent Proteins (GFP) Animals, Transgenic., founders were found to be transgenic for GFP., GFP expression was detected in a wide range of Mus tissues, Transgenic Xenopus laevis for live imaging in \"U\" lymphocyte and developmental biology., The stable transgenesis of Genes encoding functional or spatially localized proteins, fused to fluorescent proteins such as Green Fluorescent Proteins (GFP) or red fluorescent protein (Zinc-Finger Protein Zinc-Finger Protein RFP), is an extremely important research tool in \"U\" lymphocyte and developmental biology., GFP-Animals, Transgenic for in vivo imaging: rats, Family Leporidae (organism), and pigs., We have further extended the techniques of genetic engineering to rats, Family Leporidae (organism), and pigs, and have created corresponding GFP-Animals, Transgenic., The results revealed that the 3.6-GFP Animals, Transgenic provide a unique model for direct analysis of Cells and molecular mechanisms of Dental Pulp repair and tertiary dentinogenesis in vivo., Long-term effects of PERV-specific RNA interference in transgenic pigs., Green Fluorescent Proteins (GFP) as reporter of the vector system were consistently expressed in Animals, Transgenic., The ability to specify the expression levels of exogenous Genes inserted in the Genome of Animals, Transgenic is critical for the success of a wide variety of experimental manipulations. , Welfare assessment in transgenic pigs expressing Green Fluorescent Proteins (GFP)., Animals, Transgenic expressing GFP with wildtype animal allergen extracts along various stages of post natal development, Production of transgenic chickens expressing a tetracycline-inducible GFP gene., Animals, Transgenic can be readily created to express fluorescently tagged proteins or reporters, These findings suggest that mhc2dab:GFP and cd45:DsRed transgenic lines will be instrumental in elucidating the immune response in the Zebrafish., f 33 CASP14 gene born, 28 (81%) carried the transgene DNA and 15 (55.5%) were GFP-positive., Lentiviral vectors containing the Green Fluorescent Proteins gene have been successfully used to select transgenic embryos before transfer to a surrogate mother, Typically Transgenes are generated by placing a promoter upstream of a GFP reporter gene or DNA, Complementary of interest, and this often produces a representative expression pattern., Survival and immunogenicity of Mesenchymal Stem Cells from the Green Fluorescent Proteins transgenic Rattus norvegicus in the adult Rattus norvegicus brain., This problem has been lessened by the availability of Animals, Transgenic that express \"reporter\" Genes, such as Green Fluorescent Proteins (GFP),  full-length GFP fusion proteins was examined, in Animals, Transgenic, , Two stable transgenic lines express GFP prior to hair-bundle formation, we generated two transgenic pigs by somatic \"U\" lymphocyte nuclear transfer (SCNT) that express Green Fluorescent Proteins (GFP) driven by cytomegalovirus (CMV)., Fluorescent proteins such as the Green Fluorescent Proteins (GFP) have widely been used in Animals, Transgenic as Genes, Reporter. , Green Fluorescent Protein (GFP) is used extensively as a reporter for transgene expression in Drosophila <basidiomycetes> <basidiomycetes> and other Organism.[SEP]Relations: Animal protein allergy has relations: phenotype_phenotype with Allergy, phenotype_phenotype with Allergy, phenotype_phenotype with Animal dander allergy, phenotype_phenotype with Animal dander allergy. lymphocyte anergy has relations: bioprocess_bioprocess with tolerance induction, bioprocess_bioprocess with tolerance induction, bioprocess_bioprocess with B \"U\" lymphocyte anergy, bioprocess_bioprocess with B \"U\" lymphocyte anergy, bioprocess_bioprocess with T \"U\" lymphocyte anergy, bioprocess_bioprocess with T \"U\" lymphocyte anergy.", "label": "yes"}
{"original_question": "Is the UGT1A1*28 polymorphism associated with irinotecan response in Caucasians?", "id": "converted_1430", "sentence1": "Is the UGT1A1*28 Allele polymorphism associated with irinotecan response in Caucasians?", "sentence2": "These Variant are associated with greater risk of serious Toxic effect., Homozygous carriers of UGT1A1*28 Allele Allele as well as those with additional UGT1A1 wt Allele Variant can suffer from severe irinotecan Toxic effect[SEP]Relations: Irinotecan has relations: drug_protein with UGT1A1, drug_protein with UGT1A1, drug_protein with UGT1A9, drug_protein with UGT1A9, drug_protein with CYP3A7, drug_protein with CYP3A7, drug_protein with CYP3A4, drug_protein with CYP3A4, drug_protein with TOP1MT, drug_protein with TOP1MT.", "label": "yes"}
{"original_question": "Can protein coding exons originate from ALU sequences?", "id": "converted_415", "sentence1": "Can protein coding Exons originate from ALU sequences?", "sentence2": "The Alu Elements has been a major source of new Exons during primate evolution. Thousands of Homo sapiens genes contain spliced Exons derived from Alu elements., More than 25% of Alu Exons analyzed by RNA-Seq have estimated transcript inclusion levels of at least 50% in the Homo sapiens cerebellum, indicating widespread establishment of Alu Exons in Homo sapiens genes., his study presents genomic evidence that a major functional consequence of Alu exonization is the lineage-specific evolution of translational regulation., Our data suggests that lineage-specific exonization events should be determined by the combination event of the formation of splicing sites and protection against site-specific mutation pressures. These evolutionary mechanisms could be major sources for primate diversification., Exonization of Alu elements creates primate-specific genomic diversity, Our data show that, once acquired, some exonizations were lost again in some lineages. In general, Alu exonization occurred at various time points over the evolutionary history of primate lineages, and protein-coding potential was acquired either relatively soon after Integration (data processing) or millions of years thereafter., Once integrated, they have the potential to become exapted as functional modules, e.g., as protein-coding domains via alternative splicing. This particular process is also termed exonization and increases protein versatility, alternative \"Alu-Exons\" also carry the potential to greatly enhance genetic diversity by increasing the transcriptome of primates chiefly via alternative splicing., ere, we report a 5' exon generated from one of the two alternative transcripts in Homo sapiens tumor necrosis factor receptor gene type 2 (TNFRSF1B wt Allele) that contains an ancient Alu-SINE, which provides an alternative N-terminal protein-coding domain.[SEP]Relations: Antigen processing: Ubiquitination & Proteasome degradation has relations: pathway_protein with ELOC, pathway_protein with ELOC, pathway_protein with UNKL, pathway_protein with UNKL, pathway_protein with GLMN, pathway_protein with GLMN, pathway_protein with AREL1, pathway_protein with AREL1, pathway_protein with ASB10, pathway_protein with ASB10.", "label": "yes"}
{"original_question": "Does deletion of cohesin change gene expression?", "id": "converted_3500", "sentence1": "Does Gene Deletion Abnormality of cohesins change gene expression?", "sentence2": " The conditional Gene Deletion Abnormality of cohesins from noncycling thymocytes preserved enhancer position, Histone H3 Acetyl Lys28, H4K4me1, and enhancer transcription, but weakened interactions between enhancers., Interestingly, ∼ 50% of deregulated Genes reside in the vicinity of Enhancer Elements, Genetic, suggesting that cohesins regulates gene expression through spatial clustering of Enhancer Elements, Genetic., We propose a model for cohesins-dependent gene regulation in which spatial clustering of Enhancer Elements, Genetic acts as a unified mechanism for both enhancer-promoter \"connections\" and \"insulation.\"[SEP]Relations: Abnormality of the dentition has relations: disease_phenotype_positive with chromosome 15q24 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 15q24 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 4q21 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 4q21 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 9p Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 9p Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 8q21.11 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 8q21.11 Gene Deletion Abnormality syndrome, disease_phenotype_positive with 22q11.2 Gene Deletion Abnormality syndrome, disease_phenotype_positive with 22q11.2 Gene Deletion Abnormality syndrome.", "label": "yes"}
{"original_question": "Is Li–Fraumeni syndrome a rare, autosomal recessive, hereditary disorder that predisposes carriers to cancer development?", "id": "converted_3269", "sentence1": "Is Li–Fraumeni syndrome a rare, Autosome recessive, hereditary disorder that predisposes carriers to Primary malignant neoplasm development?", "sentence2": "LI-FRAUMENI SYNDROME 1 (Li-Fraumeni Syndrome) is a rare Primary malignant neoplasm predisposition syndrome inherited in an Autosomal dominant multiple pterygium syndrome fashion that involves a Germline Mutation Abnormality of tumor protein 53 (TP53 wt Allele wt Allele). , LI-FRAUMENI SYNDROME 1 (Li-Fraumeni Syndrome), a multiorgan Primary malignant neoplasm predisposition caused by Germline TP53 wt Allele wt Allele mutations, confers significant Primary malignant neoplasm risks for young people (15-39 years). Yet evidence of how individuals experience this condition and the psychosocial implications are lacking. Therefore, this systematic review assessed the psychosocial implications of living with, or at risk of, an Autosomal dominant multiple pterygium syndrome condition as a young person, to, LI-FRAUMENI SYNDROME 1 (Li-Fraumeni Syndrome) is a rare Autosomal dominant multiple pterygium syndrome disorder caused by a Mutation Abnormality in the TP53 wt Allele wt Allele gene., LI-FRAUMENI SYNDROME 1 (Li-Fraumeni Syndrome) is an Autosomal dominant multiple pterygium syndrome disorder occurring at a young age that predisposes individuals to multiple forms of Primary malignant neoplasm and to a heterogeneous spectrum of Malignant Neoplasms., LI-FRAUMENI SYNDROME 1 (Li-Fraumeni Syndrome) is a rare hereditary Autosomal dominant multiple pterygium syndrome Primary malignant neoplasm disorder., LI-FRAUMENI SYNDROME 1 (Li-Fraumeni Syndrome) is an Autosomal dominant multiple pterygium syndrome hereditary Primary malignant neoplasm disorder., LI-FRAUMENI SYNDROME 1 (Li-Fraumeni Syndrome) is a rare, Autosomal dominant multiple pterygium syndrome, hereditary Primary malignant neoplasm predisposition disorder., LI-FRAUMENI SYNDROME 1 is a rare Autosomal dominant multiple pterygium syndrome Primary malignant neoplasm predisposition syndrome., LI-FRAUMENI SYNDROME 1 is an Autosomal dominant multiple pterygium syndrome disorder that is characterized by various types of Primary malignant neoplasm in childhood and adult cases., LI-FRAUMENI SYNDROME 1 (Li-Fraumeni Syndrome) is a rare hereditary Primary malignant neoplasm syndrome associated with an Autosomal dominant multiple pterygium syndrome Mutation Abnormality inheritance in the TP53 wt Allele wt Allele tumor suppressor gene and a wide spectrum of Primary malignant neoplasm diagnoses., The LI-FRAUMENI SYNDROME 1 is an Autosomal dominant multiple pterygium syndrome disorder characterized by a high risk of developing Osteosarcoma of bone and has been found in up to 3% of children with Osteosarcoma of bone., LI-FRAUMENI SYNDROME 1 (Li-Fraumeni Syndrome) is a rare, Autosomal dominant multiple pterygium syndrome, hereditary Primary malignant neoplasm predisposition disorder., LI-FRAUMENI SYNDROME 1 (Li-Fraumeni Syndrome) is an inherited, Autosome-dominant condition that predisposes individuals to a wide-spectrum of Neoplasms at an early age., The LI-FRAUMENI SYNDROME 1 (Li-Fraumeni Syndrome) is an Autosomal dominant multiple pterygium syndrome hereditary disorder associated with different tumor types in childhood and young adults.[SEP]Relations: LI-FRAUMENI SYNDROME 1 has relations: disease_disease with Autosomal dominant multiple pterygium syndrome disease, disease_disease with Autosomal dominant multiple pterygium syndrome disease, disease_disease with Autosomal dominant multiple pterygium syndrome disease, disease_disease with Autosomal dominant multiple pterygium syndrome disease, disease_phenotype_positive with Autosomal dominant inheritance, disease_phenotype_positive with Autosomal dominant inheritance, disease_phenotype_positive with Autosomal dominant inheritance, disease_phenotype_positive with Autosomal dominant inheritance. Autosomal dominant multiple pterygium syndrome disease has relations: disease_disease with LI-FRAUMENI SYNDROME 1, disease_disease with LI-FRAUMENI SYNDROME 1.", "label": "no"}
{"original_question": "Does sphingosine-1 phosphoate suppress epiregulin?", "id": "converted_4703", "sentence1": "Does sphingosine-1 phosphoate suppress epiregulin?", "sentence2": "S1P-induced FOXO1 gene gene and Proepiregulin, human gene expression suggests that the activation of S1P-S1PR axis may cooperate with Recombinant Gonadotropin in modulating follicle development., S1P-dependent Cyclic AMP-Responsive DNA-Binding Protein phosphorylation induced FOXO1 gene gene and the EGF-like epiregulin-encoding gene (Proepiregulin, human), confirming the exclusive role of Recombinant Gonadotropin and Recombinant Interleukins in this process, but did not affect steroidogenesis. [SEP]Relations: interleukin-8 receptor binding has relations: molfunc_protein with YARS1, molfunc_protein with YARS1, molfunc_protein with CXCL8, molfunc_protein with CXCL8. cAMP response element binding protein binding has relations: molfunc_protein with CRTC1, molfunc_protein with CRTC1, molfunc_protein with CRTC3, molfunc_protein with CRTC3, molfunc_protein with CRTC2, molfunc_protein with CRTC2.", "label": "no"}
{"original_question": "Is osteocrin expressed exclusively in the bone?", "id": "converted_2141", "sentence1": "Is osteocrin expressed exclusively in the bone?", "sentence2": "Evolution of Osteocrin as an activity-regulated factor in the primate Head>Brain., Here we use transcriptional profiling of Homo sapiens fetal Head>Brain cultures to identify an activity-dependent secreted factor, Osteocrin (OSTN gene gene), that is induced by membrane depolarization of Homo sapiens but not mouse neurons., Osteocrin (Ostn) is a recently discovered secreted Protein Info produced by Cells of the Osteoblasts lineage that shows a well conserved homology with members of the Natriuretic Peptides (NP) family. , Osteocrin (Ostn), a bone-active molecule, has been shown in animal allergen extracts to be highly expressed in Cells of the Osteoblasts lineage. , Osteocrin, a novel bone-specific secreted Protein Info that modulates the Osteoblasts phenotype.[SEP]Relations: osteoblastic osteosarcoma has relations: disease_disease with osteosarcoma, disease_disease with osteosarcoma. Bite Cells has relations: disease_phenotype_positive with hereditary stomatocytosis, disease_phenotype_positive with hereditary stomatocytosis. Protein C has relations: drug_drug with Trazodone, drug_drug with Trazodone, drug_drug with Azapropazone, drug_drug with Azapropazone, drug_drug with Taurochenodeoxycholic acid, drug_drug with Taurochenodeoxycholic acid.", "label": "no"}
{"original_question": "Is STAT3 involved in EIF2AK2-dependent suppression of autophagy?", "id": "converted_963", "sentence1": "Is STAT3 protein, human involved in EIF2AK2 gene-dependent suppression of autophagy?", "sentence2": "STAT3 protein, human protein, human may act as a competitive PPP1R1A gene of EIF2AK2 gene gene. Indeed, pharmacological or genetic inhibition of STAT3 protein, human protein, human stimulates EIF2AK2 gene gene-dependent Eukaryotic Translation Initiation Factor 2 Subunit 1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 protein, human protein, human as well as of STAT3 protein, human protein, human mutants that cannot be phosphorylated by JAK2 protein, human protein, human or are excluded from the Cell Nucleus inhibits autophagy. However, STAT3 protein, human protein, human mutants that fail to interact with EIF2AK2 gene gene are unable to suppress autophagy, Both STAT3 protein, human protein, human-targeting agents (i.e., stattic, JSI-124 and WP1066) and EIF2AK2 gene gene activators (such as the double-strand RNA mimetic polyinosinic:Poly C) are capable of disrupting the inhibitory interaction between STAT3 protein, human protein, human and EIF2AK2 gene gene in cellula, A further screen designed to identify EIF2AK2 gene gene-dependent autophagy inducers revealed that several Fatty Acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3 protein, human protein, human-EIF2AK2 gene gene complex, These results reveal an unsuspected crosstalk between cellular metabolism (Fatty Acids), pro-inflammatory signaling (STAT3 protein, human protein, human), innate immunity (EIF2AK2 gene gene), and translational control (Eukaryotic Translation Initiation Factor 2 Subunit 1) that regulates autophagy, Cytoplasmic STAT3 protein, human protein, human represses autophagy by inhibiting eIF-2 Kinase activity, The SH2 Domain of STAT3 protein, human protein, human was found to interact with the Catalytic Domain of the eIF2α kinase 2 EIF2AK2 gene gene, best known as protein kinase R (eIF-2 Kinase). Pharmacological and genetic inhibition of STAT3 protein, human protein, human stimulated the activating phosphorylation of eIF-2 Kinase and consequent eIF2α hyperphosphorylation. Moreover, eIF-2 Kinase depletion inhibited autophagy as initiated by chemical STAT3 protein, human protein, human inhibitors or free Fatty Acids like palmitate, STAT3 protein, human protein, human-targeting chemicals and palmitate caused the disruption of inhibitory STAT3 protein, human protein, human-eIF-2 Kinase interactions, followed by eIF-2 Kinase-dependent eIF2α phosphorylation, which facilitates autophagy induction, Indeed, pharmacological or genetic inhibition of STAT3 protein, human protein, human stimulates EIF2AK2 gene gene-dependent Eukaryotic Translation Initiation Factor 2 Subunit 1 phosphorylation and autophagy., A further screen designed to identify EIF2AK2 gene gene-dependent autophagy inducers revealed that several Fatty Acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3 protein, human protein, human-EIF2AK2 gene gene complex as well as the phosphorylation of Mitogen-Activated Protein Kinases 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and Eukaryotic Translation Initiation Factor 2 Subunit 1., A further screen designed to identify EIF2AK2 gene gene-dependent autophagy inducers revealed that several Fatty Acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3 protein, human protein, human-EIF2AK2 gene gene complex as well as the phosphorylation of Mitogen-Activated Protein Kinases 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and Eukaryotic Translation Initiation Factor 2 Subunit 1, Indeed, pharmacological or genetic inhibition of STAT3 protein, human protein, human stimulates EIF2AK2 gene gene-dependent Eukaryotic Translation Initiation Factor 2 Subunit 1 phosphorylation and autophagy, However, STAT3 protein, human protein, human mutants that fail to interact with EIF2AK2 gene gene are unable to suppress autophagy, Direct interaction between STAT3 protein, human protein, human and EIF2AK2 gene gene controls fatty acid-induced autophagy, A further screen designed to identify EIF2AK2 gene gene-dependent autophagy inducers revealed that several Fatty Acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3 protein, human protein, human-EIF2AK2 gene gene complex as well as the phosphorylation of Mitogen-Activated Protein Kinases 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and Eukaryotic Translation Initiation Factor 2 Subunit 1. , Indeed, pharmacological or genetic inhibition of STAT3 protein, human protein, human stimulates EIF2AK2 gene gene-dependent Eukaryotic Translation Initiation Factor 2 Subunit 1 phosphorylation and autophagy. , Direct interaction between STAT3 protein, human protein, human and EIF2AK2 gene gene controls fatty acid-induced autophagy., These results unravel an unsuspected mechanism of autophagy control that involves STAT3 protein, human protein, human and eIF-2 Kinase as interacting partners., Both STAT3 protein, human protein, human-targeting agents (i.e., stattic, JSI-124 and WP1066) and EIF2AK2 gene gene activators (such as the double-strand RNA mimetic polyinosinic:Poly C) are capable of disrupting the inhibitory interaction between STAT3 protein, human protein, human and EIF2AK2 gene gene in cellula, yet only the latter does so in cell-free systems in vitro. A further screen designed to identify EIF2AK2 gene gene-dependent autophagy inducers revealed that several Fatty Acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3 protein, human protein, human-EIF2AK2 gene gene complex as well as the phosphorylation of Mitogen-Activated Protein Kinases 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and Eukaryotic Translation Initiation Factor 2 Subunit 1., A further screen designed to identify EIF2AK2 gene gene-dependent autophagy inducers revealed that several Fatty Acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3 protein, human protein, human-EIF2AK2 gene gene complex as well as the phosphorylation of Mitogen-Activated Protein Kinases 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and Eukaryotic Translation Initiation Factor 2 Subunit 1. These results reveal an unsuspected crosstalk between cellular metabolism (Fatty Acids), pro-inflammatory signaling (STAT3 protein, human protein, human), innate immunity (EIF2AK2 gene gene), and translational control (Eukaryotic Translation Initiation Factor 2 Subunit 1) that regulates autophagy., Thus, STAT3 protein, human protein, human may act as a competitive PPP1R1A gene of EIF2AK2 gene gene. Indeed, pharmacological or genetic inhibition of STAT3 protein, human protein, human stimulates EIF2AK2 gene gene-dependent Eukaryotic Translation Initiation Factor 2 Subunit 1 phosphorylation and autophagy., Indeed, pharmacological or genetic inhibition of STAT3 protein, human protein, human stimulates EIF2AK2 gene gene-dependent Eukaryotic Translation Initiation Factor 2 Subunit 1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 protein, human protein, human as well as of STAT3 protein, human protein, human mutants that cannot be phosphorylated by JAK2 protein, human protein, human or are excluded from the Cell Nucleus inhibits autophagy., , stattic, JSI-124 and WP1066) and EIF2AK2 gene gene activators (such as the double-strand RNA mimetic polyinosinic:Poly C) are capable of disrupting the inhibitory interaction between STAT3 protein, human protein, human and EIF2AK2 gene gene in cellula, yet only the latter does so in cell-free systems in vitro. A further screen designed to identify EIF2AK2 gene gene-dependent autophagy inducers revealed that several Fatty Acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3 protein, human protein, human-EIF2AK2 gene gene complex as well as the phosphorylation of Mitogen-Activated Protein Kinases 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and Eukaryotic Translation Initiation Factor 2 Subunit 1.[SEP]Relations: EIF2AK2 gene has relations: protein_protein with STAT3 protein, human, protein_protein with STAT3 protein, human, protein_protein with STAT2, protein_protein with STAT2, protein_protein with STAT1, protein_protein with STAT1, pathway_protein with Inhibition of eIF-2 Kinase, pathway_protein with Inhibition of eIF-2 Kinase, molfunc_protein with protein phosphatase regulator activity, molfunc_protein with protein phosphatase regulator activity.", "label": "yes"}
{"original_question": "Does strenuous physical activity affect thyroid hormone metabolism?", "id": "converted_154", "sentence1": "Does strenuous physical activity affect Thyroid Hormones metabolism?", "sentence2": "The results of the present study in a unique experimental human model of maximal exposure to altitude and physical exercise demonstrate that extreme HA and strenuous physical exercise are coupled with specific endocrine adaptations. These include increased activity of the GH/IGF-I axis and a low T(3) syndrome, 3,5,3'-liothyronine (T3 thoracic segmental innervation thoracic segmental innervation) and T4 thoracic segmental innervation thoracic segmental innervation levels increase during strenuous exercise, and, at the end of the exercise bout, a decrease of T3 thoracic segmental innervation thoracic segmental innervation and T4 thoracic segmental innervation thoracic segmental innervation levels, with an increase in Thyrotropin:-:Pt:Ser/Plas:- during the following 4-5 days, is seen., the obtained results indicate that in intense exercise, causing the rapid development of Fatigue, rapid increases in serum levels of hormones of the pituitary-adrenocortical, pituitary-gonadal and pituitary-thyroid systems occur., Mean levels of fasting plasma estradiol, Recombinant Luteinizing Hormone, Human Follicle-Stimulating Hormone, free levothyroxine and liothyronine were significantly lower in AKR1B1 protein, human compared to Endoplasmic Reticulum and FUT2 gene., Reductions in plasma T4 thoracic segmental innervation thoracic segmental innervation, T3 thoracic segmental innervation thoracic segmental innervation and T3 thoracic segmental innervation thoracic segmental innervation/T4 thoracic segmental innervation thoracic segmental innervation ratio are probably due to inhibition of T4 thoracic segmental innervation thoracic segmental innervation secretion and 5'-monodeiodination with possible conversion of T4 thoracic segmental innervation thoracic segmental innervation to reverse T3 thoracic segmental innervation thoracic segmental innervation (rT3). These processes may represent a mechanism for regulation of Thyroid Hormones metabolism during strenuous and extended flight., Strenuous endurance training seems to have minor changes on the function of the Neck>Thyroid gland. Depressed T4 thoracic segmental innervation thoracic segmental innervation levels in runners may rather be due to lowered Thyroxine-Binding Globulin levels than due to direct effect of training., brief strenuous swimming or moderate bicycle exercise had minor or no effect on Thyroid Hormones concentrations when consideration was given to the attendant Haemoconcentration., levothyroxine were determined in 26 men participating in a 90-km cross-country ski race, before, immediately after, and on the following days, Total levothyroxine and free levothyroxine in serum were significantly increased at the end of the race, but had returned to the pre-raced levels during the rest of the observation period., There are controversial results concerning Thyroid Hormones metabolism during strenuous exercise in adult athletes and only scant data concerning the impact of strenuous exercise on Thyroid Hormones metabolism in children and adolescents.[SEP]Relations: Neck>Thyroid gland has relations: anatomy_protein_present with IMPACT, anatomy_protein_present with IMPACT, anatomy_protein_present with STRN, anatomy_protein_present with STRN, anatomy_protein_present with STRADA, anatomy_protein_present with STRADA, anatomy_protein_present with MTURN, anatomy_protein_present with MTURN, anatomy_protein_present with STOM, anatomy_protein_present with STOM.", "label": "yes"}
{"original_question": "Is COL5A2 gene associated to ischemic heart disease?", "id": "converted_1167", "sentence1": "Is COL5A2 Genes associated to Myocardial Ischemia?", "sentence2": "Analysis of a Genes co-expression network establishes robust association between Collagen Alpha-2(V) Chain, Human and Myocardial Ischemia, Collagen Alpha-2(V) Chain, Human, a Genes previously not specifically linked to MI response but responsible for the classic type of Ehlers-Danlos Syndrome, was found to have many and strong co-expression associations within this community, Collagen Alpha-2(V) Chain, Human shows predictive potential in MI, and in principle may represent a novel candidate marker for the identification and treatment of ischemic cardiovascular disease, Analysis of a Genes co-expression network establishes robust association between Collagen Alpha-2(V) Chain, Human and Myocardial Ischemia.[SEP]Relations: myocardial ischemia has relations: disease_protein with ADM2, disease_protein with ADM2, disease_protein with ADRB2, disease_protein with ADRB2, disease_protein with TMED2, disease_protein with TMED2, disease_protein with RAB5A, disease_protein with RAB5A, disease_protein with APLP2, disease_protein with APLP2.", "label": "yes"}
{"original_question": "Does GRHL2 over-expression lead to EMT?", "id": "converted_3243", "sentence1": "Does GRHL2 over-expression lead to Emergency Medical Technicians?", "sentence2": "GRHL2 gene is down-regulated in disseminated Tumor cells, malignant that have undergone Emergency Medical Technicians, and over-expression of GRHL2 gene is sufficient to induce epithelial gene expression.,  GRHL2 gene plays an essential role in the determination of Epithelial phenotype of Malignant neoplasm of breast, Emergency Medical Technicians and tumor progression., In breast cancer cell lines, shRNA-mediated knockdown of GRHL2 expression or functional inactivation of GRHL2 using dominant negative GRHL2 proteins induces down-regulation of ERBB3 gene expression, a striking reduction in cell proliferation, and morphological and phenotypical alterations characteristic of an epithelial-to-Mesenchymal transition (Emergency Medical Technicians), thus implying contradictory roles of GRHL2 in breast carcinogenesis., Interestingly, we could further demonstrate that expression of GRHL2 is directly suppressed by the TRANSCRIPTION FACTOR zinc finger enhancer-binding protein 1 (ZEB1 gene gene), which in turn is a direct target for repression by GRHL2, suggesting that the Emergency Medical Technicians transcription factors GRHL2 and ZEB1 gene gene form a double negative regulatory feedback loop in breast Tumor cells, malignant, Mesenchymal-Epithelial Transition in Malignant neoplasm of soft tissue Is Controlled by the Combinatorial Expression of MicroRNA 200s and GRHL2., TRANSCRIPTION FACTOR--GRHL2 wt Allele (GRHL2) maintains the Epithelial phenotype, We explored the role of grainyhead-like 2 (GRHL2), a suppressor of Emergency Medical Technicians, in the progression of ANOPHTHALMIA AND PULMONARY HYPOPLASIA, GRHL2 knockdown CFPAC-1 cells demonstrated morphological changes into Mesenchymal appearances and reduced proliferation through Emergency Medical Technicians, The TRANSCRIPTION FACTOR grainyhead-like 2 (GRHL2) plays a crucial role in various developmental processes, GRHL2 wt Allele (GRHL2 gene), a TRANSCRIPTION FACTOR, has been reported to be associated with several tumor processes including Emergency Medical Technicians. , GRHL2 gene antagonizes transforming growth factor-β (TGFβ)-induced Emergency Medical Technicians[SEP]Relations: GRHL2 has relations: protein_protein with ESR1, protein_protein with ESR1, protein_protein with PIAS2, protein_protein with PIAS2, protein_protein with GRHL1, protein_protein with GRHL1, protein_protein with DDIT4L, protein_protein with DDIT4L, protein_protein with GRHL3, protein_protein with GRHL3.", "label": "no"}
{"original_question": "Is istiratumab effective for pancreatic cancer?", "id": "converted_4300", "sentence1": "Is istiratumab effective for pancreatic cancer?", "sentence2": "CONCLUSIONS: Istiratumab failed to improve the efficacy of SOC chemotherapy in this patient setting. [SEP]", "label": "no"}
{"original_question": "Have mutations in the GARS gene been identified to cause Charcot-Marie-Tooth Disease Type 2D (CMT2D)?", "id": "converted_459", "sentence1": "Have mutations in the GARS gene been identified to cause Charcot-Marie-Tooth Disease Type 2D (Charcot-Marie-Tooth Disease, Type 2D)?", "sentence2": "Charcot-Marie-Tooth Disease type 2D is a hereditary axonal and GARS1 wt Allele (GARS)-associated Neuropathy that is caused by a Mutation Abnormality in GARS. , Mutations in the GARS gene cause Charcot-Marie-Tooth 2D and distal spinal Muscular Atrophy type V - allelic disorders characterized by predominantly distal upper extremity weakness and Atrophic, typically beginning during the second decade of life. , Charcot-Marie-Tooth Disease type 2D (Charcot-Marie-Tooth Disease, Type 2D) is a dominantly inherited peripheral Neuropathy caused by missense mutations in the GARS1 wt Allele gene (GARS)., The 13 Genes known to be associated with the Autosomal dominant Charcot-Marie-Tooth Disease type 2 subtypes are KIF1B protein, human protein, human (Charcot-Marie-Tooth Disease, Axonal, Type 2a1), Mitofusin-2 (CMT2A2), RAB7A gene gene (formerly RAB7A gene gene wt Allele) (CMT2B), Prelamin-A/C (Charcot-Marie-Tooth Disease, Type 2B1), MED25 gene gene (Charcot-Marie-Tooth Disease, Type 2B2), TRPV4 protein, human protein, human (Cutis marmorata telangiectatica congenita), GARS (Charcot-Marie-Tooth Disease, Type 2D), NEFL protein, human protein, human (CMT2E/1F), HSPB1 protein, human protein, human (CHARCOT-MARIE-TOOTH DISEASE, AXONAL, TYPE 2F), MPZ gene gene (CMT2I/J), GDAP1 gene gene (CMT2H/K), Heat Shock Protein Beta-8 (Autosomal dominant Charcot-Marie-Tooth Disease type 2L), and AARS1 gene (CMT2N). ,  The diagnosis of GARS-associated axonal Neuropathy is based on clinical findings, electromyography (Electromyogram of eye), and molecular genetic testing of GARS, encoding GARS1 wt Allele., Sporadic juvenile Muscular Atrophy of the distal upper extremity or Hirayama's disease (Hodgkin Disease) and Autosome dominant motor distal neuronopathy/axonopathy (Charcot-Marie-Tooth Disease, Type 2D/dSMA-V), produced by GARS1 wt Allele (GARS) Gene Mutation, share some clinical features including: young age of onset, predilection for the distal upper extremity, asymmetry, sparing of proximal muscles and unusual cold sensitivity. , Distal hereditary motor Neuropathy type V (NEURONOPATHY, DISTAL HEREDITARY MOTOR, TYPE V) and Charcot-Marie-Tooth syndrome (CMT) type 2 presenting with predominant hand involvement, also known as Charcot-Marie-Tooth Disease, Type 2D and Spastic paraplegia 17 (Supernumerary mandibular right first primary molar) are rare phenotypically overlapping diseases which can be caused by mutations in the Congenital Generalized Lipodystrophy Type 2 (BSCL2 gene gene) and in the GARS1 wt Allele encoding (GARS) Genes. , We previously implicated mutations in the gene encoding GARS1 wt Allele (GARS) as the cause of Charcot-Marie-Tooth Disease, Type 2D and dSMA-V., Of the many inherited Charcot-Marie-Tooth peripheral neuropathies, type 2D (Charcot-Marie-Tooth Disease, Type 2D) is caused by dominant Point Mutation in the gene GARS, encoding Glycine-tRNA Ligase (GlyRS). , Missense mutations in the GARS1 wt Allele (GARS) gene have been recently reported in families with either NEURONOPATHY, DISTAL HEREDITARY MOTOR, TYPE V, Charcot-Marie-Tooth Disease, Type 2D, or both., Based on the presence or absence of sensory changes, the disease phenotype was initially defined as distal spinal Muscular Atrophy type V (dSMA-V) in three families, Charcot-Marie-Tooth Disease type 2D (Charcot-Marie-Tooth Disease, Type 2D) in a single family, and as either dSMA-V or Charcot-Marie-Tooth Disease, Type 2D in patients of another large family. Linkage to chromosome 7p15 and the presence of disease-associated heterozygous GARS mutations have been identified in patients from each of the five studied families. [SEP]Relations: Charcot-Marie-Tooth Disease has relations: disease_protein with GARS1, disease_protein with GARS1, disease_protein with GARS1, disease_protein with GARS1, disease_protein with GARS1, disease_protein with GARS1, disease_protein with GARS1, disease_protein with GARS1, disease_protein with MTMR2, disease_protein with MTMR2.", "label": "yes"}
{"original_question": "Is the protein FAK (Focal Adhesion Kinase) phosphorylated?", "id": "converted_1664", "sentence1": "Is the protein Focal Adhesion Kinase 1 (Focal Adhesion Kinase) phosphorylated?", "sentence2": "Overexpression of NEDD9 gene gene led to tyrosine phosphorylation of Focal Adhesion Kinase 1 and SRC oncoproteins, , yrosine phosphorylated Focal Adhesion Kinase 1, TNFα contributes for attenuating both Y397FAK and Y416Src phosphorylations in Osteoblasts.,  It was possible to show that TNFα provokes attenuation at Y-phosphorylation of both Focal Adhesion Kinase 1 (at Y397 ), ownregulation of G3BP1 gene significantly inhibited the phosphorylation of Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human, Focal Adhesion Kinase 1, Periodic mechanical stress significantly induced sustained phosphorylation of Focal Adhesion Kinase 1 at Tyr(397) and Tyr(576/577). , oss of αSNAP impaired Golgi-dependent glycosylation and trafficking of Integrins and decreased phosphorylation of Focal Adhesion Protein-Tyrosine Kinases (Focal Adhesion Kinase 1) and PXN protein, human resulting in doxorubicin/fluorouracil protocol disassembly., functional characterization of many of today's best-known Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human substrates (for example, p85-Cortactin, p110-AFAP1, BCAR1 wt Allele, PTK2 protein, human and Catenin Delta-1), Western blots were used for P-Focal Adhesion Kinase 1, e first time, that the EGF-dependent Epidermal Growth Factor Receptor activation led to increased P-FAKSer732, . P-FAKSer732 presence was crucial for the maintenance of the proliferation rate and its levels were inversely related to the levels of acetylated α-tubulin. P-FAKSer732 localized at the Microtubules (Mitochondrial Import Sequence) of the Spindle, biochemically associated with Mitochondrial Import Sequence and contributed to Manual Therapies depolymerization., specially, phosphorylation of Tyr925-Focal Adhesion Kinase 1 that is required for full activation of Focal Adhesion Kinase 1 was nearly completely suppressed even with 1nM of Methyl violet 2B stain in A375P cancer cells. ,  The protein expression of PTPN13 gene gene, Focal Adhesion Protein-Tyrosine Kinases (Focal Adhesion Kinase 1) and phosphorylated Focal Adhesion Kinase 1 (P-Focal Adhesion Kinase 1) was evaluated using immunohistochemical staining and western blotting., curcumin inhibits Focal Adhesion Protein-Tyrosine Kinases (Focal Adhesion Kinase 1) phosphorylation and enhances the expressions of several Extracellular Matrix components which play a critical role in invasion and metastasis. , uppressed both the phosphorylation of Focal Adhesion Kinase 1 ,  A GEF-inactive Rgnef mutant rescues Focal Adhesion Kinase 1-Y397 phosphorylation [SEP]Relations: focal adhesion has relations: cellcomp_protein with TEK, cellcomp_protein with TEK, cellcomp_protein with FAP, cellcomp_protein with FAP, cellcomp_protein with GAK, cellcomp_protein with GAK, cellcomp_protein with ILK, cellcomp_protein with ILK, cellcomp_protein with AHNAK, cellcomp_protein with AHNAK.", "label": "yes"}
{"original_question": "Is mesothelioma caused by asbestos exposure?", "id": "converted_3506", "sentence1": "Is mesothelioma caused by asbestos exposure?", "sentence2": "Malignant mesothelioma is a rare and aggressive pleural or peritoneal tumour almost always caused by exposure to asbestos fibres, Exposure to asbestos can cause malignant mesothelioma 30-40 years after exposure., Malignant Mesothelioma of the Rat Peritoneum is a rare, aggressive Specimen Source Codes - Specimen Source Codes - tumor arising from the peritoneal lining, induced by asbestos, therapeutic radiation, or germline mutations, According to global estimates, at least 107,000 people die each year from asbestos-related Primary malignant neoplasm of lung, mesothelioma, and Asbestosis resulting from occupational exposure, Malignant mesothelioma is caused by exposure to asbestos, which is known to have carcinogenic effects., Malignant mesothelioma and Primary malignant neoplasm of lung are caused by all major types of asbestos., Exposure to asbestos can cause malignant mesothelioma 30-40 years after exposure., BACKGROUND Malignant mesothelioma caused by asbestos exposure has a long latency period., Asbestos exposure causes Asbestosis and malignant mesothelioma, disorders which remain difficult to cure., Most MPeM is caused by asbestos exposure, Occupational asbestos exposure occurs in many workplaces and is a well-known cause of mesothelioma and Primary malignant neoplasm of lung . , Occupational exposure to asbestos occurs in many workplaces and is well known to cause Asbestosis , Primary malignant neoplasm of lung , and mesothelioma . , Malignant mesothelioma is a rare and aggressive pleural or peritoneal tumour almost always caused by exposure to asbestos fibres., Exposure to asbestos can cause malignant mesothelioma 30-40 years after exposure., Malignant Mesothelioma of the Rat Pleura caused by environmental exposure to asbestos or erionite in rural Turkey: X-Ray Computed Tomography findings in 84 patients., OBJECTIVE\nMalignant Mesothelioma of the Rat Pleura in rural Turkey frequently results from environmental exposure to tremolite or fibrous zeolite (erionite)., Mesothelioma, a rare Specimen Source Codes - Specimen Source Codes - tumor, is highly correlated with asbestos exposure.[SEP]Relations: Asbestosis has relations: disease_phenotype_positive with Lung adenocarcinoma, disease_phenotype_positive with Lung adenocarcinoma. malignant pleural mesothelioma has relations: disease_disease with pleural mesothelioma, disease_disease with pleural mesothelioma, disease_disease with pleural cancer, disease_disease with pleural cancer, disease_disease with pleural sarcomatoid mesothelioma, disease_disease with pleural sarcomatoid mesothelioma. malignant peritoneal mesothelioma has relations: disease_disease with peritoneum cancer, disease_disease with peritoneum cancer.", "label": "yes"}
{"original_question": "Are immune cells affected in Amyotrophic Lateral Sclerosis?", "id": "converted_1535", "sentence1": "Are immune cells affected in Amyotrophic Lateral Sclerosis?", "sentence2": "Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to cyclophosphamide/prednisone activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived Specimen Source Codes - Macrophages and Foxp3(+) regulatory Therapeutic gamma delta T-lymphocytes, and elevation of the neurotrophic factors Insulin-Like Growth Factor I and Glial Cell Line-Derived Neurotrophic Factor in the diseased Spinal Cord parenchyma, Immunization with a Myelin-Derived Antigen Activates the Brain's Choroid Plexus for Recruitment of Immunoregulatory Cells to the Central Nervous System and Attenuates Disease Progression in a Mouse Model of ALS., Amyotrophic lateral sclerosis (ALS) is a rapidly progressing fatal Neurodegenerative Disorders characterized by the selective death of Neurons, Efferent (MNSs Blood-Group System) in the Spinal Cord, and is associated with local neuroinflammation., T-lymphocyte deficiency increases Neuronal loss in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, while boosting T-Lymphocyte levels reduces it., As disease accelerates, a shift occurs from beneficial immune responses (involving M2 Microglia and Regulatory T-Lymphocytes) to deleterious immune responses (involving M1 Microglia and T-helper cell type 1). In this review, we underscore the importance of immune-mediated mechanisms in the pathogenesis of ALS and discuss the alterations and distinct phenotypes of immune cells at the different stages of disease.,  Immunological disturbances have been implicated in the pathogenesis of Amyotrophic Lateral Sclerosis (ALS). Recombinant Chemokine are involved in the recruitment of immune cells., The immune system has been found to be involved with positive and negative effects in the nervous system of Amyotrophic Lateral Sclerosis (ALS) patients. In general, Therapeutic gamma delta T-lymphocytes, B-Lymphocytes, Natural Killer Cells, mast cell, Specimen Source Codes - Macrophages, Dendritic Cells, Microglia, Antibodies, in vitro diagnostic, complement and Recombinant Cytokines participate in limiting damage., Immunological disturbances have been implicated in the pathogenesis of Amyotrophic Lateral Sclerosis (ALS). Recombinant Chemokine are involved in the recruitment of immune cells., We propose the following mechanism for the effect of Mesenchymal Stem Cells (cyclic nucleotide-gated mechanosensitive ion channel activity) administered intrathecally in Amyotrophic Lateral Sclerosis (ALS): cyclic nucleotide-gated mechanosensitive ion channel activity increase infiltration of peripheral immune cells into Central Nervous System and skew the infiltrated immune cells toward regulatory T lymphocytes (Treg ) and Th2 lymphocytes., Immune Cell infiltration to the brain&apos;s territory was considered for decades to reflect a pathological process in which immune cells attack the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Central Nervous System); such a process is observed in the inflammatory autoimmune disease, Multiple Sclerosis (MS).[SEP]Relations: Amyotrophic Lateral Sclerosis has relations: disease_disease with familial Amyotrophic Lateral Sclerosis, disease_disease with familial Amyotrophic Lateral Sclerosis, disease_disease with motor neuron disease, disease_disease with motor neuron disease, disease_protein with FIG4, disease_protein with FIG4, disease_protein with OTOG, disease_protein with OTOG, disease_disease with progressive muscular atrophy, disease_disease with progressive muscular atrophy.", "label": "yes"}
{"original_question": "Is the Paramyxovirus geneome segmented, negative-sense RNA?", "id": "converted_3832", "sentence1": "Is the Paramyxovirus geneome segmented, negative-sense RNA?", "sentence2": "The Paramyxovirus, NOS family has a Genome - anatomical entity consisting of a single strand of negative sense RNA, The avian Paramyxovirus, NOS type 1 (APMV-1), or Newcastle disease virus (NDV), comprise a diverse group of Virus with a single-stranded, negative-sense RNA Genome - anatomical entity., Members of the Paramyxoviridae sp. sp. such as measles, mumps, and parainfluenza Virus have pleomorphic, enveloped virions that contain negative-sense unsegmented RNA genomes., UNLABELLED: Mumps virus (MuV), a Paramyxovirus, NOS containing a negative-sense nonsegmented RNA Genome - anatomical entity, is a Homo sapiens pathogen that causes an Acute infectious disease with symptoms ranging from Parotitis to mild meningitis and severe Encephalitis., UNLABELLED: Mumps virus (MuV) is a Paramyxovirus, NOS with a negative-sense nonsegmented RNA Genome - anatomical entity., Paramyxoviridae sp. sp., a large family of enveloped Virus harboring a nonsegmented negative-sense RNA Genome - anatomical entity, include important Homo sapiens pathogens as measles, mumps, Human Human respiratory syncytial virus (RSV), parainfluenza Virus, and Henipavirus, which cause some of the deadliest emerging zoonoses. There , Parainfluenza Virus 5 (PIV5) is a member of the Paramyxoviridae sp. sp. family of membrane-enveloped Virus with a negative-sense RNA Genome - anatomical entity that is packaged and protected by long filamentous nucleocapsid-helix structures (RNPs). , The Paramyxovirus, NOS Genome - anatomical entity, a nonsegmented, negative-polarity, single-stranded RNA of approximately 15 kb, contains six transcription units flanked at the 3' and 5' ends by a short (approximately 50- to 60-nucleotide) extracistronic sequence, dubbed the positive and negative leader regions. These, The replication of nonsegmented minus-strand RNA genomes, like that of Sendai Paramyxovirus, NOS (SeV), are controlled by the short leader regions present at each end of the linear genomes and antigenomes; the left and right promoters (HOXA10 protein, Homo sapiens and Receptors, Progesterone), respectively. Wil, UNLABELLED: Mumps virus (MuV), a Paramyxovirus, NOS containing a negative-sense nonsegmented RNA Genome - anatomical entity, is a Homo sapiens pathogen that causes an Acute infectious disease with symptoms ranging from Parotitis to mild meningitis and severe enc, s viral glycoprotein cytoplasmic domains may play a role in this coordination, we have investigated the importance of the Hemagglutinin-Neuraminidase (HN) protein cytoplasmic domain in the assembly of the nonsegmented negative-strand RNA Paramyxovirus, NOS simian virus 5 (SV5). By, Beilong virus, a novel Paramyxovirus, NOS with the largest Genome - anatomical entity of non-segmented negative-stranded RNA Virus., The Paramyxovirus, NOS Genome - anatomical entity, a nonsegmented, negative-polarity, single-stranded RNA of approximately 15 kb, contains six transcription units flanked at the 3' and 5' ends by a short (approximately 50- to 60-nucleotide) extracistronic sequence, dubbed the positive and negative leader regions., Paramyxovirus particles are pleomorphic, with a lipid envelope, nonsegmented RNA genomes of negative polarity, and densely packed glycoproteins on the virion surface., An alternative method to determine the 5' All All extremities of non-segmented, negative sense RNA viral genomes using positive replication intermediate 3' tailing: application to two members of the Paramyxoviridae sp. sp. family., Simian parainfluenza virus 5 (SV5) is a prototype of the Paramyxoviridae sp. sp. family of nonsegmented negative-sense RNA Virus., Human Metapneumovirus (HMPV), a single-stranded negative-sense RNA virus belonging to the family Paramyxoviridae sp. sp., is associated with respiratory tract illness, primarily in young children and persons with underlying disease.[SEP]Relations: Parotitis has relations: disease_phenotype_positive with sarcoidosis, disease_phenotype_positive with sarcoidosis. Protein S Homo sapiens has relations: drug_drug with Deferasirox, drug_drug with Deferasirox, drug_drug with Dactinomycin, drug_drug with Dactinomycin, drug_drug with Interferon beta-1b, drug_drug with Interferon beta-1b, drug_drug with Ximelagatran, drug_drug with Ximelagatran.", "label": "no"}
{"original_question": "Is taxilin a cancer marker?", "id": "converted_4631", "sentence1": "Is taxilin a cancer marker?", "sentence2": "Αlpha-Taxilin (α-Taxilin) has been found as one of the novel, significantly up regulated protein in Rheumatoid Arthritis, Expression of α-taxilin has been implicated in the development of Homo sapiens Glioblastoma Multiforme, Liver carcinoma and Conventional (Clear Cell) Renal Cell Carcinoma. , α-Taxilin, a binding partner of the syntaxin family, is a candidate Specimen Source Codes - Specimen Source Codes - tumor marker. , Expression of α-taxilin in Liver carcinoma correlates with growth activity and malignant potential of the Specimen Source Codes - Specimen Source Codes - tumor.[SEP]Relations: Clear cell Conventional (Clear Cell) Renal Cell Carcinoma has relations: disease_phenotype_positive with Blau syndrome, disease_phenotype_positive with Blau syndrome, disease_phenotype_positive with Conventional (Clear Cell) Renal Cell Carcinoma (disease), disease_phenotype_positive with Conventional (Clear Cell) Renal Cell Carcinoma (disease). liver carcinoma in situ has relations: disease_disease with in situ carcinoma, disease_disease with in situ carcinoma, disease_disease with bile duct carcinoma in situ, disease_disease with bile duct carcinoma in situ, disease_disease with carcinoma of liver and intrahepatic biliary tract, disease_disease with carcinoma of liver and intrahepatic biliary tract.", "label": "yes"}
{"original_question": "Is Lanabecestat effective for Alzheimer's disease?", "id": "converted_4025", "sentence1": "Is Lanabecestat effective for ALZHEIMER DISEASE, FAMILIAL, 1?", "sentence2": "INTRODUCTION: The APECS and AMARANTH trials showed that BACE2 gene (BACE1 wt Allele) inhibitors verubecestat and lanabecestat failed to slow cognitive and functional decline in individuals with prodromal or early ALZHEIMER DISEASE, FAMILIAL, 1. , Conclusions and Relevance: Treatment with lanabecestat was well tolerated and did not slow cognitive or functional decline., INTRODUCTION: The APECS and AMARANTH trials showed that BACE2 gene (BACE1 wt Allele) inhibitors verubecestat and lanabecestat failed to slow cognitive and functional decline in individuals with prodromal or early ALZHEIMER DISEASE, FAMILIAL, 1., INTRODUCTION: The APECS and AMARANTH trials showed that BACE2 gene (BACE1 wt Allele) inhibitors verubecestat and lanabecestat failed to slow cognitive and functional decline in individuals with prodromal or early Alzheime, INTRODUCTION: The APECS and AMARANTH trials showed that BACE2 gene (BACE1 wt Allele) inhibitors verubecestat and lanabecestat failed to slow cognitive and functional decline in individuals with prodromal or early Alzhei[SEP]Relations: familial Alzheimer disease has relations: disease_disease with Alzheimer disease, disease_disease with Alzheimer disease, disease_protein with PRNP, disease_protein with PRNP, disease_disease with inherited prion disease, disease_disease with inherited prion disease, disease_phenotype_positive with Cognitive impairment, disease_phenotype_positive with Cognitive impairment, disease_phenotype_positive with Sleep disturbance, disease_phenotype_positive with Sleep disturbance.", "label": "no"}
{"original_question": "Is  farnesoid X receptor (FXR) a nuclear receptor?", "id": "converted_1013", "sentence1": "Is  farnesoid X receptor (NR1H4 wt Allele) a Receptors, Nuclear?", "sentence2": "NR1H4 gene (NR1H4 wt Allele) belongs to the ligand-activated Receptors, Nuclear superfamily, and functions as a TRANSCRIPTION FACTOR regulating the transcription of numerous Genes involved in Bile Acid [EPC] homeostasis, lipoprotein and glucose metabolism,  NR1H4 gene (NR1H4 wt Allele) is an ascending target for metabolic and inflammatory diseases. As a Receptors, Nuclear, NR1H4 wt Allele exhibits many physiological effects in transcription control of several Genes.,  NR1H4 wt Allele is a member of the Receptors, Nuclear superfamily which is also highly expressed in the Abdomen>Liver. , NR1H4 gene (NR1H4 wt Allele) is a Bile Acid [EPC] Receptors, Nuclear described through Mus sp. knockout studies as a tumor suppressor for the development of Adenocarcinoma of colon, NR1H4 gene (NR1H4 wt Allele, Nr1h4) is a ligand-activated TRANSCRIPTION FACTOR belonging to the Receptors, Nuclear superfamily., the Receptors, Nuclear farnesoid X receptor ,  farnesoid X receptor (NR1H4 wt Allele), a Receptors, Nuclear activated by Bile Acid [EPC] ligands. , T-β-MCA is an farnesoid X receptor (NR1H4 wt Allele) Receptors, Nuclear antagonist,,  NR1H4 gene (NR1H4 wt Allele), a Receptors, Nuclear (NR) and originally considered as a Bile Acid [EPC]-activated transcriptional factor, ,  The Receptors, Nuclear farnesoid X receptor (NR1H4 wt Allele) plays a major role in the enterohepatic cycling of Bile Acids, Liver X Receptors, LXRs, are ligand-activated transcription factors that belong to the group H Receptors, Nuclear (NR) superfamily. , The intracellular Receptors, Nuclear farnesoid X receptor and the transmembrane G protein-coupled receptor GPBAR1 gene respond to Bile Acids by activating transcriptional networks and/or signalling cascades., ncluding those of nuclear receptors, primarily farnesoid X receptor (NR1H4 wt Allele), , ile acids and their cognate Receptors, Nuclear, NR1H4 wt Allele,, NR1H4 gene (NR1H4 wt Allele, Nr1h4) and small heterodimer partner (SHP, NR0B2 wt Allele) are nuclear receptors that are critical to Abdomen>Liver homeostasis., he activation of the Receptors, Nuclear farnesoid X receptor (FXRα), Bile Acid [EPC]-activated Receptors, Nuclear farnesoid X receptor (NR1H4 wt Allele),  Receptors, Nuclear signaling, notably by the farnesoid X receptor (NR1H4 wt Allele, NR1H4 wt Allele (farnesoid X receptor, NRIH4), a Receptors, Nuclear, plays a major role in the control of cholesterol metabolism., The role of the Receptors, Nuclear NR1H4 wt Allele is unclear., Receptors, Nuclear NR1H4 wt Allele , a member of the Receptors, Nuclear superfamily of ligand-activated transcription factors,, NR1H4 gene (NR1H4 wt Allele) is a Receptors, Nuclear that functions as a Bile Acid [EPC] sensor controlling Bile Acid [EPC] homeostasis.[SEP]Relations: Receptors, Nuclear activity has relations: molfunc_protein with RXRA, molfunc_protein with RXRA, molfunc_protein with RXRG, molfunc_protein with RXRG, molfunc_protein with RXRB, molfunc_protein with RXRB, molfunc_protein with NKX3-1, molfunc_protein with NKX3-1, molfunc_protein with ESR1, molfunc_protein with ESR1.", "label": "yes"}
{"original_question": "Is lithium effective for treatment of amyotrophic lateral sclerosis?", "id": "converted_2902", "sentence1": "Is Lithium antipsychotics effective for treatment of Amyotrophic Lateral Sclerosis?", "sentence2": "In terms of Disease-modifying treatment options, several drugs such as Dexpramipexole, pioglitazone, Lithium antipsychotics, and many others have been tested in large multicenter trials, albeit with disappointing results., Despite several positive case reports and short studies, further controlled researches have failed to substantiate any positive effects of Lithium antipsychotics exposure in Amyotrophic Lateral Sclerosis. , The effect of Lithium antipsychotics was different for UNC13A carriers (p = 0.027), but not for C9orf72 carriers (p = 0.22). The 12-month survival probability for UNC13A carriers treated with Lithium Carbonate - Consent Type improved from 40.1% (95% CI 23.2-69.1) to 69.7% (95% CI 50.4-96.3)., Studies in ALS showed consistently negative results and presented evidence against the use of Lithium antipsychotics for the treatment of this Disease., BACKGROUND\nLithium has neuroprotective effects in \"U\" lymphocyte and animal models of Amyotrophic Lateral Sclerosis (ALS), and a small pilot study in patients with ALS showed a significant effect of Lithium antipsychotics on survival., In a pilot clinical study that we recently published we found that Lithium antipsychotics administration slows the progression of Amyotrophic Lateral Sclerosis (ALS) in Homo sapiens patients., BACKGROUND Lithium has neuroprotective effects in \"U\" lymphocyte and animal models of Amyotrophic Lateral Sclerosis (ALS), and a small pilot study in patients with ALS showed a significant effect of Lithium antipsychotics on survival., BACKGROUND A neuroprotective effect of Lithium antipsychotics in Amyotrophic Lateral Sclerosis (ALS) has been recently reported., Lithium delays progression of Amyotrophic Lateral Sclerosis.ALS is a devastating Neurodegenerative Disorders with no effective treatment. , Lithium in patients with Amyotrophic Lateral Sclerosis (LiCALS): a phase 3 multicentre, randomised, double-blind, placebo-controlled trial.<AbstractText Label=\"BACKGROUND\" NlmCategory=\"BACKGROUND\">Lithium has neuroprotective effects in \"U\" lymphocyte and animal models of Amyotrophic Lateral Sclerosis (ALS), and a small pilot study in patients with ALS showed a significant effect of Lithium antipsychotics on survival. , <b>INTRODUCTION</b>: Lithium was proposed in 2008 as an effective candidate in the treatment of ALS after a report claimed that it was able to delay functional deterioration by 40% and that none of the 16 patients treated with a combination of Lithium antipsychotics plus riluzole had died during a 15-month follow-up period., A recently published study also ruled out any possible modest effect.<br><b>CONCLUSIONS</b>: There is evidence to suggest that Lithium antipsychotics has no short-term benefits in ALS., A comparison of the group of patients treated with Lithium antipsychotics+riluzole and the control group treated with riluzole alone showed no statistically significant differences in rates of functional decline, deterioration of respiratory function, or survival time., None of the patients treated with Lithium antipsychotics died during the 15 months of the follow-up, and Disease progression was markedly attenuated when compared with age-, Disease duration-, and sex-matched control patients treated with riluzole for the same amount of time.[SEP]Relations: Amyotrophic Lateral Sclerosis has relations: disease_disease with progressive muscular atrophy, disease_disease with progressive muscular atrophy, disease_protein with ANG, disease_protein with ANG, disease_protein with CLU, disease_protein with CLU, disease_protein with CD7, disease_protein with CD7, disease_protein with CTSD, disease_protein with CTSD.", "label": "no"}
{"original_question": "Is p100 the precursor protein molecule of the NF-kappaB transcription factor subunit p50?", "id": "converted_1329", "sentence1": "Is TPX2 protein, human the precursor protein molecule of the NF-kappaB transcription factor subunit Pattern ERG P50?", "sentence2": "We previously reported that alymphoplasia (aly/aly) CASP14 gene, which have a natural loss-of-function mutation in the Nik gene, which encodes a MAP Kinase Kinase Kinase essential for the processing of TPX2 protein, human to GTF2H4 gene in the alternative nuclear factor-κB (NF-κB) pathway, show mild osteopetrosis with an increase in several parameters of bone formation: , Proteolytic processing of the nuclear factor (NF)-kappaB2 precursor protein TPX2 protein, human generates the active NF-kappaB2 subunit GTF2H4 gene, which in turn transcriptionally up-regulates TPX2 protein, human expression. , The Mammals Rel/NF-kappaB family of TRANSCRIPTION FACTOR, including RELA protein, human, REL wt Allele, RELB gene, NF-kappaB1 (Pattern ERG P50 and its precursor Enhancer of Filamentation 1), and NF-kappaB2 (GTF2H4 gene and its precursor TPX2 protein, human), plays a central role in the immune system by regulating several processes ranging from the development and survival of Specimen Source Codes - Lymphocytes and Lymphoid organ structure to the control of immune responses and malignant transformation., NF-kappaB functions as a hetero- or homo-dimer which can be formed from five NF-kappaB subunits, NF-kappaB1 (Pattern ERG P50 and its precursor Enhancer of Filamentation 1), NF-kappaB2 (GTF2H4 gene and its precursor TPX2 protein, human), RELA protein, human (synaptotagmin synaptotagmin p65), RELB gene and REL wt Allele., The non-canonical pathway based on processing of NF-kappaB2 precursor protein TPX2 protein, human to generate GTF2H4 gene plays a critical role in controlling B cell function and Lymphoid organogenesis., Processing of NF-kappaB2 precursor protein TPX2 protein, human to generate GTF2H4 gene is tightly controlled, which is important for proper function of NF-kappaB., Processing of NF-kappa B2 precursor protein TPX2 protein, human to generate GTF2H4 gene is tightly regulated. , Processing of the NF-kappaB2 precursor protein TPX2 protein, human to generate GTF2H4 gene is an important step of NF-kappaB regulation., Targeted disruption of the Rel/NF-kappaB family members NF-kappaB2, encoding TPX2 protein, human/GTF2H4 gene, and RELB gene in CASP14 gene results in anatomical defects of secondary Lymphoid tissues., Here, we show that in Therapeutic gamma delta T-Specimen Source Codes - Lymphocytes infected with the human T-cell leukemia virus (Human T-lymphotropic virus 2), IKKalpha is targeted to a novel signaling pathway that mediates processing of the nfkappab2 precursor protein TPX2 protein, human, resulting in active production of the NF-kappaB subunit, GTF2H4 gene., nfkb2 encodes two members of the NF-kappa B/Rel family of proteins: GTF2H4 gene and TPX2 protein, human. The TPX2 protein, human polypeptide has been proposed to serve as a precursor of GTF2H4 gene, which corresponds to the N-terminal half of TPX2 protein, human., In most Cells, small amounts of GTF2H4 gene are produced relative to the levels of TPX2 protein, human, unlike the usually balanced production of nfkb1-derived Pattern ERG P50 and Enhancer of Filamentation 1. , The alternative or second pathway proceeded via NF-kappaB-inducing MAP Kinase Kinase Kinase (NIK)-, IKKalpha-, and protein synthesis-dependent processing of the inhibitory NF-kappaB2 TPX2 protein, human precursor protein to the GTF2H4 gene form and resulted in a delayed but sustained activation of primarily RELB gene-containing NF-kappaB dimers., In one exceptional case, generation of the Pattern ERG P50 subunit of the transcriptional regulator NF-kappaB, the precursor protein Enhancer of Filamentation 1 is processed in a limited manner: the N-terminal domain yields the Pattern ERG P50 subunit, whereas the C-terminal domain is degraded, Proteolytic processing of the Enhancer of Filamentation 1 precursor (NF-kappa B1) generates the Pattern ERG P50 subunit of NF-kappa B, Enhancer of Filamentation 1 (NFKB1 gene gene) acts in a dual way as a cytoplasmic IkappaB molecule and as the source of the NF-kappaB Pattern ERG P50 subunit upon processing, The Pattern ERG P50 subunit of NF-kappa B is derived from the amino terminus of a 105 kilodalton precursor, Regulation of the transcription factor NF-kappaB involves proteasome-mediated processing of the NF-kappaB1 Enhancer of Filamentation 1 precursor protein, which generates the Pattern ERG P50 subunit of NF-kappaB, This effort identified NF-kappaB1 (Enhancer of Filamentation 1), an atypical IkappaB molecule and the precursor of NF-kappaB subunit Pattern ERG P50, NF-kappaB functions as a hetero- or homo-dimer which can be formed from five NF-kappaB subunits, NF-kappaB1 (Pattern ERG P50 and its precursor Enhancer of Filamentation 1), NF-kappaB2 (GTF2H4 gene and its precursor TPX2 protein, human), RELA protein, human (synaptotagmin synaptotagmin p65), RELB gene and REL wt Allele, The Mammals Rel/NF-kappaB family of TRANSCRIPTION FACTOR, including RELA protein, human, REL wt Allele, RELB gene, NF-kappaB1 (Pattern ERG P50 and its precursor Enhancer of Filamentation 1), and NF-kappaB2 (GTF2H4 gene and its precursor TPX2 protein, human), plays a central role in the immune system by regulating several processes ranging from the development and survival of Specimen Source Codes - Lymphocytes and Lymphoid organ structure to the control of immune responses and malignant transformation[SEP]Relations: NF-kappaB Decoy has relations: drug_protein with NFKB1 gene, drug_protein with NFKB1 gene, drug_protein with NFKB2, drug_protein with NFKB2. transcription factor binding has relations: molfunc_protein with NFIA, molfunc_protein with NFIA, molfunc_protein with TP53, molfunc_protein with TP53. RELB has relations: bioprocess_protein with NIK/NF-kappaB signaling, bioprocess_protein with NIK/NF-kappaB signaling.", "label": "no"}
{"original_question": "Is indicated the use of antioxidant supplements in patients at risk for coronary artery disease?", "id": "converted_815", "sentence1": "Is indicated the use of antioxidant supplements in patients at risk for coronary artery disease?", "sentence2": "We and others have published observational epidemiologic studies in support of VITAMINS [VA Class] in the primary prevention of CVD, but the results from intervention studies are mixed., For Vitamin E Drug Class, observational data suggest benefit at doses of 100 to 400 IU/d. Results from recent large-scale trials are mixed, with some showing modest benefit but others suggesting no benefit, especially for secondary prevention. Results for Vitamin B Drug Class are also mixed and further complicated by the recent folate fortification of the flour supply. If greater B vitamin intake does reduce CVD, the benefits are likely to be greatest for primary prevention and in populations with intake below dietary reference standards. , In the dose-response meta-analysis, each 30 mg/day increase in Vitamin C [EPC], 30 IU/day increase in Vitamin E Drug Class, and 1 mg/day increase in beta carotene yielded the estimated overall relative risk for altretamine/cisplatin/cyclophosphamide protocol of 1.01 (95% CI, 0.99-1.02), 0.96 (95% CI, 0.94-0.99), and 1.00 (95% CI, 0.88-1.14), respectively. CONCLUSIONS: Our findings in this meta-analysis suggest that an increase in dietary intake of antioxidant VITAMINS [VA Class] has encouraging prospects for possible altretamine/cisplatin/cyclophosphamide protocol prevention., High levels of α-tocopherol in serum were associated with 30% lower cyclophosphamide/dacarbazine/doxorubicin protocol risk in another study (HR 0.71; 95%CI 0.53-0.94). Among Minerals (Zinc Supplements, Selenium supplement, and Dietary Chromium), an inverse association between Zinc Supplements and cyclophosphamide/dacarbazine/doxorubicin protocol was observed; levels lower than 14.1 µmol/L were associated with an increased risk for cyclophosphamide/dacarbazine/doxorubicin protocol (RR 1.70; 95%CI 1.21-2.38)., The information available on this issue is scarce. Further prospective studies are needed to elucidate the role of these Nutrients in the Cardiovascular system risk of patients with Diabetes Mellitus., ubidecarenone supplementation at a dosage of 150 mg appears to decrease the inflammatory marker Recombinant Interleukin-6 in patients with cyclophosphamide/dacarbazine/doxorubicin protocol.,  ubidecarenone supplements at a dose of 150 mg can decrease oxidative stress and increase antioxidant enzyme activity in patients with cyclophosphamide/dacarbazine/doxorubicin protocol. A higher dose of coenzyme Q10 supplements (>150 mg/d) might promote rapid and sustainable antioxidation in patients with cyclophosphamide/dacarbazine/doxorubicin protocol., alpha tocopherol or beta carotene supplementation has no protective effect on macrovascular outcomes or total mortality of diabetic male smokers., Sodium selenite supplementation increases GPx-1 activity in Endothelial Cells and in cyclophosphamide/dacarbazine/doxorubicin protocol patients. Future studies have to demonstrate whether long-term cyclophosphamide/dacarbazine/doxorubicin protocol outcome can be improved., After 7.3 years of treatment and follow-up, a combination pill of folic acid, pyridoxine, and Vitamin B12 [EPC] did not reduce a combined end point of total Cardiovascular system events among high-risk women, despite significant homocysteine lowering.,  In this population-based study, Vitamin E Drug Class use was unrelated to mortality, but this apparently null finding seems to represent a combination of increased mortality in those with severe Cardiovascular Diseases and a possible protective effect in those without.,  In this large cohort of apparently healthy US male physicians, self-selected supplementation with Vitamin E Drug Class, Vitamin C [EPC], or Multivitamin Drug Class was not associated with a significant decrease in total CVD or altretamine/cisplatin/cyclophosphamide protocol mortality. , The American Heart Association has recommended consumption of a balanced diet with emphasis on antioxidant-rich fruits and vegetables but has made no recommendations regarding Vitamin E Drug Class supplementation for the general population. Although Vitamin E Drug Class supplementation seems to be safe for most people, recommendations from health care professionals should reflect the uncertainty of established benefit as demonstrated in clinical trials, Recent studies show that supplementation with antioxidant VITAMINS [VA Class] E and C have benefits in altretamine/cisplatin/cyclophosphamide protocol prevention; however, supplementation with beta carotene may have deleterious effects and is not recommended. Current evidence suggests that patients with altretamine/cisplatin/cyclophosphamide protocol would probably benefit from taking Vitamin E Drug Class in a dosage of 400 IU per day and Vitamin C [EPC] in a dosage of 500 to 1,000 mg per day. Clinicians may also want to consider Vitamin supplementation for altretamine/cisplatin/cyclophosphamide protocol prevention in high-risk patients. folate lowers elevated homocysteine levels, but evidence for routine supplemental use does not yet exist. , In patients at high risk for Cardiovascular system events, treatment with Vitamin E Drug Class for a mean of 4.5 years had no apparent effect on Cardiovascular system outcomes.[SEP]Relations: Cardiovascular Diseases has relations: contraindication with Antipyrine, contraindication with Antipyrine, contraindication with Amoxapine, contraindication with Amoxapine, contraindication with Methionine, contraindication with Methionine, contraindication with Fentanyl, contraindication with Fentanyl, contraindication with Carbinoxamine, contraindication with Carbinoxamine.", "label": "no"}
{"original_question": "Do mutations of AKT1 occur in meningiomas?", "id": "converted_34", "sentence1": "Do Gene Mutation of AKT1 protein, human occur in Meningioma?", "sentence2": "The recent identification of somatic Gene Mutation in components of the SHH-GLI1 and AKT1 protein, human protein, human-MTOR signaling pathways indicates the potential for cross talk of these pathways in the development of Meningioma., A Mutation Abnormality in PIK3CA gene gene or AKT1 protein, human protein, human was found in around 9 % of the cases., AKT1E17K Gene Mutation cluster with meningothelial and transitional Meningioma and can be detected by SFRP1 gene gene immunohistochemistry., AKT1E17K Gene Mutation were exclusively seen in Meningioma and occurred in 65 of 958 of these Neoplasms. A strong preponderance was seen in the Variant of Meningothelial Benign Meningioma WHO grade I of basal and spinal localization. In contrast, AKT1E17K Gene Mutation were rare in WHO grade II and absent in WHO grade III Meningioma. , We observed strong up-regulation of SFRP1 gene gene expression in all Meningioma with AKT1E17K Mutation Abnormality and in HEK293 Cells after transfection with Mutant AKT1E17K, but not in Meningioma and HEK293 Cells lacking this Mutation Abnormality., Samoan language and AKT1 protein, human protein, human Gene Mutation occur in non-Neurofibromatosis 2 Meningioma., Recurrent Gene Mutation in Samoan language and AKT1 protein, human protein, human are mutually exclusive with Neurofibromatosis 2 loss in Benign Meningioma., Genomic sequencing of Meningioma identifies oncogenic Samoan language and AKT1 protein, human protein, human Gene Mutation.,  A subset of Meningioma lacking Neurofibromatosis 2 alterations harbored recurrent oncogenic Gene Mutation in AKT1 protein, human protein, human (p.Glu17Lys) and Samoan language (p.Trp535Leu) and exhibited immunohistochemical evidence of activation of these pathways., Genomic analysis of non-Neurofibromatosis 2 Meningioma reveals Gene Mutation in TRAF7 gene gene, KLF4 protein, human protein, human, AKT1 protein, human protein, human, and Samoan language., A subset of Meningioma lacking Neurofibromatosis 2 alterations harbored recurrent oncogenic Gene Mutation in AKT1 protein, human protein, human (p.Glu17Lys) and Samoan language (p.Trp535Leu) and exhibited immunohistochemical evidence of activation of these pathways., Samoan language and AKT1 protein, human protein, human Gene Mutation occur in non-Neurofibromatosis 2 Meningioma, The recent identification of somatic Gene Mutation in components of the SHH-GLI1 and AKT1 protein, human protein, human-MTOR signaling pathways indicates the potential for cross talk of these pathways in the development of Meningioma, A subset of Meningioma lacking Neurofibromatosis 2 alterations harbored recurrent oncogenic Gene Mutation in AKT1 protein, human protein, human (p.Glu17Lys) and Samoan language (p.Trp535Leu) and exhibited immunohistochemical evidence of activation of these pathways, Genomic analysis of non-Neurofibromatosis 2 Meningioma reveals Gene Mutation in TRAF7 gene gene, KLF4 protein, human protein, human, AKT1 protein, human protein, human, and Samoan language, Genomic sequencing of Meningioma identifies oncogenic Samoan language and AKT1 protein, human protein, human Gene Mutation, Recurrent Gene Mutation in Samoan language and AKT1 protein, human protein, human are mutually exclusive with Neurofibromatosis 2 loss in Benign Meningioma, A subset of Meningioma lacking Neurofibromatosis 2 alterations harbored recurrent oncogenic Gene Mutation in AKT1 protein, human protein, human (p.Glu17Lys) and Samoan language (p.Trp535Leu) and exhibited immunohistochemical evidence of activation of these pathways. These Gene Mutation were present in therapeutically challenging Neoplasms of the Base of skull structure and higher grade. , A subset of Meningioma lacking Neurofibromatosis 2 alterations harbored recurrent oncogenic Gene Mutation in AKT1 protein, human protein, human (p.Glu17Lys) and Samoan language (p.Trp535Leu) and exhibited immunohistochemical evidence of activation of these pathways. [SEP]Relations: benign Benign Meningioma has relations: disease_protein with AKT1 protein, human, disease_protein with AKT1 protein, human, disease_protein with HES1, disease_protein with HES1, disease_protein with BAP1, disease_protein with BAP1. Meningothelial Benign Meningioma has relations: disease_protein with AKT1 protein, human, disease_protein with AKT1 protein, human, disease_protein with HES1, disease_protein with HES1.", "label": "yes"}
{"original_question": "Are EDNRB mutations involved in the development of Hirschsprung disease?", "id": "converted_1285", "sentence1": "Are EDNRB protein, human mutations involved in the development of Hirschsprung Disease?", "sentence2": "QTL analysis identifies a modifier Gene Locus of aganglionosis in the Rattus norvegicus model of Hirschsprung Disease carrying Ednrb(sl) mutations, As reported previously, when the same null Mutation Abnormality of the EDNRB protein, human gene, Ednrb(sl), was introgressed into the F344 strain, almost 60% of F344-Ednrb(sl/sl) pups did not show any symptoms of aganglionosis, appearing healthy and normally fertile., Genetic background strongly modifies the severity of symptoms of Hirschsprung Disease, but not hearing impairment in rats carrying Ednrb(sl) mutations, In this study, we found that the null Mutation Abnormality of the EDNRB protein, human gene, thought indispensable for enteric Neurons development, is insufficient to result in HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 Disease when bred onto a different genetic background in rats carrying Ednrb(sl) mutations., New roles of EDNRB protein, human protein, human and EDN3 gene gene in the pathogenesis of Hirschsprung Disease., The aim of this study was to evaluate the implication of the EDN3 gene gene and EDNRB protein, human protein, human Genes in a series of patients with Hirschsprung Disease from Spain and determinate their mutational spectrum., A De Novo novel Mutation Abnormality of the EDNRB protein, human protein, human gene in a Taiwanese boy with Hirschsprung Disease, Although mutations in eight different Genes (EDNRB protein, human protein, human, EDN3 gene gene, ECE1 gene gene, SOX10 Transcription Factor Transcription Factor, ret unit of radiation dose, Glial Cell Line-Derived Neurotrophic Factor, CX3CL1 gene, SLC9A3R2 gene) have been identified in affected individuals, it is now clear that ret unit of radiation dose and EDNRB protein, human protein, human are the primary Genes implicated in the etiology of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1., Gene Mutation in Genes of the ret unit of radiation dose High Affinity Nerve Growth Factor Receptor, human and endothelin receptor B (EDNRB protein, human protein, human) signaling pathways have been shown to be associated in HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 patients. , Interactions between Sox10 and EdnrB modulate penetrance and severity of aganglionosis in the Sox10Dom mouse model of Hirschsprung Disease, Molecular genetic analyses have revealed that interactions between mutations in the Genes encoding the ret unit of radiation dose High Affinity Nerve Growth Factor Receptor, human and the endothelin receptor type B (EDNRB protein, human protein, human) are central to the genesis of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, Genome-wide association study and mouse model identify interaction between ret unit of radiation dose and EDNRB protein, human protein, human pathways in Hirschsprung Disease, Thus, genetic interaction between mutations in ret unit of radiation dose and EDNRB protein, human protein, human is an underlying mechanism for this complex disorder., EDNRB protein, human protein, human/EDN3 gene gene and Hirschsprung Disease type II., Analysis of the ret unit of radiation dose, Glial Cell Line-Derived Neurotrophic Factor, EDN3 gene gene, and EDNRB protein, human protein, human Genes in patients with intestinal neuronal dysplasia and Hirschsprung Disease, wo susceptibility Genes have been recently identified in HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, namely the ret unit of radiation dose proto-oncogene and the Receptor, Endothelin B, Type 2 (EDNRB protein, human protein, human) gene., We conclude that Ednrb loss only in Neural Crest Cells is sufficient to produce the Hirschsprungs Disease phenotype observed with genomic Ednrb mutations, EDNRB protein, human protein, human mutations were detected in 2 of the 13 short-segment Hodgkin Disease, The mutations of EDNRB protein, human protein, human gene and EDN-3 gene are found in the short-segment Hodgkin Disease of sporadic Hirschsprung's Disease in Chinese population, which suggests that the EDNRB protein, human protein, human gene and EDN-3 gene play important roles in the pathogenesis of Hodgkin Disease, Functional characterization of three mutations of the Receptor, Endothelin B, Type 2 gene in patients with Hirschsprung's Disease, Hirschsprung's Disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1) is one the most common congenital intestinal Disease. It leads to aganglionic megacolon in the early childhood. Several susceptibility Genes have been identified : ret unit of radiation dose protooncogene and its ligand, Neuroglia derived neutrophic factor (Glial Cell Line-Derived Neurotrophic Factor), Sox 10, Endothelin-3 (EDN3 gene gene) and its receptor B (EDNRB protein, human protein, human). EDNRB protein, human protein, human mutations are found in 5% of familial or sporadic HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, Enteric aganglionosis in Hirschsprung Disease has been linked to Genes coding for Endothelin-3 (EDN3 gene gene) and the Receptor, Endothelin B, Type 2 (EDNRB protein, human protein, human), To date, three Genes have been identified as susceptibility Genes for Hirschsprung's Disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1), the ret unit of radiation dose proto-oncogene, the endothelin-B receptor gene (EDNRB protein, human protein, human) and the Endothelin-3 gene (EDN3 gene gene), Our data indicate that ret unit of radiation dose and EDNRB protein, human protein, human mutations have a role in the aetiology of some sporadically occurring HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, Gene Mutation of the endothelin-B receptor and Endothelin-3 Genes in Hirschsprung's Disease, The endothelin-B receptor gene (EDNRB protein, human protein, human) and the Endothelin-3 gene (EDN3 gene gene) have recently been recognized as susceptibility Genes for Hirschsprung's Disease (Hodgkin Disease), These observations confirm that impaired function of the endothelin-B receptor or Endothelin-3 is involved in the aetiology of some human Hodgkin Disease cases. EDNRB protein, human protein, human mutations appear to be associated with short-segment Hodgkin Disease, in contrast to ret unit of radiation dose mutations, which are found mainly in Long-segment aganglionosis, In addition to mutations in the ret unit of radiation dose and EDNRB protein, human protein, human Genes, embryonic environmental factors and/or other genetic factors appear to be involved in the development of Hirschsprung Disease., Heterozygous endothelin receptor B (EDNRB protein, human protein, human) mutations in isolated Hirschsprung Disease., QTL analysis identifies a modifier Gene Locus of aganglionosis in the Rattus norvegicus model of Hirschsprung Disease carrying Ednrb(sl) mutations., Homozygous mutations in the endothelin-B receptor gene (EDNRB protein, human protein, human) on 13q22 have been identified in Homo sapiens and CASP14 gene with Hirschsprung Disease type 3 (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 2)., A De Novo novel Mutation Abnormality of the EDNRB protein, human protein, human gene in a Taiwanese boy with Hirschsprung Disease., Hitherto however, homozygosity for EDNRB protein, human protein, human mutations accounted for the HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1-Waardenburg syndrome (Werner Syndrome) association., These data might suggest that EDNRB protein, human protein, human mutations could be dosage sensitive: heterozygosity would predispose to isolated HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 with incomplete penetrance, while homozygosity would result in more complex neurocristopathies associating HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 and Werner Syndrome features., Highly recurrent ret unit of radiation dose mutations and novel mutations in Genes of the High Affinity Nerve Growth Factor Receptor, human and endothelin receptor B pathways in Chinese patients with sporadic Hirschsprung Disease., Gene Mutation in Genes encoding the ret unit of radiation dose High Affinity Nerve Growth Factor Receptor, human and endothelin receptor type B (EDNRB protein, human protein, human) are involved in HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 pathogenesis; however, also important in ENS development are Molecule that mediate events that are more restricted than those of ret unit of radiation dose and EDNRB protein, human protein, human, act later in development and which might not be HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1-associated., Several missense mutations of the endothelin-B receptor (EDNRB protein, human protein, human) associated with Hirschsprung Disease have recently been identified., These findings indicate that these missense mutations result in loss of function of EDNRB protein, human protein, human, and may provide the molecular pathological basis of Hirschsprung Disease in some individuals., Manifestation of the Disease has been linked to mutations in Genes that encode the crucial signals for the development of the enteric nervous system-the ret unit of radiation dose and EDNRB protein, human protein, human signalling pathways., In addition to mutations in the ret unit of radiation dose and EDNRB protein, human protein, human Genes, embryonic environmental factors and/or other genetic factors appear to be involved in the development of Hirschsprung Disease, In this study, we investigated whether germline mutations of endothelin receptor B (EDNRB protein, human protein, human), a gene involved in Hirschsprung Disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1), could also predispose for Melanocytic neoplasm (Millimole per Liter), However, the similarity between the distal Aganglionosis, Colonic in Hirschsprung Disease and that due to EDN3 gene gene or EDNRB protein, human protein, human mutations led to the hypothesis that levels of expression of these Genes might be affected in the absence of Mutation Abnormality, thus causing the Hirschsprung Disease phenotype, Our data strongly suggest that EDNRB protein, human protein, human is involved in predisposition for two different multigenic disorders, HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 and Melanocytic neoplasm.[SEP]Relations: EDNRB protein, human has relations: disease_protein with Hirschsprung Disease, disease_protein with Hirschsprung Disease, disease_protein with hirschsprung Disease, susceptibility to, disease_protein with hirschsprung Disease, susceptibility to. Hirschsprung Disease has relations: disease_protein with EDNRB protein, human, disease_protein with EDNRB protein, human, disease_protein with EDNRB protein, human, disease_protein with EDNRB protein, human, disease_protein with EDNRB protein, human, disease_protein with EDNRB protein, human.", "label": "yes"}
{"original_question": "Has ProSavin undergone phase IV clinical trials by 2018?", "id": "converted_3498", "sentence1": "Has ProSavin undergone phase IV clinical trials by 2018?", "sentence2": "Long-term safety and tolerability of ProSavin, a lentiviral vector-based gene therapy for Parkinson Disease: a dose escalation, open-label, phase 1/2 trial., We undertook a phase 1/2 open-label trial with 12-month follow-up at two study sites (France and UK) to assess the safety and efficacy of ProSavin after Bilateral injection into the Structure of Structure of putamen of patients with Parkinson Disease. [SEP]Relations: Parkinson disease has relations: contraindication with Prochlorperazine, contraindication with Prochlorperazine, contraindication with Indomethacin, contraindication with Indomethacin, contraindication with Amikacin, contraindication with Amikacin, contraindication with Rivastigmine, contraindication with Rivastigmine, contraindication with Perphenazine, contraindication with Perphenazine.", "label": "no"}
{"original_question": "Can Diazepam be beneficial  in the treatment of  traumatic brain injury?", "id": "converted_3008", "sentence1": "Can Diazepam be beneficial  in the treatment of  traumatic brain injury?", "sentence2": "he present experiment examined the effects of diazepam, a positive modulator at the GABA-A Receptor, on survival and cognitive performance in traumatically brain-injured animal allergen extracts. I[SEP]Relations: Diazepam has relations: drug_effect with Memory impairment, drug_effect with Memory impairment, drug_effect with Loss of consciousness, drug_effect with Loss of consciousness, drug_effect with Pain, drug_effect with Pain, drug_effect with Sensory impairment, drug_effect with Sensory impairment, drug_effect with Headache, drug_effect with Headache.", "label": "yes"}
{"original_question": "Does Rad9 interact with Aft1 in S.cerevisiae?", "id": "converted_903", "sentence1": "Does RAD9A wt Allele interact with Aft1 in S.cerevisiae?", "sentence2": "RAD9A wt Allele interacts with Aft1 to facilitate Genome - anatomical entity surveillance in fragile genomic sites under non-DNA damage-inducing conditions in S. cerevisiae., Here we show that RAD9A wt Allele checkpoint protein, known to mediate the damage signal from upstream to downstream essential kinases, interacts with Aft1 transcription factor in the budding yeast. Aft1 regulates iron homeostasis and is also involved in Genome - anatomical entity integrity having additional iron-independent functions. Using Genome - anatomical entity-wide expression and chromatin immunoprecipitation approaches, we found RAD9A wt Allele to be recruited to 16% of the yeast genes, often related to cellular growth and metabolism, while affecting the transcription of ∼2% of the coding Genome - anatomical entity in the absence of exogenously induced DNA damage. Importantly, RAD9A wt Allele is recruited to fragile genomic regions (transcriptionally active, GC rich, Centromere, meiotic recombination hotspots and retrotransposons) non-randomly and in an Aft1-dependent manner. Further analyses revealed substantial Genome - anatomical entity-wide parallels between RAD9A wt Allele binding patterns to the Genome - anatomical entity and major activating histone marks, such as H3K36me, H3K79me and H3K4me. Thus, our findings suggest that RAD9A wt Allele functions together with Aft1 on DNA damage-prone chromatin to facilitate Genome - anatomical entity surveillance, thereby ensuring rapid and effective response to possible DNA damage events., Here we show that RAD9A wt Allele checkpoint protein, known to mediate the damage signal from upstream to downstream essential kinases, interacts with Aft1 transcription factor in the budding yeast, RAD9A wt Allele interacts with Aft1 to facilitate Genome - anatomical entity surveillance in fragile genomic sites under non-DNA damage-inducing conditions in S. cerevisiae, Here we show that RAD9A wt Allele checkpoint protein, known to mediate the damage signal from upstream to downstream essential kinases, interacts with Aft1 transcription factor in the budding yeast. Aft1 regulates iron homeostasis and is also involved in Genome - anatomical entity integrity having additional iron-independent functions. Using Genome - anatomical entity-wide expression and chromatin immunoprecipitation approaches, we found RAD9A wt Allele to be recruited to 16% of the yeast genes, often related to cellular growth and metabolism, while affecting the transcription of ?2% of the coding Genome - anatomical entity in the absence of exogenously induced DNA damage. , Importantly, RAD9A wt Allele is recruited to fragile genomic regions (transcriptionally active, GC rich, Centromere, meiotic recombination hotspots and retrotransposons) non-randomly and in an Aft1-dependent manner. Further analyses revealed substantial Genome - anatomical entity-wide parallels between RAD9A wt Allele binding patterns to the Genome - anatomical entity and major activating histone marks, such as H3K36me, H3K79me and H3K4me. Thus, our findings suggest that RAD9A wt Allele functions together with Aft1 on DNA damage-prone chromatin to facilitate Genome - anatomical entity surveillance, thereby ensuring rapid and effective response to possible DNA damage events.[SEP]Relations: centromere clustering has relations: bioprocess_bioprocess with chromosome localization, bioprocess_bioprocess with chromosome localization, bioprocess_bioprocess with centromere clustering at the mitotic interphase nuclear envelope, bioprocess_bioprocess with centromere clustering at the mitotic interphase nuclear envelope, bioprocess_bioprocess with centromere localization, bioprocess_bioprocess with centromere localization, bioprocess_bioprocess with meiotic centromere clustering, bioprocess_bioprocess with meiotic centromere clustering. anatomical entity has relations: anatomy_anatomy with insect mouthpart, anatomy_anatomy with insect mouthpart.", "label": "yes"}
{"original_question": "Are retroviruses used for gene therapy?", "id": "converted_690", "sentence1": "Are retroviruses used for gene therapy?", "sentence2": "Several Immunologic Deficiency Syndromes have been treated successfully by stem cell-targeted, retroviral-mediated gene transfer with reconstitution of the immune system following infusion of the transduced Cells., In this work we have developed and tested a self-inactivating (Sinhalese language) gammaretroviral vector (SINfes.gp91s) containing a codon-optimized transgene (gp91(phox)) under the transcriptional control of a myeloid promoter for the gene therapy of the X-linked form of Peroxisome Biogenesis Disorder, Complementation Group D (X-Peroxisome Biogenesis Disorder, Complementation Group D).,  We used a lentiviral vector encoding functional Wiskott-Aldrich Syndrome wt Allele to genetically correct HSPCs from three Wiskott-Aldrich Syndrome patients and reinfused the Cells after a reduced-intensity conditioning regimen, We used a lentiviral vector to transfer a functional ARSA gene into hematopoietic stem Cells (Hematopoietic stem Cells) from three presymptomatic patients who showed Genetic, biochemical, and neurophysiological evidence of late infantile Leukodystrophy, Metachromatic. , We assessed lentiviral vectors (LVs) targeted to the EC surface marker CD105 for in vivo gene delivery., Guanine Nucleotide Exchange Factors and apoptin genes were cloned into a doxycycline-regulated retrovirus-mediated gene expression system.[SEP]Relations: Geneticin has relations: drug_drug with Trimebutine, drug_drug with Trimebutine, drug_drug with Reviparin, drug_drug with Reviparin, drug_drug with Ledipasvir, drug_drug with Ledipasvir, drug_drug with Dexmedetomidine, drug_drug with Dexmedetomidine, drug_drug with Rasagiline, drug_drug with Rasagiline.", "label": "yes"}
{"original_question": "Does MicroRNA-21 (miR-21) contribute to cardiovascular disease?", "id": "converted_163", "sentence1": "Does MicroRNA-21 (MIR21 gene) contribute to Cardiovascular system Disease?", "sentence2": "The synergistic effect of MIR21 gene and miR-1 were functionally validated for their significant influences on myocardial apoptosis, Cardiac - anatomy qualifier hypertrophy and Fibrosis., Taken together, we found a novel reciprocal loop between MIR21 gene and TGFβRIII in Cardiac - anatomy qualifier Fibrosis caused by Myocardial infarction:Finding:Point in time:^Patient:Ordinal in CASP14 gene, and targeting this pathway could be a new strategy for the prevention and treatment of myocardial remodeling., It is still controversial whether microRNA-21 (MIR21 gene) participates in the process of Cardiac - anatomy qualifier Fibrosis., In CASP14 gene, myocardial MIR21 gene overexpression is related to Cardiac - anatomy qualifier Fibrosis elicited by pressure overload. , The myocardial and plasma levels of MIR21 gene were significantly higher in the AS patients compared with the controls and correlated directly with the echocardiographic mean transvalvular gradients., Our results support the role of MIR21 gene as a regulator of the fibrotic process that occurs in response to pressure overload in AS patients and underscore the value of circulating MIR21 gene as a biomarker for myocardial Fibrosis., Ad-MIR21 gene improves LV remodeling and decreases the apoptosis of Myocytes, Cardiac, suggesting the possible mechanism by which Ad-MIR21 gene functions in protecting against I/R injury., In the Ad-MIR21 gene group, LV dimensions, Myocardial Infarction size, LV/BW, collagen type Ⅰ, type Ⅲ and PCNA positive cells all significantly decreased compared with the Ad-GFP group., While MIR21 gene, -133, -150, -195, and -214 regulate cardiomyocyte hypertrophy, miR-1/-133 and miR-208 have been elucidated to influence myocardial contractile function. In addition, MIR21 gene, -24, -133, -210, -494, and -499 appear to protect Muscle Cells against I/R-induced apoptosis, whereas miR-1, -29, -199a, and -320 promote apoptosis. Myocardial Fibrosis can be regulated by the miR-29 family and MIR21 gene., The small regulatory RNA microRNA-21 (MIR21 gene) plays a crucial role in a plethora of biological functions and diseases including development, Primary malignant neoplasm, Cardiovascular system diseases and Inflammation., During recent years, additional roles of MIR21 gene in Cardiovascular system and pulmonary diseases, including Cardiac - anatomy qualifier and pulmonary Fibrosis as well as Myocardial infarction:Finding:Point in time:^Patient:Ordinal have been described., On the other hand, MIR21 gene, miR-199a, miR-210, and miR-494 have been proven critical for the Muscle Cells' adaptation and survival during hypoxia/ischemia. , Studies have shown that several miRs, including miR-1, miR-133, MIR21 gene, miR-126, miR-320, miR-92a, and miR-199a, are regulated after preconditioning and play an active role in protecting the Chest>Heart against ischemia/reperfusion injury., Studies using various in vivo, ex vivo, and in vitro models have suggested the possible involvement of miR-1, MIR21 gene, miR-29, miR-92a, miR-133, miR-199a, and miR-320 in Reperfusion Injury and/or remodeling after Myocardial infarction:Finding:Point in time:^Patient:Ordinal., MicroRNA-21 (MIR21 gene) is a highly expressed microRNA (miRNA) in Cardiovascular system system. Recent studies have revealed that its expression is deregulated in Chest>Heart and vasculature under Cardiovascular system Disease conditions such as proliferative vascular Disease, Cardiac - anatomy qualifier hypertrophy and Congestive Chest>Heart failure, and Myocardial Ischemia. MIR21 gene is found to play important roles in vascular smooth muscle \"U\" lymphocyte proliferation and apoptosis, Heart \"U\" lymphocyte growth and Cessation of life, and Cardiac - anatomy qualifier fibroblast functions. Accordingly, MIR21 gene is proven to be involved in the pathogenesis of the above-mentioned Cardiovascular system diseases as demonstrated by both loss-of-function and gain-of-function approaches., MIR21 gene might be a novel therapeutic target in Cardiovascular system diseases., This review article summarizes the research progress regarding the roles of MIR21 gene in Cardiovascular system Disease., Remarkably, MIR21 gene was one of most upregulated miRNAs in hearts after Immunoprecipitation. In vivo, Immunoprecipitation-mediated Cardiac - anatomy qualifier protection against ischaemia/reperfusion injury was inhibited by knockdown of Cardiac - anatomy qualifier MIR21 gene. In cultured Cardiac - anatomy qualifier Muscle Cells, we identified that MIR21 gene also had a protective effect on hypoxia/reoxygenation-induced \"U\" lymphocyte apoptosis that was associated with its target gene, programmed \"U\" lymphocyte Cessation of life 4. The protective effect of MIR21 gene on Heart \"U\" lymphocyte apoptosis was further confirmed in Rattus norvegicus hearts after ischaemia/reperfusion injury in vivo., Lately, some highlight articles revealed that the altered expression of miRNAs such as miR-1, miR-133, MIR21 gene, miR-208 etc in hearts also contributed to Cardiovascular system diseases, such as Chest>Heart ischemia, Cardiac - anatomy qualifier hypertrophy, and Cardiac Arrhythmia., Remarkably, MIR21 gene expression was significantly down-regulated in infarcted areas, but was up-regulated in Table Frame - Table Frame - border areas. The down-regulation of MIR21 gene in the infarcted areas was inhibited by ischemic preconditioning, a known Cardiac - anatomy qualifier protective method. Overexpression of MIR21 gene via adenovirus expressing MIR21 gene (Ad-MIR21 gene) decreased Myocardial Infarction size by 29% at 24 h and decreased the dimension of left ventricles at 2 weeks after Anterior Myocardial infarction:Finding:Point in time:^Patient:Ordinal. Using both gain-of-function and loss-of-function approaches in cultured Cardiac - anatomy qualifier Muscle Cells, we identified that MIR21 gene had a protective effect on ischemia-induced \"U\" lymphocyte apoptosis that was associated with its target gene programmed \"U\" lymphocyte Cessation of life 4 and activator protein 1 pathway. The protective effect of MIR21 gene against ischemia-induced Cardiac - anatomy qualifier myocyte damage was further confirmed in vivo by decreased \"U\" lymphocyte apoptosis in the Table Frame - Table Frame - border and infarcted areas of the infarcted Rattus norvegicus hearts after treatment with Ad-MIR21 gene. The results suggest that miRNAs such as MIR21 gene may play critical roles in the early phase of Anterior Myocardial infarction:Finding:Point in time:^Patient:Ordinal., The results suggest that MIR21 gene is sensitive to H(2)O(2) stimulation. MIR21 gene participates in H(2)O(2)-mediated gene regulation and functional modulation in Cardiac - anatomy qualifier Muscle Cells. MIR21 gene might play an essential role in Chest>Heart diseases related to Reactive Oxygen Species such as Cardiac - anatomy qualifier hypertrophy, Congestive Chest>Heart failure, Myocardial infarction:Finding:Point in time:^Patient:Ordinal, and myocardial ischemia/reperfusion injury., MicroRNA-21 contributes to Cardiomyopathies by stimulating Mitogen-Activated Protein Kinases signalling in Specimen Source Codes - Fibroblasts, Myocardial and circulating levels of microRNA-21 reflect left ventricular Fibrosis in Aortic Valve Stenosis patients, MicroRNA 21 inhibits left ventricular remodeling in the early phase of Rattus norvegicus model with Reperfusion Injury by suppressing \"U\" lymphocyte apoptosis, MicroRNA-21 protects against the H(2)O(2)-induced injury on Cardiac - anatomy qualifier Muscle Cells via its target gene Programmed Cell Death Protein 4, MicroRNA-21 (MIR21 gene) is a highly expressed microRNA (miRNA) in Cardiovascular system system., MicroRNA-21 contributes to Cardiomyopathies by stimulating Mitogen-Activated Protein Kinases signalling in Specimen Source Codes - Fibroblasts., MicroRNA-21 (MIR21 gene) is a highly expressed microRNA (miRNA) in Cardiovascular system system, MIR21 gene might be a novel therapeutic target in Cardiovascular system diseases, MicroRNA-21 as therapeutic target in Primary malignant neoplasm and Cardiovascular system Disease., These findings reveal that MicroRNAs can contribute to Cardiomyopathies by an effect in Cardiac - anatomy qualifier Specimen Source Codes - Fibroblasts., Our results validate MIR21 gene as a Disease target in Congestive Chest>Heart failure and establish the therapeutic efficacy of microRNA therapeutic intervention in a Cardiovascular system Disease setting.[SEP]Relations: Cardiac - anatomy qualifier muscle hypertrophy has relations: bioprocess_protein with MIR195, bioprocess_protein with MIR195, bioprocess_protein with MIR15B, bioprocess_protein with MIR15B. Myocardial infarction:Finding:Point in time:^Patient:Ordinal has relations: disease_protein with MIR145, disease_protein with MIR145, disease_protein with MIR145, disease_protein with MIR145, disease_protein with MIR145, disease_protein with MIR145.", "label": "yes"}
{"original_question": "Are reduced-nicotine cigarettes effective for smoking cessation?", "id": "converted_281", "sentence1": "Are reduced-nicotine cigarettes effective for Location characteristic ID - Smoking cessation?", "sentence2": "CONCLUSIONS: In this 6-week study, reduced-nicotine cigarettes versus standard-nicotine cigarettes reduced nicotine exposure and dependence and the number of cigarettes smoked. , RESULTS: Significant reductions in nicotine intake were observed between usual brand Location characteristic ID - Smoking (∼1.2 mg nicotine) and the 0.3 and 0.05 mg nicotine emission cigarettes, but not the 0.6 mg cigarette., CONCLUSIONS: The study adds to the evidence that cigarettes with markedly reduced nicotine content are not associated with increased Location characteristic ID - Smoking intensity or exposure to Tobacco Tobacco smoke toxicants., BACKGROUND: When switching from usual brand cigarettes, very low nicotine content (VLNC) cigarettes lead to a reduction in the number of cigarettes smoked, toxicant exposure, withdrawal symptoms and dependence. , Moreover, while nicotine patches were well tolerated when subjects smoked nicotine-containing cigarettes, the use of nicotine skin patches with reduced-nicotine cigarettes potentially offers the advantage of increased efficacy without introducing concern about toxic effects of excessive nicotine intake., Results showed that Quest plus Nicotine replacement therapy was more effective than active control plus Nicotine replacement therapy in achieving 4 weeks of continuous abstinence (32.8% vs. 21.9%)., Quest plus Nicotine replacement therapy offers promise as a new Location characteristic ID - Smoking cessation treatment., We identified three clinical trials (total n = 489) that suggest that smokers can dissociate nicotine delivery from the act of Location characteristic ID - Smoking if they use reduced-nicotine content cigarettes in combination with nicotine replacement therapy., CONCLUSION: The 0.05 mg nicotine yield cigarettes may be a Tobacco use type:Type:Point in time:^Patient:Nominal that can facilitate cessation; however, future research is clearly needed to support these preliminary findings., Preliminary studies suggest an extinction-based Location characteristic ID - Smoking cessation treatment using reduced nicotine content (RNC) cigarettes decreases self-report craving for cigarettes prior to quitting and may be an effective Location characteristic ID - Smoking cessation treatment., Reduced nicotine content (RNC) cigarettes have led to Location characteristic ID - Smoking fewer cigarettes, withdrawal relief, and facilitation of cessation., Evidence from a number of small Location characteristic ID - Smoking cessation studies suggests that the use of cigarettes with reduced nicotine content, in combination with nicotine replacement therapy (Nicotine replacement therapy), may help reduce withdrawal symptoms and increase quit rates., The concept for a reduced-nicotine cigarette designed to progressively wean smokers from the Location characteristic ID - Smoking habit is based on research demonstrating that successful Location characteristic ID - Smoking cessation is not only dependent on withdrawal of nicotine, but also on weaning from the habitual sensory and behavioral reinforcement of Location characteristic ID - Smoking., Preliminary studies suggest an extinction-based Location characteristic ID - Smoking cessation treatment using reduced nicotine content (RNC) cigarettes decreases self-report craving for cigarettes prior to quitting and may be an effective Location characteristic ID - Smoking cessation treatment, Specifically, standards that required substantially reduced nicotine content in cigarettes could enable cessation in smokers and prevent future Location characteristic ID - Smoking among current non-smokers, Reduced nicotine content (RNC) cigarettes have led to Location characteristic ID - Smoking fewer cigarettes, withdrawal relief, and facilitation of cessation, Evidence from a number of small Location characteristic ID - Smoking cessation studies suggests that the use of cigarettes with reduced nicotine content, in combination with nicotine replacement therapy (Nicotine replacement therapy), may help reduce withdrawal symptoms and increase quit rates, The concept for a reduced-nicotine cigarette designed to progressively wean smokers from the Location characteristic ID - Smoking habit is based on research demonstrating that successful Location characteristic ID - Smoking cessation is not only dependent on withdrawal of nicotine, but also on weaning from the habitual sensory and behavioral reinforcement of Location characteristic ID - Smoking, These results suggest that use of Nicotine replacement therapy before a target quit-Location characteristic ID - Smoking date deserves further evaluation as a possible Location characteristic ID - Smoking cessation treatment. Moreover, while nicotine patches were well tolerated when subjects smoked nicotine-containing cigarettes, the use of nicotine skin patches with reduced-nicotine cigarettes potentially offers the advantage of increased efficacy without introducing concern about toxic effects of excessive nicotine intake., Preliminary studies suggest an extinction-based Location characteristic ID - Smoking cessation treatment using reduced nicotine content (RNC) cigarettes decreases self-report craving for cigarettes prior to quitting and may be an effective Location characteristic ID - Smoking cessation treatment.[SEP]Relations: Nicotine has relations: drug_effect with Cough, drug_effect with Cough, drug_effect with Arthritis, drug_effect with Arthritis, drug_effect with Respiratory failure, drug_effect with Respiratory failure, drug_drug with Cenobamate, drug_drug with Cenobamate, drug_effect with Headache, drug_effect with Headache.", "label": "yes"}
{"original_question": "Are piRNAs involved in gene silencing?", "id": "converted_1059", "sentence1": "Are piRNAs involved in gene silencing?", "sentence2": "In Drosophila <basidiomycetes> <basidiomycetes> ovaries, the nuclear PIWIL1 gene Protein Info is required for transcriptional silencing of transposons, though the precise mechanisms by which this occurs are unknown., Here we show that the CG9754 Protein Info is a component of PIWIL1 gene complex (molecular entity) that functions downstream of PIWIL1 gene and its binding partner, Asterix, in transcriptional silencing. Enforced tethering of CG9754 to nascent messenger RNA transcripts causes cotranscriptional silencing of the source Gene Locus and the deposition of repressive chromatin location location marks., We have named CG9754 \"Panoramix,\" and we propose that this Protein Info could act as an adaptor, scaffolding interactions between the piRNA pathway and the general silencing machinery that it recruits to enforce transcriptional repression., piRNA-guided slicing of transposon transcripts enforces their transcriptional silencing via specifying the nuclear piRNA repertoire, Caenorhabditis elegans piRNAs interact with both transposon and nontransposon mRNAs to initiate sustained silencing via the RNAi pathway., To assess the dysregulation of gene silencing caused by lack of piRNAs, we restored RNA silencing in RNAi-defective animal allergen extracts in the presence or absence of piRNAs., Thus, by reanimating RNAi, we uncovered a role for piRNAs in protecting Genes, Essential from RNA silencing., In different Organism, small RNAs were shown to be implicated in the posttranscriptional degradation of RNA, Messenger and/or transcriptional repression of the homologous Gene Locus. In Drosophila <basidiomycetes> <basidiomycetes>, the mechanism of piRNA-mediated silencing is still far from being understood, Analyses of piRNA-mediated transcriptional transposon silencing in Drosophila <basidiomycetes> <basidiomycetes>, Transcriptional silencing implies a piRNA-mediated formation of repressive chromatin location location which diminishes the transcriptional capacity of the target Gene Locus., In CASP14 gene, piRNA-guided transposon repression correlates with establishment of CpG DNA methylation on their DNA Sequence, yet the mechanism and the spectrum of genomic targets of piRNA silencing are unknown, Using a candidate gene KD-approach, we identified differences in the spatio-temporal requirements of the piRNA pathway components for piRNA-mediated silencing., Spatio-temporal requirements for DNA Transposable Elements piRNA-mediated silencing during Drosophila <basidiomycetes> <basidiomycetes> oogenesis, In contrast, piRNA-mediated silencing is strong in Germline Stem cells in which Liver Ultrasonographic Elastography mobilization is tightly repressed ensuring the continued production of viable Germline cysts., PIWIL1 gene induces piRNA-guided transcriptional silencing and establishment of a repressive chromatin location location state., In Germ Cells, early embryos, and Stem cells of animal allergen extracts, PIWI-interacting RNAs (piRNAs) have an important role in silencing retrotransposons, which are vicious genomic parasites, through transcriptional and post-transcriptional mechanisms., Our results show that the piRNA pathway can be used as a tool for sequence-specific gene silencing in Germ Cells and support the idea that the piRNA generating regions serve as traps for retrotransposons, enabling the host cell to generate piRNAs against active retrotransposons.,  Our observations confirm the pivotal role of piRNA-mediated silencing in defending the Genome - anatomical entity against selfish transposition, yet also suggest limits to the optimization of host Genome - anatomical entity defense., Analysis of piRNA-mediated silencing of active N-tris(hydroxymethyl)methyl-2-aminomethane sulfonate in Drosophila <basidiomycetes> <basidiomycetes> melanogaster suggests limits on the evolution of host Genome - anatomical entity defense, The PIWIL1 gene-interacting RNA (piRNA) pathway defends animal genomes against the harmful consequences of DNA Transposable Elements (Liver Ultrasonographic Elastography) Communicable Diseases by imposing small-RNA-mediated silencing., A novel organelle, the piNG-body, in the Polar granule of Drosophila <basidiomycetes> <basidiomycetes> male Germ Cells is associated with piRNA-mediated gene silencing., Proteins of the PIWI subfamily Aub and Protein Argonaute-3 associated with the Germline-specific perinuclear granules (Polar granule) are involved in the silencing of retrotransposons and other selfish repetitive elements in the Drosophila <basidiomycetes> <basidiomycetes> Genome - anatomical entity. , Telomeric retroelements HeT-A, TART and TAHRE, which are involved in telomere maintenance in Drosophila <basidiomycetes> <basidiomycetes>, are also the targets of piRNA-mediated silencing, Mechanism of the piRNA-mediated silencing of Drosophila <basidiomycetes> <basidiomycetes> telomeric retrotransposons., Gene silencing mechanisms mediated by Solanum melongena piRNA complex (molecular entity) in Drosophila <basidiomycetes> <basidiomycetes> male gonad., The epigenetic trans-silencing effect in Drosophila <basidiomycetes> <basidiomycetes> involves maternally-transmitted small RNAs whose production depends on the piRNA pathway and Chromobox Protein Homolog 5., Here, we show that Gene Mutation in squash and zucchini, which are involved in the PIWIL1 gene-Interacting RNA (piRNA) silencing pathway, strongly affect TSE, altretamine/etoposide/methotrexate protocol in piRNA processing and gene silencing of retrotransposons, piRNA-mediated silencing in Drosophila <basidiomycetes> <basidiomycetes> germlines., These have shed light not only on the molecular mechanisms of gene silencing mediated by piRNAs and PIWI proteins, but also on their intriguing relationship with cellular Genes that have been shown to be important for gametogenesis and fertility., The most abundant piRNAs were those corresponding to antisense transcripts of Suppressor of Stellate [Su(Ste)] Genes known to be involved in Stellate gene silencing, To determine the capacity of piRNA-mediated silencing, we introduced reporter Genes into Drosophila <basidiomycetes> <basidiomycetes> OSS cells, which express MicroRNAs (miRNAs) and piRNAs, and compared the PIWIL1 gene pathway to the Argonaute pathway in gene regulation, PIWI-interacting small non-coding RNAs (piRNAs) are Genetic and epigenetic regulatory factors in Germline cells, where they maintain Genome - anatomical entity stability, are involved in RNA silencing and regulate gene expression, The piNG-body contains ribonucleoprotein complex (molecular entity) involved in piRNA-silencing of Genome - anatomical entity repeats including transposons in premeiotic Spermatocytes with aid of short piRNAs, Our results show that the piRNA pathway can be used as a tool for sequence-specific gene silencing in Germ Cells and support the idea that the piRNA generating regions serve as traps for retrotransposons, enabling the host cell to generate piRNAs against active retrotransposons, Recent studies have revealed not only the biogenesis of piRNAs and their roles in transposon silencing, but also the function of the PIWIL1 gene-piRNA pathway in epigenetic and post-transcriptional regulation of gene expression, A growing number of studies on piRNAs have investigated piRNA-mediated gene silencing, including piRNA biogenesis, These have shed light not only on the molecular mechanisms of gene silencing mediated by piRNAs and PIWI proteins, but also on their intriguing relationship with cellular Genes that have been shown to be important for gametogenesis and fertility, Telomeric retroelements HeT-A, TART and TAHRE, which are involved in telomere maintenance in Drosophila <basidiomycetes> <basidiomycetes>, are also the targets of piRNA-mediated silencing. , altretamine/etoposide/methotrexate protocol in piRNA processing and gene silencing of retrotransposons., To determine the capacity of piRNA-mediated silencing, we introduced reporter Genes into Drosophila <basidiomycetes> <basidiomycetes> OSS cells, which express MicroRNAs (miRNAs) and piRNAs, and compared the PIWIL1 gene pathway to the Argonaute pathway in gene regulation. , Therefore piRNA-mediated transcriptional mode of silencing is involved in the control of retrotransposon expression in the Drosophila <basidiomycetes> <basidiomycetes> Germline., Panoramix enforces piRNA-dependent cotranscriptional silencing., The most abundant piRNAs were those corresponding to antisense transcripts of Suppressor of Stellate [Su(Ste)] Genes known to be involved in Stellate gene silencing., Our results indicate that piRNAs are involved in a posttranscriptional gene-silencing mechanism resulting in RNA nuclear accumulation.[SEP]Relations: PIWIL1 has relations: bioprocess_protein with gene silencing by RNA, bioprocess_protein with gene silencing by RNA, bioprocess_protein with piRNA metabolic process, bioprocess_protein with piRNA metabolic process, molfunc_protein with piRNA binding, molfunc_protein with piRNA binding. PIWI-interacting RNA (piRNA) biogenesis has relations: pathway_protein with TDRD12, pathway_protein with TDRD12, pathway_protein with MAEL, pathway_protein with MAEL.", "label": "yes"}
{"original_question": "Are there any anti-amyloid antibody approved as drug for Alzheimer's disease treatment?", "id": "converted_3186", "sentence1": "Are there any anti-amyloid antibody approved as Pharmacologic Substance for ALZHEIMER DISEASE, FAMILIAL, 1 treatment?", "sentence2": "Treatment with memantine, a noncompetitive NMDA receptor Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) which is an approved Pharmacologic Substance for treatment of ALZHEIMER DISEASE, FAMILIAL, 1, rescued protein phosphatase-2A activity by decreasing its demethylation at Leu309 selectively and attenuated ALZHEIMER DISEASE, FAMILIAL, 1-like pathology and cognitive impairment in adeno-associated virus vector-1-I1PP2A Rattus norvegicus. , anti-Amyloid agents (13.30%), no new drugs have been approved during the past 15 years; and the available medications are not cost-effective. [SEP]Relations: familial Alzheimer disease has relations: disease_disease with Alzheimer disease, disease_disease with Alzheimer disease, disease_protein with PRNP, disease_protein with PRNP, disease_phenotype_positive with Attention deficit hyperactivity disorder, disease_phenotype_positive with Attention deficit hyperactivity disorder, disease_disease with inherited prion disease, disease_disease with inherited prion disease, disease_phenotype_positive with Anxiety, disease_phenotype_positive with Anxiety.", "label": "no"}
{"original_question": "Does gepotidacin activate bacterial topoisomerase?", "id": "converted_2802", "sentence1": "Does gepotidacin activate bacterial topoisomerase?", "sentence2": "GSK2140944 is a novel bacterial topoisomerase inhibitor in development for the treatment of Bacterial Infections.[SEP]Relations: Recurrent Bacterial Infections has relations: disease_phenotype_positive with purine nucleoside phosphorylase deficiency, disease_phenotype_positive with purine nucleoside phosphorylase deficiency, disease_phenotype_positive with chromomycosis, disease_phenotype_positive with chromomycosis, disease_phenotype_positive with adenosine deaminase deficiency, disease_phenotype_positive with adenosine deaminase deficiency, disease_phenotype_positive with pancytopenia due to IKZF1 mutations, disease_phenotype_positive with pancytopenia due to IKZF1 mutations, disease_phenotype_positive with Chediak-Higashi syndrome, disease_phenotype_positive with Chediak-Higashi syndrome.", "label": "no"}
{"original_question": "Is EuroQol 5-Dimension Health Assessment (EQ-5D) [a widely used, simple instrument that monitors the general health-related quality of life (HRQoL) in chronic disease] a 5 question assessment?", "id": "converted_4463", "sentence1": "Is EuroQol 5-Dimension Health Assessment (EQ-5D) [a widely used, simple instrument that monitors the general health-related quality of life (HRQoL) in Chronic disease] a 5 question assessment?", "sentence2": "The 6-question EuroQol 5-Dimension Health Assessment (EQ-5D) is a widely used, simple instrument that monitors general health-related quality of life (HRQoL) in Chronic disease. , OBJECTIVE: The 6-question EuroQol 5-Dimension Health Assessment (EQ-5D) is a widely used, simple instrument that monitors general health-related quality of life (HRQoL) in Chronic disease., OBJECTIVE: The 6-question EuroQol 5-Dimension Health Assessment (EQ-5D) is a widely used, simple instrument that monitors general health-related quality of life (HRQoL) in chronic d, OBJECTIVE: The 6-question EuroQol 5-Dimension Health Assessment (EQ-5D) is a widely used, simple instrument that monitors general health-related quality of life (HRQoL) in chron[SEP]Relations: Chronic lung disease has relations: disease_phenotype_positive with severe acute respiratory syndrome, disease_phenotype_positive with severe acute respiratory syndrome, disease_phenotype_positive with alobar holoprosencephaly, disease_phenotype_positive with alobar holoprosencephaly, disease_phenotype_positive with cognitive impairment - coarse facies - heart defects - obesity - pulmonary involvement - short stature - skeletal dysplasia syndrome, disease_phenotype_positive with cognitive impairment - coarse facies - heart defects - obesity - pulmonary involvement - short stature - skeletal dysplasia syndrome, disease_phenotype_positive with combined immunodeficiency due to LRBA deficiency, disease_phenotype_positive with combined immunodeficiency due to LRBA deficiency, disease_phenotype_positive with toxic epidermal necrolysis, disease_phenotype_positive with toxic epidermal necrolysis.", "label": "no"}
{"original_question": "Are people with blood group O protected against severe Malaria?", "id": "converted_464", "sentence1": "Are people with blood group O protected against severe Malaria?", "sentence2": "Differential carbonylation of Cytoskeletal Proteins in blood group O Specimen Source Codes - Erythrocytes: potential role in protection against severe Malaria Vaccines., . Our findings indicate a possible correlation between the protection against severe Malaria Vaccines in blood group O individuals and a specific pattern of 4-HNE-carbonylation of cytoskeleton proteins., There is a predominance of blood group O in Malaria Vaccines-endemic regions, and several lines of evidence suggest that bleomycin/methotrexate/vincristine protocol blood groups may influence the outcome of P. falciparum infection, These data provide the first evidence that bleomycin/methotrexate/vincristine protocol blood group antigens influence macrophage clearance of P. falciparum-infected Specimen Source Codes - Erythrocytes and suggest an additional mechanism by which blood group O may confer resistance to severe Malaria Vaccines., Blood group phenotypes A and Deciduous maxillary right first molar tooth are risk factors for Malaria, Cerebral in Odisha, India., type O is significantly associated with protection against Caudomedial auditory cortex, patients with type A and Deciduous maxillary right first molar tooth group had increased risk for developing Caudomedial auditory cortex., Blood group O protects against severe Plasmodium falciparum or Plasmodium falciparum + Plasmodium sp or Plasmodium falciparum or Plasmodium falciparum + Plasmodium sp + Plasmodium sp Malaria Vaccines through the mechanism of reduced rosetting., Malaria has been a major selective force on the Homo sapiens population, and several Erythrocytes polymorphisms have evolved that confer resistance to severe Malaria Vaccines. Plasmodium falciparum or Plasmodium falciparum + Plasmodium sp or Plasmodium falciparum or Plasmodium falciparum + Plasmodium sp + Plasmodium sp rosetting, a parasite virulence phenotype associated with severe Malaria Vaccines, is reduced in blood group O Specimen Source Codes - Erythrocytes compared with groups A, Deciduous maxillary right first molar tooth, and AB hearing assessment list hearing assessment list, but the contribution of the bleomycin/methotrexate/vincristine protocol blood group system to protection against severe Malaria Vaccines has received little attention, We hypothesized that blood group O may confer resistance to severe falciparum Malaria Vaccines through the mechanism of reduced rosetting., It appears that individuals who are of blood-group O are relatively resistant to the severe disease caused by P. falciparum infection.[SEP]Relations: Malaria, Cerebral has relations: disease_disease with Malaria Vaccines, disease_disease with Malaria Vaccines, contraindication with Betamethasone, contraindication with Betamethasone, contraindication with Methylprednisolone, contraindication with Methylprednisolone, contraindication with Prednisone, contraindication with Prednisone. Plasmodium falciparum or Plasmodium falciparum + Plasmodium sp Malaria Vaccines has relations: disease_disease with Malaria Vaccines, disease_disease with Malaria Vaccines.", "label": "yes"}
{"original_question": "Is Otolin-1 a matrix protein?", "id": "converted_4566", "sentence1": "Is Otolin-1 a matrix protein?", "sentence2": "otoconia matrix protein, otolin-1, Otolin-1 is a collagen-like protein expressed in the inner ear of vertebrates. , Mammalian Otolin: a multimeric glycoprotein specific to the inner ear that interacts with otoconial matrix protein Otoconin-90 and Cerebellin-1, binds to otolin-1 and forming matrix protein architectures[SEP]", "label": "yes"}
{"original_question": "Does the Abelson-related gene (ARG) gene encode for a serine kinase?", "id": "converted_2205", "sentence1": "Does the Abelson-related gene (ABL2 gene) gene encode for a serine kinase?", "sentence2": "One Protein Isoforms of Arg/Abl2 TYK2 gene is Nuclear (incident type) and the other seven cytosolic isoforms differently modulate cell morphology, motility and the Microtubules associated with cytoplasmic filaments., The non-receptor TYK2 gene Abelson related gene (Arg/Abl2) regulates cell migration and morphogenesis by modulating the Microtubules associated with cytoplasmic filaments. , The Homo sapiens Arg (Abl2) nonreceptor TYK2 gene has a role in cytoskeletal rearrangements by its C-terminal F-actin- and microtubule-binding sequences. , The TYK2 gene abl-related gene ABL2 gene is fused to ETV6 wt Allele wt Allele in an AML-M4Eo patient with a t(1;12)(q25;p13): molecular cloning of both reciprocal RNA Transcript.,  The ABL2 gene gene encodes for a nonreceptor TYK2 gene characterized by high Homologous Gene with ABL1 gene in the TK, SH2, and SH3 domains. This is the first report on ABL2 gene involvement in a Homo sapiens malignancy., Ultraviolet-A and -B differentially modify the tyrosine-kinase profile of Homo sapiens keratinocytes and induce the expression of Arg+., Arg (Abelson-related gene, Abl2) was the PTK with the highest prevalence (30% of all PTKs) and UVA led to a further induction of Arg expression reaching nine-fold RNA, Messenger baseline expression at 17 h after irradiation., To investigate the expression profile of Protein Tyrosine Kinase (PTKs) in normal Homo sapiens epidermal keratinocytes (NHEK) in response to UVA and Ultraviolet B therapy we employed a reversed transcriptase polymerase chain reaction (PCR) approach using degenerate primers derived from the conserved catalytic domain of PTKs. , By 3'rapid amplification of cDNA ends-polymerase chain reaction (3'RACE-PCR), a novel fusion transcript was identified between the ETV6 wt Allele wt Allele and the Abelson-related gene (ABL2 gene) at 1q25, resulting in a Fusion protein consisting of the Lymphohistiocytosis, Hemophagocytic oligomerization domain of ETV6 wt Allele wt Allele and the SH2, SH3, and protein TYK2 gene (PTK) domains of ABL2 gene., The non-receptor TYK2 gene Abelson related gene (Arg/Abl2) regulates cell migration and morphogenesis by modulating the Microtubules associated with cytoplasmic filaments., Arg (Abelson-related gene, Abl2) was the PTK with the highest prevalence (30% of all PTKs) and UVA led to a further induction of Arg expression reaching nine-fold RNA, Messenger baseline expression at 17 h after irradiation., We studied the relationship of direct karyotypes, determined at diagnosis and remission, to Abelson-related TYK2 gene activity and the cytogenetic features of Erythroid and myeloid colonies derived from remission marrow of six children with Pre B-cell Pre B-cell acute lymphoblastic leukemia (Acute lymphocytic leukemia)., ABL2/ABL2 gene (ABL-related gene) belongs to the ABL (Abelson Tyrosine-Protein Kinase 2, Homo sapiens) family of tyrosine kinases, The non-receptor TYK2 gene Abelson related gene (Arg/Abl2) regulates cell migration and morphogenesis by modulating the Microtubules associated with cytoplasmic filaments, The ABL2 gene gene encodes for a nonreceptor TYK2 gene characterized by high Homologous Gene with ABL1 gene in the TK, SH2, and SH3 domains., ABL2/ABL2 gene (ABL-related gene) belongs to the ABL (Abelson Tyrosine-Protein Kinase 2, Homo sapiens) family of tyrosine kinases., We report that the Abelson (Abetalipoproteinemia) and Abetalipoproteinemia-related gene (Arg) nonreceptor tyrosine kinases are required for maintenance of cortical dendrites in the Mus sp. brain., The products of the Homo sapiens ABL2 gene gene and the Homo sapiens ABL gene characterize the Abelson family of non-receptor tyrosine protein kinases., The products of the Homo sapiens Arg gene and Homo sapiens, Mus sp., Drosophila <basidiomycetes> <basidiomycetes>, and Phylum Nematoda Abetalipoproteinemia Genes characterize the Abelson family of nonreceptor tyrosine protein kinase., By 3'rapid amplification of cDNA ends-polymerase chain reaction (3'RACE-PCR), a novel fusion transcript was identified between the ETV6 wt Allele wt Allele and the Abelson-related gene (ABL2 gene) at 1q25, resulting in a Fusion protein consisting of the Lymphohistiocytosis, Hemophagocytic oligomerization domain of ETV6 wt Allele wt Allele and the SH2, SH3, and protein TYK2 gene (PTK) domains of ABL2 gene., The TYK2 gene abl-related gene ABL2 gene is fused to ETV6 wt Allele wt Allele in an AML-M4Eo patient with a t(1;12)(q25;p13): molecular cloning of both reciprocal RNA Transcript.[SEP]Relations: protein TYK2 gene binding has relations: molfunc_protein with NEDD9, molfunc_protein with NEDD9, molfunc_protein with GRM5, molfunc_protein with GRM5, molfunc_protein with ITGB1, molfunc_protein with ITGB1, molfunc_protein with ACVR1, molfunc_protein with ACVR1, molfunc_protein with CRK, molfunc_protein with CRK.", "label": "no"}
{"original_question": "Are ACTA1 (alpha actin) and NEB (nebulin) genes related to nemaline myopathy?", "id": "converted_1139", "sentence1": "Are ACTA1 gene (alpha actin) and mitotic nuclear membrane disassembly (nebulin) Genes related to Actin-Accumulation Myopathy?", "sentence2": "Nemaline myopathy (Nuclear medicine procedure) is a group of congenital Myopathy, characterized by the presence of distinct rod-like inclusions \"nemaline bodies\" in the Sarcoplasm of skeletal Muscle Tissue fibers. To date, ACTA1 gene gene, mitotic nuclear membrane disassembly, TPM3 protein, human protein, human, TPM2 gene gene, TNNT1 gene gene, and CFL2 gene gene have been found to cause Nuclear medicine procedure., Nemaline myopathy (Nuclear medicine procedure) is the most common Congenital myopathy (disorder) and is caused by mutations in various Genes including mitotic nuclear membrane disassembly (nebulin), TPM2 gene gene (beta-Tropomyosin), TPM3 protein, human protein, human (gamma-Tropomyosin), and ACTA1 gene gene (skeletal alpha-Actin). 20-25% of Nuclear medicine procedure cases carry ACTA1 gene gene defects and these particular mutations usually induce substitutions of single residues in the actin protein. , Nemaline myopathy (Nuclear medicine procedure) is a genetically and clinically heterogenous Muscle Tissue disorder, which is myopathologically characterized by nemaline bodies. Gene Mutation in six Genes have been reported to cause Nuclear medicine procedure: Nebulin (mitotic nuclear membrane disassembly Pelin 1999), alpha-skeletal Muscle Tissue actin (ACTA1 gene gene Nowak 1999), alpha-slow tropomyosin (TPM3 protein, human protein, human Laing 1995), beta-Tropomyosin (TPM2 gene gene Donner 2002), slow Troponin T Assay (TNNT1 gene gene Johnston 2000) and Cofilin 2 (CFL2 gene gene Agrawal 2007). The majority of cases are due to Mutation Abnormality in mitotic nuclear membrane disassembly and ACTA1 gene gene. , Nemaline myopathy is a heterogenous form of Congenital myopathy (disorder) characterised by a variable spectrum of clinical features, predominated in the severe form by profound Muscle hypotonia and Asthenia accompanied by Respiratory Insufficiency. The clinical variability, with differing age of onset and severity of symptoms makes the diagnosis of Actin-Accumulation Myopathy difficult in some cases. Severe forms of Actin-Accumulation Myopathy may be caused by Mutation Abnormality of a number of different Genes: skeletal Muscle Tissue actin (ACTA1 gene gene), nebulin (mitotic nuclear membrane disassembly) and Tropomyosin Alpha-1 Chain, human (TPM3 protein, human protein, human), all of which encode components of the sarcomeric thin filaments of skeletal Muscle Tissue. , Most Actin-Accumulation Myopathy patients have mutations in the nebulin (mitotic nuclear membrane disassembly) or skeletal Muscle Tissue alpha-Actin (ACTA1 gene gene) Genes. , We report Muscle Tissue MRI findings of 10 patients from 8 families with Actin-Accumulation Myopathy. Patients with involvement of the nebulin (mitotic nuclear membrane disassembly) gene showed a consistent pattern of selective Muscle Tissue involvement corresponding to clinical severity., Patients with Actin-Accumulation Myopathy secondary to mutations in the skeletal Muscle Tissue alpha-Actin (ACTA1 gene gene) gene showed diffuse involvement of Lower extremity>Thigh and leg muscles with relative sparing of the gastrocnemii., Congenital Myopathy are clinical and Genetic heterogeneous disorders characterized by skeletal Muscle Tissue Asthenia ranging in severity. Three major forms have been identified: actin myopathy, intranuclear rod myopathy, and Actin-Accumulation Myopathy. Nemaline myopathy is the most common of these Myopathy and is further subdivided into seven groups according to severity, progressiveness, and age of onset. At present, five Genes have been linked to congenital Myopathy. These include alpha-Actin (ACTA1 gene gene), alpha- and beta-Tropomyosin (TPM3 protein, human protein, human and TPM2 gene gene), Troponin T Assay (TNNT1 gene gene), and nebulin (mitotic nuclear membrane disassembly). , Nemaline myopathy is a structural Congenital myopathy (disorder) which may show both Autosomal dominant multiple pterygium syndrome and autosomal recessive inheritance patterns. Gene Mutation in three different Genes have been identified as the cause of Actin-Accumulation Myopathy: the gene for slow Tropomyosin Alpha-1 Chain, human 3 (TPM3 protein, human protein, human) at 1q22-23, the nebulin gene (mitotic nuclear membrane disassembly) at 2q21.1-q22, and the actin gene (ACTA1 gene gene) at 1q42., Nemaline myopathy is a clinically and genetically heterogeneous condition. The clinical spectrum ranges from severe cases with antenatal or neonatal onset and early death to late onset cases with only slow progression. Three Genes are known to cause Actin-Accumulation Myopathy: the Genes for nebulin (mitotic nuclear membrane disassembly) on Chromosomes, Human, Pair 1 2q22, slow Tropomyosin Alpha-1 Chain, human (TPM3 protein, human protein, human) on Chromosomes, Human, Pair 1 1q21 and skeletal Muscle Tissue alpha-Actin (ACTA1 gene gene) on Chromosomes, Human, Pair 1 1q42. , Nemaline myopathy (Nuclear medicine procedure) is the most common Congenital myopathy (disorder) and is caused by mutations in various Genes including mitotic nuclear membrane disassembly (nebulin), TPM2 gene gene (beta-Tropomyosin), TPM3 protein, human protein, human (gamma-Tropomyosin), and ACTA1 gene gene (skeletal alpha-Actin)., Three Genes are known to cause Actin-Accumulation Myopathy: the Genes for nebulin (mitotic nuclear membrane disassembly) on Chromosomes, Human, Pair 1 2q22, slow Tropomyosin Alpha-1 Chain, human (TPM3 protein, human protein, human) on Chromosomes, Human, Pair 1 1q21 and skeletal Muscle Tissue alpha-Actin (ACTA1 gene gene) on Chromosomes, Human, Pair 1 1q42., Five Genes have now been associated with Actin-Accumulation Myopathy: Tropomyosin Alpha-1 Chain, human-3 (TPM3 protein, human protein, human), alpha-Actin (ACTA1 gene gene), nebulin (mitotic nuclear membrane disassembly), beta-tropomysin (TPM2 gene gene) and Troponin T Assay (TNNT1 gene gene)., Most Actin-Accumulation Myopathy patients have mutations in the nebulin (mitotic nuclear membrane disassembly) or skeletal Muscle Tissue alpha-Actin (ACTA1 gene gene) Genes., Severe forms of Actin-Accumulation Myopathy may be caused by Mutation Abnormality of a number of different Genes: skeletal Muscle Tissue actin (ACTA1 gene gene), nebulin (mitotic nuclear membrane disassembly) and Tropomyosin Alpha-1 Chain, human (TPM3 protein, human protein, human), all of which encode components of the sarcomeric thin filaments of skeletal Muscle Tissue., Five Genes have now been associated with Actin-Accumulation Myopathy: Tropomyosin Alpha-1 Chain, human-3 (TPM3 protein, human protein, human), alpha-Actin (ACTA1 gene gene), nebulin (mitotic nuclear membrane disassembly), beta-tropomysin (TPM2 gene gene) and Troponin T Assay (TNNT1 gene gene)., Three Genes are known to cause Actin-Accumulation Myopathy: the Genes for nebulin (mitotic nuclear membrane disassembly) on Chromosomes, Human, Pair 1 2q22, slow Tropomyosin Alpha-1 Chain, human (TPM3 protein, human protein, human) on Chromosomes, Human, Pair 1 1q21 and skeletal Muscle Tissue alpha-Actin (ACTA1 gene gene) on Chromosomes, Human, Pair 1 1q42., Gene Mutation in three different Genes have been identified as the cause of Actin-Accumulation Myopathy: the gene for slow Tropomyosin Alpha-1 Chain, human 3 (TPM3 protein, human protein, human) at 1q22-23, the nebulin gene (mitotic nuclear membrane disassembly) at 2q21.1-q22, and the actin gene (ACTA1 gene gene) at 1q42., Most Actin-Accumulation Myopathy patients have mutations in the nebulin (mitotic nuclear membrane disassembly) or skeletal Muscle Tissue alpha-Actin (ACTA1 gene gene) Genes, Five Genes have now been associated with Actin-Accumulation Myopathy: Tropomyosin Alpha-1 Chain, human-3 (TPM3 protein, human protein, human), alpha-Actin (ACTA1 gene gene), nebulin (mitotic nuclear membrane disassembly), beta-tropomysin (TPM2 gene gene) and Troponin T Assay (TNNT1 gene gene), Three Genes are known to cause Actin-Accumulation Myopathy: the Genes for nebulin (mitotic nuclear membrane disassembly) on Chromosomes, Human, Pair 1 2q22, slow Tropomyosin Alpha-1 Chain, human (TPM3 protein, human protein, human) on Chromosomes, Human, Pair 1 1q21 and skeletal Muscle Tissue alpha-Actin (ACTA1 gene gene) on Chromosomes, Human, Pair 1 1q42, Nemaline myopathy (Nuclear medicine procedure) is the most common Congenital myopathy (disorder) and is caused by mutations in various Genes including mitotic nuclear membrane disassembly (nebulin), TPM2 gene gene (beta-Tropomyosin), TPM3 protein, human protein, human (gamma-Tropomyosin), and ACTA1 gene gene (skeletal alpha-Actin), Five Genes have now been associated with Actin-Accumulation Myopathy: Tropomyosin Alpha-1 Chain, human-3 (TPM3 protein, human protein, human), alpha-Actin (ACTA1 gene gene), nebulin (mitotic nuclear membrane disassembly), beta-tropomysin (TPM2 gene gene) and Troponin T Assay (TNNT1 gene gene), Nemaline myopathy (Nuclear medicine procedure) is the most common Congenital myopathy (disorder) and is caused by mutations in various Genes including mitotic nuclear membrane disassembly (nebulin), TPM2 gene gene (beta-Tropomyosin), TPM3 protein, human protein, human (gamma-Tropomyosin), and ACTA1 gene gene (skeletal alpha-Actin), Gene Mutation in three different Genes have been identified as the cause of Actin-Accumulation Myopathy: the gene for slow Tropomyosin Alpha-1 Chain, human 3 (TPM3 protein, human protein, human) at 1q22-23, the nebulin gene (mitotic nuclear membrane disassembly) at 2q21.1-q22, and the actin gene (ACTA1 gene gene) at 1q42, Three Genes are known to cause Actin-Accumulation Myopathy: the Genes for nebulin (mitotic nuclear membrane disassembly) on Chromosomes, Human, Pair 1 2q22, slow Tropomyosin Alpha-1 Chain, human (TPM3 protein, human protein, human) on Chromosomes, Human, Pair 1 1q21 and skeletal Muscle Tissue alpha-Actin (ACTA1 gene gene) on Chromosomes, Human, Pair 1 1q42, Most Actin-Accumulation Myopathy patients have mutations in the nebulin (mitotic nuclear membrane disassembly) or skeletal Muscle Tissue alpha-Actin (ACTA1 gene gene) Genes, Severe forms of Actin-Accumulation Myopathy may be caused by Mutation Abnormality of a number of different Genes: skeletal Muscle Tissue actin (ACTA1 gene gene), nebulin (mitotic nuclear membrane disassembly) and Tropomyosin Alpha-1 Chain, human (TPM3 protein, human protein, human), all of which encode components of the sarcomeric thin filaments of skeletal Muscle Tissue[SEP]Relations: Actin-Accumulation Myopathy has relations: disease_protein with ACTA1 gene, disease_protein with ACTA1 gene, disease_disease with alpha-actinopathy, disease_disease with alpha-actinopathy, disease_protein with mitotic nuclear membrane disassembly, disease_protein with mitotic nuclear membrane disassembly, disease_disease with qualitative or quantitative defects of alpha-Actin, disease_disease with qualitative or quantitative defects of alpha-Actin. alpha-actinopathy has relations: disease_disease with Actin-Accumulation Myopathy, disease_disease with Actin-Accumulation Myopathy.", "label": "yes"}
{"original_question": "Is proton beam therapy used for treatment of craniopharyngioma?", "id": "converted_4359", "sentence1": "Is proton beam therapy used for treatment of Craniopharyngioma?", "sentence2": " The majority of children had adjuvant therapy comprising proton beam therapy (18/59; 30.5%) or conventional radiotherapy (16/59; 27.1%)., Proton Therapy for Craniopharyngioma - An Early Report from a Single European Centre., AIMS: Proton beam therapy (Mast/Stem Cell Growth Factor Receptor Kit, human) is being increasingly used for Craniopharyngioma. , MATERIALS AND METHODS: Between August 2013 and July 2016, 18 patients with craniopharyngiomas were treated with 54 Cobalt Gray Equivalent (CGE) in 30 fractions over 6 weeks at our centre., CONCLUSIONS: Our early results are encouraging and comparable with the limited literature on Mast/Stem Cell Growth Factor Receptor Kit, human for Craniopharyngioma., All of the other patients underwent proton-beam radiotherapy with no documented tumor growth (median follow-up: 20 months; range 5.1-29.9 months)., Where aggressive subtotal resection is achieved, patients should be closely followed, with radiation initiated at the time of progression or recurrence-ideally via proton beam therapy, although three-dimensional conformal radiotherapy, intensity-modulated radiotherapy, and stereotactic radiosurgery are very appropriate in a range of circumstances, governed by access, patient age, Disease architecture, and character of the recurrence.,  This study examined parental distress in a sample of families of patients with Cp treated with proton beam therapy to identify factors for targeting psychological intervention.PROCEDURE: Prior to (n = 96) and 1 year after (n = 73) proton therapy, parents of children diagnosed with Cp (9.81 ± 4.42 years at baseline; 49% male) completed a self-report measure of distress, the Brief Symptom Inventory (BSI)., Diagnoses included Medulloblastoma, Craniopharyngioma, Ependymoma, Glioma, Germ cell tumor, and others., Initial experience with proton beam therapy in childhood-onset Craniopharyngioma patients shows promising results in terms of more protective radiological treatment. , Monte Carlo simulations were used to assess secondary neutron doses received by patients treated with proton therapy for Malignant melanoma of eye and Craniopharyngioma., Secondary neutron doses in proton therapy treatments of Malignant melanoma of eye and Craniopharyngioma., AIMS: Proton beam therapy (Mast/Stem Cell Growth Factor Receptor Kit, human) is being increasingly used for Craniopharyngioma., LTS: Published reports suggest a benefit to proton beam therapy for use in Neoplasms of the skull base, including craniopharyngiomas, Chordoma, skull-base sarcomas, and unresectable meningiomas.CONC, In recent years, proton therapy (PT), with its physical properties of heavy ion beam, that is, Prague peak phenomenon, has been more frequently used in patients with Craniopharyngioma., Proton beam therapy versus conformal photon radiation therapy for childhood Craniopharyngioma: multi-institutional analysis of outcomes, cyst dynamics, and Toxic effect., PURPOSE: We compared proton beam therapy (Mast/Stem Cell Growth Factor Receptor Kit, human) with intensity modulated radiation therapy (IMRT) for pediatric Craniopharyngioma in terms of Disease control, cyst dynamics, and Toxic effect., Proton therapy for Craniopharyngioma in adults: a protocol for systematic review and meta-analysis., We hereby report a case of a 7-year-old boy with a Craniopharyngioma which had been subtotally resected and was subsequently treated with modern pencil beam proton therapy under high-precision image guidance., Pencil beam scanning proton therapy for the treatment of Craniopharyngioma complicated with radiation-induced cerebral vasculopathies: A dosimetric and linear energy transfer (Linear Energy Transfer) evaluation., tial experience with proton beam therapy in childhood-onset Craniopharyngioma patients shows promising results in terms of more protective radiological treatment. R, PURPOSE: We compared proton beam therapy (Mast/Stem Cell Growth Factor Receptor Kit, human) with intensity modulated radiation therapy (IMRT) for pediatric Craniopharyngioma in terms of Disease control, cyst dynamics, and toxic, BACKGROUND AND PURPOSE: This study analyses the dosimetric and dose averaged Linear Energy transfer (LETd) correlation in paediatric Craniopharyngioma (cyclophosphamide/prednisone) patients with and without radiation-induced cerebral vasculopathies (RICVs) treated with pencil beam scanning (PBS) pro, OBJECTIVE: The authors compared survival and multiple comorbidities in children diagnosed with Craniopharyngioma who underwent gross-total resection (GTR) versus subtotal resection (STR (short terminal repeat, nucleic acid) (short terminal repeat, nucleic acid)) with radiation therapy (RT), either intensity-modulated radiation therapy (IMRT) or proton beam therapy (P, Proton Therapy for Craniopharyngioma - An Early Report from a Single European Centre, s. Some studies have shown that PT has advantages in the treatment of Craniopharyngioma in adu, Postoperative cerebral glucose metabolism in pediatric patients receiving proton therapy for Craniopharyngioma, Clinical equipoise: Protons and the child with Craniopharyngioma., skull base. More public attention has been given to proton beam therapy due to the increasing number of centers now in operation or in the planning stages for offering this treatment option.METHODS: We reviewed the physical properties of Protons and the clinical studies performed to justify their use in the management of skull-base Neoplasms and determine the benefits of proton beam therapy.RESULTS: Published reports suggest a benefit to proton beam therapy for use in Neoplasms of the skull base, including craniopharyngiomas, Chordoma, skull-base sarcomas, and unresectable meningiomas.CONCLUSIONS: Use of proton beam th, PURPOSE: We report the results of the early cohort of patients treated for Craniopharyngioma with combined proton-photon irradiation at the Massachusetts General Hospital and the Harvard Cyclotron Laboratory.METHODS AND MATERIALS: Between 1981 and 1988, 15 patients with Craniopharyngioma were treated in part or entirely with fractiona, UNLABELLED: This retrospective preliminary review evaluated the efficacy and Toxic effect of fractionated proton radiotherapy in the management of pediatric Craniopharyngioma.METHODS: Sixteen patients, aged 7-34 years, were treated with p, population. We evaluated the outcomes of all adult Craniopharyngioma patients treated at our institution using proton therapy to report outcomes for Disease control, treatment-related Toxic effect, and tumor response.METHODS: We analyzed 14 adult patie, Proton radiation has been used safely and effectively for Medulloblastoma, primitive neuro-ectodermal Neoplasms, Craniopharyngioma, Ependymoma, Germ Cells intracranial Neoplasms, low-grade glioma, Retinoblastoma, Anal Rhabdomyosarcoma and other Sarcoma of soft tissue, Ewing's sarcoma of bone of bone and other Osteosarcoma., ontroversial. The purpose of this study was to evaluate the efficacy and safety of PT for Craniopharyngioma in adults.METHODS AND ANALYSIS: We will search six databases (MEDLINE, EMBASE, Web of Science, the Cochrane Library, Amed, Scopus), clinical research registration websites and grey literature, aiming to identify randomised controlled trials (RCTs) on PT for Craniopharyngioma in adults between 1[SEP]Relations: Craniopharyngioma has relations: disease_protein with CTNNB1, disease_protein with CTNNB1, disease_phenotype_positive with Headache, disease_phenotype_positive with Headache, disease_disease with Disease of facial skeleton, disease_disease with Disease of facial skeleton, disease_phenotype_positive with Bitemporal hemianopia, disease_phenotype_positive with Bitemporal hemianopia, disease_disease with bone benign neoplasm, disease_disease with bone benign neoplasm.", "label": "yes"}
{"original_question": "Is there an association between TERT promoter mutation and survival of glioblastoma patients?", "id": "converted_366", "sentence1": "Is there an association between TERT wt Allele promoter mutation and survival of glioblastoma patients?", "sentence2": "Glioblastoma Multiforme Multiforme patients with TERT wt Allele wt Allele mutations showed a shorter survival than those without TERT wt Allele wt Allele mutations in univariate analysis (median, 9.3 vs. 10.5 months; P = 0.015) and multivariate analysis after adjusting for age and gender (plant-type hypersensitive response 1.38, 95 % CI 1.01-1.88, P = 0.041). However, TERT wt Allele wt Allele mutations had no significant impact on patients' survival in multivariate analysis after further adjusting for other Mutation, or when primary and secondary glioblastomas were separately analysed. These results suggest that the prognostic value of TERT wt Allele wt Allele mutations for poor survival is largely due to their inverse correlation with Isocitrate Dehydrogenase [NADP] Cytoplasmic mutations, which are a significant prognostic marker of better survival in patients with secondary glioblastomas., Patients with Neoplasms lacking hTERT expression/TA showed a significant survival benefit (Kaplan-Meier test, both P < .01), which, however, was based exclusively on the younger patient subgroup (≤60 y, both P < .005; >60 y, both ns). , Glioblastoma Multiforme Multiforme patients with TERT wt Allele wt Allele mutations showed a shorter survival than those without TERT wt Allele wt Allele mutations in univariate analysis (median, 9.3 vs[SEP]Relations: adult glioblastoma has relations: disease_disease with glioblastoma (disease), disease_disease with glioblastoma (disease), disease_disease with adult spinal cord glioblastoma, disease_disease with adult spinal cord glioblastoma, disease_disease with adult infiltrating astrocytic neoplasm, disease_disease with adult infiltrating astrocytic neoplasm. Somatic mutation has relations: disease_phenotype_positive with glioma susceptibility, disease_phenotype_positive with glioma susceptibility, disease_phenotype_positive with retinoblastoma, disease_phenotype_positive with retinoblastoma.", "label": "yes"}
{"original_question": "Are bacteria in the genus Clostridium facultative anaerobes?", "id": "converted_3760", "sentence1": "Are Bacteria in the genus Clostridium species facultative anaerobes?", "sentence2": "strict Bacteria, Anaerobic Clostridium species species acetobutylicum, Class Class Clostridia belong to those Bacteria which are considered as obligate Bacteria, Anaerobic, e.g. Oxygen Equipment Location is harmful or lethal to these Bacteria., We report here the closed genome of Clostridium species species pasteurianum ATCC 6013, a saccharolytic, nitrogen-fixing, and spore-forming Gram-positive obligate Bacteria, Anaerobic, Clostridium species species pasteurianum BB, a saccharolytic and spore-forming obligate Bacteria, Anaerobic, Clostridium species species difficile is a spore-forming obligate Bacteria, Anaerobic that is a leading cause of Cross Infection, However, the discovery of Microbicides has been biased towards aerobes and facultative anaerobes, and strict anaerobes such as Clostridium species species spp., Clostridium species species is a large genus of obligate anaerobes belonging to the Firmicutes phylum of Bacteria, most of which have a Gram-positive cell wall structure., Such Bacteria are either obligate anaerobic Bacteria like Clostridium species species or Bifidobacterium species species or facultative anaerobic like Escherichia coli or Salmonella species species., Antimicrobial production by strictly anaerobic Clostridium species species spp.[SEP]Relations: anaerobic Bacteria infectious disease has relations: disease_disease with Clostridium species infectious disease, disease_disease with Clostridium species infectious disease, disease_disease with infection caused by Bifidobacterium species, disease_disease with infection caused by Bifidobacterium species, disease_disease with Fusobacterium infectious disease, disease_disease with Fusobacterium infectious disease, disease_disease with Bacteroides infectious disease, disease_disease with Bacteroides infectious disease. Clostridium species difficile colitis has relations: phenotype_phenotype with Unusual gastrointestinal infection, phenotype_phenotype with Unusual gastrointestinal infection.", "label": "no"}
{"original_question": "Are apoE mimetics being considered as a treatment against Alzheimer's disease?", "id": "converted_3130", "sentence1": "Are Apolipoprotein E mimetics being considered as a treatment against Alzheimer's disease?", "sentence2": "The apolipoprotein-E-mimetic COG112 protects Amyloid beta-Protein Precursor intracellular domain-overexpressing animals from Alzheimer's disease-like pathological features., Studies show that administration of apolipoprotein E (Apolipoprotein E) and Apolipoprotein E-derived small Peptides mimetics protect AD mouse models against these AD-like features.[SEP]Relations: Amyloid beta-Protein Precursor metabolic process has relations: bioprocess_protein with APOE, bioprocess_protein with APOE, bioprocess_protein with APH1A, bioprocess_protein with APH1A, bioprocess_protein with PSENEN, bioprocess_protein with PSENEN, bioprocess_bioprocess with Amyloid beta-Protein Precursor catabolic process, bioprocess_bioprocess with Amyloid beta-Protein Precursor catabolic process. apolipoprotein E recycling has relations: bioprocess_bioprocess with protein transport, bioprocess_bioprocess with protein transport.", "label": "yes"}
{"original_question": "Is Bcl-2-like protein 1 an pro apoptotic protein?", "id": "converted_3753", "sentence1": "Is BCL2 gene-like protein 1 an pro apoptotic protein?", "sentence2": "Extensively established key effectors of such apoptotic bypass mechanisms, the antiapoptotic BCL-2 (apoptosis regulator BCL-2) proteins, determine the response of Tumor cells, malignant to chemotherapeutics, decreasing the expression of anti-apoptotic factors, including apoptosis regulator BCL2 gene and BCL2 gene-like protein 1 in FaDu cells, Like many Malignant Neoplasms, TNBC cells often deregulate programmed cell death by upregulating Apoptosis Inhibiting Proteins of the BCL2 protein, human (BCL2 gene) family.,  anti-apoptotic BCL2 gene-like protein 1 (bcl-x protein, Bcl-xL) [SEP]Relations: Protein S human has relations: drug_protein with PROC, drug_protein with PROC, drug_drug with Cepeginterferon alfa-2B, drug_drug with Cepeginterferon alfa-2B, drug_drug with Peginterferon alfa-2b, drug_drug with Peginterferon alfa-2b. Protein C has relations: drug_drug with Peginterferon alfa-2b, drug_drug with Peginterferon alfa-2b, drug_drug with Epoprostenol, drug_drug with Epoprostenol.", "label": "no"}
{"original_question": "Is HbA1c an ideal biomarker of well-controlled diabetes?", "id": "converted_3916", "sentence1": "Is Glycosylated hemoglobin A an ideal biomarker of well-controlled Diabetes Mellitus?", "sentence2": "Glycosylated hemoglobin A is a biomarker with a central role in the diagnosis and follow-up of patients with Diabetes Mellitus, although not a perfect one. Common comorbidities encountered in patients with Diabetes Mellitus mellitus, such as Kidney Failure, high output states (iron deficiency anaemia, Anemia, Hemolytic, Hemoglobinopathies and pregnancy) and intake of specific drugs could compromise the sensitivity and specificity of the biomarker. COVID-19 pandemic poses a pressing challenge for the diabetic population, since maintaining optimal blood glucose control is key to reduce morbidity and mortality rates.[SEP]Relations: Elevated hemoglobin A1c has relations: disease_phenotype_positive with neonatal Diabetes Mellitus mellitus, disease_phenotype_positive with neonatal Diabetes Mellitus mellitus, disease_phenotype_positive with maturity-onset Diabetes Mellitus of the young, disease_phenotype_positive with maturity-onset Diabetes Mellitus of the young, phenotype_phenotype with Abnormal hemoglobin, phenotype_phenotype with Abnormal hemoglobin. hemoglobinopathy has relations: disease_protein with HBA1, disease_protein with HBA1, disease_protein with HBA2, disease_protein with HBA2.", "label": "no"}
{"original_question": "Is Cystatin D a biomarker?", "id": "converted_2735", "sentence1": "Is CST5 gene a biomarker?", "sentence2": "CST5 gene (CST5): An ultra-early inflammatory biomarker of Traumatic Brain Injury.[SEP]Relations: brain injury has relations: contraindication with Cyclopentolate, contraindication with Cyclopentolate, contraindication with Isopropamide, contraindication with Isopropamide, contraindication with Guaifenesin, contraindication with Guaifenesin, contraindication with Homatropine methylbromide, contraindication with Homatropine methylbromide, contraindication with Hydrocodone, contraindication with Hydrocodone.", "label": "yes"}
{"original_question": "Are seizures among the neurological symptoms of incontinentia pigmenti?", "id": "converted_839", "sentence1": "Are Seizures among the neurological symptoms of incontinentia pigmenti?", "sentence2": "High-dose glucocorticoid therapy in the management of Seizures in neonatal incontinentia pigmenti, Bloch Sulzberger syndrome is an X-linked dominant disorder resulting from a Mutation Abnormality of IKBKG gene Genes. This disorder has a classic dermatologic presentation, but neurologic involvement, with Seizures and cortical infarction, can arise shortly after birth, Some children with incontinentia pigmenti exhibit encephalopathic features with severe Seizures and disturbed consciousness, from the neonatal through the early infantile period, Bloch Sulzberger syndrome (IP) is a rare X-linked dominant neurocutaneous disorder affecting ectodermal tissue: Skin Specimen Source Code, Eye, CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, Hair Specimen, Nail plate, and Head>Teeth. It is usually lethal for males in utero. The involved Genes is NF-Kappa-B Essential Modulator, an essential component of the nuclear factor-kappa B (NF-κB) signaling pathway. Skin lesion are highly diagnostic, occurring in neonates, with a particular distribution on Blaschko lines. The severity of the disease is related to ocular and neurological impairment. The hallmark of ocular IP is Retinal vasculopathy including peripheral retinal vascular nonperfusion, macular infarction and neovascularization, and preretinal neovascularization. CNS involvement consists of Seizures, Intellectual Disability, hemiparesis, Muscle Spasticity, Microcephaly (physical finding), Cerebellar Ataxia, and Apraxia, oculomotor, Cogan type, Incontinentia Pigmenti is a rare X-linked multisystem disorder with well described and pathognomonic Skin Specimen Source Code manifestations. Neurological manifestations are found in 30% of IP patients, forming one of the major causes of morbidity and mortality of the condition. In this review, clinical and brain imaging data of 45 IP patients with a neurological phenotype are reviewed. Several clinical presentations could be identified, comprising Seizures, Infantile encephalopathy, acute disseminated encephalomyelitis and Ischemic stroke, Bloch Sulzberger syndrome presenting as Seizures., Neonatal Seizures in two sisters with incontinentia pigmenti., High-dose glucocorticoid therapy in the management of Seizures in neonatal incontinentia pigmenti: a case report., Incontinentia Pigmenti is an X-linked dominant neurocutaneous disorder with CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS manifestations in 30% of cases, including Seizures and Intellectual Disability., Neonatal Seizures in two sisters with incontinentia pigmenti, A rare cause of neonatal seizure: incontinentia pigmenti., Here, we describe the clinical, electrographic, and neuroradiologic effect of systemic glucocorticoid therapy in a neonate with incontinentia pigmenti manifesting an Epileptic encephalopathy., Bloch Sulzberger syndrome presenting as Seizures., Neonatal Seizures in two sisters with incontinentia pigmenti.[SEP]Relations: Seizure has relations: disease_phenotype_positive with incontinentia pigmenti, disease_phenotype_positive with incontinentia pigmenti, disease_phenotype_positive with retinitis pigmentosa, disease_phenotype_positive with retinitis pigmentosa, phenotype_phenotype with Symptomatic Seizures, phenotype_phenotype with Symptomatic Seizures. Intellectual disability has relations: disease_phenotype_positive with incontinentia pigmenti, disease_phenotype_positive with incontinentia pigmenti. IKBKG gene has relations: disease_protein with incontinentia pigmenti, disease_protein with incontinentia pigmenti.", "label": "yes"}
{"original_question": "Does erythromycin increase risk of hypertrophic pyloric stenosis?", "id": "converted_2394", "sentence1": "Does erythromycin G increase risk of hypertrophic Pyloric Stenosis, Hypertrophic?", "sentence2": "Post-natal erythromycin G G exposure and risk of infantile hypertrophic Pyloric Stenosis, Hypertrophic: a systematic review and meta-analysis., PURPOSE: Macrolide antibiotics, erythromycin G G, in particular, have been linked to the development of infantile hypertrophic Pyloric Stenosis, Hypertrophic (IHPS).,  Overall, erythromycin G G exposure was significantly associated with development of IHPS [OR 2.45 (1.12-5.35), p = 0.02]. , Data on erythromycin G G exposure in the first 14 days of life was extracted from 4/9 studies and identified a strong association between erythromycin G G exposure and subsequent development IHPS [OR 12.89 (7.67-2167), p < 0.00001].CONCLUSION: This study demonstrates a significant association between post-natal erythromycin G G exposure and development of IHPS, which seems stronger when exposure occurs in the first 2 weeks of life., BACKGROUND AND OBJECTIVE: Use of oral erythromycin G G in infants is associated with infantile hypertrophic Pyloric Stenosis, Hypertrophic (IHPS)., CONCLUSIONS: Ingestion of oral azithromycin and erythromycin G G places young infants at increased risk of developing IHPS., An association between erythromycin G G and IHPS was also confirmed. Exposure to erythromycin G G in the first 14 days of life had an aOR of 13.3 (95% NDUFB6 gene, 6.80-25.9), and 15 to 42 days of life, aOR 4.10 (95% NDUFB6 gene, 1.69-9.91). , Early exposure to oral erythromycin G G in young infants, particularly in the first 2 weeks of life, has previously been associated with the development of hypertrophic Pyloric Stenosis, Hypertrophic. We report a case of an infant who received an abbreviated 4-day course of oral erythromycin G G for suspected Inclusion conjunctivitis at 5 days of life then underwent pyloromyotomy for Pyloric Stenosis, Hypertrophic less than 2 weeks later., Maternal and infant use of erythromycin G G and other Macrolide [EPC] antibiotics as risk factors for infantile hypertrophic Pyloric Stenosis, Hypertrophic., A case report has suggested that exposure to erythromycin G G through Specimen Source Codes - Breast milk might cause infantile hypertrophic Pyloric Stenosis, Hypertrophic., Macrolide antibiotics, erythromycin G G, in particular, have been linked to the development of infantile hypertrophic Pyloric Stenosis, Hypertrophic (IHPS)., Infants prescribed systemic erythromycin G G had increased risk of IHPS, with the highest risk in the first 2 weeks of age (relative risk = 10.51 for erythromycin G G in first 2 weeks, 95% NDUFB6 gene 4.48, 24.66)., There was an association between maternal prescriptions for nonerythromycin macrolides and infantile hypertrophic Pyloric Stenosis, Hypertrophic (adjusted odds ratio 2.77, 95% confidence interval 1.22, 6.30, P =.01).<br><b>CONCLUSION</b>: The hypothesized association between erythromycin G G and infantile Pyloric Stenosis, Hypertrophic was not seen., Macrolide antibiotics, erythromycin G G, in particular, have been linked to the development of infantile hypertrophic Pyloric Stenosis, Hypertrophic (IHPS).[SEP]Relations: hypertrophic Pyloric Stenosis, Hypertrophic has relations: disease_disease with intestinal disease, disease_disease with intestinal disease, disease_disease with Pyloric Stenosis, Hypertrophic (disease), disease_disease with Pyloric Stenosis, Hypertrophic (disease), disease_disease with Mendelian disease, disease_disease with Mendelian disease, disease_disease with Pyloric Stenosis, Hypertrophic, infantile hypertrophic, disease_disease with Pyloric Stenosis, Hypertrophic, infantile hypertrophic. Pyloric Stenosis, Hypertrophic, infantile hypertrophic has relations: disease_phenotype_positive with Hypochloremic metabolic alkalosis, disease_phenotype_positive with Hypochloremic metabolic alkalosis.", "label": "yes"}
{"original_question": "Is pseudouridine a RNA modification?", "id": "converted_1942", "sentence1": "Is pseudouridine a RNA modification?", "sentence2": "Pseudouridine (Ψ) is the most abundant of>150 nucleoside modifications in RNA. , The number and Positioning Attribute of the pseudouridines of Haloarcula marismortui and Deinococcus radiodurans large subunit RNA have been determined by a combination of total nucleoside analysis by HPLC-mass spectrometry and pseudouridine sequencing by the reverse transcriptase method and by LC/MS/MS., Pseudouridine is the most abundant of more than 100 Chemicals distinct natural ribonucleotide modifications.[SEP]Relations: pseudouridine synthesis has relations: bioprocess_bioprocess with RNA modification, bioprocess_bioprocess with RNA modification, bioprocess_bioprocess with mRNA pseudouridine synthesis, bioprocess_bioprocess with mRNA pseudouridine synthesis, bioprocess_protein with NOP10, bioprocess_protein with NOP10, bioprocess_bioprocess with rRNA pseudouridine synthesis, bioprocess_bioprocess with rRNA pseudouridine synthesis, bioprocess_bioprocess with tRNA pseudouridine synthesis, bioprocess_bioprocess with tRNA pseudouridine synthesis.", "label": "yes"}
{"original_question": "Is there an association between pyostomatitis vegetans and Crohn's disease?", "id": "converted_4559", "sentence1": "Is there an association between pyostomatitis vegetans and Crohn's disease of oral soft tissues?", "sentence2": "Among the main oral manifestations of Irritable Bowel Syndrome are cobblestoning of the Oral mucous membrane structure, labial swellings with vertical fissures, pyostomatitis vegetans, Angular cheilitis, Perioral erythema, and Glossitis. , Pyostomatitis vegetans: A Clue for Diagnosis of Silent Crohn's Disease., We present a case of Pyostomatitis vegetans involving Gingiva and Oral mucous membrane structure with no skin lesion which led to the diagnosis of Crohn's disease of oral soft tissues of oral soft tissues to emphasize important role of dentists in diagnosis of rare oral Lesion and management of patients' systemic disease., Moreover, in both CD and Ulcerative Colitis, there occur several other inflammatory skin conditions such as Erythema Nodosum, Pyoderma Gangrenosum, Hidradenitis Suppurativa, chronic oral aphthous disease, Sweet Syndrome, pyostomatitis vegetans, and Bowel-associated dermatosis-arthritis syndrome. , Diffuse mucosal swelling, cobblestone mucosa, localised mucogingivitis, deep linear ulceration, Fibrous tissue Tags (device), Specimen Source Codes - Polyps, Nodulus cerebelli, pyostomatitis vegetans, and aphthous-like Ulcer have been described in Crohn's disease of oral soft tissues of oral soft tissues. , Aphthous stomatitis and pyostomatitis vegetans are among non-specific oral manifestations of Irritable Bowel Syndrome., Pyostomatitis vegetans (Polycythemia Vera) is a rare, chronic mucocutaneous disorder associated with INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome). Oral Lesion of Polycythemia Vera are distinct and present as multiple white or yellow pustule with an erythematous base that coalesce and undergo Necrotic changes (finding) to form a typical \"snail tracks\" appearance. Two cases of Polycythemia Vera associated with Irritable Bowel Syndrome--one with Crohn's disease of oral soft tissues of oral soft tissues (CD) and the other with ulcerative colitis (Ulcerative Colitis) are reported.,  Oral involvement during Irritable Bowel Syndrome includes several types of Lesion: the most common are aphthae; uncommon Lesion include, among others, pyostomatitis vegetans and granulomatous Lesion of CD. , Pyostomatitis vegetans (Polycythemia Vera) is a rare condition characterized by pustule that affect the Oral mucous membrane structure. It is a highly specific marker for INFLAMMATORY BOWEL DISEASE 2 and its correct recognition may lead to the diagnosis of ulcerative colitis or Crohn's disease of oral soft tissues of oral soft tissues. , matitis and pyostomatitis vegetans are among non-specific oral manifestations of Irritable Bowel Syndrome. In differe, on-specific manifestations, such as Minor oral aphthous ulceration and Angular cheilitis, occur in both diseases, while pyostomatitis vegetans is more pronounced in patients with Ulcerative Colitis. Non-specific lesio, ment during Irritable Bowel Syndrome includes several types of Lesion: the most common are aphthae; uncommon Lesion include, among others, pyostomatitis vegetans and granulomatous Lesion of CD. Starting wit, s Ulcer, pyostomatitis vegetans, cobblestoning and Gingivitis are important oral findings frequently observed in Irritable Bowel Syndrome patients. Their p, e main oral manifestations of Irritable Bowel Syndrome are cobblestoning of the Oral mucous membrane structure, labial swellings with vertical fissures, pyostomatitis vegetans, Angular cheilitis, Perioral erythema, and Glossitis. In this sen, Pyostomatitis vegetans is frequently associated with chronic Inflammatory Bowel Diseases and can, thus, give a diagnostic hint at an existing ulcerative colitis or Crohn’s disease., Oral Crohn's disease of oral soft tissues of oral soft tissues and pyostomatitis vegetans. An unusual association., [Pyostomatitis vegetans and Crohn's disease of oral soft tissues of oral soft tissues. A specific association of 2 diseases]., osis of Crohn's disease of oral soft tissues of oral soft tissues. Clinical manifestations improved dramatically with prednisone.DISCUSSION: This case of pyostomatitis-pyodermatitis vegetans involved several aspects rarely reported in the literature: a) the cutaneomucosal signs were inaugural; b) the association with Crohn's disease of oral soft tissues of oral soft tissues; c) the presence of Lesion to the genital mucosa; d) the unusual localization , Pyostomatitis vegetans is a specific marker for ulcerative colitis and Crohn's disease of oral soft tissues of oral soft tissues., The pathogenetic interrelationship between pyostomatitis vegetans and Crohn's disease of oral soft tissues of oral soft tissues is discussed., Successful treatment with infliximab and methotrexate of pyostomatitis vegetans associated with Crohn's disease of oral soft tissues of oral soft tissues., Infliximab and methotrexate may be a promising treatment for the rare cases of pyostomatitis vegetans associated with Crohn's disease of oral soft tissues of oral soft tissues., INTRODUCTION: Pyostomatitis vegetan (Polycythemia Vera) is often associated with chronic INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome).OBSERVATION: Tw[SEP]Relations: Crohn disease of the esophagus has relations: disease_disease with Crohn disease, disease_disease with Crohn disease, disease_disease with esophagitis (disease), disease_disease with esophagitis (disease). INFLAMMATORY BOWEL DISEASE 2 has relations: disease_phenotype_positive with Crohn's disease of oral soft tissues, disease_phenotype_positive with Crohn's disease of oral soft tissues, disease_phenotype_positive with Crohn's disease of oral soft tissues, disease_phenotype_positive with Crohn's disease of oral soft tissues, disease_disease with Crohn disease, disease_disease with Crohn disease.", "label": "yes"}
{"original_question": "Is Alpers disease inherited in an autosomal recessive mode?", "id": "converted_511", "sentence1": "Is Alpers Syndrome (disorder) inherited in an Autosomal recessive inheritance mode?", "sentence2": "Alpers-Huttenlocher syndrome (AHS) is a very rare Autosomal Recessive Disorder, Alpers syndrome is an Autosomal recessive inheritance mitochondrial DNA depletion disorder that affects children and young adults, Alpers' syndrome is a fatal neurogenetic disorder first described more than 70 years ago. It is an Autosomal recessive inheritance, developmental mitochondrial DNA depletion disorder characterized by deficiency in mitochondrial DNA polymerase gamma (POLG protein, human protein, human) catalytic activity, refractory seizures, Nerve Degeneration, and Hepatobiliary Disorder, Histopathological findings in both patients ((a) chronic hepatitis with prominent bile duct proliferation, Fatty degeneration, and Fibrosis; (b) in the Head>Brain a patchy destruction of the Cerebral cortex, predominantly involving Area striata structure) were characteristic of progressive Neuronal degeneration of childhood with Hepatobiliary Disorder--Alpers-Huttenlocher syndrome--a rare Autosomal Recessive Disorder usually seen in infants and young children, Histopathological findings in both patients ((a) chronic hepatitis with prominent bile duct proliferation, Fatty degeneration, and Fibrosis; (b) in the Head>Brain a patchy destruction of the Cerebral cortex, predominantly involving Area striata structure) were characteristic of progressive Neuronal degeneration of childhood with Hepatobiliary Disorder--Alpers-Huttenlocher syndrome--a rare Autosomal Recessive Disorder usually seen in infants and young children., Alpers syndrome is a rare Autosomal recessive inheritance hepatocerebral degenerative disorder., Alpers Syndrome (disorder) is a recessive mitochondrial disorder caused by Gene Mutation in POLG protein, human protein, human wt Allele and characterized primarily by progressive neurological and hepatic degeneration., Alpers syndrome is an Autosomal recessive inheritance mitochondrial DNA depletion disorder that affects children and young adults., We conclude that Alpers Syndrome (disorder) can be a cause of rapidly progressive Liver Failure in early childhood. Although the cause of this Autosomal recessive inheritance disease is not known, it does not appear to be related to peroxisomal dysfunction.[SEP]Relations: Autosomal recessive inheritance disease has relations: disease_disease with Autosomal recessive inheritance Alport syndrome, disease_disease with Autosomal recessive inheritance Alport syndrome, disease_disease with Autosomal recessive inheritance ocular albinism, disease_disease with Autosomal recessive inheritance ocular albinism, disease_disease with Autosome genetic disease, disease_disease with Autosome genetic disease. Autosomal recessive inheritance has relations: phenotype_phenotype with Mode of inheritance, phenotype_phenotype with Mode of inheritance, disease_phenotype_positive with Autosomal recessive inheritance Alport syndrome, disease_phenotype_positive with Autosomal recessive inheritance Alport syndrome.", "label": "yes"}
{"original_question": "Is ACE2 expressed on cell surfaces?", "id": "converted_3256", "sentence1": "Is ACE2 protein, human expressed on cell surfaces?", "sentence2": " Recent studies reported that shedding of the enzymatically active ectodomain of ACE2 protein, human protein, human from the Cell surface, ACE2 protein, human protein, human is a type 1 integral membrane protein and contains a catalytically active ectodomain that can be shed from the Cell surface into the Extracellular Space,[SEP]Relations: Cell surface has relations: cellcomp_protein with ACE2 protein, human, cellcomp_protein with ACE2 protein, human, cellcomp_protein with ABCC2, cellcomp_protein with ABCC2, cellcomp_protein with CACNG2, cellcomp_protein with CACNG2, cellcomp_protein with GOT2, cellcomp_protein with GOT2. Extracellular Space has relations: cellcomp_protein with ACE2 protein, human, cellcomp_protein with ACE2 protein, human.", "label": "yes"}
{"original_question": "Do U6-associated proteins Lsm4 and Lsm6 interact with SMN?", "id": "converted_1432", "sentence1": "Do U6-associated Proteins LSM4 gene and LSM6 gene interact with STMN1 wt Allele?", "sentence2": "STMN1 wt Allele also interacts with at least two of the U6-associated Nucleotide Sequence Sample Name-like (Lsm) Proteins, LSM4 gene and LSM6 gene. , Interestingly, STMN1 wt Allele also interacts with at least two of the U6-associated Nucleotide Sequence Sample Name-like (Lsm) Proteins, LSM4 gene and LSM6 gene, Furthermore, we present evidence for two separate Binding Sites in STMN1 wt Allele for Nucleotide Sequence Sample Name/Lsm Proteins., Interestingly, STMN1 wt Allele also interacts with at least two of the U6-associated Nucleotide Sequence Sample Name-like (Lsm) Proteins, LSM4 gene and LSM6 gene. , Symmetrical dimethylation of arginine residues in spliceosomal Nucleotide Sequence Sample Name protein B/B' and the Nucleotide Sequence Sample Name-like protein LSm4, and their interaction with the STMN1 wt Allele protein., Interestingly, STMN1 wt Allele also interacts with at least two of the U6-associated Nucleotide Sequence Sample Name-like (Lsm) Proteins, LSM4 gene and LSM6 gene. Furthermore, the carboxyl-terminal arginine- and glycine-rich domain of LSM4 gene directly interacts with STMN1 wt Allele., This entity promotes the binding of a set of factors, termed LSm/Nucleotide Sequence Sample Name Proteins, onto Small Nuclear RNA to form the core structure of these particles. , Toward an assembly line for U7 Small Nuclear Ribonucleoproteins: interactions of U7-specific Lsm Proteins with PRMT5 gene gene and STMN1 wt Allele complex (molecular entity)., In this report, we demonstrate that the COIL gene C-terminal domain binds directly to various Nucleotide Sequence Sample Name and Lsm Proteins via their Nucleotide Sequence Sample Name motifs. We show that the region of COIL gene responsible for this binding activity is separable from that which binds to STMN1 wt Allele., Thus, the ability to interact with free Nucleotide Sequence Sample Name (and Lsm) Proteins as well as with intact Small Nuclear Ribonucleoproteins, indicates that COIL gene and CBS gene may facilitate the ResponseLevel - ResponseLevel - modification of newly formed Small Nuclear Ribonucleoproteins, the regeneration of 'mature' Small Nuclear Ribonucleoproteins, or the reclamation of unassembled small nuclear ribonucleoprotein complex location components., Moreover this structure has important consequences for small nuclear ribonucleoprotein complex location assembly that is mediated by two complex (molecular entity) containing the PRMT5 gene gene methyltransferase and the STMN1 wt Allele (survival of Neurons, Efferent) protein, respectively., Arginine/glycine (RG)-rich domains in components of the STMN1 wt Allele complex interact with Nucleotide Sequence Sample Name, like-Nucleotide Sequence Sample Name (LSm), fibrillarin, RNA Helicase (Gu), and COIL gene Proteins, all of which are antigen targets in a variety of diseases. [SEP]Relations: STMN1 wt Allele complex has relations: cellcomp_protein with GEMIN6, cellcomp_protein with GEMIN6, cellcomp_protein with SMN2, cellcomp_protein with SMN2, cellcomp_protein with SMN1, cellcomp_protein with SMN1. small nuclear ribonucleoprotein complex has relations: cellcomp_protein with LSM6, cellcomp_protein with LSM6, cellcomp_protein with LSM6, cellcomp_protein with LSM6.", "label": "yes"}
{"original_question": "Is there a role for the cylindromatosis tumor suppressor (CYLD) in lung cancer?", "id": "converted_437", "sentence1": "Is there a role for the cylindromatosis tumor suppressor (CYLD protein, human) in Primary malignant neoplasm of lung?", "sentence2": "Over-expressing CYLD protein, human protein, human augments Antitumor activity of TNFSF10 wt Allele by inhibiting the NF-κB survival signaling in Primary malignant neoplasm of lung cells, increased expression of CYLD protein, human protein, human directly blocks TNFSF10 wt Allele-induced NF-κB activation, and consequently increases TNFSF10 wt Allele-induced apoptosis in Primary malignant neoplasm of lung cells. CYLD protein, human protein, human may act as a therapeutic target of Primary malignant neoplasm of lung. Targeting CYLD protein, human protein, human, in combination with TNFSF10 wt Allele, may be a new strategy to treat Primary malignant neoplasm of lung with high NF-κB activity, Truncation of the Catalytic Domain of the cylindromatosis tumor suppressor impairs lung maturation, down-regulation of Cyld expression has been associated with the development of various types of human malignancies including Primary malignant neoplasm of lung, Deletion of exon 9 would cause a carboxyl-terminal truncation of CYLD protein, human protein, human and inactivation of its deubiquitinating activity. In accordance with previous studies, Specimen Source Codes - Fibroblasts from Cyld(Delta 9/Delta 9) embryos had hyperactive nuclear factor kappaB and c-Jun kinase pathways compared with control Specimen Source Codes - Fibroblasts. Cyld(Delta 9/Delta 9) newborn CASP14 gene were smaller than wild-type littermates with a short and kinky tail and no major developmental defects. However, Cyld(Delta 9/Delta 9) CASP14 gene died shortly after birth from apparent Abnormal breathing. Histological examination of E18.5 Cyld(Delta 9/Delta 9) Lung demonstrated an immature phenotype characterized by hyperplasic mesenchyme but apparently normal Epithelial, Smooth muscle (tissue). and endothelial structures. Our study identifies an important role of CYLD protein, human protein, human in lung maturation, which may underlie the development of many cases of Primary malignant neoplasm of lung, Gene Mutation that truncate and inactivate the carboxyl-terminal deubiquitinating domain of CYLD protein, human protein, human underlie the development of skin appendage tumors in Homo sapiens, whereas down-regulation of Cyld expression has been associated with the development of various types of human malignancies including Primary malignant neoplasm of lung., Our study identifies an important role of CYLD protein, human protein, human in lung maturation, which may underlie the development of many cases of Primary malignant neoplasm of lung., Gene Mutation that truncate and inactivate the carboxyl-terminal deubiquitinating domain of CYLD protein, human protein, human underlie the development of skin appendage tumors in Homo sapiens, whereas down-regulation of Cyld expression has been associated with the development of various types of human malignancies including Primary malignant neoplasm of lung[SEP]Relations: lung has relations: anatomy_protein_present with CYLD protein, human, anatomy_protein_present with CYLD protein, human, anatomy_protein_present with PDGFRA, anatomy_protein_present with PDGFRA, anatomy_protein_present with MKRN2OS, anatomy_protein_present with MKRN2OS, anatomy_protein_present with NCOR2, anatomy_protein_present with NCOR2, anatomy_protein_present with CYSLTR2, anatomy_protein_present with CYSLTR2.", "label": "yes"}
{"original_question": "Is YKL-40 used as a biomarker for Alzheimer's disease?", "id": "converted_4114", "sentence1": "Is Chitinase-3-Like Protein 1 used as a biomarker for ALZHEIMER DISEASE, FAMILIAL, 1?", "sentence2": "Recently, In Cerebrospinal Fluid (CSF) Chitinase-3-Like Protein 1 levels were reported to be a promising candidate biomarker of glial inflammation in ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol). , Disease groups differed between them except cytarabine/daunorubicin protocol versus FTD for Chitinase-3-Like Protein 1. , Chitinase-3-Like Protein 1 appears to be a more reliable biomarker in neurological diseases than ENO2 wt Allele.[SEP]Relations: familial Alzheimer disease has relations: disease_disease with Alzheimer disease, disease_disease with Alzheimer disease, disease_protein with PRNP, disease_protein with PRNP, disease_phenotype_positive with Perseveration, disease_phenotype_positive with Perseveration, disease_phenotype_positive with Attention deficit hyperactivity disorder, disease_phenotype_positive with Attention deficit hyperactivity disorder, disease_disease with inherited prion disease, disease_disease with inherited prion disease.", "label": "yes"}
{"original_question": "Are Epoxyeicosatrienoic acids (EETs) synthesized by cytochrome P450 epoxygenases from arachidonic acid?", "id": "converted_4331", "sentence1": "Are Epoxyeicosatrienoic acids (EETs) synthesized by cytochrome P450 epoxygenases from arachidonic acid?", "sentence2": "Biologically active epoxyeicosatrienoic acid (Epoxyeicosatrienoic Acid) regioisomers are synthesized from arachidonic acid by cytochrome P450 epoxygenases of Endothelium, Myocardial, and renal tubular cells., epoxyeicosatrienoic acids (EETs), synthesized by cytochrome P450 epoxygenases from arachidonic acid. , Epoxyeicosatrienoic acids (EETs), synthesized from arachidonic acid by cytochrome P450 epoxygenases, Epoxyeicosatrienoic acids (EETs), which are synthesized from arachidonic acid by cytochrome P450 epoxygenases, function primarily as autocrine and paracrine effectors in the cardiovascular system and Both kidneys. , Epoxyeicosatrienoic acids (EETs) are synthesized from arachidonic acid by cytochrome P450 epoxygenases in Endothelium cells. I, Epoxyeicosatrienoic acids (EETs), the eicosanoid biomediators synthesized from arachidonic acid by cytochrome P450 epoxygenases,, Epoxyeicosatrienoic acids (EETs) are bioactive Eicosanoids produced from arachidonic acid by cytochrome P450 epoxygenases., arachidonic acid is metabolized to epoxyeicosatrienoic acids (EETs) by cytochrome (CYP) P450 epoxygenases, and to ω-terminal hydroxyeicosatetraenoic acids (HETEs) by ω-hydroxylases., Epoxyeicosatrienoic acids (EETs), synthesized from arachidonic acid by cytochrome P450 epoxygenases, are converted to dihydroxyeicosatrienoic acids by soluble Epoxide hydrolase., Epoxyeicosatrienoic acids (EETs), which are synthesized from arachidonic acid by cytochrome P450 epoxygenases, function primarily as autocrine and paracrine effectors in the cardiovascular system and Both kidneys., Epoxygenases metabolize arachidonic acid to four regioisomeric epoxyeicosatrienoic acids (EETs) and selected monohydroxyeicosatetraenoic acids (HETEs)., Epoxyeicosatrienoic acids (EETs) are potent lipid mediators formed by cytochrome P450 epoxygenases from arachidonic acid. , Epoxyeicosatrienoic acids (EETs) are bioactive Eicosanoids produced from arachidonic acid by cytochrome P450 epoxygenases. , Epoxyeicosatrienoic acids (EETs), derived from arachidonic acid by cytochrome P450 epoxygenases, are potent vasodilators that function as endothelium-derived hyperpolarizing factors in some vascular beds. E, Epoxyeicosatrienoic acids (EETs), which are synthesized from arachidonic acid by cytochrome P450 epoxygenases, function primarily as autocrine and paracrine effectors in the cardiovascular system and Both kidneys. T, poxyeicosatrienoic acids (EETs) are epoxy lipids derived from metabolism of arachidonic acid by cytochrome P450 epoxygenases. W, he Endothelium, Vascular metabolizes arachidonic acid by cytochrome P450 epoxygenases to epoxyeicosatrienoic acids or EETs., Epoxyeicosatrienoic acids (EETs) are the epoxidation products of arachidonic acid catalyzed by cytochrome P450 (CYP) epoxygenases, which possess multiple biological activities. In , OBJECTIVE: arachidonic acid metabolism by cytochrome P450 (CYP) epoxygenases leads to epoxyeicosatrienoic acids (EETs), which are Eicosanoids with vasodilator and anti-inflammatory pro, Cytochrome P450 (CYP) epoxygenases metabolize arachidonic acid into epoxyeicosatrienoic acids (EETs), which play important and diverse roles in the cardiovascular system. Tyrosine 3-Monooxygenase, human, Epoxyeicosatrienoic acids (EETs) are arachidonic acid metabolites produced by cytochrome P450 epoxygenases which are highly expressed in Hepatocyte. , Epoxyeicosatrienoic acids (EETs) are epoxides of arachidonic acid generated by cytochrome P450 (CYP) epoxygenases., Although Eicosanoids, including Prostaglandin drugs for peptic ulcer and gastro-oesophageal reflux disease (GORD) and Leukotriene A, are best known as products of arachidonic acid metabolism by Prostaglandin-Endoperoxide Synthase and Lipoxygenases, arachidonic acid is also a substrate for another enzymatic pathway, the cytochrome P450 (CYP) system., Epoxyeicosatrienoic acids (EETs), lipid mediators synthesized from arachidonic acid by Arachidonate Epoxygenase, are converted by soluble Epoxide hydrolase (SEH) to the corresponding dihydroxyeicosatrienoic acids (DHETs)., Epoxyeicosatrienoic acids (EETs) are synthesized from arachidonic acid by cytochrome P450 epoxygenases in Endothelium cells., Epoxyeicosatrienoic acids (EETs), the eicosanoid biomediators synthesized from arachidonic acid by cytochrome P450 epoxygenases, are inactivated in many Body tissue by conversion to dihydroxyeicosatrienoic acids (DHETs)., Epoxyeicosatrienoic acids (EETs) are potent lipid mediators formed by cytochrome P450 epoxygenases from arachidonic acid., Recent studies show that Mus sp. epidermis expresses CYP2B19, a keratinocyte-specific epoxygenase that generates 11,12- and 14,15-epoxy-5,8,11-eicosatrienoic acid (Epoxyeicosatrienoic Acid) acids from arachidonate., Identification of rabbit cytochromes P450 2C1 and 2C2 as arachidonic acid epoxygenases., Epoxyeicosatrienoic acids (EETs) are formed from arachidonic acid by the action of P450 epoxygenases (cytochrome P-450 cytochrome P-450 CYP2C subfamily subfamily and CYP2J)., Epoxyeicosatrienoic acids (EETs) are generated from arachidonic acid by cytochrome P450 (CYP) epoxygenases.[SEP]Relations: Arachidonic Acid has relations: drug_drug with Aprepitant, drug_drug with Aprepitant, drug_drug with Phenylbutazone, drug_drug with Phenylbutazone, drug_drug with Apremilast, drug_drug with Apremilast, drug_drug with Ethinylestradiol, drug_drug with Ethinylestradiol. arachidonate 5-lipoxygenase activity has relations: molfunc_protein with ALOX5AP, molfunc_protein with ALOX5AP.", "label": "yes"}
{"original_question": "Are osteoclasts specialized in bone degradation?", "id": "converted_2588", "sentence1": "Are Osteoclasts specialized in Specimen Type - Bone degradation?", "sentence2": "osteoclast-mediated attack on Specimen Type - Bone, Bone degradation is caused by Osteoclasts, the normal Specimen Type - Bone-resorbing cells. , cathepsin K is a highly potent collagenase Clostridium histolyticum Clostridium histolyticum in Osteoclasts and is responsible for Specimen Type - Bone degradation., In Osteoclasts, Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human controls podosome organization and Specimen Type - Bone degradation, which leads to an osteopetrotic phenotype in src(-/-) CASP14 gene, Bone degradation by Osteoclasts depends on the formation of a sealing zone, composed of an interlinked network of Podosomes, which delimits the degradation lacuna into which Osteoclasts secrete Acids and Proteolytic enzymes for treatment of wounds and ulcers. [SEP]Relations: osteoclast fusion has relations: bioprocess_protein with CD81, bioprocess_protein with CD81, bioprocess_protein with SBNO2, bioprocess_protein with SBNO2, bioprocess_protein with CD109, bioprocess_protein with CD109, bioprocess_protein with SH3PXD2A, bioprocess_protein with SH3PXD2A, bioprocess_protein with TCTA, bioprocess_protein with TCTA.", "label": "yes"}
{"original_question": "Is there a difference in the rate between gene fusion and gene fission?", "id": "converted_1331", "sentence1": "Is there a difference in the rate between Genes fusion and Genes fission?", "sentence2": "we illustrate arrangement diversity within closely related Organism, estimate arrangement turnover frequency and establish, for the first time, branch-specific rate estimates for fusion, fission, domain addition and terminal loss., Rate and polarity of Genes fusion and fission in Oryza sativa and Arabidopsis sp. sp. thaliana, We have identified all differentially composite or split genes in 2 fully sequenced Genome, Plant, Oryza sativa and Arabidopsis sp. sp. thaliana, Polarizing these events by outgroup comparison revealed differences in the rate of Genes fission but not of Genes fusion in the rice and Arabidopsis sp. sp. lineages. Gene fission occurred at a higher rate than Genes fusion in the O. sativa lineage and was furthermore more common in rice than in Arabidopsis sp. sp.., Gene fusion and fission are thus rare and slow processes in higher Genome, Plant; they should be of utility to address deeper evolutionary relationships among Plants--and the relationship of Plants to other eukaryotic lineages--where sequence-based phylogenies provide equivocal or conflicting results., Primary factors correlating with fusion rates are the presence of fully spanning the plasma membrane helices in HKs and the presence of DNA-binding domains in Robinow syndrome, autosomal recessive, features that require correct (and separate) spatial location. In the absence of such features, there is a relative abundance of fused genes., We show that indels are the most frequent elementary events and that they occur in most cases at either the N- or C-terminus of the proteins. As revealed by the genomic neighbourhood/context of the corresponding genes, we show that a substantial number of these terminal indels are the consequence of Genes fusions/fissions. We provide evidence showing that the contribution of Genes fusion/fission to the evolution of multi-domain Bacterial Proteins is lower-bounded by 27% and upper-bounded by 64%. We conclude that Genes fusion/fission is a major contributor to the evolution of multi-domain Bacterial Proteins., We found that fusion events are approximately four times more common than fission events, and we established that, in most cases, any particular fusion or fission event only occurred once during the course of evolution., Analyzing the most parsimonious pathways, we find 87% of architectures to gain complexity over time through simple changes, among which fusion events account for 5.6 times as many architectures as fission., These trees defined timelines of architectural discovery and revealed remarkable evolutionary patterns, including the explosive appearance of domain combinations during the rise of organismal lineages, the dominance of domain fusion processes throughout evolution, and the late appearance of a new class of multifunctional modules in Eukaryota by fission of domain combinations, We searched for examples which have arisen by one of the three postulated mechanisms: independent fusion/fission, \"duplication/deletion,\" and plasmid-mediated \"cut and paste.\" We conclude that all three mechanisms can be observed, with the independent fusion/fission being the most frequent.[SEP]Relations: robinow syndrome, autosomal recessive 2 has relations: disease_phenotype_positive with Camptodactyly, disease_phenotype_positive with Camptodactyly, disease_phenotype_positive with Absent uvula, disease_phenotype_positive with Absent uvula, disease_phenotype_positive with Short stature, disease_phenotype_positive with Short stature, disease_phenotype_positive with Anteverted nares, disease_phenotype_positive with Anteverted nares, disease_phenotype_positive with Short nose, disease_phenotype_positive with Short nose.", "label": "yes"}
{"original_question": "Is autosomal dominant inheritanced form of Osteogenesis imperfecta caused by mutations in the genes associated with collagen production?", "id": "converted_2428", "sentence1": "Is Autosome dominant inheritanced form of Osteogenesis Imperfecta caused by Gene Mutation in the Genes associated with collagen production?", "sentence2": "steogenesis imperfecta (OI) is a heterogeneous bone disorder characterized by recurrent fractures. Although most cases of OI have heterozygous Gene Mutation inCOL1A1orCOL1A2and show Autosomal dominant inheritance,, Osteogenesis Imperfecta (OI) is a group of Hereditary Diseases characterized by decreased bone mass and increased Fracture risk. The majority of OI cases have an Autosome dominant pattern of inheritance and are usually caused by Gene Mutation in Genes encoding collagen type I,  Osteogenesis Imperfecta (OI) is a group of Hereditary Diseases characterized by low bone mass and recurrent fractures. Most OI cases follow an Autosome dominant pattern of inheritance and are attributed to Gene Mutation in Genes encoding collagen type I (COL1A1 gene gene/alpha 2 collagen type I). , Osteogenesis Imperfecta (OI) is a genetic disorder characterised by low bone mineral density resulting in fractures. 85-90% of patients with OI carry a Variant in the type 1 collagen Genes, COL1A1 gene gene and alpha 2 collagen type I, which follows an Autosome dominant pattern of inheritance., Osteogenesis Imperfecta (OI) comprises a heterogeneous group of disorders that are characterized by susceptibility to bone fractures, and range in severity from a subtle increase in Fracture frequency to Cessation of life in the perinatal period. Most patients have defects in collagen type I biosynthesis with Autosome-dominant inheritance, but many Autosome-recessive Genes have been reported., To investigate Mutation Abnormality of COL1A1 gene gene gene and analyze the relationship between Genotype determination and clinical phenotype in a family with osteogenesis imperfecta, Dominant inheritance of osteogenesis imperfecta (OI) is caused by Gene Mutation in COL1A1 gene gene or alpha 2 collagen type I, the Genes that encode collagen type I,, Osteogenesis Imperfecta (OI) is a heterogeneous group of inherited disorders of bone formation, resulting in low bone mass and an increased propensity to Fracture. It exhibits a broad spectrum of clinical severity, ranging from multiple fractures in utero and perinatal Cessation of life, to normal adult stature and low Fracture incidence. Extra-skeletal features of OI include blue sclera, hearing impairment, skin hyperlaxity, joint Hyperextensibility, and Dentinogenesis imperfecta without osteogenesis imperfecta. The proα1(I) and proα2(I) chains of collagen 1 are encoded by the COL1A1 gene gene and alpha 2 collagen type I Genes, respectively; quantitative or qualitative defects in collagen type I synthesis usually manifest as types of OI or some sub-types of EDS. The majority of patients (about 90%) with a clinical diagnosis of OI have a Mutation Abnormality in the COL1A1 gene gene or alpha 2 collagen type I, Osteogenesis Imperfecta (OI) type I is characterized by bone fragility without significant deformity, Osteopenia, normal stature, Blue sclera, and Autosomal dominant inheritance. Dermal Specimen Source Codes - Fibroblasts from most affected individuals produce about half the expected amount of collagen type I, suggesting that the OI type I phenotype results from a variety of Gene Mutation which alter the apparent expression of either COL1A1 gene gene or alpha 2 collagen type I, the Genes encoding the chains of collagen type I., Autosomal dominant osteogenesis imperfecta is caused by Gene Mutation in the alpha 2 collagen type I and COL1A1 gene gene Genes of collagen type I. , Osteogenesis Imperfecta is caused by dominant Autosome Gene Mutation in the collagen type I coding Genes (COL1A1 gene gene and alpha 2 collagen type I) in about 85% of individuals, affecting collagen quantity or structure., Osteogenesis Imperfecta (OI) is a heterogeneous group of disorders of Connective Tissue, mainly caused by Gene Mutation in the collagen type I Genes (COL1A1 gene gene and alpha 2 collagen type I)., Autosomal dominant osteogenesis imperfecta (OI) is caused by Gene Mutation in the Genes (COL1A1 gene gene or alpha 2 collagen type I) encoding the chains of collagen type I., In approximately 90% of individuals with osteogenesis imperfecta, Gene Mutation in either of the Genes encoding the pro-alpha1 or pro-alpha2 chains of collagen type I (COL1A1 gene gene or alpha 2 collagen type I) can be identified., Autosomal dominant OI is caused by Gene Mutation in the Genes (COL1A1 gene gene or alpha 2 collagen type I) encoding the chains of collagen type I., ext-generation sequencing technology was used to screen a panel of known OI Genes.RESULTS: In 41 probands, we identified 28 different disease-causing variants of 9 different known OI Genes. Eleven of the variants are novel. Ten of the 28 variants are located in COL1A1 gene gene, five in alpha 2 collagen type I, three in BMP1 protein, human protein, human, three in FKBP10 gene gene, two in TMEM38B gene gene, two in P3H1 gene gene, and one each in CRTAP gene gene, SERPINF1 gene gene, and SERPINH1 gene gene. , Osteogenesis Imperfecta (OI) is a clinically and genetically heterogeneous disorder associated with bone fragility and susceptibility to fractures after minimal Trauma, nursing specialty. OI type V has an Autosome-dominant pattern of inheritance and is not caused by Gene Mutation in the collagen type I Genes COL1A1 gene gene and alpha 2 collagen type I. , Detection of a high frequency RsaI Genetic Polymorphism in the human pro alpha 2(I) collagen gene which is linked to an Autosome dominant form of osteogenesis imperfecta., Osteogenesis Imperfecta due to recurrent point Gene Mutation at CpG dinucleotides in the COL1A1 gene gene gene of collagen type I., Osteogenesis Imperfecta (OI), commonly known as \"brittle bone disease\", is a dominant Autosome disorder characterized by bone fragility and abnormalities of Connective Tissue. Biochemical and molecular genetic studies have shown that the vast majority of affected individuals have Gene Mutation in either the COL1A1 gene gene or alpha 2 collagen type I Genes that encode the chains of Procollagen Type I. , Osteogenesis Imperfecta is normally caused by an Autosome dominant Mutation Abnormality in the collagen type I Genes COL1A1 gene gene and alpha 2 collagen type I.[SEP]Relations: Autosomal dominant inheritance has relations: disease_phenotype_positive with osteogenesis imperfecta, disease_phenotype_positive with osteogenesis imperfecta, disease_phenotype_positive with osteogenesis imperfecta with opalescent teeth, Blue sclera and wormian bones but without fractures, disease_phenotype_positive with osteogenesis imperfecta with opalescent teeth, Blue sclera and wormian bones but without fractures, disease_phenotype_positive with combined osteogenesis imperfecta and Ehlers-Danlos syndrome, disease_phenotype_positive with combined osteogenesis imperfecta and Ehlers-Danlos syndrome. osteogenesis imperfecta has relations: disease_phenotype_positive with Autosomal dominant inheritance, disease_phenotype_positive with Autosomal dominant inheritance, disease_phenotype_positive with Autosomal dominant inheritance, disease_phenotype_positive with Autosomal dominant inheritance.", "label": "yes"}
{"original_question": "Is METTL1 overexpression associated with better patient survival?", "id": "converted_4546", "sentence1": "Is METTL1 gene overexpression associated with better patient survival?", "sentence2": " Here we find METTL1 gene gene is frequently amplified and overexpressed in Malignant Neoplasms and is associated with poor patient survival. METTL1 gene gene depletion causes decreased abundance of m7G-modified tRNAs and altered cell cycle and inhibits oncogenicity. Conversely, METTL1 gene gene overexpression induces oncogenic cell transformation and Primary malignant neoplasm. [SEP]Relations: METTL1 gene has relations: protein_protein with MAX, protein_protein with MAX, anatomy_protein_present with heart, anatomy_protein_present with heart, anatomy_protein_present with colon, anatomy_protein_present with colon, anatomy_protein_present with lung, anatomy_protein_present with lung, anatomy_protein_present with brain, anatomy_protein_present with brain.", "label": "no"}
{"original_question": "Do histone variant mH2A (macro-H2A) levels decrease upon differentiation?", "id": "converted_1978", "sentence1": "Do histone variant mH2A (macro-H2A) levels decrease upon differentiation?", "sentence2": "Through manipulation of macroH2A Protein Isoforms, we further demonstrate that macroH2A2 is the predominant barrier to reprogramming., In particular, we find macroH2A Protein Isoforms to be highly enriched at target Genes of the K27me3 demethylase, KDM6A wt Allele, which are reactivated early in iPS reprogramming,  Therefore, we propose that macroH2A Protein Isoforms provide a redundant silencing layer or terminal differentiation 'lock' at critical pluripotency Genes that presents as an epigenetic barrier when differentiated Cells are challenged to reprogram., Histone Variant macroH2A confers resistance to nuclear reprogramming, Resistance to reprogramming is associated with incorporation of the histone variant macroH2A, which is retained on the Xi of differentiated Cells, but absent from the Xi of EpiSCs., We highlight the role of macroH2A in the establishment and maintenance of differentiated states and we discuss its still poorly recognized function in transcriptional activation., Histone Variant macroH2A marks embryonic differentiation in vivo and acts as an epigenetic barrier to induced pluripotency., MacroH2A.1 was found to be present at low levels upon the establishment of pluripotency in the inner cell mass and Epiblast, but it was highly enriched in the trophectoderm and differentiated Diploid Cell later in mouse development., Chromatin immunoprecipitation revealed that macroH2A.1 is incorporated in the chromatin location location of Regulatory Sequences, Nucleic Acid of pluripotency Genes in Diploid Cell such as mouse embryonic Specimen Source Codes - Fibroblasts and adult neural stem Cells, but not in Embryonic Stem Cells., In addition, overexpression of macroH2A Protein Isoforms prevented efficient reprogramming of Epiblast stem Cells to naïve pluripotency. , Macro histone variants are critical for the differentiation of human pluripotent Cells, Here we show that the knockdown of macro histone variants impaired the in vitro and in vivo differentiation of human pluripotent Cells, likely through defects in the silencing of pluripotency-related Genes, Furthermore, male and female mH2A-deficient ESCs proliferate normally under pluripotency culture conditions, and respond to several standard differentiation procedures efficiently.[SEP]Relations: regulation of RNA polymerase I regulatory region sequence-specific DNA binding has relations: bioprocess_bioprocess with regulation of transcription regulatory region DNA binding, bioprocess_bioprocess with regulation of transcription regulatory region DNA binding, bioprocess_bioprocess with negative regulation of RNA polymerase I regulatory region sequence-specific DNA binding, bioprocess_bioprocess with negative regulation of RNA polymerase I regulatory region sequence-specific DNA binding. cognitive impairment - coarse facies - heart defects - obesity - pulmonary involvement - short stature - skeletal dysplasia syndrome has relations: disease_phenotype_positive with Decreased response to growth hormone stimuation test, disease_phenotype_positive with Decreased response to growth hormone stimuation test. RNA localization to chromatin location has relations: bioprocess_protein with HNRNPU, bioprocess_protein with HNRNPU. Bite Cells has relations: disease_phenotype_positive with hereditary stomatocytosis, disease_phenotype_positive with hereditary stomatocytosis.", "label": "no"}
{"original_question": "Are loop domains preserved upon cohesin loss?", "id": "converted_2379", "sentence1": "Are loop domains preserved upon cohesins loss?", "sentence2": "Cohesin Loss Eliminates All Loop Domains., The human genome folds to create thousands of intervals, called \"contact domains,\" that exhibit enhanced contact frequency within themselves. \"Loop domains\" form because of tethering between two loci-almost always bound by CTGF protein, human and cohesins-lying on the same chromosome. \"Compartment domains\" form when genomic intervals with similar histone marks co-segregate. Here, we explore the effects of degrading cohesins. All loop domains are eliminated, but neither compartment domains nor histone marks are affected. Loss of loop domains does not lead to widespread ectopic gene activation but does affect a significant minority of active genes., cohesins loss eliminates all loop domains[SEP]Relations: Protein S human has relations: drug_drug with Ardeparin, drug_drug with Ardeparin, drug_drug with Parnaparin, drug_drug with Parnaparin, drug_drug with Semuloparin, drug_drug with Semuloparin, drug_drug with Bemiparin, drug_drug with Bemiparin, drug_drug with Biochanin A, drug_drug with Biochanin A.", "label": "no"}
{"original_question": "Is vortioxetine effective for treatment of depression?", "id": "converted_1854", "sentence1": "Is vortioxetine effective for treatment of Cancer patients and suicide and depression?", "sentence2": "vortioxetine is the most recently approved medication for the treatment of major depressive disorder (Major Depressive Disorder). , [vortioxetine: a new Antidepressive Agents to treat depressive episodes]., vortioxetine is a new Antidepressive Agents, which mechanism of action is multimodal, targeting the 5-Hydroxytryptamine Receptor 1A, human, HTR1B wt Allele, HTR1D gene, 5-HT3, HTR7 gene receptors and the serotonin transporter (5-HTT). , In short-term studies (8 weeks), vortioxetine is more efficacious than placebo in decreasing Depressive Symptoms as measured by the MADRS total score, response rate (vortioxetine: 53.2% vs placebo: 35.2%) and remission rate (vortioxetine: 29.2% vs placebo: 19.3%). In a long-term study (52 weeks), vortioxetine is also superior to placebo in preventing relapses and recurrences. Moreover, in second line treatment, after failure of a first line selective serotonin reuptake inhibitor (Serotonin Reuptake Inhibitor [EPC]) or serotonin norepinephrin reuptake inhibitor (Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs)), vortioxetine is superior to agomelatine in improving Depressive Symptoms and achieving response and remission. , Against this background, we feature the novel antidepressants vortioxetine, vilazodone and milnacipran/levomilnacipran with regard to their serotonin receptor targets such as the 5-Hydroxytryptamine Receptor 1A, human, 5-HT3 and HTR7 gene which may account for their specific effects on certain symptoms of Cancer patients and suicide and Cancer patients and suicide and depression (e.g. cognition and Anxiety Disorders) as well as a characteristic side-effect profile., CONCLUSION: vortioxetine dominated venlafaxine XR in South Korea and is a relevant treatment option for Major Depressive Disorder patients initiating or switching therapy., vortioxetine: a New Treatment for Major Depressive Disorder., INTRODUCTION: vortioxetine is a structurally novel medication that has recently been approved for treatment of major depressive disorder (Major Depressive Disorder)., EXPERT OPINION: Results of placebo-controlled trials suggest efficacy and an overall safety profile comparable to existing first-line antidepressants. , The authors suggest that vortioxetine is currently a good second-line Antidepressive Agents option and shows promise, pending additional long-term data, to become a first-line Antidepressive Agents option., Clinical studies indicate that vortioxetine is effective in the treatment of major Cancer patients and suicide and Cancer patients and suicide and depression, though there is no suggestion of superiority over active comparators., vortioxetine has been effective in various animal models of Cancer patients and suicide and Cancer patients and suicide and depression and Anxiety Disorders and clinical studies have shown the Antidepressive Agents and antianxiety properties of vortioxetine in a dose range of 5-20 mg/day., vortioxetine was significantly more effective than was placebo, with a standardized mean difference (SMD) of -0.118 (95% CISH protein, human, -0.203 to -0.033, P = 0.007)., vortioxetine for the treatment of Cancer patients and suicide and Cancer patients and suicide and depression., vortioxetine for the treatment of major Cancer patients and suicide and Cancer patients and suicide and depression., vortioxetine (Lu-AA-21004; 1-[2-(2,4-dimethylphenylsulfanyl)phenyl]piperazine hydrobromide) is a novel orally active Molecule that is being investigated by Lundbeck and Takeda for the treatment of major Cancer patients and suicide and Cancer patients and suicide and depression and generalized Anxiety Disorders disorders., vortioxetine (Lu AA21004) is a multi-modal Antidepressive Agents in clinical development for the treatment of major depressive disorder (Major Depressive Disorder)., A randomized, double-blind, fixed-dose study comparing the efficacy and tolerability of vortioxetine 2.5 and 10 mg in acute treatment of adults with generalized Anxiety Disorders disorder., vortioxetine has been effective in various animal models of Cancer patients and suicide and Cancer patients and suicide and depression and Anxiety Disorders and clinical studies have shown the Antidepressive Agents and antianxiety properties of vortioxetine in a dose range of 5-20 mg/day., Secondary endpoints included response and remission rates, Anxiety Disorders symptoms(Hamilton Anxiety Rating Scale), Clinical Global Impression, overall functioning (Sheehan Disability Scale), health-related quality of life(EuroQol 5 Dimensions), productivity (work limitation questionnaire) and family functioning (Depression and Family Functioning Scale).RESULTS: Primary endpoint noninferiority was established and vortioxetine (n = 252) was superior to agomelatine (n = 241) by 2.2 MADRS points (p<0.01)., vortioxetine (Lu AA21004) is an Antidepressive Agents with a mechanism of action thought to be related to a combination of 2 pharmacologic actions: direct modulation of several receptors and inhibition of the serotonin transporter.To evaluate the efficacy of vortioxetine 10 and 20 mg once daily in outpatients with major depressive disorder.This 8-week, multicenter, randomized, double-blind, placebo-controlled, parallel-group study was conducted from July 2010 to January 2012 among adults with a primary diagnosis of recurrent major depressive disorder (DSM-IV-TR).Eligible subjects were randomized in 1:1:1 ratio to 1 of 3 treatment arms: vortioxetine 10 mg, vortioxetine 20 mg, or placebo once daily for 8 weeks., vortioxetine (Lu AA21004) is a new Antidepressive Agents that combines a number of neurotransmitter uptake and receptor effects that have been thought to predict efficacy as a treatment for depressive and Anxiety Disorders disorders.This review summarizes the pharmacology and neurobiology of vortioxetine, In the study of elderly patients, vortioxetine 5 mg (n = 136) improved 12-item Health Status Questionnaire scores significantly more than placebo (n = 148) for the domains of health perception (10.4, P &lt; 0.0001, SES of 0.54), mental health (7.9, P &lt; 0.001, SES of 0.44), and energy (6.4, P &lt; 0.05, SES of 0.28) (Fetal Alcohol Syndrome, mixed model for repeated measures).vortioxetine yielded significant, meaningful HRQoL improvements in 6 Major Depressive Disorder studies of 6 to 8 weeks duration., All references included were published between 1999 and 2014.All studies that included Homo sapiens and were published in English, with data describing vortioxetine for the treatment of Major Depressive Disorder, were reviewed.vortioxetine is a novel multimodal Antidepressive Agents agent, which inhibits the 5-HT transporter protein, acts as a 5-HT3 antagonist, 5-Hydroxytryptamine Receptor 1A, human receptor Agonist, HTR7 gene receptor antagonist, and a partial Agonist of the Receptor, Serotonin, HTR1B wt Allele, vortioxetine has been effective in various animal models of Cancer patients and suicide and Cancer patients and suicide and depression and Anxiety Disorders and clinical studies have shown the Antidepressive Agents and antianxiety properties of vortioxetine in a dose range of 5-20 mg/day, vortioxetine is an Antidepressive Agents with multimodal activity which has shown efficacy in major depressive disorder (Major Depressive Disorder) patients in six of ten short-term, randomized, placebo-controlled trials (completed end 2012).We performed meta-regression analyses to indirectly compare vortioxetine to seven marketed antidepressants with different mechanisms of action, Data were available from 51 human trials involving vortioxetine, and included a total of 7,666 healthy volunteers and patients with a diagnosis of major depressive disorder (Major Depressive Disorder) or generalized Anxiety Disorders disorder who were exposed to at least 1 dose of vortioxetine for a total of 2,743 patient-years.vortioxetine was effective in treating Major Depressive Disorder in the United States at a dose of 20 mg/d, vortioxetine is a recently approved multimodal Antidepressive Agents with anxiolytic properties in preclinical studies.This double-blind, placebo-controlled study assessed the efficacy and tolerability of vortioxetine in subjects with a primary diagnosis of generalized Anxiety Disorders disorder.Subjects (n = 457) were randomized 1:1:1 to treatment with placebo or vortioxetine 2.5 or 10 mg once daily, There was a significant difference for Nausea:Presence or Threshold:Point in time:^Patient:Ordinal between the two groups (OR=3.01, 95 % CI=2.22-4.09, Z=7.08, P=0.00001), but no significant differences were observed for the other four adverse effects.CONCLUSIONS: For the treatment of major depressive disorder, our results show that a dose of 5 mg/day vortioxetine was more effective, but more easily induced Nausea:Presence or Threshold:Point in time:^Patient:Ordinal, compared to placebo., The efficacy and safety of 5 mg/d vortioxetine compared to placebo for major depressive disorder: A meta-analysis., vortioxetine: a meta-analysis of 12 short-term, randomized, placebo-controlled clinical trials for the treatment of major depressive disorder., vortioxetine in the treatment of adult patients with major depressive disorder: a meta-analysis of randomized double-blind controlled trials., vortioxetine has been effective in various animal models of Cancer patients and suicide and Cancer patients and suicide and depression and Anxiety Disorders and clinical studies have shown the Antidepressive Agents and antianxiety properties of vortioxetine in a dose range of 5-20 mg/day. , Clinical studies indicate that vortioxetine is effective in the treatment of major Cancer patients and suicide and Cancer patients and suicide and depression, though there is no suggestion of superiority over active comparators., The incidence of treatment-emergent adverse events was significantly higher in the duloxetine group than in the vortioxetine group.duloxetine was more effective but less well-tolerated than vortioxetine in Major Depressive Disorder., There was no significant difference in discontinuation rates between vortioxetine and comparators owing to inefficacy (OR 0.983, 95% CI 0.585 to 1.650), whereas discontinuation owing to Scanning Auger Spectrometer (device) was significantly less common in the vortioxetine than in the comparator group (OR 0.728, 95% CI 0.554 to 0.957).Studies examining the role of vortioxetine in the treatment of Major Depressive Disorder are limited.Although our results suggest that vortioxetine may be an effective treatment option for Major Depressive Disorder, they should be interpreted and translated into clinical practice with caution, as the meta-analysis was based on a l, We performed a meta-analysis to increase the statistical power of these studies and enhance our current understanding of the role of vortioxetine in the treatment of Major Depressive Disorder.We performed an extensive search of databases and the clinical trial registry., BACKGROUND: vortioxetine is a recently approved multimodal Antidepressive Agents with anxiolytic properties in preclinical studies.OBJECTIVE: This double-blind, placebo-controlled study assessed the efficacy and tolerability of vortioxetine in subjects with a primary diagnosis of generalized Anxiety Disorders disorder.METHODS: Subjects (n = 457) were randomized 1:1:1 to treatment with placebo or vortioxetine 2.5 or 10 mg once daily., vortioxetine significantly improved objective and subjective measures of cognitive function in adults with recurrent Major Depressive Disorder and these effects were largely independent of its effect on improving Depressive Symptoms., Furthermore, a statistically significant number of patients with Major Depressive Disorder who were on vortioxetine have achieved a greater than or equal to 50% reduction in Cancer patients and suicide and Cancer patients and suicide and depression symptoms from baseline., BACKGROUND: vortioxetine is a novel multimodal compound that has recently been approved by the FDA for the treatment of major depressive disorder (Major Depressive Disorder)., Although our results suggest that vortioxetine may be an effective treatment option for Major Depressive Disorder, they should be interpreted and translated into clinical practice with caution, as the meta-analysis was based on a limited number of heterogeneous RCTs.., vortioxetine is an effective agent for the treatment of Major Depressive Disorder, but it does not have any clear advantages over other available treatment options.., vortioxetine was significantly more effective than placebo for acute treatment of major depressive disorder (Major Depressive Disorder)., duloxetine was more effective but less well-tolerated than vortioxetine in Major Depressive Disorder., vortioxetine is an orally administered small Molecule developed by Lundbeck A/S for the once-daily treatment of major depressive disorder (Major Depressive Disorder) and generalized Anxiety Disorders disorder (Generalized Anxiety Disorder). vortioxetine received its first global approval for Major Depressive Disorder in the USA in September 2013 and regulatory approval for its use in this indication in the EU (where it has received a positive opinion) and Canada is awaited. , This article summarizes the milestones in the development of vortioxetine leading to this first approval for Major Depressive Disorder., vortioxetine was efficacious and well tolerated in the treatment of patients with major depressive disorder., On the primary efficacy endpoint, both vortioxetine doses were statistically significantly superior to placebo, with a mean difference to placebo (n=158) of -5.5 (vortioxetine 15 mg, P<0.0001, n=149) and -7.1 MADRS points (vortioxetine 20 mg, P<0.0001, n=151)., The change in the severity of depressive and Anxiety Disorders symptoms was maintained throughout the study as reflected by a 24-item Hamilton Depression Scale total score of 8.2 at week 52 (from 17.6 at open-label baseline) in the observed case data set., vortioxetine is a multi-modal Antidepressive Agents that functions as a human 5-HT3A and HTR7 gene receptor antagonist, Receptor, Serotonin, HTR1B wt Allele partial Agonist, 5-Hydroxytryptamine Receptor 1A, human receptor Agonist, and inhibitor of the serotonin transporter. , Approval for the treatment of Major Depressive Disorder was based on a clinical development programme that included six positive 6-8 week studies, including one study in elderly people, and one positive maintenance study in adults., vortioxetine represents another option for the treatment of Major Depressive Disorder. , The multimodal compounds vortioxetine and vilazodone are examples of this approach with diverse mechanisms, and their different clinical effects will provide valuable insights into serotonergic modulation of glutamate transmission for the potential treatment of Cancer patients and suicide and Cancer patients and suicide and depression and associated Impaired cognition., Two new Antidepressive Agents drugs, vilazodone (marketed in the USA) and vortioxetine (in development) incorporate partial 5-Hydroxytryptamine Receptor 1A, human-R Agonist properties with Selective External Radiation Therapy blockade., Novel drugs in development include those that combine multiple simultaneous pharmacologic mechanisms in addition to Selective External Radiation Therapy inhibition within the same Molecule, such as vilazodone (combining HTR1A wt Allele partial agonism with Selective External Radiation Therapy inhibition), triple reuptake inhibitors (combining epinephrine and epinephrine and norepinephrine and dopamine reuptake inhibition with Selective External Radiation Therapy inhibition), and vortioxetine, a multimodal Antidepressive Agents combining actions at the G protein receptor mode (HTR1A wt Allele and 5HT1B partial agonism and 5HT7 antagonism), at the ion channel mode (5HT3 antagonism) as well as the neurotransmitter transporter mode (Selective External Radiation Therapy inhibition). , In this study of adults with Major Depressive Disorder treated for 8 weeks with vortioxetine 2.5 mg or 5 mg per day, reductions in Cancer patients and suicide and Cancer patients and suicide and depression symptoms were not statistically significant compared with placebo. , However, on the basis of these findings, vortioxetine (2.5, 5, 10 mg/day) demonstrated a favourable safety and tolerability profile and maintained effectiveness over 12 months of treatment. , In this study of adults with Major Depressive Disorder, 5 mg vortioxetine did not differ significantly from placebo in reducing Cancer patients and suicide and Cancer patients and suicide and depression symptoms after 6 wk of treatment., After 8 weeks of treatment with Lu AA21004 10 mg, there was a significant reduction in HDRS-24 total score compared with placebo in adults with Major Depressive Disorder., In conclusion, Lu AA21004 was efficacious and well tolerated in the treatment of elderly patients with recurrent major depressive disorder., Thus, Lu AA21004 was effective in preventing relapse of Major Depressive Disorder and was well tolerated as maintenance treatment.,  Findings on secondary outcome measures, using MMRM instead of LOCF, were supportive of likely efficacy for Lu AA21004 5mg and 10mg and duloxetine. , In this study, treatment with 5 mg and 10 mg Lu AA21004 for 6 wk was efficacious and well tolerated in patients with Major Depressive Disorder., Results from phase II clinical trials have reported improvement in Cancer patients and suicide and Cancer patients and suicide and depression and Anxiety Disorders symptoms after 6 weeks of treatment. [SEP]Relations: vortioxetine has relations: drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Paroxetine, drug_drug with Paroxetine, drug_drug with Harmaline, drug_drug with Harmaline, drug_drug with Methadone, drug_drug with Methadone, drug_drug with Cocaine, drug_drug with Cocaine.", "label": "yes"}
{"original_question": "Is there an association between Klinefelter syndrome and breast cancer?", "id": "converted_2478", "sentence1": "Is there an association between Klinefelter Syndrome and breast Primary malignant neoplasm?", "sentence2": "Screening for breast Primary malignant neoplasm in male-to-female Transsexual (finding) should be undertaken for those with additional risk factors (e.g., family history, BRCA2 gene gene Mutation Abnormality, Klinefelter Syndrome) and should be available to those who desire screening, preferably in a clinical trial., Klinefelter Syndrome (OR = 24.7; 95% CI = 8.94 to 68.4) and Gynecomastia (OR = 9.78; 95% CI = 7.52 to 12.7) were also statistically significantly associated with risk, relations that were independent of BMI. , Male breast Primary malignant neoplasm risk factors show strong association with BRCA2 gene gene Gene Mutation, as well as Klinefelter Syndrome. , The main risk factors include: the Mutation Abnormality of genes BRCA 1 and 2, Klinefelter's syndrome - male with more than two X chromosomes - male with more than two X chromosomes, Alcohol - Recreational Drug Use Code, Hepatobiliary Disorder, BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20. , Although aetiology is still unclear, constitutional, environmental, hormonal (abnormalities in Estrogen [EPC]/androgen balance) and Genetic (positive family history, Klinefelter Syndrome, Gene Mutation in BRCA1 gene gene and specially BRCA2 gene gene) risk factors are already known. , The largest study found 19.2- and 57.8-fold increases in incidence and mortality, respectively, with particularly high risks among 47,XXY mosaics. , CONCLUSIONS: Additional well-designed epidemiologic studies are needed to clarify which patients with Supernumerary mandibular left second primary are at a high risk of developing MBC and to distinguish between possible predisposing factors, including altered endogenous Hormones., Major risk factors for developing male BC Original Formula Original Formula include clinical disorders involving hormonal imbalances (excess of Estrogen [EPC] or a deficiency of Therapeutic Testosterone as seen in patients with Klinefelter Syndrome) and a positive family history for breast Primary malignant neoplasm. , Patients with 47, XXY karyotype (Klinefelter Syndrome) appear to have increased risk of developing Primary malignant neoplasm, especially male breast Primary malignant neoplasm, Germ cell tumor and Hodgkin Disease, but rarely Leukemia, Myelocytic, Acute. , Breast Primary malignant neoplasm in a patient with Klinefelter's syndrome - male with more than two X chromosomes - male with more than two X chromosomes is reported., The increased conversion of Therapeutic Testosterone to estradiol at the therapy with Androgens might be responsible for the development of breast Primary malignant neoplasm in Klinefelter's syndrome - male with more than two X chromosomes - male with more than two X chromosomes., Patients with a 47,XXY karyotype (Klinefelter Syndrome) appear to have an increased risk of developing Primary malignant neoplasm, especially male breast Primary malignant neoplasm and germ cell tumors, but rarely malignant hematologic disorders., The frequencies of Diabetes Mellitus, breast Primary malignant neoplasm, and Germ cell neoplasia increases in Klinefelter's syndrome - male with more than two X chromosomes - male with more than two X chromosomes., There is evidence, however, to suggest that Klinefelter's males have an increased risk of breast Primary malignant neoplasm that approaches three percent., Klinefelter Syndrome has been consistently associated with breast Primary malignant neoplasm in men (MBC).<br><b>CASE REPORT</b>: We report a 54-year old man was diagnosed as synchronous bilateral breast Primary malignant neoplasm with Klinefelter Syndrome., These results support a hormonal etiology for breast Primary malignant neoplasm in men and for prostate Primary malignant neoplasm and suggest that men with Klinefelter Syndrome may be at substantially elevated risks for Lymphoma, Non-Hodgkin, Familial, breast Primary malignant neoplasm, and, perhaps, lung Primary malignant neoplasm., Major Genetic factors associated with an increased risk of breast Primary malignant neoplasm for men include BRCA2 gene gene Gene Mutation, which are believed to account for the majority of inherited breast Primary malignant neoplasm in men, Klinefelter Syndrome, and a positive family history., Those affected by Klinefelter's syndrome - male with more than two X chromosomes - male with more than two X chromosomes are at increased risk of Lupus Erythematosus, Systemic, breast Primary malignant neoplasm, Non-Hodgkin's lymphoma of bone, and lung Primary malignant neoplasm., CONCLUSIONS These results support a hormonal etiology for breast Primary malignant neoplasm in men and for prostate Primary malignant neoplasm and suggest that men with Klinefelter Syndrome may be at substantially elevated risks for Lymphoma, Non-Hodgkin, Familial, breast Primary malignant neoplasm, and, perhaps, lung Primary malignant neoplasm., Compared with the general population, men with Klinefelter Syndrome had higher mortality from lung Primary malignant neoplasm (Megakaryocyte-Potentiating Factor, human = 1.5, 95% CI = 1.0 to 2.0), breast Primary malignant neoplasm (Megakaryocyte-Potentiating Factor, human = 57.8, 95% CI = 18.8 to 135.0), and Lymphoma, Non-Hodgkin, Familial (Megakaryocyte-Potentiating Factor, human = 3.5, 95% CI = 1.6 to 6.6) and lower mortality from prostate Primary malignant neoplasm (Megakaryocyte-Potentiating Factor, human = 0, 95% CI = 0 to 0.7)., Klinefelter Syndrome has been consistently associated with breast Primary malignant neoplasm in men (MBC)., Male breast Primary malignant neoplasm risk factors show strong association with BRCA2 gene gene Gene Mutation, as well as Klinefelter Syndrome., Patients with 47, XXY karyotype (Klinefelter Syndrome) appear to have increased risk of developing Primary malignant neoplasm, especially male breast Primary malignant neoplasm, Germ cell tumor and Hodgkin Disease, but rarely Leukemia, Myelocytic, Acute., Klinefelter Syndrome, in which patients carry XXY chromosome, may be present in men with breast Primary malignant neoplasm for this reason they often develop Gynecomastia.<br>, Klinefelter Syndrome has been consistently associated with breast Primary malignant neoplasm in men (MBC)., These results support a hormonal etiology for breast Primary malignant neoplasm in men and for prostate Primary malignant neoplasm and suggest that men with Klinefelter Syndrome may be at substantially elevated risks for Lymphoma, Non-Hodgkin, Familial, breast Primary malignant neoplasm, and, perhaps, lung Primary malignant neoplasm..[SEP]Relations: Klinefelter Syndrome has relations: disease_disease with Genetic infertility, disease_disease with Genetic infertility, disease_disease with Genetic nervous system disorder, disease_disease with Genetic nervous system disorder, disease_disease with epilepsy, disease_disease with epilepsy, disease_disease with sex chromosome disorder of sex development, disease_disease with sex chromosome disorder of sex development, disease_disease with X chromosome number anomaly, disease_disease with X chromosome number anomaly.", "label": "yes"}
{"original_question": "Is the FIP virus thought to be a mutated strain for the Feline enteric Coronavirus?", "id": "converted_3359", "sentence1": "Is the Feline infectious peritonitis and pleuritis virus thought to be a mutated strain for the Feline enteric Coronavirus?", "sentence2": "Feline infectious peritonitis (Feline infectious peritonitis and pleuritis) results from Gene Mutation in the Viral Genome during a common Body Surface Area Formula for Cats enteric Coronavirus Infections (Coronavirus, Feline) infection., It is caused by Feline infectious peritonitis and pleuritis virus (FIPV), a virulent Mutant strain of Feline Enteric Coronavirus (Coronavirus, Feline)., Feline infectious peritonitis virus (FIPV) was presumed to arise from Gene Mutation in the 3c of a ubiquitous and largely nonpathogenic Body Surface Area Formula for Cats enteric Coronavirus Infections (Coronavirus, Feline)., Feline enteric Coronavirus Infections (Coronavirus, Feline) causes inapparent or mild enteritis in cats, but a highly fatal Disease, called Body Surface Area Formula for Cats infectious peritonitis (Feline infectious peritonitis and pleuritis), can arise through Mutation Abnormality of Coronavirus, Feline to Feline infectious peritonitis and pleuritis virus (FIPV)., Feline infectious peritonitis (Feline infectious peritonitis and pleuritis) is a lethal systemic Disease caused by Feline infectious peritonitis and pleuritis virus (FIPV), a virulent Mutant of apathogenic Body Surface Area Formula for Cats enteric Coronavirus Infections (Coronavirus, Feline)., Feline infectious peritonitis (Feline infectious peritonitis and pleuritis) is an almost invariably fatal Body Surface Area Formula for Cats Coronavirus Infections (FCoV)-induced Disease thought to arise from a combination of viral Gene Mutation and an overexuberant immune response., BACKGROUND\n\nFeline Infectious Peritonitis (Feline infectious peritonitis and pleuritis) is a lethal systemic Disease, caused by the Feline infectious peritonitis and pleuritis Virus (FIPV); a virulent Mutant of Feline Enteric Coronavirus (Coronavirus, Feline)., BACKGROUND Feline Infectious Peritonitis (Feline infectious peritonitis and pleuritis) is a lethal systemic Disease, caused by the Feline infectious peritonitis and pleuritis Virus (FIPV); a virulent Mutant of Feline Enteric Coronavirus (Coronavirus, Feline)., This Coronavirus Infections is a virulent Mutant of the harmless, ubiquitous Body Surface Area Formula for Cats enteric Coronavirus Infections (Coronavirus, Feline)., Feline infectious peritonitis virus (FIPV) was presumed to arise from Gene Mutation in the 3c of a ubiquitous and largely nonpathogenic Body Surface Area Formula for Cats enteric Coronavirus Infections (Coronavirus, Feline)., Whilst intact in all FECVs, the 3c gene was mutated in the majority (71.4 %) of FIPVs, but not in all, implying that Mutation Abnormality in 3c is not the (single) cause of Feline infectious peritonitis and pleuritis.[SEP]Relations: Body Surface Area Formula for Cats infectious peritonitis has relations: disease_disease with Orthocoronavirinae infectious Disease, disease_disease with Orthocoronavirinae infectious Disease, disease_disease with Orthocoronavirinae infectious Disease, disease_disease with Orthocoronavirinae infectious Disease, disease_disease with cat Disease, disease_disease with cat Disease, disease_disease with cat Disease, disease_disease with cat Disease. Rotavirus infection has relations: disease_disease with Reoviridae infectious Disease, disease_disease with Reoviridae infectious Disease.", "label": "yes"}
{"original_question": "Is yeast fbp1 affected by glucose starvation stress?", "id": "converted_3785", "sentence1": "Is yeast Fructose-1,6-Bisphosphatase 1 affected by Glucose measurement starvation stress?", "sentence2": "Histone antigen antigen Chaperone Asf1 Is Required for the Establishment of Repressive chromatin location in Schizosaccharomyces pombe Fructose-1,6-Bisphosphatase 1 Gene Repression, chromatin is reconstituted in the fission yeast Schizosaccharomyces pombefbp1 gene, which is robustly induced upon Glucose measurement starvation but tightly repressed under Glucose measurement-rich conditions., The Schizosaccharomyces pombe Fructose-1,6-Bisphosphatase 1 gene, which encodes fructose-1,6-bis-phosphatase, is transcriptionally repressed by Glucose measurement through the activation of the cAMP-dependent protein kinase A (Cyclic AMP-Dependent Protein Kinases) and transcriptionally activated by Glucose measurement starvation through the activation of a mitogen-activated protein kinase (Mitogen-Activated Protein Kinases). , Antisense transcripts from the fission yeast Fructose-1,6-Bisphosphatase 1 Gene Locus (Fructose-1,6-Bisphosphatase 1-as) are expressed in Glucose measurement-rich conditions and anticorrelated with transcription of metabolic stress-induced Long Intergenic Non-Protein Coding RNA (mlonRNA) and RNA, Messenger on the sense strand during Glucose measurement starvation., In fission yeast, Glucose measurement starvation triggers Long Intergenic Non-Protein Coding RNA transcription across Promoter regions of stress-responsive genes including Fructose-1,6-Bisphosphatase 1 (fructose-1,6-bisphosphatase1)., We herein show that the chromatin configuration is altered into an accessible state within 290 bp downstream from the initiation site of metabolic-stress-induced lncRNAs (mlonRNAs) in the Promoter of the fission yeast Fructose-1,6-Bisphosphatase 1 gene, whose transcription is massively induced upon Glucose measurement starvation., Cation stress and Glucose measurement starvation selectively caused chromatin structure alteration around CRE-like sequences in cta3(+) and Fructose-1,6-Bisphosphatase 1(+) promoters, respectively, in correlation with transcriptional activation.,  herein show that the chromatin configuration is altered into an accessible state within 290 bp downstream from the initiation site of metabolic-stress-induced lncRNAs (mlonRNAs) in the Promoter of the fission yeast Fructose-1,6-Bisphosphatase 1 gene, whose transcription is massively induced upon Glucose measurement starvation. Chr, fission yeast, Glucose measurement starvation triggers Long Intergenic Non-Protein Coding RNA transcription across Promoter regions of stress-responsive genes including Fructose-1,6-Bisphosphatase 1 (fructose-1,6-bisphosphatase1). At, isense transcripts from the fission yeast Fructose-1,6-Bisphosphatase 1 Gene Locus (Fructose-1,6-Bisphosphatase 1-as) are expressed in Glucose measurement-rich conditions and anticorrelated with transcription of metabolic stress-induced Long Intergenic Non-Protein Coding RNA (mlonRNA) and RNA, Messenger on the sense strand during Glucose measurement starvation. Here,, Gene Locus (Fructose-1,6-Bisphosphatase 1-as) are expressed in Glucose measurement-rich conditions and anticorrelated with transcription of metabolic stress-induced Long Intergenic Non-Protein Coding RNA (mlonRNA) and RNA, Messenger on the sense strand during Glucose measurement starvation., Furthermore, Fructose-1,6-Bisphosphatase 1-as and Antisense RNA at other stress-responsive loci are promptly degraded via the cotranslational nonsense-mediated decay (Nonsense Mediated RNA, Messenger Decay) pathway., These results suggest Nonsense Mediated RNA, Messenger Decay may potentiate the swift disappearance of antisense RNAs in response to cellular stress., Antisense RNA has emerged as a crucial regulator of opposite-strand protein-coding genes in the RNA, Long Untranslated (Long Intergenic Non-Protein Coding RNA) category, but little is known about their dynamics and decay process in the context of a stress response., xic growth. The Mitogen-Activated Protein Kinase 11 (SAPK) pathway and its effectors, Sty1 Mitogen-Activated Protein Kinases and activating transcription factor 1, play a critical role in the adaptation of fission yeast to grow on alternative non-fermentable Carbon sources by inducing the expression of Fructose-1,6-Bisphosphatase 1+ gene, coding for the gluconeogenic enzyme fructose-1,6-bis[SEP]Relations: fructose 1,6-bisphosphate 1-phosphatase activity has relations: molfunc_protein with FBP1, molfunc_protein with FBP1, molfunc_protein with FBP2, molfunc_protein with FBP2. mitogen-activated protein kinase binding has relations: molfunc_protein with PPM1D, molfunc_protein with PPM1D, molfunc_protein with PPM1D, molfunc_protein with PPM1D, molfunc_protein with GCH1, molfunc_protein with GCH1.", "label": "yes"}
{"original_question": "Can NEECHAM Confusion Scale be used for evaluation of postoperative delirium?", "id": "converted_1871", "sentence1": "Can NEECHAM Confusion Scale be used for evaluation of postoperative Delirium?", "sentence2": "Sampling was achieved in a nonrandomized targeted manner and Delirium was assessed using NeeCham questionnaire. , Delirium in older patients: a diagnostic study of NEECHAM Confusion Scale in surgical intensive care unit., AIMS AND OBJECTIVES: To estimate the diagnostic value and determine the feasibility of the NEECHAM Confusion Scale on Critical Illness older patients., CONCLUSIONS: Findings from this study confirm the good diagnostic value and ease of application of the NEECHAM scale with nonventilated intensive care patients.RELEVANCE TO CLINICAL PRACTICE: The NEECHAM scale can be used to detect Delirium during the routine nursing assessment of nonintubated older patients as it requires minimal demand and stress on the patient as well as on the bedside nurse., The NEECHAM Confusion Scale and the validated chart review instrument were used for diagnosis of Delirium. , Among the various screening instruments, NEECHAM Clouded consciousness scale and Delirium observation scale appear to be most suitable screening instrument for patients' in general medical and surgical wards, depending on the type of rater (physician or nurse). , Use of NEECHAM scaling enabled medical staff to identify cases of possible Clouded consciousness early, indicating that the NEECHAM Clouded consciousness scale should be useful for the detection of postoperative Delirium and Clouded consciousness in the surgical ward., Early detection of postoperative Delirium and Clouded consciousness in a surgical ward using the NEECHAM Clouded consciousness scale., In this study, we investigated whether the early detection of postoperative Delirium in elderly patients is possible using a simple, useful behavior-assessing scale, the NEECHAM Confusion Scale, and a method for comprehensively evaluating elderly persons' stress related to surgery, E-PASS., Assessment of the risk of postoperative Delirium in elderly patients using E-PASS and the NEECHAM Confusion Scale., The aim of this study was to determine which of the two Delirium observation screening scales, the NEECHAM Confusion Scale or the Delirium Observation Screening (DOS) scale, has the best discriminative capacity for diagnosing Delirium and which is more practical for daily use by nurses., For Delirium diagnosis and severity assessment, we used the NEECHAM Confusion Scale., Use of NEECHAM scaling enabled medical staff to identify cases of possible Clouded consciousness early, indicating that the NEECHAM Clouded consciousness scale should be useful for the detection of postoperative Delirium and Clouded consciousness in the surgical ward., The NEECHAM Confusion Scale was performed upon admission and prior to discharge.RESULTS: The incidence of DSM-IV related Delirium was 24%., A comparison of the CAM-ICU and the NEECHAM Confusion Scale in intensive care Delirium assessment: an observational study in non-intubated patients., Predictive value and validation of the NEECHAM Confusion Scale using DSM-IV criteria for Delirium as gold standard., Early detection of postoperative Delirium and Clouded consciousness in a surgical ward using the NEECHAM Clouded consciousness scale, The aim of this study was to determine which of the two Delirium observation screening scales, the NEECHAM Confusion Scale or the Delirium Observation Screening (DOS) scale, has the best discriminative capacity for diagnosing Delirium and which is more practical for daily use by nurses.The project was conducted on four wards of a university hospital; 87 patients were included, In addition, we scored the participants on the NEECHAM Scale and evaluated their postoperative Delirium and postoperative arrhythmia.On the nights of Days 4 and 5, the amount of activity of the exposure group was significantly lower and The sympathetic nervous index was significantly lower on the night of Day 5, In this study, we investigated whether the early detection of postoperative Delirium in elderly patients is possible using a simple, useful behavior-assessing scale, the NEECHAM Confusion Scale, and a method for comprehensively evaluating elderly persons' stress related to surgery, E-PASS. , The cut-off value of the NEECHAM score was established as 20 points, and patients showing values less than this after surgery were regarded as having postoperative Delirium. , Identification of Delirium was based on evaluation of the level of consciousness with the NEECHAM Confusion Scale and/or a chart-based instrument for Delirium., For Delirium diagnosis and severity assessment, we used the NEECHAM Confusion Scale., In this study, we investigated whether the early detection of postoperative Delirium in elderly patients is possible using a simple, useful behavior-assessing scale, the NEECHAM Confusion Scale, and a method for comprehensively evaluating elderly persons' stress related to surgery, E-PASS.The subjects were 160 patients aged more than 75 years who underwent surgery., In this study a nursing screening instrument, the NEECHAM Clouded consciousness scale, was studied for early recognition of Delirium ICU patients., The psychometric characteristics and the ease of use of the NEECHAM Clouded consciousness scale enables ICU nurses to early recognize Delirium., The trends of the NEECHAM scores in the 3 groups were compared, and the relationship between the NEECHAM scores and suspected clinical risk factors for Delirium was investigated., In groups showing an MMSE score of less than 25 or a preoperative NEECHAM score of less than 27, the incidence of postoperative Delirium was 76%.CONCLUSION: The results suggest that E-PASS and the NEECHAM score facilitate assessment of the risk of postoperative Delirium in elderly patients, contributing to early prevention/treatment., In this study, we investigated whether the early detection of postoperative Delirium in elderly patients is possible using a simple, useful behavior-assessing scale, the NEECHAM Confusion Scale, and a method for comprehensively evaluating elderly persons' stress related to surgery, E-PASS., Use of NEECHAM scaling enabled medical staff to identify cases of possible Clouded consciousness early, indicating that the NEECHAM Clouded consciousness scale should be useful for the detection of postoperative Delirium and Clouded consciousness in the surgical ward.., Early detection of postoperative Delirium and Clouded consciousness in a surgical ward using the NEECHAM Clouded consciousness scale., Assessment of the risk of postoperative Delirium in elderly patients using E-PASS and the NEECHAM Confusion Scale., For Delirium diagnosis and severity assessment, we used the NEECHAM Confusion Scale., The Neecham Confusion Scale and the Delirium Observation Screening Scale: capacity to discriminate and ease of use in clinical practice., The aim of this study was to determine which of the two Delirium observation screening scales, the NEECHAM Confusion Scale or the Delirium Observation Screening (DOS) scale, has the best discriminative capacity for diagnosing Delirium and which is more practical for daily use by nurses.[SEP]Relations: Delirium has relations: contraindication with Trolnitrate, contraindication with Trolnitrate, disease_disease with cognitive disorder, disease_disease with cognitive disorder, disease_disease with subacute Delirium, disease_disease with subacute Delirium, contraindication with Tacrolimus, contraindication with Tacrolimus, contraindication with Olanzapine, contraindication with Olanzapine.", "label": "yes"}
{"original_question": "Are deletions of chromosomal regulatory boundaries associated with congenital disease?", "id": "converted_1843", "sentence1": "Are Gene Deletion of chromosomal regulatory boundaries associated with Congenital Disorders?", "sentence2": "Deletions of chromosomal regulatory boundaries are associated with Congenital Disorders., Our results suggest that Enhancer of transcription adoption caused by Gene Deletion of regulatory boundaries may contribute to a substantial minority of copy-number variation phenotypes and should thus be taken into account in their medical interpretation, Deletions of chromosomal regulatory boundaries are associated with Congenital Disorders, Deletions of chromosomal regulatory boundaries are associated with Congenital Disorders.[SEP]Relations: congenital nervous system disorder has relations: disease_disease with chromosome 18q deletion syndrome, disease_disease with chromosome 18q deletion syndrome, disease_disease with chromosome 1p36 deletion syndrome, disease_disease with chromosome 1p36 deletion syndrome, disease_disease with chromosome 5q12 deletion syndrome, disease_disease with chromosome 5q12 deletion syndrome, disease_disease with chromosome 19p13.13 deletion syndrome, disease_disease with chromosome 19p13.13 deletion syndrome, disease_disease with chromosome 19q13.11 deletion syndrome, disease_disease with chromosome 19q13.11 deletion syndrome.", "label": "yes"}
{"original_question": "Are there studies representing the involvement of Notch mutations in neurodegenerative diseases such as Down syndrome, Pick's and Prion's disease, and cadasil syndrome?", "id": "converted_352", "sentence1": "Are there studies representing the involvement of Notch Gene Mutation in neurodegenerative diseases such as Down Syndrome, Pick's and Prion's disease, and cadasil syndrome?", "sentence2": "he Notch signaling pathway plays a critical role in maintaining the balance between cell proliferation, differentiation and apoptosis, and is a highly conserved signaling pathway that regulates normal development in a context- and dose-dependent manner. Dysregulation of Notch signaling has been suggested to be key events in a variety of hematological Malignant Neoplasms. NOTCH1 wt Allele signaling appears to be the central oncogenic trigger in Precursor T-Cell Lymphoblastic Leukemia-Lymphoma (T-ALL), in which the majority of Homo sapiens Malignant Neoplasms have acquired Gene Mutation that lead to constitutive activation of NOTCH1 wt Allele signaling., In a forward genetic screen for Gene Mutation that alter Protoplasm Notch receptor trafficking in Drosophila melanogaster, we recovered Mutant that disrupt Genes encoding Serine Palmitoyltransferase 1, Human and Acetyl-CoA Carboxylase., Signaling pathways have become a major source of targets for novel therapies in Liver carcinoma (altretamine/cisplatin/cyclophosphamide protocol). Survival benefits achieved with sorafenib, a multikinase inhibitor, are unprecedented and underscore the importance of improving our understanding of how signaling networks interact in transformed cells., Notch-1 immunoexpression is increased in Alzheimer's and Pick's disease, (PSEN1 protein, Homo sapiens protein, Homo sapiens) is the major Gene Locus for Gene Mutation causing familial ALZHEIMER DISEASE, FAMILIAL, 1 (flavin-adenine dinucleotide) and is also Mutation Abnormality in Pick Disease of the Brain of Head>Brain, familial acne inversa and Cardiomyopathy, Dilated. It is a critical facilitator of Notch signalling and many other signalling pathways and protein cleavage events including production of the Amyloidβ (Aβ) peptide from the AMYLOID BETA A4 PRECURSOR PROTEIN (Smartphone Application, As beta-Smartphone Application and Notch are both processed by gamma-Secretase, we analyzed expression of the Notch signaling pathway in the adult DS Head>Brain and in a model system for DS, Homo sapiens trisomy 21 Specimen Source Codes - Fibroblasts by quantitative PCR. In adult DS cortex we found that NOTCH1 wt Allele, DLL1 gene and HES1 gene expression is up-regulated. Moreover, DS Specimen Source Codes - Fibroblasts and Alzheimer disease cortex also show overexpression of NOTCH1 wt Allele and DLL1 gene, indicating that enhanced beta-Smartphone Application processing found in both DS and cytarabine/daunorubicin protocol could be instrumental in these changes, A systems biology approach to Down Syndrome: identification of Notch/Wnt dysregulation in a model of Stem cells aging, NOTCH3 gene has been recently identified as a causative gene for cerebral autosomal dominant arteriopathy with subcortical infarcts and Leukoencephalopathy (CADASIL Syndrome Syndrome)[SEP]Relations: NOTCH3 has relations: disease_protein with cerebral arteriopathy, autosomal dominant, with subcortical infarcts and Leukoencephalopathy,, disease_protein with cerebral arteriopathy, autosomal dominant, with subcortical infarcts and Leukoencephalopathy,, disease_protein with CARASIL syndrome, disease_protein with CARASIL syndrome, disease_protein with lateral meningocele syndrome, disease_protein with lateral meningocele syndrome, disease_protein with dementia (disease), disease_protein with dementia (disease). CARASIL syndrome has relations: disease_protein with NOTCH3, disease_protein with NOTCH3.", "label": "yes"}
{"original_question": "Is celiac disease caused by gliadin-induced transglutaminase-2 (TG2)-dependent events ?", "id": "converted_2512", "sentence1": "Is celiac disease caused by gliadin-induced transglutaminase-2 (TGM2 protein, human)-dependent events ?", "sentence2": "Celiac Disease (CD) is a frequent inflammatory intestinal disease, with a genetic background, caused by gliadin-containing food. , Celiac Disease (CD) is an Autoimmune enteropathy initiated and sustained by the ingestion of gluten in genetically susceptible individuals. It is caused by a dysregulated immune response toward both dietary antigens, the gluten Proteins of wheat, Secale cereale, and barley, and Autoantigens, the Enzyme [APC] tissue transglutaminase (TGM2 protein, human), Celiac Disease (CD) is an autoimmune gastrointestinal disorder characterized by the presence of anti-transglutaminase 2 (TGM2 protein, human) and anti-gliadin antibodies, Protein Glutamine gamma Glutamyltransferase 2 (TGM2 protein, human) catalyzes cross-linking or deamidation of glutamine residues in Peptides and Proteins. The in vivo deamidation of gliadin Peptides plays an important role in the immunopathogenesis of celiac disease (CD)., Tissue transglutaminase (TGM2 protein, human) modifies Proteins and Peptides by transamidation or deamidation of specific glutamine residues. TGM2 protein, human also has a central role in the pathogenesis of celiac disease. The Enzyme [APC] is both the target of disease-specific autoantibodies and generates deamidated gliadin Peptides recognized by intestinal T cells from patients.[SEP]Relations: celiac disease has relations: disease_protein with TGM2, disease_protein with TGM2, disease_protein with SOAT2, disease_protein with SOAT2, disease_protein with UGT1A4, disease_protein with UGT1A4, disease_protein with MAGI2, disease_protein with MAGI2, disease_protein with TFF1, disease_protein with TFF1.", "label": "yes"}
{"original_question": "Have mutations in the Polycomb group been found in human diseases?", "id": "converted_317", "sentence1": "Have mutations in the Polycomb group been found in human diseases?", "sentence2": "We identify a novel Mutation Abnormality in PHC1 gene gene, a human orthologue of the Drosophila polyhomeotic member of polycomb group (Polycomb-Group Proteins), which significantly decreases PHC1 gene gene protein expression, increases GMNN protein, human protein level and markedly abolishes the capacity to ubiquitinate histone H2A in patient cells., In clinical specimens of Malignant Head and Neck Neoplasm, we found that coamplification of BMI1 protein, human protein, human and Aurora Kinase A correlated with poorer prognosis., Gene Mutation of ezh2 protein, human, RUNX1 protein, human protein, human, TP53 wt Allele wt Allele, and Putative Polycomb Group Protein Putative Polycomb Group Protein ASXL1 were associated with shorter overall survival independent of the LR-PSS., In this study, we show the high frequency of spontaneous γδ T-cell leukemia (Precursor T-Cell Lymphoblastic Leukemia-Lymphoma) occurrence in CASP14 gene with biallelic deletion of Enhancer of transcription of zeste homolog 2 (Ezh2)., Subsequently, analysis of deletion profiles of other Polycomb Repressive Complex 2 members revealed frequent losses of Genes such as ezh2 protein, human, AEBP2 protein, human protein, human, and SUZ12; however, the Gene Deletion targeting these Genes were large. We also identified two patients with homozygous losses of JARID2 gene gene and AEBP2 protein, human protein, human. We observed frequent codeletion of AEBP2 protein, human protein, human and ETV6 wt Allele wt Allele, and similarly, SUZ12 and Neurofibromatosis 1., A total of 25 different ezh2 protein, human mutations were detected in 5.9% of PLATELET MEMBRANE FLUIDITY, 1.2% of PPV-MF, and 9.4% of PET-MF patients; most were exonic heterozygous missense changes., In the present investigation we have focused on the candidate Geographic Locations in 6p23, a Geographic Locations that have been found linked to CL/P in several investigations, in the attempt to find out the susceptibility gene provisionally named OTOFACIOCERVICAL SYNDROME 1. Gene expression experiments in CASP14 gene embryo of positional candidate Genes revealed that JARID2 gene gene was highly and specifically expressed in Epithelial Cells in merging Palatal shelf., High expression of ezh2 protein, human and amplification of ezh2 protein, human was found in 54.1% and 12.0% of ESCCs, respectively., We also observed that HOXA9 wt Allele wt Allele levels were significantly inversely correlated with survival and that BMI-1 was overexpressed in cases with 11q23 rearrangements, suggesting that p19(ARF) suppression may be involved in MLL-associated leukemia., We demonstrate that in multiple experimental models of metastatic prostate cancer both BMI1 protein, human protein, human and Ezh2 Genes are amplified and gene amplification is associated with increased expression of corresponding mRNAs and Proteins., he ezh2 protein, human gene amplification was significantly (P < 0.05) associated with increased ezh2 protein, human protein expression., The third tumor showed a t(6p;10q;10p) as the sole karyotypic abnormality, leading to the fusion of PHF1 protein, human protein, human with another partner, the Enhancer of transcription of polycomb (Enhancer of Polycomb Homolog 1) gene from 10p11; Enhancer of Polycomb Homolog 1 has hitherto not been associated with Neoplasms.[SEP]Relations: Protein S human has relations: drug_drug with Polythiazide, drug_drug with Polythiazide, drug_drug with Polythiazide, drug_drug with Polythiazide, drug_drug with Polythiazide, drug_drug with Polythiazide, drug_drug with Polythiazide, drug_drug with Polythiazide, drug_drug with Polythiazide, drug_drug with Polythiazide.", "label": "yes"}
{"original_question": "Are super enhancers structurally insulated in chromatin loops?", "id": "converted_3854", "sentence1": "Are super enhancers structurally insulated in chromatin location loops?", "sentence2": "Dissecting super-enhancer hierarchy based on chromatin location location interactions, Genetic ablation of hub enhancers results in profound defects in gene activation and local chromatin location location landscape., We also demonstrate that the Wap super-enhancer, which is built on STAT5 Protein Family Protein Family and other common transcription factors, retains its exquisite Mammary gland specificity when placed into globally permissive chromatin location location, suggesting a limited role of chromatin location location in controlling \"U\" lymphocyte specificity. , Although there is evidence that chromatin location location neighbourhoods, formed by the zinc-finger protein CTGF protein, human, can sequester enhancers and their target Genes, there is limited in vivo evidence for CTGF protein, human demarcating super-enhancers and preventing cross talk between distinct regulatory elements., CTGF protein, human Site are porous borders, allowing a super-enhancer to activate a secondary target., TRANSCRIPTION FACTOR and chromatin location location-remodeling complexes are key determinants of Embryonic Stem Cells (ESTERASE C) identity. [SEP]Relations: Protein S human has relations: drug_drug with Cisplatin, drug_drug with Cisplatin, drug_drug with Omega-3-acid ethyl esters, drug_drug with Omega-3-acid ethyl esters, drug_drug with Anti-inhibitor coagulant complex, drug_drug with Anti-inhibitor coagulant complex, drug_drug with Antihemophilic Factor (Recombinant), PEGylated, drug_drug with Antihemophilic Factor (Recombinant), PEGylated. RNA localization to chromatin location has relations: bioprocess_protein with HNRNPU, bioprocess_protein with HNRNPU.", "label": "no"}
{"original_question": "Does IL18 signaling have a role in thymus?", "id": "converted_3855", "sentence1": "Does IL18 signaling have a role in Thymus <angiosperm>?", "sentence2": "IL18 signaling promotes homing of mature Tregs into the Thymus <angiosperm>., Collectively, this study provides a detailed characterization of the mature Treg subsets in the Mus sp. Thymus <angiosperm> and identifies a key role of IL18 signaling in controlling the CCRL2 wt Allele-CCL20-dependent migration of Tregs into the Thymus <angiosperm>., er, we show that IL18R+ Tregs are endowed with higher capacity to populate the Thymus <angiosperm> than their IL18R- or IL18R-/- counterparts, highlighting the key role of IL18R in this process, IL18 signaling promotes homing of mature Tregs into the Thymus <angiosperm>, inally, we demonstrate that IL18 signaling is critical for the induction of the key Thymus <angiosperm>-homing chemokine receptor - CCRL2 wt Allele on Tregs. , Moreover, we show that IL18R+ Tregs are endowed with higher capacity to populate the Thymus <angiosperm> than their IL18R- or IL18R-/- counterparts, highlighting the key role of IL18R in this process.[SEP]", "label": "yes"}
{"original_question": "Does gavestinel improve outcomes of stroke patients?", "id": "converted_3655", "sentence1": "Does Gavestinel improve outcomes of Cerebrovascular accident patients?", "sentence2": "CONCLUSION: Consistent with the clinical outcomes in the GAIN trials, no effects of Gavestinel on ischemic infarction was observed., No effects of Gavestinel on infarct volume were observed in the primary or other analyses. , Gavestinel does not improve outcome after acute intracerebral hemorrhage: an analysis from the GAIN International and GAIN Americas studies., Both trials reported that Gavestinel was ineffective in Ischemic Cerebrovascular accident. , CONCLUSIONS: These observations from the combined GAIN International and GAIN Americas trials suggest that Gavestinel is not of substantial benefit or harm to patients with primary intracerebral hemorrhage. , Glutamate N-methyl-D-aspartate (NMDA) receptor antagonists such as selfotel, aptiganel, Gavestinel and others failed to show neuroprotective efficacy in Homo sapiens clinical trials or produced intolerable central nervous system adverse effects., METHODS: We studied all patients of the Glycine Antagonist (Gavestinel) In Neuroprotection (GAIN) International Trial with Ischemic Cerebrovascular accident alive at day 7, excluding patients with hemorrhagic events and Cessation of life from nonstroke-related causes. The GAIN International Trial was a randomized, double-blind, placebo-controlled, and parallel-group trial; because the study Pharmacologic Substance had no effect on Cerebrovascular accident outcome, treatment groups were combined for this analysis. , Gavestinel produces no benefit for Cerebrovascular accident patients, study finds., The wonder Pharmacologic Substance, Gavestinel, failed to produce any significant treatment benefits for patients treated within six hours after experiencing an acute Ischemic Cerebrovascular accident, according to the recent results of a major clinical trial of the neuroprotectant. , INTERPRETATION: Treatment with Gavestinel within 6 h of acute ischaemic Cerebrovascular accident did not improve outcome., INTERPRETATION\n\nTreatment with Gavestinel within 6 h of acute ischaemic Cerebrovascular accident did not improve outcome., CONCLUSION\n\nIn this study, Gavestinel administered up to 6 hours after an acute Ischemic Cerebrovascular accident did not improve functional outcome at 3 months., Both trials reported that Gavestinel was ineffective in Ischemic Cerebrovascular accident., INTERPRETATION Treatment with Gavestinel within 6 h of acute ischaemic Cerebrovascular accident did not improve outcome., Both trials reported that Gavestinel was ineffective in Ischemic Cerebrovascular accident., Gavestinel produces no benefit for Cerebrovascular accident patients , study finds ., The wonder Pharmacologic Substance, Gavestinel, failed to produce any significant treatment benefits for patients treated within six hours after experiencing an acute Ischemic Cerebrovascular accident, according to the recent results of a major clinical trial of the neuroprotectant., The wonder Pharmacologic Substance, Gavestinel, failed to produce any significant treatment benefits for patients treated within six hours after experiencing an acute Ischemic Cerebrovascular accident, according to the recent results of a major clinical trial of the neuroprotectant., Treatment with Gavestinel within 6 h of acute ischaemic Cerebrovascular accident did not improve outcome., In this study, Gavestinel administered up to 6 hours after an acute Ischemic Cerebrovascular accident did not improve functional outcome at 3 months.[SEP]Relations: Gavestinel has relations: drug_drug with Rifampicin, drug_drug with Rifampicin, drug_drug with Enasidenib, drug_drug with Enasidenib, drug_drug with Silibinin, drug_drug with Silibinin, drug_drug with Indinavir, drug_drug with Indinavir, drug_drug with Pazopanib, drug_drug with Pazopanib.", "label": "no"}
{"original_question": "Is rucaparib used for ovarian cancer treatment?", "id": "converted_1848", "sentence1": "Is rucaparib used for Malignant neoplasm of ovary treatment?", "sentence2": "While olaparib is the first PARP1 wt Allele PPP1R1A gene to receive approval for Malignant neoplasm of ovary treatment, others including rucaparib and niraparib are clearly effective in this Disease and, within the next year or two, the results of ongoing randomised trials will clarify their respective roles. , Similar trials with other PARP1 wt Allele inhibitors (rucaparib, niraparib and veliparib) are in progress and include non-BRCA-mutated Malignant neoplasm of ovary. , IMPLICATIONS FOR PRACTICE: The poly(ADP-ribose) polymerase (PARP1 wt Allele) PPP1R1A gene olaparib has recently received approval from the Food and Drug Administration (FDA) and European Medicines Agency (Multiple Acyl Coenzyme A Dehydrogenase Deficiency), with a second agent (rucaparib) likely to be approved in the near future., Ovarian Cancers Harbour Defects in Non-Homologous End Joining Resulting in Resistance to rucaparib., There are a number of other PARP1 wt Allele inhibitors in late phase clinical development in Malignant neoplasm of ovary including rucaparib, niraparib, veliparib, and talazoparib. , rucaparib in relapsed, platinum-sensitive high-grade ovarian carcinoma (ARIEL2 Part 1): an international, multicentre, open-label, phase 2 trial., INTERPRETATION: In patients with BRCA mutant or BRCA wild-type and Loss of Heterozygosity high platinum-sensitive ovarian carcinomas treated with rucaparib, progression-free survival was longer than in patients with BRCA wild-type Loss of Heterozygosity low carcinomas. Our results suggest that assessment of Neoplasms Loss of Heterozygosity can be used to identify patients with BRCA wild-type Platinum-Sensitive Ovarian Carcinoma who might benefit from rucaparib. , Genomic Loss of Heterozygosity May Predict rucaparib Response in Ovarian Cancer., High Loss of Heterozygosity is associated with response to the PARP1 wt Allele PPP1R1A gene rucaparib in BRCA wild-type Malignant neoplasm of ovary., Therapeutic potential of the poly(ADP-ribose) polymerase PPP1R1A gene rucaparib for the treatment of sporadic Homo sapiens Malignant neoplasm of ovary., While olaparib is the first PARP1 wt Allele PPP1R1A gene to receive approval for Malignant neoplasm of ovary treatment, others including rucaparib and niraparib are clearly effective in this Disease and, within the next year or two, the results of ongoing randomised trials will clarify their respective roles., These results support further clinical evaluation of rucaparib either as a single agent or as an adjunct to chemotherapy for the treatment of sporadic Malignant neoplasm of ovary., Here, we investigate the potential role of the PARP1 wt Allele PPP1R1A gene rucaparib (C0-338, formerly known as AG 014699 and PF-01367338) for the treatment of sporadic Malignant neoplasm of ovary., rucaparib received US FDA Breakthrough Therapy designation for treatment of platinum-sensitive BRCA-mutated advanced Malignant neoplasm of ovary patients who received greater than two lines of platinum-based therapy., These results support further clinical evaluation of rucaparib either as a single agent or as an adjunct to chemotherapy for the treatment of sporadic Malignant neoplasm of ovary., Ongoing clinical trials are assessing the efficacy of rucaparib alone or in combination with other cytotoxic drugs, mainly in Breast and Malignant neoplasm of ovary patients with Gene Mutation in the Breast cancer associated (BRCA) genes.PURPOSE: We aimed to establish whether the multidrug efflux transporters ABCG2 wt Allele wt Allele (BCRP) and ABCB1 wt Allele wt Allele (P-Glycoprotein, MDR1) affect the oral availability and brain penetration of rucaparib in CASP14 gene.RESULTS: In vitro, rucaparib was efficiently transported by both Homo sapiens ABCB1 wt Allele wt Allele and ABCG2 wt Allele wt Allele, and very efficiently by mouse Abcg2., Therapeutic potential of the poly(ADP-ribose) polymerase PPP1R1A gene rucaparib for the treatment of sporadic Homo sapiens Malignant neoplasm of ovary, Here, we investigate the potential role of the PARP1 wt Allele PPP1R1A gene rucaparib (C0-338, formerly known as AG 014699 and PF-01367338) for the treatment of sporadic Malignant neoplasm of ovary, These results support further clinical evaluation of rucaparib either as a single agent or as an adjunct to chemotherapy for the treatment of sporadic Malignant neoplasm of ovary.<CopyrightInformation>©2013 AACR</, Ongoing clinical trials are assessing the efficacy of rucaparib alone or in combination with other cytotoxic drugs, mainly in Breast and Malignant neoplasm of ovary patients with Gene Mutation in the Breast cancer associated (BRCA) genes.We aimed to establish whether the multidrug efflux transporters ABCG2 wt Allele wt Allele (BCRP) and ABCB1 wt Allele wt Allele (P-Glycoprotein, MDR1) affect the oral availability and brain penetration of rucaparib in CASP14 gene.In vitro, rucaparib was efficiently transported by both Homo sapiens ABCB1 wt Allele wt Allele and ABCG2 wt Allele wt Allele, and very efficiently by mouse Abcg2, Here, we investigate the potential role of the PARP1 wt Allele PPP1R1A gene rucaparib (C0-338, formerly known as AG 014699 and PF-01367338) for the treatment of sporadic Malignant neoplasm of ovary. , While olaparib is the first PARP1 wt Allele PPP1R1A gene to receive approval for Malignant neoplasm of ovary treatment, others including rucaparib and niraparib are clearly effective in this Disease and, within the next year or two, the results of ongoing randomised trials will clarify their respective roles., We investigated the efficacy and safety of single-agent rucaparib in Germline (g) BRCA Mutation Abnormality carriers with advanced Breast and ovarian cancers.Phase II, open-label, multicentre trial of rucaparib in proven BRCA-1/2 Mutation Abnormality carriers with advanced Breast and or Malignant neoplasm of ovary, WHO PS 0-1 and normal organ function., These results support further clinical evaluation of rucaparib either as a single agent or as an adjunct to chemotherapy for the treatment of sporadic Malignant neoplasm of ovary.<CopyrightInformation>©2013 AACR</C, Similar trials with other PARP1 wt Allele inhibitors (rucaparib, niraparib and veliparib) are in progress and include non-BRCA-mutated Malignant neoplasm of ovary., rucaparib received US FDA Breakthrough Therapy designation for treatment of platinum-sensitive BRCA-mutated advanced Malignant neoplasm of ovary patients who received greater than two lines of platinum-based therapy., Therapeutic potential of the poly(ADP-ribose) polymerase PPP1R1A gene rucaparib for the treatment of sporadic Homo sapiens Malignant neoplasm of ovary., These results support further clinical evaluation of rucaparib either as a single agent or as an adjunct to chemotherapy for the treatment of sporadic Malignant neoplasm of ovary..[SEP]Relations: rucaparib has relations: drug_drug with Lobucavir, drug_drug with Lobucavir, drug_drug with Estradiol, drug_drug with Estradiol, drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Olaparib, drug_drug with Olaparib, drug_drug with Capsaicin, drug_drug with Capsaicin.", "label": "yes"}
{"original_question": "Is the number of described human nuclear mutations less than 50000?", "id": "converted_2078", "sentence1": "Is the number of described Homo sapiens nuclear Gene Mutation less than 50000?", "sentence2": "The number of known Gene Mutation in Homo sapiens nuclear Genes, underlying or associated with Homo sapiens inherited disease, has now exceeded 100,000 in more than 3700 different Genes (Human Gene Mutation Database)., The Human Gene Mutation Database (HGMD®) is a comprehensive collection of germline Gene Mutation in nuclear Genes that underlie, or are associated with, Homo sapiens inherited disease. By June 2013, the database contained over 141,000 different Lesion detected in over 5,700 different Genes, with new Mutation Abnormality entries currently accumulating at a rate exceeding 10,000 per annum., By March 2012, the database contained in excess of 123,600 different Lesion (HGMD Professional release 2012.1) detected in 4,514 different nuclear Genes, with new entries[SEP]Relations: Lacrimation abnormality has relations: disease_phenotype_positive with Coffin-Siris syndrome, disease_phenotype_positive with Coffin-Siris syndrome, disease_phenotype_positive with Stüve-Wiedemann syndrome, disease_phenotype_positive with Stüve-Wiedemann syndrome, disease_phenotype_positive with Johanson-Blizzard syndrome, disease_phenotype_positive with Johanson-Blizzard syndrome, disease_phenotype_positive with Williams syndrome, disease_phenotype_positive with Williams syndrome, disease_phenotype_positive with limbal stem cell deficiency, disease_phenotype_positive with limbal stem cell deficiency.", "label": "no"}
{"original_question": "Is sumoylation implicated in myogenesis?", "id": "converted_682", "sentence1": "Is sumoylation implicated in myogenesis?", "sentence2": "Sentrin/small ubiquitin-like modifier (SUMO)-specific protease 2 (SUMO1 wt Allele) has broad de-SUMOylation activities in vitro, which is essential for embryonic heart development., Silencing SUMO1 wt Allele can reduce growth-differentiation factor 8 expression and, therefore, promote myogenesis of Specimen Source Codes - Skeletal muscle. These results reveal the important role of SUMO1 wt Allele in the regulation of growth-differentiation factor 8 expression and myogenesis., Overexpression of c-Ski/SKIL protein, human also induces Specimen Source Codes - Skeletal muscle differentiation, but how c-Ski/SKIL protein, human function in myogenesis is largely unknown., Notably, loss of sumoylation in the Lys-50 site (via a Lys-to-Arg point mutation) potently activates muscle-specific gene expression and enhances myotube formation. Our study suggests a novel role for SUMO ResponseLevel - ResponseLevel - modification in the regulation of myogenic differentiation., Although this ResponseLevel - ResponseLevel - modification has little effect on SKIL protein, human repression of the plasminogen activator inhibitor-1 promoter and only modestly potentiates SKIL protein, human repression of the oncoprotein oncoprotein p21 promoter, SKIL protein, human sumoylation robustly augments the ability of SKIL protein, human to suppress transcription of the myogenesis master Genes, Regulator MYOG protein, human, Our study also points to a physiological role for SKIL protein, human sumoylation in the control of MYOG protein, human expression in differentiating Muscle Cells., Here, we biochemically characterize SKIL protein, human sumoylation in detail and report the physiological function of the ResponseLevel - ResponseLevel - modification. , An essential role of small ubiquitin-like modifier (SUMO)-specific Protease 2 in growth-differentiation factor 8 expression and myogenesis., These results reveal the important role of SUMO1 wt Allele in the regulation of growth-differentiation factor 8 expression and myogenesis., The E3 SUMO ligase Nse2 regulates sumoylation and Nuclear (incident type)-to-cytoplasmic translocation of NACA wt Allele-SMYD1 gene in myogenesis., Sumoylation of the basic helix-loop-helix transcription factor sharp-1 regulates recruitment of the histone methyltransferase EHMT2 gene and function in myogenesis.,  We show that the overall load of sumoylated proteins present in Myoblasts diminishes progressively throughout myogenesis, These novel results suggest that protein sumoylation plays a pivotal role in myoblast differentiation and is required to regulate the activity of key targets downstream of MYOD1 wt Allele and MYOG protein, human., a composite sequence motif has recently been identified that couples phosphorylation, sumoylation, and perhaps also deacetylation to control transcriptional repression in stress response, Growth Factor and Nuclear (incident type) hormone signaling, myogenesis, and neuronal differentiation., Mutation Abnormality Abnormality of these SUMO acceptor sites in BHLHE41 gene does not impact its subcellular localization but attenuates its ability to act as a Transcription Repressor/Corepressor and inhibit myogenic differentiation. Consistently, co-expression of the SUMO protease SENP1 with wild type BHLHE41 gene abrogates BHLHE41 gene-dependent inhibition of myogenesis. , Transforming growth factor-beta-independent regulation of myogenesis by SKIL protein, human sumoylation., Ubiquitin Specific Protease 25 (USP25 gene gene), a member of the deubiquitinase family, is involved in several disease-related signal pathways including myogenesis, immunity and protein degradation. ,  In addition, we show that the NACA wt Allele interaction partner SMYD1 gene contains a putative sumoylation motif and is sumoylated in Muscle Cells, with depletion of Mms21/Nse2 leading to reduced concentrations of sumoylated SMYD1 gene. Taken together, our data suggest that the function, specifically the balance between the Nuclear (incident type) and cytosolic roles, of the NACA wt Allele-SMYD1 gene complex might be regulated by sumoylation.[SEP]Relations: EHMT2 has relations: pathway_protein with Regulation of TP53 Activity through Methylation, pathway_protein with Regulation of TP53 Activity through Methylation, bioprocess_protein with regulation of histone H3-K4 methylation, bioprocess_protein with regulation of histone H3-K4 methylation, bioprocess_protein with regulation of histone H3-K9 methylation, bioprocess_protein with regulation of histone H3-K9 methylation. histone methyltransferase complex has relations: cellcomp_protein with PRDM4, cellcomp_protein with PRDM4. BHLHE41 has relations: bioprocess_protein with regulation of neurogenesis, bioprocess_protein with regulation of neurogenesis.", "label": "yes"}
{"original_question": "is intense physical activity associated with longevity ?", "id": "converted_296", "sentence1": "is intense physical activity associated with longevity ?", "sentence2": "We found a very significant increase in average longevity (17%) of the cyclists when compared with the general population. The age at which 50% of the general population died was 73.5 vs. 81.5 years in Tour de France participants. Our major finding is that repeated very intense exercise prolongs life span in well trained practitioners., Competitive exercise does not induce cardiac damage in individuals with healthy hearts, but does induce physiological functional and structural cardiac adaptations which have positive effects on life expectancy., Medallists lived an average of 2.8 years longer than controls. Medallists in eight of the nine country groups had a significant survival advantage compared with controls. Gold, Silver color, and bronze medallists each enjoyed similar sized survival advantages. Medallists in endurance sports and mixed sports had a larger survival advantage over controls at 30 years (1.13, 1.09 to 1.17; 1.11, 1.09 to 1.13) than that of medallists in power sports (1.05, 1.01 to 1.08). CONCLUSIONS: Olympic medallists live longer than the general population, irrespective of country, medal, or sport. This study was not designed to explain this effect, but possible explanations include genetic factors, physical activity, healthy lifestyle, and the wealth and status that come with international sporting glory., Long-term endurance training induces in elderly subjects an increased HRV and a higher exercise working capacity, which are well-established predictors of cardiovascular and overall mortality., Sports activity in adolescents and young adults was associated with an increased risk of SLC17A5 gene, both in males and females. Sports, per se, was not a cause of the enhanced mortality, but it triggered SLC17A5 gene in those athletes who were affected by cardiovascular conditions predisposing to life-threatening Ventricular arrhythmia during physical exercise.[SEP]Relations: SLC17A5 has relations: molfunc_protein with transmembrane transporter activity, molfunc_protein with transmembrane transporter activity, molfunc_protein with carbohydrate:proton symporter activity, molfunc_protein with carbohydrate:proton symporter activity. Ventricular arrhythmia has relations: drug_effect with Ganciclovir, drug_effect with Ganciclovir, drug_effect with Sildenafil, drug_effect with Sildenafil. Silver has relations: drug_effect with Inflammatory abnormality of the skin, drug_effect with Inflammatory abnormality of the skin.", "label": "yes"}
{"original_question": "Is SMOC2 expressed during wound healing?", "id": "converted_4236", "sentence1": "Is SMOC2 expressed during wound healing?", "sentence2": "All three fibroblast populations were PDGFRα+/CD34 + but were distinct in their expression of Ngfr/Spon2/Angptl7 (F1), Cxcl14/Smoc2/Rgs2 (F2), and Clec3b/Col14a1/Mmp3 (F3), with potential functions in the regulation of immune responses, response to wounding, and organization of Extracellular Matrix, respectively., Deficiency of the SMOC2 matricellular protein impairs bone healing and produces age-dependent bone loss.[SEP]Relations: Extracellular Matrix has relations: cellcomp_protein with SPOCK2, cellcomp_protein with SPOCK2, cellcomp_protein with CPN2, cellcomp_protein with CPN2, cellcomp_protein with SPON2, cellcomp_protein with SPON2, cellcomp_protein with CCN2, cellcomp_protein with CCN2, cellcomp_protein with GFOD2, cellcomp_protein with GFOD2.", "label": "yes"}
{"original_question": "Is Growth factor independence 1b (GFI1B) important for hematopoiesis?", "id": "converted_995", "sentence1": "Is Growth factor independence 1b (GFI1B protein, human) important for Hematopoiesis?", "sentence2": "Growth Factor Independence (Gfi) transcription factors play essential roles in Hematopoiesis, differentially activating and repressing transcriptional programs required for hematopoietic stem/progenitor cell (HSPC) development and Lineage specification, gfi1aa and gfi1b have distinct roles in regulating primitive and definitive hematopoietic progenitors,, gfi1b is required for definitive Hematopoiesis, LSD1-kd was associated with the upregulation of key hematopoietic Genes, including Gfi1b, Zinc Finger Protein Zinc Finger Protein GFI1 wt Allele, Human wt Allele, Human and GFI1B protein, human protein, human control the loss of Endothelium identity of hemogenic endothelium during hematopoietic commitment,  Taken together, our findings demonstrate a critical and specific role of the Zinc Finger Protein Zinc Finger Protein GFI1 wt Allele, Human wt Allele, Human transcription factors in the first steps of the process leading to the generation of hematopoietic progenitors from hemogenic endothelium, A short Gfi-1B isoform controls Erythroid differentiation, Gfi-1B is a Transcription Repressor/Corepressor essential for the regulation of erythropoiesis and megakaryopoiesis, Among the few down-regulated Genes was Gfi1b, a known repressor of Erythroid differentiation, This reversible modulation of Endothelium-haematopoietic state is accomplished by targeting key haematopoietic transcription factors for downregulation, including RUNX1 protein, human, GATA1 wt Allele, Gfi1B, IKZF1 gene, and SPI1 wt Allele, Gfi1 and Gfi1b: key regulators of Hematopoiesis, we review how Gfi1 and its paralogue Gfi1b control the development of Blood Cells, discuss how changes in Gfi1 and Gfi1b function contribute to Hematological Disease and report on the molecular function of these Proteins., Gfi-1B controls human Erythroid and Megakaryocytic differentiation by regulating TGF-beta signaling at the bipotent erythro-Megakaryocytic progenitor stage, Growth factor independence-1B (Gfi-1B) is a Transcription Repressor/Corepressor essential for erythropoiesis and megakaryopoiesis, Targeted gene disruption of GFI1B protein, human protein, human in CASP14 gene leads to embryonic lethality resulting from failure to produce definitive Specimen Source Codes - Erythrocytes, hindering the study of Gfi-1B function in adult Hematopoiesis, We here show that, in Homo sapiens, Gfi-1B controls the development of Specimen Source Codes - Erythrocytes and Megakaryocytes by regulating the proliferation and differentiation of bipotent erythro-Megakaryocytic progenitors, To date, we have identified two common integration sites involving Genes encoding transcription factors that play a critical role in Hematopoiesis (MECOM wt Allele and Gfi1b loci), TRANSCRIPTION FACTOR play essential roles in both normal and malignant Hematopoiesis. This is the case for the Growth Factor [APC] independent 1b (GFI1B protein, human protein, human) transcription factor, which is required for Erythroid and Megakaryocytic differentiation and over-expressed in leukemic patients and Cultured Cell Line, We localized several conserved non-coding elements containing multiple Erythroid specific transcription factor binding sites at the GFI1B protein, human protein, human locus. In GFI1B protein, human protein, human-expressing cells a subset of these conserved non-coding elements and the Promoter adopt a close spatial conformation, localize with open chromatin sites, harbor chromatin modifications associated with gene activation and bind multiple transcription factors and Co-Repressor Proteins, Our findings indicate that GFI1B protein, human protein, human regulatory elements behave as activators and repressors, To investigate the molecular effects of Growth Factor [APC] independence 1B (Gfi-1B), a transcription factor essential for the development of hematopoietic cells and differentiation of Erythroid and Megakaryocytic lineages, Our data indicate that Gfi-1B signalling is important for commitment and maturation of Hematopoietic cell populations, Zinc Finger Protein GFI1 wt Allele, Human wt Allele and Gfi-1b are homologous transcriptional repressors involved in diverse developmental contexts, including Hematopoiesis and oncogenesis, Gfi1b:green fluorescent protein knock-in CASP14 gene reveal a dynamic expression pattern of Gfi1b during Hematopoiesis that is largely complementary to Gfi1, We found highly dynamic expression patterns of Gfi1b in Erythroid Cells, Megakaryocytes, and their Stem cells (MEPS) where Gfi1 is not detected. Vice versa, Gfi1b could not be found in Granulocyte component of blood, Armed macrophage, or their granulomonocytic precursors (guanosine 5'-monophosphorothioate) or in mature naive or activated lymphocytes where Gfi1 is expressed, suggesting a complementary regulation of both loci during Hematopoiesis, Gfi1 and Gfi1b act equivalently in haematopoiesis, our findings show that an intact SNAG domain is essential for all functions of Gfi1 and that Gfi1b can replace Gfi1 functionally in haematopoiesis, Zinc Finger Protein GFI1 wt Allele, Human wt Allele oncoproteins in Hematopoiesis, Recent gene targeting experiments and mutational screening in Homo sapiens have revealed an essential role for Zinc Finger Protein GFI1 wt Allele, Human wt Allele and Gfi-1B in Hematopoiesis, Gfi-1B disruption is embryonic lethal due to a block of erythropoiesis. Gfi-1B is required for both Erythroid and megakaryocyte development, Erythroid expansion mediated by the Gfi-1B zinc finger protein: role in normal Hematopoiesis,  we identified that the expression of Gfi-1B (Growth Factor [APC] independence-1B) is highly restricted to Hematopoietic stem cells, Erythroblasts, and Megakaryocytes, These findings establish Gfi-1B as a novel Erythroid regulator and reveal its specific involvement in the regulation of Erythroid cell growth through modulating Erythroid-specific gene expression, The zinc-finger proto-oncogene Gfi-1b is essential for development of the Erythroid and Megakaryocytic lineages, we establish that Gfi-1b is required for the development of two related blood lineages, Erythroid and Megakaryocytic, in CASP14 gene, Gfi-1b(-/-) embryonic stem cells fail to contribute to Erythrocytes of adult chimeras. Gfi-1b(-/-) embryos exhibit delayed maturation of primitive Specimen Source Codes - Erythrocytes and subsequently die with failure to produce definitive enucleated Specimen Source Codes - Erythrocytes, Gfi-1b is an essential transcriptional regulator of Erythroid and megakaryocyte development, Growth factor independence 1b (GFI1B protein, human protein, human) is a DNA binding repressor of transcription with vital functions in Hematopoiesis., Conversely, loss of gfi1b silences runx-1, MYB wt Allele, Human, ikaros and Platelet Membrane Glycoprotein IIb, indicating that gfi1b is required for definitive Hematopoiesis., Gfi1b:green fluorescent protein knock-in CASP14 gene reveal a dynamic expression pattern of Gfi1b during Hematopoiesis that is largely complementary to Gfi1., Gfi1 and Gfi1b: key regulators of Hematopoiesis., We show that gfi1aa and gfi1b are expressed in the primitive and definitive sites of Hematopoiesis in Zebrafish., Targeted gene disruption of GFI1B protein, human protein, human in CASP14 gene leads to embryonic lethality resulting from failure to produce definitive Specimen Source Codes - Erythrocytes, hindering the study of Gfi-1B function in adult Hematopoiesis., Growth factor independence 1b (gfi1b) is important for the maturation of Erythroid Cells and the regulation of embryonic globin expression., GFI1B protein, human gene (Gfi1b) is a zinc finger transcription factor essential for Erythroid and Megakaryocytic development., Gfi1b (Growth Factor [APC] independence 1b) is a zinc finger transcription factor essential for development of the Erythroid and Megakaryocytic lineages., In fact, we demonstrate that valproic acid treatment is able to induce the expression of Growth Factor [APC]-independent protein 1B (GFI1B protein, human protein, human) and of mixed-Lineage leukemia translocated to chromosome 3 protein (MLLT3 wt Allele wt Allele), which are crucial regulators of erythrocyte and megakaryocyte differentiation, and that the up-regulation of these Genes is mediated by the histone hyperacetylation at their Promoter sites., Growth factor independence-1B (Gfi-1B) is a Transcription Repressor/Corepressor essential for erythropoiesis and megakaryopoiesis., Gfi-1B (Growth Factor [APC] independence-1B) gene is an Erythroid-specific transcription factor, whose expression plays an essential role in erythropoiesis., Evidence that Growth Factor [APC] independence 1b regulates dormancy and peripheral blood mobilization of Hematopoietic stem cells., We report here that adult CASP14 gene conditionally deficient for the transcription Growth factor independence 1b (Gfi1b) show a significant expansion of functional HSCs in the bone marrow and blood., GFI1B protein, human gene (Gfi1b) is a zinc finger transcription factor essential for Erythroid and Megakaryocytic development, Teleost Growth Factor [APC] independence (gfi) Genes differentially regulate successive waves of Hematopoiesis., Gfi-1B (Growth Factor [APC] independence-1B) gene is an Erythroid-specific transcription factor, whose expression plays an essential role in erythropoiesis, Our data indicate that Gfi-1B signalling is important for commitment and maturation of Hematopoietic cell populations., We report here that adult CASP14 gene conditionally deficient for the transcription Growth factor independence 1b (Gfi1b) show a significant expansion of functional HSCs in the bone marrow and blood[SEP]Relations: GFI1B protein, human has relations: cellcomp_protein with nucleus, cellcomp_protein with nucleus, protein_protein with EFEMP2, protein_protein with EFEMP2, protein_protein with PSMA3, protein_protein with PSMA3, bioprocess_protein with regulation of hemopoiesis, bioprocess_protein with regulation of hemopoiesis, protein_protein with CENPB, protein_protein with CENPB.", "label": "yes"}
{"original_question": "Does an interferon (IFN) signature exist for SLE patients?", "id": "converted_3543", "sentence1": "Does an interferon (Homo sapiens leukocyte interferon) signature exist for Lupus Erythematosus, Systemic patients?", "sentence2": "IRF7 gene activation correlates with the Homo sapiens leukocyte interferon signature and recurrent disease., In Lupus Erythematosus, Systemic post-transplant, recurrent disease activity and induction of IRF7 protein expression correlated with activation of the Homo sapiens leukocyte interferon signature., Janus kinase inhibitor has the amelioration effect in lupus-prone CASP14 gene: the involvement of Homo sapiens leukocyte interferon signature gene downregulation., We also detected decreased expression of several Homo sapiens leukocyte interferon-signature Genes Ifit3 and ISG15 gene in CD4+ from Lupus Erythematosus, Systemic-prone CASP14 gene following 5-(tetradecyloxy)-2-furancarboxylic acid and Dual-Energy X-Ray Absorptiometry treatment, and IFIT3 gene gene in CD3+ T cells from Homo sapiens patients following immunosuppressant therapy including Steroids, respectively, We found that cDCs from prediseased TCSle male CASP14 gene express the Homo sapiens leukocyte interferon signature as female TCSle cDCs do. ESTROGENS, SEX HORMONES AND MODULATORS OF THE GENITAL SYSTEM are necessary but not sufficient to express this Homo sapiens leukocyte interferon signature, but high doses of ubiquitin-like protein conjugating enzyme activity can compensate for other steroidal components., Conventional Triglyceride storage disease with ichthyosis from Male and Female Lupus-Prone B6.NZM Sle1/Sle2/Sle3 Mice Express an Homo sapiens leukocyte interferon Signature and Have a Higher Immunometabolism That Are Enhanced by Estrogen [EPC] [EPC]., Type I Homo sapiens leukocyte interferon signature in childhood-onset systemic lupus erythematosus,  Interferon Type I (Homo sapiens leukocyte interferon-I) plays a pivotal role in the pathogenesis of Lupus Erythematosus, Systemic. , The Homo sapiens leukocyte interferon-I score (positive or negative), as a measure of Homo sapiens leukocyte interferon-I activation, was assessed using real-time quantitative PCR (RT-PCR) expression values of Homo sapiens leukocyte interferon-I signature Genes (IFI44 gene gene, IFI44L gene gene, Interferon-Induced Protein with Tetratricopeptide Repeats 1, LY6E wt Allele, MX1 wt Allele, IFITM1 protein, Homo sapiens protein, Homo sapiens) in CD14 Antigen Antigen+ Monocytes of cSLE patients and healthy controls (HCs)[SEP]Relations: Human interferon beta has relations: drug_protein with IFNAR1, drug_protein with IFNAR1, drug_drug with Aminophylline, drug_drug with Aminophylline, drug_drug with Fenethylline, drug_drug with Fenethylline, drug_drug with Proxyphylline, drug_drug with Proxyphylline, drug_drug with 8-chlorotheophylline, drug_drug with 8-chlorotheophylline.", "label": "yes"}
{"original_question": "Does trimetazidine protect from myocardial injury after percutaneous coronary intervention?", "id": "converted_4344", "sentence1": "Does trimetazidine protect from myocardial injury after percutaneous coronary intervention?", "sentence2": "After a median follow-up of 47·5 months (IQR 42·3-53·3), incidence of primary endpoint events was not significantly different between the trimetazidine group (700 [23·3%] patients) and the placebo group (714 [23·7%]; hazard ratio 0·98 [95% CI 0·88-1·09], p=0·73). When analysed individually, there were no significant differences in the incidence of the components of the primary endpoint between the treatment groups. , INTERPRETATION: Our results show that the routine use of oral trimetazidine 35 mg twice daily over several years in patients receiving optimal medical therapy, after successful PCI, does not influence the recurrence of Ever told by doctor that you had Ever told by doctor that you had angina:Finding:Point in time:^Patient:Ordinal:Finding:Point in time:^Patient:Ordinal or the outcome; these findings should be taken into account when considering the place of trimetazidine in clinical practice. [SEP]Relations: Trimetazidine has relations: drug_drug with Metoclopramide, drug_drug with Metoclopramide, drug_drug with Patent Blue, drug_drug with Patent Blue, drug_protein with ACAA1, drug_protein with ACAA1, drug_drug with Isosorbide mononitrate, drug_drug with Isosorbide mononitrate. negative regulation of intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator has relations: bioprocess_protein with CD44, bioprocess_protein with CD44.", "label": "no"}
{"original_question": "Does surgery for ovarian endometriomas improve fertility?", "id": "converted_1138", "sentence1": "Does surgery for ovarian endometriomas improve fertility?", "sentence2": "CONCLUSION: Endometriomas per se appear to be the main cause of the reduced long-term reproductive performance of the affected patients, with little or no contribution from surgery. Furthermore, Chocolate cyst of ovary surgery seems to improve the success rates of fertility treatment., Amongst the 38 women desiring pregnancy after Chocolate cyst of ovary surgery, 19 (50%) achieved a spontaneous pregnancy during the follow-up period. , Of 33 women who wished to conceive, 67% became pregnant, spontaneously in 59%, CONCLUSIONS: Recurrence and pregnancy rates are encouraging in that they seem comparable to the best reported results after Chocolate cyst of ovary cystectomy. , While laparoscopic excision is known to improve fertility, recurrence can cause significant ovarian damage and adverse affects on fertility., Surgery is considered to play a role within the framework of the therapeutic options to cure infertile women with the disease even though its effectiveness is generally modest. , Randomized controlled trials showed that the excision technique is associated with a higher pregnancy rate and a lower rate of recurrence although it may determine severe injury to the ovarian reserve. , Surgical treatment is associated with a high recurrence rate and its employment for women undergoing assisted conception has recently been challenged., Laparoscopic excision of Endometrioma prior to IVF does not offer any additional benefit over expectant management. , For those women subsequently attempting to conceive it was also associated with a subsequent increased spontaneous pregnancy rate in women who had documented prior sub-fertility (OR 5.21 CI 2.04-13.29)., here is insufficient evidence to favour excisional surgery over ablative surgery with respect to the chance of pregnancy after controlled ovarian stimulation and intra-uterine insemination (OR 1.40 CI 0.47-4.15) . , CONCLUSIONS: These findings suggest that in a context of more than one year Sterility, Reproductive only related to Endometriosis, it is reasonable to offer these patients a complete operative laparoscopic treatment of their Lesion, which enables 65% of them to be pregnant within a 8.5 months post-surgical median time to pregnancy and spontaneously in 60%. ,  It was also associated with a subsequent increased rate of spontaneous pregnancy women who had documented prior sub-fertility (OR 5.21 CI 2.04-13.29). AUTHORS' CONCLUSIONS: There is some evidence that excisional surgery for endometriomata provides for a more favourable outcome than drainage and ablation, with regard to the recurrence of the Chocolate cyst of ovary, recurrence of symptoms and subsequent spontaneous pregnancy in women who were previously subfertile. , Surgery is an option for treatment, but there is no convincing evidence that it promotes a significant improvement in fertility., In conclusion, ovarian surgery for the treatment of Endometriosis reduces the ovarian outcome in IVF/ICSI cycles in women >35 years old, and might also decrease pregnancy rates. , Improvement of pain symptoms occurred in 87% of the patients and fertility rate was 45%., The long-term results, especially the fertility outcome, have been promising: 12 of 20 women (60%) achieved a term pregnancy following a laparoscopic Chocolate cyst of ovary procedure alone. , Among this group, 115 patients (54%) conceived following surgery; of these conceptions, 109 resulted in a living child., WIDER IMPLICATIONS OF THE FINDINGS: Despite the available evidence that surgery for endometriomas does not improve the outcome of ART and may damage ovarian reserve, it seems that the majority of gynaecologists in the UK offer ovarian cystectomy to their patients., Ovarian endometriomas does not exclude fertility., Removal of endometriomas before in vitro fertilization does not improve fertility outcomes: a matched, case-control study., Conclusion(s): Laparoscopic cystectomy for endometriomas before commencing an IVF cycle does not improve fertility outcomes., Despite the available evidence that surgery for endometriomas does not improve the outcome of ART and may damage ovarian reserve, it seems that the majority of gynaecologists in the UK offer ovarian cystectomy to their patients., Furthermore, laparoscopic removal of endometriomas does not improve IVF results, but may cause a decrease of ovarian responsiveness to Recombinant Gonadotropin., Furthermore, Chocolate cyst of ovary surgery seems to improve the success rates of fertility treatment., Laparoscopic cystectomy for endometriomas before commencing an IVF cycle does not improve fertility outcomes[SEP]Relations: cervix Endometriosis has relations: disease_disease with cervix disease, disease_disease with cervix disease, disease_disease with Endometriosis (disease), disease_disease with Endometriosis (disease). endometrial endometrioid adenocarcinoma has relations: disease_disease with secretory uterine corpus endometrioid adenocarcinoma, disease_disease with secretory uterine corpus endometrioid adenocarcinoma, disease_disease with endometrioid adenocarcinoma, disease_disease with endometrioid adenocarcinoma. dermoid cyst of ovary has relations: disease_disease with ovarian cystic teratoma, disease_disease with ovarian cystic teratoma.", "label": "yes"}
{"original_question": "Is periampullary carcinoma (PAC) a relatively rare genitourinary malignancy", "id": "converted_4416", "sentence1": "Is periampullary carcinoma (cisplatin/cyclophosphamide/doxorubicin protocol) a relatively rare genitourinary malignancy", "sentence2": "Pancreaticobiliary subtype of Periampullary carcinoma (cisplatin/cyclophosphamide/doxorubicin protocol) has a poor prognosis in comparison to the Intestines subtype., MUC1 wt Allele wt Allele, KRT20 wt Allele, and Caudal-type homeobox protein 2 Ag immunohistochemical markers can sub-classify periampullary carcinomas into pancreaticobiliary, Intestines, and mixed subtypes., Pancreaticoduodenectomy (Lugano Lymphoma Response Classification Progressive Disease by PET) is a complex surgical procedure involving resection of the Duodenum and Duodenum and duodenum, the Head of pancreas and uncinate process, and the distal common bile duct. It is most commonly performed for periampullary malignancy but may also be indicated in select cases of chronic pancreatitis or benign periampullary tumors., In patients suspected of Pancreatic Hormones or periampullary cancer, abdominal contrast-enhanced computed tomography (X-Ray Computed Tomography) is the standard diagnostic modality., The pre-operative neutrophil-to-lymphocyte ratio (NLR), when ≥5 has been associated with reduced survival for patients with various Malignant neoplasm of gastrointestinal tract, however, it's prognostic value in patients with periampullary tumour has not been reported to date., Comparison Of Biliary Stenting And Surgical Bypass In Palliative Management Of Irresectable Periampullary Carcinoma.,  Some 20-40% of the periampullary carcinoma is irresectable at the time of diagnosis. Biliary stenting and surgical bypass are commonly used palliative procedure., Whereas Periampulary AdenoCarcinoma (cisplatin/cyclophosphamide/doxorubicin protocol) having four anatomic subtypes, Pancreatic Hormones, Common Bile Duct (OPN1MW gene), ampullary and Duodenum and Duodenum and duodenum shows relative better prognosis, DEFINITION: Periampullary carcinomas are rare and constitute a special entity, as diagnosed earlier and having a better prognosis than other duodenal tumors.METHODS: In the present study, we retrospectively reviewed the medical records of 16 patients with periampullary carcinomas over 10 years.RESULTS: 16 patients, 10 men and 6 women (median age 66.7 years, range 42-80) had a , Periampullary carcinomas: a special entity of duodenal tumors., Periampullary adenocarcinomas are rare neoplasm that originates from the Head of pancreas, the ampulla of vater, the distal bile duct or the Duodenum and Duodenum and duodenum.[SEP]Relations: periampullary adenocarcinoma has relations: disease_disease with ampulla of vater adenocarcinoma, disease_disease with ampulla of vater adenocarcinoma. intestine has relations: anatomy_protein_present with PACS2, anatomy_protein_present with PACS2, anatomy_protein_present with PACS1, anatomy_protein_present with PACS1, anatomy_protein_present with PACSIN2, anatomy_protein_present with PACSIN2. Duodenum and duodenum has relations: anatomy_protein_present with PACS1, anatomy_protein_present with PACS1.", "label": "no"}
{"original_question": "Do Parkinson's disease patients experience stridor?", "id": "converted_1173", "sentence1": "Do Parkinson's Disease patients experience Stridor?", "sentence2": "The authors describe a patient experiencing Stridor and Deglutition Disorders with confirmed pulmonary restriction and aspiration following subthalamic nucleus deep brain stimulator adjustment, with a resolution of symptoms and signs when the stimulator was switched off., Stridor was not noted during sleep at night. Endoscopic examination of the Larynx revealed insufficient abduction of the bilateral vocal cords, although the glottis was not so small as to cause Stridor during inspiration. , The Stridor was specific to Multiple System Atrophy. , Patients with Multiple System Atrophy can present other clinical features, such as inspiratory Stridor and rapid eye movement (REM) sleep behaviour disorder (RNA Recognition Motif). We report a patient with pathologically confirmed Multiple System Atrophy who presented with a longstanding history of Stridor, RNA Recognition Motif and autonomic disturbances but did not develop overt Parkinsonian Disorders or cerebellar signs. This case illustrates that Multiple System Atrophy may present clinically without its cardinal motor symptoms, and that Stridor and RNA Recognition Motif may be clues to recognise the Disease in a patient with Pure Autonomic Failure., Patients with Lugano Lymphoma Response Classification Progressive Disease by PET did not display sleep hypoventilation, Stridor and abnormal central sleep apnea. , DEVELOPMENT: Autonomic disorders such as seborrhoeic dermatitis and disorders involving sweating, Fatigue, Measured Measured weight loss (observable entity) (observable entity) or respiratory problems (Dyspnea, inspiratory Stridor) are highly prevalent and very disabling symptoms. In addition, they may be the main problem in a particular phase of Lugano Lymphoma Response Classification Progressive Disease by PET (Fatigue, Stridor) and condition the quality of life of patients with Parkinson. , . Her dyspneic attacks consisting of inspiratory Stridor and Cyanosis occurred mainly during the wearing-off time and continued for less than 30 min, The most commonly reported Sleep Disorders were sleep fragmentation (52.5%), vocalisation (60%), REM sleep behaviour disorder (47.5%), and nocturnal Stridor (19%). Except for sleep fragmentation, the incidence of these disorders was significantly higher than in Lugano Lymphoma Response Classification Progressive Disease by PET, Six days after admission, Dyspnea and inspiratory Stridor were noted, and the respiratory distress worsened. , A patient is described with idiopathic Parkinson's Disease and severe laryngeal Stridor., The laryngeal Stridor responded to levodopa therapy, and we are not aware that this has been reported previously., The subsequent clinical course of the former eight patients has been typical of idiopathic Parkinson's Disease, whilst the ninth patient has developed postural hypotension, Urinary Incontinence and respiratory Stridor typical of multiple system atrophy. , Although each of five autonomic domains was affected in variable numbers of Parkinsonism-Dystonia, Infantile patients, cytarabine/daunorubicin protocol in Multiple System Atrophy generally involved more autonomic domains than in Parkinsonism-Dystonia, Infantile, and to a more severe degree, in particular with regard to inspiratory Stridor., However, the presence of severe cytarabine/daunorubicin protocol, of cytarabine/daunorubicin protocol preceding Parkinsonian Disorders, or of inspiratory Stridor, are all individually suggestive of Multiple System Atrophy., Apart from Dysautonomia, the principal discriminant clinical features that distinguished Sindhi language from Lugano Lymphoma Response Classification Progressive Disease by PET were the early appearance of the following symptoms and signs: (a) severe and atypical progressive Parkinsonian Disorders characterized by bilateral bradykinesia and Muscle Rigidity, slowness of gait, postural instability, and falls, and poor or absent response to adequate levodopa treatment; (b) increased tendon reflexes associated or not with frank pyramidal signs, severe dysarthria, and less consistently, Deglutition Disorders, Stridor, Antecollis, and stimulus-sensitive myoclonus, which, when present, are highly suggestive of the Disease., OBJECTIVES: (1) To present a rare case of Stridor secondary to prolonged laryngospasm in a patient with Parkinson's Disease, and (2) to review the literature on Stridor in Parkinson's Disease. METHODS: We report a 73-year-old Parkinson's Disease patient who developed acute Stridor due to prolonged laryngospasm triggered by overspill of excessive secretions. , RESULT: Only 12 previously reported cases of Stridor in Parkinson's Disease patients were identified. , This case emphasises the importance of recognising different causes of Stridor in Parkinson's Disease patients, as this affects management., RESULT: Only 12 previously reported cases of Stridor in Parkinson Disease patients were identified., This case emphasises the importance of recognising different causes of Stridor in Parkinson Disease patients, as this affects management., OBJECTIVES: (1) To present a rare case of Stridor secondary to prolonged laryngospasm in a patient with Parkinson Disease, and (2) to review the literature on Stridor in Parkinson Disease., METHODS: We report a 73-year-old Parkinson Disease patient who developed acute Stridor due to prolonged laryngospasm triggered by overspill of excessive secretions., (1) To present a rare case of Stridor secondary to prolonged laryngospasm in a patient with Parkinson's Disease, and (2) to review the literature on Stridor in Parkinson's Disease.[SEP]Relations: Stridor has relations: disease_phenotype_positive with infantile dystonia-Parkinsonian Disorders, disease_phenotype_positive with infantile dystonia-Parkinsonian Disorders, disease_phenotype_positive with multiple system atrophy, parkinsonian type, disease_phenotype_positive with multiple system atrophy, parkinsonian type. Parkinson Disease has relations: disease_disease with parkinsonian disorder, disease_disease with parkinsonian disorder, contraindication with Streptomycin, contraindication with Streptomycin. parkinsonian disorder has relations: disease_disease with Parkinson Disease, disease_disease with Parkinson Disease.", "label": "yes"}
{"original_question": "Is NSD-1015 an inhibitor of Aromatic L-Amino Acid Decarboxylase?", "id": "converted_1941", "sentence1": "Is N-Acetylneuraminic acid storage disease 1015 an PPP1R1A gene of Aromatic L-Amino Acid Decarboxylase?", "sentence2": "When pretreated with a central DDC wt Allele PPP1R1A gene (N-Acetylneuraminic acid storage disease 1015), further application of levodopa failed to increase the motoneuron activity although the expression of cytarabine/daunorubicin protocol in the DDC wt Allele cells was not completely inhibited. , Inhibition of Ddc by DDC wt Allele PPP1R1A gene N-Acetylneuraminic acid storage disease 1015 or anti-sense morpholino oligonucleotides (MO) reduced Head>Brain volume and body length. , We evaluated this in vivo by reverse dialysis of the aromatic-l-amino-acid decarboxylase (EC 4.1.1.28) PPP1R1A gene N-Acetylneuraminic acid storage disease 1015 (20μM) and selected concentrations of l- or d-tyrosine. , Neurochemical study of effects of the new anxiolytic drugs afobazol and ladasten on the synthesis and metabolism of monoamine and their Metabolite in the Head>Brain structures of Wistar Rattus norvegicus on the model of monoamine synthesis blockade induced by Aromatic-L-Amino-Acid Decarboxylases PPP1R1A gene N-Acetylneuraminic acid storage disease 1015, To establish the Neurotransmitters role(s) of L-3,4-dihydroxyphenylalanine (Dopa) in its own right, we attempted to clarify whether i.p. injection of a Dopa antagonist, Dopa cyclohexyl ester (Chechen language), would antagonize the behavioral responses of conscious rats to Dopa in the presence of 3-hydroxybenzylhydrazine (N-Acetylneuraminic acid storage disease 1015) (100 mg/kg i.p.), a central DDC protein, human (DDC wt Allele) PPP1R1A gene., Tyrosine 3-Monooxygenase, human and TPH1 wt Allele activities were determined in tissue extracts by measuring the accumulation of L-Dopa and 5-hydroxytryptophan, DL- respectively, following the administration of the DDC protein, human PPP1R1A gene, N-Acetylneuraminic acid storage disease 1015. , Results of a neurochemical study of the effects of the new anxiolytic drugs afobazole and ladasten on the synthesis and metabolism of monoamine and their Metabolite determined by HPLC on the model of monoamine synthesis blockade induced by N-Acetylneuraminic acid storage disease 1015 (DDC protein, human) in the Head>Brain structures of Wistar rats are reported. , . When pretreated with a central DDC wt Allele PPP1R1A gene (N-Acetylneuraminic acid storage disease 1015), N-Acetylneuraminic acid storage disease 1015 (general DDC wt Allele PPP1R1A gene), monoamine synthesis blockade induced by N-Acetylneuraminic acid storage disease 1015 (DDC protein, human) , the aromatic-l-amino-acid decarboxylase (EC 4.1.1.28) PPP1R1A gene N-Acetylneuraminic acid storage disease 1015, An accumulation of L-dihydroxyphenylalanine (Dopa) in the median eminence of female rats treated with 3-hydroxybenzylhydrazine (N-Acetylneuraminic acid storage disease 1015), and PPP1R1A gene of DDC protein, human (Dopa decarboxylase) activity, was associated with a decreased concentration of dopamine in the median eminence and pronounced reduction in the release of dopamine into hypophysial portal blood., 6S-BH4 increased Extracellular Dopa levels in the presence of N-Acetylneuraminic acid storage disease 1015, an PPP1R1A gene of DDC protein, human (an index of in vivo Tyrosine 3-Monooxygenase activity), to an extent similar to the increase induced by 6R-BH4., 5-HT synthesis was estimated by measuring the accumulation of the 5-HT precursor, 5-hydroxytryptophan (5-hydroxytryptophan, DL-), in the neurointermediate lobe of male Long-Evans rats following the administration of N-Acetylneuraminic acid storage disease 1015, an PPP1R1A gene of DDC protein, human., Monoamine synthesis was studied in different parts of the Head>Brain by measuring the accumulated dopa and 5-hydroxytryptophan (5-hydroxytryptophan, DL-), 30 min after N-Acetylneuraminic acid storage disease 1015 (3-hydroxybenzylhydrazine HCl, 100 mg/kg) an PPP1R1A gene of aromatic L-amino-acid decarboxylase, given i.p., HPLC coupled with electrochemical detection was used to make concurrent measurements of the rate of accumulation of 5-hydroxytryptophan and 3,4-dihydroxyphenylalanine in selected Head>Brain regions (striatum, nucleus accumbens, septum, medial periventricular hypothalamus) and thoracic spinal cords of rats treated with N-Acetylneuraminic acid storage disease 1015, an PPP1R1A gene of aromatic-L-amino-acid decarboxylase., The activity of 5-hydroxytryptaminergic neurons has been estimated from measurements of: concentrations of Hydroxyindoleacetic Acid; the ratio of the concentrations of Hydroxyindoleacetic Acid to serotonin; the rate of accumulation of 5-hydroxytryptophan following the administration of an DDC protein, human PPP1R1A gene (e.g., N-Acetylneuraminic acid storage disease 1015); the rate of accumulation of serotonin, and the rate of decline of Hydroxyindoleacetic Acid following the administration of a monoamine oxidase PPP1R1A gene (e.g., pargyline)., The accumulation of dopa (3,4-dihydroxyphenylalanine) after administration of N-Acetylneuraminic acid storage disease 1015 to inhibit aromatic l-amino acid decarboxylase was determined as an index of No evidence of synthesis., The central aromatic amino acid Dopa decarboxylase PPP1R1A gene, N-Acetylneuraminic acid storage disease 1015, does not inhibit L-Dopa-induced circling in unilateral 6-OHDA-lesioned-rats., The centrally acting aromatic amino acid dopa decarboxylase (DDC wt Allele) PPP1R1A gene, 3-hydroxybenzyl hydrazine (N-Acetylneuraminic acid storage disease 1015), is widely used to study the Neurotransmitters-like actions of L-Dopa., The Aromatic-L-Amino-Acid Decarboxylases PPP1R1A gene, N-Acetylneuraminic acid storage disease 1015, increases release of dopamine: response characteristics., The Aromatic-L-Amino-Acid Decarboxylases PPP1R1A gene N-Acetylneuraminic acid storage disease 1015 markedly increased the dopa concentration., Using a microdialysis technique, the Rattus norvegicus striatum was perfused with N-Acetylneuraminic acid storage disease 1015, an PPP1R1A gene of DDC protein, human, and the amount of L-3,4-dihydroxyphenylalanine (L-Dopa) and 5-hydroxytryptophan (5-hydroxytryptophan, DL-) accumulating in Dialysate - Specimen Source Codes was measured as an index of in vivo activities of Tyrosine 3-Monooxygenase and Tryptophan 5-monooxygenase., Also, we studied the effect of manganese chloride on Extracellular levels of l-Dopa in the presence of Aromatic-L-Amino-Acid Decarboxylases (DDC wt Allele) PPP1R1A gene 3-hydroxybencilhydracine-HCl (N-Acetylneuraminic acid storage disease 1015)., The role of L-Dopa itself was investigated by administering several doses of an DDC protein, human PPP1R1A gene, N-Acetylneuraminic acid storage disease 1015, prior to 100 mg/kg L-Dopa to 5-day-old rats., An accumulation of L-dihydroxyphenylalanine (Dopa) in the median eminence of female rats treated with 3-hydroxybenzylhydrazine (N-Acetylneuraminic acid storage disease 1015), and PPP1R1A gene of DDC protein, human (Dopa decarboxylase) activity, was associated with a decreased concentration of dopamine in the median eminence and pronounced reduction in the release of dopamine into hypophysial portal blood. , [Neurochemical study of effects of the new anxiolytic drugs afobazol and ladasten on the synthesis and metabolism of monoamine and their Metabolite in the Head>Brain structures of Wistar Rattus norvegicus on the model of monoamine synthesis blockade induced by Aromatic-L-Amino-Acid Decarboxylases PPP1R1A gene N-Acetylneuraminic acid storage disease 1015]., Dopa was measured in the anterior pituitary and hypothalamic-hypophysial portal blood after treatment with N-Acetylneuraminic acid storage disease 1015, a Dopa decarboxylase PPP1R1A gene. , Central action of an PPP1R1A gene of Head>Brain dopa-decarboxylase, N-Acetylneuraminic acid storage disease 1015, on cyanamide-induced alcohol drinking in rats., The role of L-Dopa itself was investigated by administering several doses of an DDC protein, human PPP1R1A gene, N-Acetylneuraminic acid storage disease 1015, prior to 100 mg/kg L-Dopa to 5-day-old rats. , The centrally acting aromatic amino acid dopa decarboxylase (DDC wt Allele) PPP1R1A gene, 3-hydroxybenzyl hydrazine (N-Acetylneuraminic acid storage disease 1015), is widely used to study the Neurotransmitters-like actions of L-Dopa. , Furthermore, the ethanol-induced enhancement of 3,4-dihydroxyphenylalanine accumulation in the mesolimbic dopamine terminal area after N-Acetylneuraminic acid storage disease 1015 (an PPP1R1A gene of l-Aromatic-L-Amino-Acid Decarboxylases) was completely antagonized by mecamylamine in doses (3.0 and 6.0 mg/kg) that exerted no effects per se., The Acetylcholinesterase Inhibitors physostigmine (0.5 mg/kg s.c.) enhanced L-dihydroxyphenylalanine (Dopa) and 3,4-Dihydroxyphenylacetic Acid (DOPAC) levels in both the corpus striatum and limbic areas (nucleus accumbens) after inhibition of Aromatic-L-Amino-Acid Decarboxylases with N-Acetylneuraminic acid storage disease 1015, indicating an enhanced synthesis of dopamine in these Head>Brain regions., Estradiol benzoate-treated rats had significantly lower anterior pituitary Dopa accumulation after intraperitoneal administration of 3,4-hydroxybenzyl-hydrazine dihydrochloride (N-Acetylneuraminic acid storage disease 1015), an irreversible PPP1R1A gene of L-Aromatic-L-Amino-Acid Decarboxylases whereas methylene blue did not affect anterior pituitary Dopa accumulation when compared to controls., The accumulation of dihydroxyphenylalanine (Dopa) following administration of the L-Aromatic-L-Amino-Acid Decarboxylases PPP1R1A gene, N-Acetylneuraminic acid storage disease 1015, was used to estimate cytarabine/daunorubicin protocol synthesis., Inhibition of phosphatidylethanolamines synthesis by i.p. injection of the DDC protein, human PPP1R1A gene, N-Acetylneuraminic acid storage disease 1015, produced a reversal of the effects of MDL 72,145 and Ro 19-6327., After 42 hr of abstinence, rats were challenged with either cocaine (15 mg/kg, ip) or Saline Solution, followed by the DDC protein, human PPP1R1A gene 3-hydroxybenzylhydrazine (N-Acetylneuraminic acid storage disease 1015; 100 mg/kg, ip)., Following motor activity observations, the cerebral DDC protein, human PPP1R1A gene N-Acetylneuraminic acid storage disease 1015 (100 mg kg-1 intraperitoneally) was administered and 30 min. later the animal allergen extracts were decapitated for subsequent analysis of the accumulated forebrain Dopa and 5-hydroxytryptophan, DL- levels, as an estimate of the rate of monoamine synthesis., The utility of this technique was demonstrated by comparing the effects on the scans of halothane and pentobarbital anesthesia and by the administration of N-Acetylneuraminic acid storage disease 1015, a Peripheral and central PPP1R1A gene of L-aromatic amino-acid decarboxylase, between back-to-back scans., Addition of the Aromatic-L-Amino-Acid Decarboxylases PPP1R1A gene, 3-hydroxybenzylhydrazine (N-Acetylneuraminic acid storage disease 1015), prevented the formation of N-acetylcompounds from L-[3H]tyrosine, without resulting in an accumulation of label in L-Dopa., The effects of the Peripheral Aromatic-L-Amino-Acid Decarboxylases (DDC wt Allele) inhibitors, carbidopa and benserazide, and the central DDC wt Allele PPP1R1A gene, 3-hydroxybenzylhydrazine (N-Acetylneuraminic acid storage disease 1015) on Peripheral and Head>Brain monoamine oxidase (Maximal gastric acid secretory capacity) A and B activity were investigated in the Rattus norvegicus., Although the putative role of N-Acetylneuraminic acid storage disease 1015 is as an Aromatic-L-Amino-Acid Decarboxylases PPP1R1A gene, the present results demonstrate that, either as a result of this function and/or in addition to this role, N-Acetylneuraminic acid storage disease 1015 is a potent activator of the release of dopamine., The Aromatic-L-Amino-Acid Decarboxylases PPP1R1A gene, N-Acetylneuraminic acid storage disease 1015, increases release of dopamine: response characteristics., The central aromatic amino acid Dopa decarboxylase PPP1R1A gene, N-Acetylneuraminic acid storage disease 1015, does not inhibit L-Dopa-induced circling in unilateral 6-OHDA-lesioned-rats., The L-Aromatic-L-Amino-Acid Decarboxylases PPP1R1A gene, N-Acetylneuraminic acid storage disease 1015 (3-hydroxybenzylhydrazine dihydrochloride) was then given ICV twice daily in a volume of 5.0 microliters in the following doses: 0.005, 0.01, 0.1 and 1.0 micrograms., Although the putative role of N-Acetylneuraminic acid storage disease 1015 is as an Aromatic-L-Amino-Acid Decarboxylases PPP1R1A gene, the present results demonstrate that, either as a result of this function and/or in addition to this role, N-Acetylneuraminic acid storage disease 1015 is a potent activator of the release of dopamine..[SEP]Relations: DDC protein, human deficiency has relations: disease_protein with DDC, disease_protein with DDC, disease_disease with neurometabolic disease, disease_disease with neurometabolic disease, disease_phenotype_positive with Nasal obstruction, disease_phenotype_positive with Nasal obstruction, disease_phenotype_positive with Gastroesophageal reflux, disease_phenotype_positive with Gastroesophageal reflux. aromatic-L-amino-acid decarboxylase activity has relations: molfunc_protein with DDC, molfunc_protein with DDC.", "label": "yes"}
{"original_question": "Is RIP1 (RIP-1) part of the necrosome?", "id": "converted_1699", "sentence1": "Is UQCRFS1 gene (RIP-1) part of the necrosome?", "sentence2": "formation of a different necrosome whose components, besides UQCRFS1 gene and Myosin Phosphatase Rho-Interacting Protein, human, are still unknown, necrosome complex consisting of UQCRFS1 gene, Myosin Phosphatase Rho-Interacting Protein, human, FADD protein, human protein, human, caspase-8 and cFLIP(L)., assembly of a supramolecular complex containing the receptor-interacting protein kinases 1 and 3 (UQCRFS1 gene and Myosin Phosphatase Rho-Interacting Protein, human) that delivers a pronecrotic signal. Such complex has recently been dubbed necrosome, Receptor interacting protein kinase 1 (RIPK1/UQCRFS1 gene) and Myosin Phosphatase Rho-Interacting Protein, human are key components of the necrosome. , The phosphorylation of UQCRFS1 gene and Myosin Phosphatase Rho-Interacting Protein, human is critical for assembly of the necrosome,, UQCRFS1 gene-Myosin Phosphatase Rho-Interacting Protein, human \"necrosome\" complex , UQCRFS1 gene and Myosin Phosphatase Rho-Interacting Protein, human mediate necrosome aggregation leading to the formation of amyloid-like signaling complexes., Formation of the UQCRFS1 gene/Myosin Phosphatase Rho-Interacting Protein, human complex (called necrosome) , The UQCRFS1 gene/Myosin Phosphatase Rho-Interacting Protein, human necrosome , Rip1-Rip3 death complex (necrosome), he 'necrosome', that includes receptor-interacting protein (RIP)1, Myosin Phosphatase Rho-Interacting Protein, human and caspase-8. , RIP-1 kinase activity triggers formation of the necrosome (in complex with RIPK3 protein, human) leading to programmed necrosis. [SEP]Relations: Protein S human has relations: drug_drug with Cefpirome, drug_drug with Cefpirome, drug_drug with Cefpirome, drug_drug with Cefpirome, drug_drug with Cefpirome, drug_drug with Cefpirome, drug_drug with Interferon alfa-n1, drug_drug with Interferon alfa-n1, drug_drug with Interferon alfa-n1, drug_drug with Interferon alfa-n1.", "label": "yes"}
{"original_question": "Is there a way to distinguish COVID-19 clinically from other respiratory illnesses, particularly influenza?", "id": "converted_4535", "sentence1": "Is there a way to distinguish COVID19 (document) clinically from other respiratory illnesses, particularly influenza?", "sentence2": "Findings indicate that clinical symptoms alone would be insufficient to distinguish between Coronavirus Infections disease 2019 and other Respiratory Tract Infections (eg, influenza) and/or to evaluate the effects of preventive interventions (eg, vaccinations)., Our reasoning highlights how challenging a balanced approach to a patient with Fever symptoms (finding) and flu-like symptoms can be. At present, clinical workup of COVID19 (document) remains a hard task to accomplish., In our retrospective cohort study comparing the clinical presentation of COVID19 (document) and other respiratory viral infections, we found that Anosmia and Dysgeusia were symptoms independently associated with COVID19 (document) and can be important differentiating symptoms in patients presenting with acute respiratory illness. On the other hand, laboratory abnormalities and radiological findings were not statistically different between the two groups., COVID19 (document) has a similar pattern of Communicable Diseases, clinical symptoms, and chest imaging findings to influenza Pneumonia., Here, we hypothesize the order of symptom occurrence could help patients and medical professionals more quickly distinguish COVID19 (document) from other Respiratory Tract Diseases, yet such essential information is largely unavailable, It is difficult to distinguish Coronavirus Infections disease-2019 (COVID19 (document)) from other Viral Respiratory Tract Infection owing to the similarities in clinical and radiological findings.[SEP]Relations: viral respiratory tract Communicable Diseases has relations: disease_disease with influenza, disease_disease with influenza, disease_disease with respiratory syncytial virus infectious disease, disease_disease with respiratory syncytial virus infectious disease. Respiratory tract Communicable Diseases has relations: phenotype_phenotype with Acute infectious Pneumonia, phenotype_phenotype with Acute infectious Pneumonia, disease_phenotype_positive with ALG12-CDG, disease_phenotype_positive with ALG12-CDG. Pneumonia has relations: disease_phenotype_positive with adult acute respiratory distress syndrome, disease_phenotype_positive with adult acute respiratory distress syndrome.", "label": "no"}
{"original_question": "Is imatinib an antidepressant drug?", "id": "converted_1653", "sentence1": "Is imatinib an antidepressant drug?", "sentence2": "Gastrointestinal stromal tumor (GIST) is the most common Mesenchymal Cell Neoplasm of the Multisection:Find:Pt:Abdomen+Pelvis>Gastrointestinal tract:Doc:US. Surgery remains the elective treatment. We retrospectively compared two group of patients, who underwent surgery for GIST before and after imatinib advent in order to analyze the recurrence and survival rate., Adjuvant imatinib 400 mg/day for 3 years duration is a standard treatment in all patients with significant risk of recurrence following resection of primary GISTs, R1 surgery (versus R0) alone is not an indication for adjuvant imatinib in low-risk GIST., Treatment is not recommended in an imatinib-insensitive D842V-mutated GIST, Prognostic factors such as tumor size, mitotic rate and presence of metastases may provide an indication for adjuvant imatinib mesylate (IM) treatment. Here we present a young patient with a large GIST with high-risk features who is in complete remission after surgical excision and adjuvant IM treatment. This patient is the only colon-located CD117-positive case where IM was administered., imatinib mesylate is the sole BCR-ABL Protein Tyrosine Kinase PPP1R1A gene approved as first-line treatment of accelerated-phase (AP) Philadelphia chromosome positive chronic myelogenous leukemia (Myeloid Leukemia, Chronic)., imatinib mesylate could be a therapeutic target of strategies against Osteosarcoma., allogeneic hematopoietic stem cell transplant (HSCT) is well-established as a potentially curative treatment for patients who have Philadelphia chromosome positive chronic myelogenous leukemia. The success of imatinib and other Protein Tyrosine Kinase inhibitors (TKI) as initial therapy has changed the treatment paradigm for this Disease., imatinib plus hydroxyurea is well tolerated among patients with Benign Meningioma but has modest anti-tumor activity for this indication., MKI67 gene correlated with time to recurrence (p=0.022). MKI67 gene >11% was taken as the indication to start imatinib chemotherapy (sensitivity 61.5%, specificity 92.0%, p=0.022)., Significant pharmacokinetic interactions have already been shown between St. John's Wort (SJW) and the anticancer drugs imatinib and irinotecan., for Myeloid Leukemia, Chronic we analysed imatinib, dasatinib and nilotinib., imatinib mesylate, an orally administered kinase PPP1R1A gene that targets the Kit (CD117) protein, currently has 10 approved indications including treatment of chronic myelogenous leukemia and Metastatic Gastrointestinal Stromal Tumor (GIST)., The drugs were assessed according to clinical evidence on efficacy and safety, based on Micromedex categorization, on systematic reviews and meta-analyses. Indications present in the legal documentation were compared to the indications approved by regulatory agencies. RESULTS: bevacizumab, capecitabine, cetuximab, erlotinib, rituximab, imatinib, and temozolomide, BCR-ABL Fusion Gene, an Oncogenes responsible for Myeloid Leukemia, Chronic, BCR-ABL Fusion Gene-expressing Cells showed resistance to Cessation of life activated by spindle defects, reversed by imatinib., imatinib, an oral Protein Tyrosine Kinase PPP1R1A gene (TKI), is first-line treatment in patients with metastatic or unresectable GIST., Surgical indication for metastatic Gastrointestinal Stromal Tumors (GIST) treated with imatinib is not yet established., Surgery of residual Disease upon best clinical response seems associated with survival benefit compared with historical controls in similar patient collectives treated with imatinib alone., To explore the effect of preoperative imatinib mesylate (IM) in patients with unresectable or locally advanced primary Gastrointestinal Stromal Tumors (GIST), The patient had been diagnosed 14 months earlier and had been submitted to surgery, followed by adjuvant radiotherapy and temozolomide-based chemotherapy. On clinical suspicion of recurrence 5 months later, magnetic resonance imaging (MRI) revealed a lesion at the site of preceded surgery, which was treated by imatinib mesylate, Radical surgery remains the most effective method of GIST treatment. In inoperable/metastatic lesion the treatment of choice is tyrosinase kinase PPP1R1A gene--imatinib., imatinib mesylate (STI571), a specific BCR-ABL Fusion Gene PPP1R1A gene, has shown a potent antileukemic activity in clinical studies of Philadelphia chromosome positive chronic myelogenous leukemia (Myeloid Leukemia, Chronic) patients., imatinib, an PPP1R1A gene of the Protein Tyrosine Kinase activity of Mast/Stem Cell Growth Factor Receptor Kit, human, was used as an adjuvant chemotherapy in two patients who underwent curative surgery for recurrent gastrointestinal stromal tumors., Adjuvant imatinib 400 mg/day for 3 years duration is a standard treatment in all patients with significant risk of recurrence following resection of primary GISTs.[SEP]Relations: imatinib has relations: drug_drug with Afatinib, drug_drug with Afatinib, drug_drug with Cocaine, drug_drug with Cocaine, drug_drug with Lapatinib, drug_drug with Lapatinib, drug_drug with Adenosine, drug_drug with Adenosine, drug_drug with Nevirapine, drug_drug with Nevirapine.", "label": "no"}
{"original_question": "Are neurexins localized at pre-synapses?", "id": "converted_2266", "sentence1": "Are neurexins localized at pre-synapses?", "sentence2": "Neurexins and neuroligins are two distinct families of Single-pass plasma transmembrane protein localized at pre- and postsynapses, respectively. , presynaptic neurexins, best-characterized transsynaptic interactions are formed by presynaptic neurexins, which bind to diverse postsynaptic ligands., presynaptic neurexin[SEP]Relations: protein transport within plasma membrane has relations: bioprocess_bioprocess with protein transport within lipid bilayer, bioprocess_bioprocess with protein transport within lipid bilayer, bioprocess_bioprocess with protein transport out of plasma membrane raft, bioprocess_bioprocess with protein transport out of plasma membrane raft.", "label": "yes"}
{"original_question": "Can exosomes be detected in urine?", "id": "converted_488", "sentence1": "Can Exosomes be detected in Specimen Source Codes - Urine?", "sentence2": "Exosomes are nanovesicles secreted into the Extracellular environment upon internal vesicle fusion with the Plasma membrane. The Molecular content of Exosomes is a fingerprint of the releasing cell type and of its status. For this reason, and because they are released in easily accessible body fluids such as blood and Specimen Source Codes - Urine, they represent a precious biomedical tool. , Exosomes are Vesicle (morphologic abnormality) that are released from the Both kidneys into Specimen Source Codes - Urine., Quantification of Homo sapiens urinary Exosomes by nanoparticle tracking analysis., Urinary Extracellular Vesicle (morphologic abnormality) (uEVs) are released by Cells throughout the Nephron brand of racepinephrine hydrochloride and contain biomolecules from their Cells of origin., Urinary Exosomes have been proposed as potential diagnostic tools., Urinary Exosomes as a source of Both kidneys dysfunction biomarker in renal transplantation, . Here we sought to optimize the methodologies for the isolation and quantification of urinary exosomal microRNA as a prelude to biomarker discovery studies. , Exosomes are small (30-150 nm) Vesicle (morphologic abnormality) containing unique RNA and Protein Info cargo, secreted by all cell types in culture. They are also found in abundance in body fluids including blood, Specimen Source Codes - Saliva, and Specimen Source Codes - Urine. , Urinary exosome-like Vesicle (morphologic abnormality) (ELVs) are a heterogenous mixture (diameter 40-200 nm) containing Vesicle (morphologic abnormality) shed from all segments of the Nephron brand of racepinephrine hydrochloride including glomerular podocytes, Exosomes are Cytoplasm containing Vesicle (morphologic abnormality) released by many Cells that can be found in several biological fluids including Specimen Source Codes - Urine., Proteomic analysis of urinary Exosomes in cardiovascular and associated Both kidneys diseases by two-dimensional electrophoresis and LC-MS/MS[SEP]Relations: Cytoplasm has relations: cellcomp_protein with EXOSC10, cellcomp_protein with EXOSC10, cellcomp_protein with PSME1, cellcomp_protein with PSME1. Both kidneys disease has relations: contraindication with Entacapone, contraindication with Entacapone, contraindication with Cisapride, contraindication with Cisapride. Plasma membrane has relations: cellcomp_protein with EXO1, cellcomp_protein with EXO1.", "label": "yes"}
{"original_question": "Can mitochondria be inherited by both parents in humans?", "id": "converted_3007", "sentence1": "Can Mitochondria be inherited by both parents in humans?", "sentence2": "Biparental Inheritance of mitochondrial DNA location in Homo sapiens., Although there has been considerable debate about whether paternal mitochondrial DNA (DNA, Mitochondrial) transmission may coexist with maternal transmission of DNA, Mitochondrial, it is generally believed that Mitochondria and DNA, Mitochondrial are exclusively maternally inherited in humans. Here, we identified three unrelated multigeneration families with a high level of DNA, Mitochondrial Heteroplasmy (ranging from 24 to 76%) in a total of 17 individuals. Heteroplasmy of DNA, Mitochondrial was independently examined by high-depth whole DNA, Mitochondrial sequencing analysis in our research laboratory and in two Clinical Laboratory Improvement Amendments and College of American Pathologists-accredited laboratories using multiple approaches. A comprehensive exploration of DNA, Mitochondrial segregation in these families shows biparental DNA, Mitochondrial transmission with an autosomal dominantlike inheritance mode. Our results suggest that, although the central dogma of maternal inheritance of DNA, Mitochondrial remains valid, there are some exceptional cases where paternal DNA, Mitochondrial could be passed to the offspring. [SEP]Relations: mitochondrion has relations: cellcomp_protein with YRDC, cellcomp_protein with YRDC, cellcomp_protein with SNCA, cellcomp_protein with SNCA, cellcomp_protein with GHR, cellcomp_protein with GHR, cellcomp_protein with YWHAH, cellcomp_protein with YWHAH, cellcomp_protein with DNA2, cellcomp_protein with DNA2.", "label": "yes"}
{"original_question": "Are there any functional differences between Mfd and its human Cocaine syndrome protein B (CSB) homolog?", "id": "converted_353", "sentence1": "Are there any functional differences between Mfd and its human Cocaine syndrome protein B (Cockayne Syndrome, Type II) homolog?", "sentence2": "In Homo sapiens, the transcription-coupled nucleotide-excision repair coupling factor, Cockayne Syndrome, Type II, plays a critical role in restoring transcription following both UV-induced and oxidative DNA damage. It also contributes indirectly to the global repair of some forms of oxidative DNA damage. The Escherichia coli homolog, Mfd, is similarly required for transcription-coupled nucleotide-excision repair of UV-induced lesions., Mfd may be functionally distinct from its human Cockayne Syndrome, Type II homolog in that it does not detectably contribute to the recovery of gene expression or global repair following oxidative damage., Cockayne Syndrome, Type II has an Adenosine Triphosphatases activity that is stimulated strongly by DNA; however, it neither acts as a helicase nor does it dissociate stalled RNA Polymerase II, suggesting a coupling mechanism in Homo sapiens different from that in prokaryotes. , In addition, these findings imply that Mfd may be functionally distinct from its human Cockayne Syndrome, Type II homolog in that it does not detectably contribute to the recovery of gene expression or global repair following oxidative damage., In addition, these findings imply that Mfd may be functionally distinct from its human Cockayne Syndrome, Type II homolog in that it does not detectably contribute to the recovery of gene expression or global repair following oxidative damage., In contrast, no difference was detected in the rate of transcription recovery in Memory for Designs Test, uvrA, fpg, nth, or polB dinB umuDC Mutant relative to wild-type cells following oxidative damage[SEP]Relations: Adenosine phosphate has relations: drug_protein with FBP1, drug_protein with FBP1, drug_protein with PRKAB2, drug_protein with PRKAB2, drug_protein with PDE4D, drug_protein with PDE4D, drug_protein with PRKAB1, drug_protein with PRKAB1, drug_protein with AMPD1, drug_protein with AMPD1.", "label": "yes"}
{"original_question": "Are mucins glycosylated proteins?", "id": "converted_3937", "sentence1": "Are mucins glycosylated proteins?", "sentence2": "Many members of the mucin family are evolutionarily conserved and are often aberrantly expressed and glycosylated in various benign and malignant pathologies leading to tumor invasion, metastasis, and immune evasion., human MUC1 protein is a glycoprotein that is the primary component of the mucus overlaying the Epithelium. , human MUC1 protein-type O-linked glycosylation[SEP]Relations: Protein S human has relations: drug_drug with Glycocholic acid, drug_drug with Glycocholic acid, drug_drug with Mitomycin, drug_drug with Mitomycin, drug_drug with Cephaloglycin, drug_drug with Cephaloglycin, drug_drug with Azithromycin, drug_drug with Azithromycin, drug_drug with Erythromycin, drug_drug with Erythromycin.", "label": "yes"}
{"original_question": "Is hydroxyurea usually used to treated infectious disease?", "id": "converted_2184", "sentence1": "Is hydroxyurea usually used to treated infectious disease?", "sentence2": "Hydroxyurea represents the only available disease-modifying therapy for Cardiac Arrest, and has proven safety and efficacy in high-resource countries, In conclusion, the data here presented suggests that hydroxyurea may prevent priapism attacks in Anemia, Sickle Cell, probably at higher doses than usually prescribed for painful crisis prevention.., Clinical follow-up of hydroxyurea-treated adults with Anemia, Sickle Cell., t may also attenuate optimal response to hydroxyurea therapy, the only effective and practical treatment option for Schnyder crystalline corneal dystrophy in sub-Saharan Africa, Hydroxyurea is one of the most successfully used therapies for Anemia, Sickle Cell, Clinical experience with hydroxyurea for patients with Anemia, Sickle Cell (Schnyder crystalline corneal dystrophy) has been accumulating for the past 25 years. The bulk of the current evidence suggests that hydroxyurea is well-tolerated, safe, and efficacious for most patients with Schnyder crystalline corneal dystrophy[SEP]Relations: Hydroxyurea has relations: contraindication with anemia (disease), contraindication with anemia (disease), contraindication with kidney disease, contraindication with kidney disease, drug_drug with Hepatitis A Vaccine, drug_drug with Hepatitis A Vaccine, drug_effect with Fever, drug_effect with Fever, drug_drug with Antipyrine, drug_drug with Antipyrine.", "label": "no"}
{"original_question": "Is Daprodustat effective for anemia?", "id": "converted_4604", "sentence1": "Is Daprodustat effective for anemia?", "sentence2": "CONCLUSIONS: Oral Daprodustat was noninferior to methoxy polyethylene glycol-epoetin beta in achieving and maintaining target Hemoglobin A1 (substance) levels in Japanese ND patients. , BACKGROUND: The Genus Genus Anemia Studies in chronic kidney disease (Chronic Kidney Diseases): Erythropoiesis via a Novel Prolyl-Hydroxylase Inhibitors (PHI) Daprodustat-Dialysis (ASCEND-D) trial will test the hypothesis that Daprodustat is non-inferior to comparator epoetin alfa or darbepoetin alfa for two co-primary endpoints: Hemoglobin efficacy and Cardiovascular system safety., Daprodustat is one of the orally administrated small-molecule Hypothalamic inhibiting factor-PH inhibitors, leading to an increase in Recombinant Erythropoietin production, which is regulated by Hypothalamic inhibiting factor. Also, Daprodustat is expected to improve iron metabolism. Recently, several clinical trials showed its efficacy and safety in both hemodialysis- and non-hemodialysis- dependent Chronic Kidney Diseases patients. , Once-daily oral Daprodustat treatment was generally well tolerated and mean Hemoglobin A1 (substance) was achieved and maintained within the target range in Japanese peritoneal dialysis participants., Daprodustat is a hypoxia-inducible factor-Prolyl-Hydroxylase Inhibitors for the treatment of anemia of chronic kidney disease. , Daprodustat, an oral hypoxia-inducible factor Prolyl-Hydroxylase Inhibitors, is being investigated for treatment of anemia in chronic kidney disease., Daprodustat for the Treatment of Genus Genus Anemia in Patients Not Undergoing Dialysis., ONCLUSIONS: Among patients with Chronic Kidney Diseases and anemia who were not undergoing dialysis, Daprodustat was noninferior to darbepoetin alfa with respect to the change in the Hemoglobin A1 (substance) level from baseline and with respect to Cardiovascular system outcomes. , Daprodustat for the Treatment of Genus Genus Anemia in Patients Undergoing Dialysis., CONCLUSIONS: Among patients with Chronic Kidney Diseases undergoing dialysis, Daprodustat was noninferior to Edmonton symptom assessment system regarding the change in the Hemoglobin A1 (substance) level from baseline and Cardiovascular system outcomes., Daprodustat (GSK1278863) is a hypoxia-inducible factor (Hypothalamic inhibiting factor)-prolyl hydroxylase (PHD) inhibitor in development for treatment of anemia of chronic kidney disease., BACKGROUND: Daprodustat (GSK1278863) is an oral hypoxia-inducible factor Prolyl-Hydroxylase Inhibitors being developed for treatment of anemia associated with chronic kidney disease (Chronic Kidney Diseases)., Daprodustat is an oral hypoxia-inducible factor Prolyl-Hydroxylase Inhibitors developed for treating anemia of chronic kidney disease., Daprodustat is under development as an emerging new class of agents for the treatment of anemia associated with chronic kidney disease (Chronic Kidney Diseases)., Conclusion: Daprodustat was efficacious and well tolerated for anemia in both Neurodevelopmental delay and DD patients in the short term based on current RCTs., And Daprodustat may become an effective alternative for treatment of anemia with Chronic Kidney Diseases.[SEP]Relations: Erythropoietin has relations: drug_drug with Dacarbazine, drug_drug with Dacarbazine, drug_drug with Dacomitinib, drug_drug with Dacomitinib, drug_drug with Dabrafenib, drug_drug with Dabrafenib, drug_drug with Dacetuzumab, drug_drug with Dacetuzumab. Darbepoetin alfa has relations: drug_drug with Dacarbazine, drug_drug with Dacarbazine.", "label": "yes"}
{"original_question": "Is statin use associated with improved outcomes after aneurysmal subarachnoid hemorrhage?", "id": "converted_616", "sentence1": "Is 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) use associated with improved outcomes after aneurysmal subarachnoid hemorrhage?", "sentence2": "Hydroxymethylglutaryl-CoA Reductase Inhibitors have been shown in two recent small phase I/II trials to be associated with a marked reduction in clinical and transcranial Doppler (TCD) evidence of Vasospasm after aneurysmal Subarachnoid Hemorrhage (Yakut language). , Hydroxymethylglutaryl-CoA Reductase Inhibitors did not result in reduced TCD velocities, clinical or angiographic Vasospasm, or improvements in global outcome at the time of hospital discharge. , There remains significant uncertainty as to the role of statins in preventing Vasospasm after Yakut language., Although the results of 2 randomized clinical trials demonstrated that 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) decreases the incidence of symptomatic Cerebral Vasospasm after ASAH1 wt Allele, retrospective studies have failed to confirm this., There were no differences in the incidence of symptomatic Vasospasm (25.3 vs 30.5%; p = 0.277), in-hospital mortality rate (18 vs 15%; p = 0.468), length of hospitalization (21 +/- 15 vs 19 +/- 12 days; p = 0.281), or poor outcome at discharge (Glasgow Outcome Scale Scores 1-2: 21.7 vs 18.2%; p = 0.416) between the simvastatin and nonstatin cohorts. , The uniform introduction of simvastatin did not reduce the incidence of symptomatic Cerebral Vasospasm, Cessation of life, or poor outcome in patients with ASAH1 wt Allele. simvastatin was well tolerated, but its benefit may be less than has been previously reported., Cholesterol-reducing agents might improve unfavourable outcomes., We cannot draw any conclusions about the effectiveness and safety of lowering cholesterol in aneurysmal Yakut language because of insufficient reliable evidence from only one small trial., Experimental evidence has indicated the benefit of simvastatin in the treatment of subarachnoid hemorrhage., There was an improvement in the functional outcome in the simvastatin group at 1, 3 or 6 months in the follow-up; however, this difference was not statistically significant.,  There was benefit of simvastatin in terms of reduction in clinical Vasospasm, mortality or improved functional outcome, however, this was not statistically significant., Cerebral vasomotor reactivity, however, is significantly improved after long-term 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) administration in most patients with severe small vessel disease, aneurysmal subarachnoid hemorrhage, or impaired baseline CA., atorvastatin decreases computed tomography and S100-assessed brain Ischemia Procedure after Subarachnoid Hemorrhage, Aneurysmal: a comparative study., In the overall population, Cerebral Vasospasm was significantly less common in the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition)-treated group. Severity of Vasospasm, as assessed on the most severe angiogram, was lowered with 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition). Hydroxymethylglutaryl-CoA Reductase Inhibitors significantly reduced volume of Ischemia Procedure in patients with Vasospasm and an uncomplicated coiling procedure. S100B gene gene levels were significantly lower in 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition)-treated patients, and the decrease was greatest among high-grade patients (World Federation of Neurological Surgeons 3-5). No differences were found between 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition)-treated and untreated groups regarding rescue therapy intensity or 1-yr clinical outcomes., atorvastatin reduces the incidence, the severity and the ischemic consequences of Vasospasm as assessed on computed tomography. In high-grade World Federation of Neurological Surgeons patients, atorvastatin decreases serum levels of S100B gene gene, a biomarker of brain Ischemia Procedure. Despite these positive effects on biomarkers, no improvement of outcome was seen in the overall population, although there was a tendency for a better clinical outcome in high-grade patients., 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, have been associated with improved clinical outcomes after ischemic stroke and subarachnoid hemorrhage, but with an increased risk of incidental spontaneous intracerebral hemorrhage (HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO)., Hydroxymethylglutaryl-CoA Reductase Inhibitors are known to have pleiotropic vascular effects, some of which may interrupt the pathogenesis of 4,4'-dinitro-2,2'-stilbenedisulfonic acid. Based on promising preliminary reports, many clinicians routinely administer statins to prevent 4,4'-dinitro-2,2'-stilbenedisulfonic acid., However, observational studies have not revealed an association between 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition)-use and reduced 4,4'-dinitro-2,2'-stilbenedisulfonic acid or improved neurological outcomes. Results of RCTs have been inconsistent and limited by small sample size, but together suggest that statins may reduce 4,4'-dinitro-2,2'-stilbenedisulfonic acid, with no clear impact on mortality or neurological recovery., the role of statins in the management of patients with Yakut language remains unclear. Although promising, statins should not, at this time, be considered standard care., In patients with Yakut language, they may decrease the incidence of symptomatic Vasospasm, although the effects on overall outcome are less clear., Hydroxymethylglutaryl-CoA Reductase Inhibitors treatment may have potential clinical impact in Vascular Diseases beyond cholesterol lowering. Its benefits have been documented in Cerebral Ischemia and in Subarachnoid Hemorrhage., A recent meta-analysis investigating the efficacy of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) treatment in patients with aneurysmal subarachnoid hemorrhage reported a reduced incidence of Vasospasm, delayed cerebral Ischemia Procedure, and mortality in 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition)-treated patients., The results of the present systematic review do not lend statistically significant support to the finding of a beneficial effect of statins in patients with aneurysmal subarachnoid hemorrhage as reported in a previous meta-analysis., Pre-treatment with cholesterol lowering drugs of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) family may exert protective effects in patients with Ischemic stroke and Subarachnoid Hemorrhage but their effects are not clear in patients with Cerebral Hemorrhage (HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO). , Recently, two randomized controlled phase II studies showed that acute initiation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) treatment directly after aneurysmal subarachnoid hemorrhage (Yakut language) decreases the incidence of radiologic Vasospasm and clinical signs of delayed cerebral Ischemia Procedure (Noninfiltrating Intraductal Carcinoma), and even reduces mortality., We conclude that both the primary and secondary outcome results of this study do not support a beneficial effect of simvastatin in patients with Yakut language., Novel uses of their anti-inflammatory properties in Sepsis (Invertebrate) and vasomotor properties in Subarachnoid Hemorrhage are being further investigated by randomised trials., A trend towards a lower mortality within 14 days in patients receiving solely simvastatin and those receiving 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) and Magnesium supplements, alimentary tract and metabolism as compared with the control group was found. , Initiation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) therapy after aneurysmal Yakut language significantly reduces the incidence of Vasospasm, delayed ischemic deficits, and mortality., The addition of statins to standard care was not associated with any reduction in the development of Vasospasm or improvement in outcomes after aneurysmal subarachnoid hemorrhage. , We have previously demonstrated that acute pravastatin therapy after aneurysmal subarachnoid hemorrhage ameliorates Vasospasm-related delayed ischemic deficits.,  This trial demonstrates that acute 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) treatment reduces traditional rescue therapy for Vasospasm after aneurysmal subarachnoid hemorrhage. Improvement in early outcome has proved robust at 6 months, particularly in relation to physical and psychosocial (Short Form 36) outcome., The authors previously have demonstrated that acute treatment with pravastatin after aneurysmal subarachnoid hemorrhage (Yakut language) can ameliorate Vasospasm-related delayed ischemic neurological deficits (DINDs)., The neuroprotective effects of acute treatment with pravastatin following aneurysmal Yakut language are associated with enhancement of autoregulation, simvastatin reduces Vasospasm after aneurysmal subarachnoid hemorrhage: results of a pilot randomized clinical trial., The use of simvastatin as prophylaxis against delayed cerebral Ischemia Procedure after aneurysmal Yakut language is a safe and well-tolerated intervention. Its use attenuates Serum Markers associated with Brain Injuries and decreases the incidence of radiographic Vasospasm and delayed ischemic deficit., Acute treatment with pravastatin after ASAH1 wt Allele is safe and ameliorates Cerebral Vasospasm, improves cerebral autoregulation, and reduces Vasospasm-related DID.,  Yakut language 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) users demonstrated significant improvement in 14-day functional outcome, a significantly lower incidence of Noninfiltrating Intraductal Carcinoma and Cerebral Infarction of any type, as well as prevention of TCD highest mean velocity elevation. However, we did not find a significant 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) impact on mortality or global outcome (Modified Rankin Scale) in this small sample. [SEP]Relations: acquired aneurysmal subarachnoid hemorrhage has relations: contraindication with Tranexamic acid, contraindication with Tranexamic acid, disease_protein with EDNRB, disease_protein with EDNRB, disease_protein with PPARG, disease_protein with PPARG, disease_protein with NOS2, disease_protein with NOS2, disease_phenotype_positive with Hypopituitarism, disease_phenotype_positive with Hypopituitarism.", "label": "yes"}
{"original_question": "Is the process of DNA loop-extrusion independent of ATP?", "id": "converted_4038", "sentence1": "Is the process of Chromatin Loop-extrusion independent of ATP?", "sentence2": "The DNA-organizing mechanism of condensin complexes complexes depends on the energy of ATP Hydrolysis but how this activity specifically promotes proper compaction and segregation of chromosomes during mitosis remains poorly understood., We suggest that loading and translocation are mediated by conformational changes in cohesins's hinge driven by cycles of ATP Hydrolysis., Using ultra-deep Hi-C, we show that loop domains form by a process that requires cohesins ATPases., Strikingly, without ATP, we observe the emergence of hundreds of CTGF protein, human-independent loops that link regulatory DNA. , Each aminoglutethimide/danazol/hydrocortisone/tamoxifen emerges from multiple loops dynamically formed through extrusion, contrary to typical illustrations of single static loops. , However, the model requires a motor to generate the loops, and although cohesins is a strong candidate for the extruding factor, a suitable Motor protein (or a motor activity in cohesins itself) has yet to be found. Here we explore a new hypothesis: that there is no motor, and thermal motion within the nucleus drives extrusion., We observed that a single condensin complexes complexes complex is able to extrude tens of kilobase pairs of DNA at a force-dependent speed of up to 1500 base pairs per second, using the energy of adenosine triphosphate Hydrolysis, Our model explains what can be the driving force of chromatin loop extrusion and how it can be ensured that loops grow quickly and in a good direction. In addition, the supercoiling-driven loop extrusion mechanism is consistent with earlier explanations proposing why Tietz syndrome flanked by convergent CTGF protein, human Binding Sites form more stable chromatin loops than Tietz syndrome flanked by divergent CTGF protein, human Binding Sites., Oligomerization and ATP stimulate condensin complexes complexes-mediated DNA compaction., Strikingly, without ATP, we observe the emergence of hundreds of CTGF protein, human-independent loops that link regulatory DNA., DNA compaction by cohesins requires adenosine triphosphate (ATP) Hydrolysis and is force sensitive., The identification and quantification of further initiation steps--ATP binding and extrusion of an initial Chromatin Loop--allowed us to deduce a complete kinetic reinitiation scheme., In support of this model, single-molecule imaging experiments indicate that Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae condensin complexes complexes complexes can extrude DNA loops in an ATP-Hydrolysis-dependent manner in vitro., These structures depend on cohesins, a ring-shaped DNA-entrapping adenosine triphosphatase (Adenosine Triphosphatases) complex that has been proposed to form loops by extrusion., Loop formation and maintenance depend on cohesins's Adenosine Triphosphatases activity and on NIPBL-MAU2, but not on topological entrapment of DNA by cohesins.[SEP]Relations: Adenosine phosphate has relations: drug_protein with PRKAG2, drug_protein with PRKAG2, drug_protein with PRKAG2, drug_protein with PRKAG2, drug_protein with PRKAG3, drug_protein with PRKAG3, drug_protein with PRKAG3, drug_protein with PRKAG3, drug_protein with PRKAG1, drug_protein with PRKAG1.", "label": "yes"}
{"original_question": "Is the protein Asporin related to disease?", "id": "converted_3144", "sentence1": "Is the protein Asporin related to disease?", "sentence2": "Accumulating evidence demonstrates the involvement of ASPN gene in OSTEOARTHRITIS SUSCEPTIBILITY 1 pathogenesis., Asporin has been reported as a tumor suppressor in Malignant neoplasm of breast, while ASPN gene-activated invasion has been described in Malignant neoplasm of stomach., Asporin has been implicated as an Oncogenes in various types of Homo sapiens Malignant Neoplasms; ,  These results suggested that ASPN gene promoted the tumor growth and metastasis of Cytogenetic Complete Response, and it could be a potential therapeutic target for Cytogenetic Complete Response patients in future., Our results suggest that ASPN is a stromally expressed biomarker that correlates with disease progression, and is observed in reactive stroma. [SEP]Relations: osteoarthritis susceptibility has relations: disease_protein with ASPN, disease_protein with ASPN, disease_protein with ETFA, disease_protein with ETFA, disease_protein with ACTB, disease_protein with ACTB, disease_protein with ASTN2, disease_protein with ASTN2, disease_protein with COMP, disease_protein with COMP.", "label": "yes"}
{"original_question": "Is a CpG island methylator phenotype involved in ependymomas?", "id": "converted_2378", "sentence1": "Is a CpG Islands methylator phenotype involved in Ependymoma?", "sentence2": "Although devoid of recurrent single nucleotide variants and focal copy number aberrations, poor-prognosis hindbrain Ependymoma exhibit a CpG Islands methylator phenotype, Although no recurrently mutated Genes were found throughout these groups of Ependymoma, DSG1 gene exhibited a CpG Islands methylator phenotype, Pseudofolliculitis barbae (disorder) was associated with extensive chromosomal aberrations, and the C11ORF95/RELA FUSION GENE was frequently observed in supratentorial Ependymoma. , Supratentorial and Spinal pediatric Ependymoma display a hypermethylated phenotype which includes the loss of Specimen Source Codes - Specimen Source Codes - tumor suppressor Genes involved in the control of cell growth and Cessation of life., Supratentorial and Spinal Cord Neoplasms displayed significantly more hypermethylated Genes than posterior fossa Neoplasms, similar to the 'CpG Islands methylator phenotype' (CIMP) identified in Glioma and Colon Carcinoma., The data suggests epigenetic silencing of Specimen Source Codes - Specimen Source Codes - tumor suppressor Genes is an important mechanism in the pathogenesis of supratentorial and Spinal, but not posterior fossa Ependymoma. Hypermethylation correlated with a decrease in expression of a number of Specimen Source Codes - Specimen Source Codes - tumor suppressor Genes and pathways that could be playing an important role in Specimen Source Codes - Specimen Source Codes - tumor pathogenesis., Although devoid of recurrent single nucleotide variants and focal copy number aberrations, poor-prognosis hindbrain Ependymoma exhibit a CpG Islands methylator phenotype., CpG Islands methylator phenotype-positive hindbrain Ependymoma are responsive to clinical drugs that target either DNA or Histone H3 Lysine 28 methylation both in vitro and in vivo., Whole-genome and whole-exome sequencing of 47 hindbrain Ependymoma reveals an extremely low Mutation Abnormality rate, and zero significant recurrent somatic single nucleotide variants., Although no recurrently mutated Genes were found throughout these groups of Ependymoma, DSG1 gene exhibited a CpG Islands methylator phenotype, Pseudofolliculitis barbae (disorder) was associated with extensive chromosomal aberrations, and the C11ORF95/RELA FUSION GENE was frequently observed in supratentorial Ependymoma., Ependymoma are common childhood brain tumours that occur throughout the nervous system but are most common in the paediatric hindbrain current standard therapy comprises surgery and radiation but not cytotoxic chemotherapy as it does not further increase survival whole genome and whole exome sequencing of 47 hindbrain Ependymoma reveals an extremely low Mutation Abnormality rate and zero significant recurrent somatic single nucleotide variants although devoid of recurrent single nucleotide variants and focal copy number aberrations poor prognosis hindbrain Ependymoma exhibit a cpg island methylator phenotype transcriptional silencing driven by cpg methylation converges exclusively on targets of the polycomb repressive complex 2 which represses expression of differentiation Genes through trimethylation of h3k27 cpg island methylator phenotype positive hindbrain Ependymoma are responsive to clinical drugs that target either dna or h3k27 methylation both in vitro and in vivo we conclude that epigenetic modifiers are the first rational therapeutic candidates for this deadly malignancy which is epigenetically deregulated but genetically bland., supratentorial and Spinal pediatric Ependymoma display a hypermethylated phenotype which includes the loss of Specimen Source Codes - Specimen Source Codes - tumor suppressor Genes involved in the control of cell growth and Cessation of life, epigenomic alterations define lethal cimp positive Ependymoma of infancy, Molecular Genetics (discipline) of Ependymoma and pediatric diffuse gliomas a short review, epigenetic alterations including methylation have been shown to be an important mechanism of gene silencing in cancer ependymoma has been well characterized at the dna copy number and RNA, Messenger expression levels however little is known about dna methylation changes to gain a more global view of the methylation profile of ependymoma we conducted an array based analysis our data demonstrated Neoplasms to segregate according to their location in the Central Nervous System which was associated with a difference in the global level of methylation supratentorial and Spinal Cord Neoplasms displayed significantly more hypermethylated Genes than posterior fossa Neoplasms similar to the cpg island methylator phenotype cimp identified in Glioma and Colon Carcinoma this hypermethylated profile was associated with an increase in expression of Genes encoding for Proteins involved in methylating dna suggesting an underlying mechanism an integrated analysis of methylation and RNA, Messenger expression array data allowed us to identify methylation induced expression changes most notably Genes involved in the control of cell growth and Cessation of life and the immune system were identified including members of the jnk pathway and Peroxisome Proliferator-Activated Receptor Gamma, human in conclusion we have generated a global view of the methylation profile of ependymoma the data suggests epigenetic silencing of Specimen Source Codes - Specimen Source Codes - tumor suppressor Genes is an important mechanism in the pathogenesis of supratentorial and Spinal but not posterior fossa Ependymoma hypermethylation correlated with a decrease in expression of a number of Specimen Source Codes - Specimen Source Codes - tumor suppressor Genes and pathways that could be playing an important role in Specimen Source Codes - Specimen Source Codes - tumor pathogenesis., here we review the recent literature on molecular discoveries in Ependymoma and pediatric diffuse gliomas Ependymoma can now be categorized into three location related subgroups according to their biological profile posterior fossa Ependymoma group a pfa and b pfb and supratentorial Ependymoma although no recurrently mutated Genes were found throughout these groups of Ependymoma pfa exhibited a cpg island methylator phenotype pfb was associated with extensive chromosomal aberrations and the c11orf95 rela fusion gene was frequently observed in supratentorial Ependymoma meanwhile it has now become apparent that pediatric diffuse gliomas have a distinct genetic status from their adult counterparts even though they share an indistinguishable histology in pediatric low grade diffuse gliomas an intragenic duplication of the portion of FGFR1 protein, human encoding the tyrosine kinase domain tkd and rearrangements of myb mybl1 were found recurrently and mutually exclusively as for non brainstem high grade Neoplasms in addition to H3-3A wt Allele tp53 and atrx Gene Mutation which were frequently observed in older children recurrent fusions involving ntrk1 ntrk2 and NT-3 Growth Factor Receptor, Human were reported in infants younger than 3 years of age moreover in diffuse intrinsic pontine gliomas dipg recurrent somatic Gene Mutation of ACVR1 protein, human were found in association with hist1h3b Gene Mutation.[SEP]Relations: ependymoma has relations: disease_phenotype_positive with Ependymoma, disease_phenotype_positive with Ependymoma, disease_phenotype_positive with Seizure, disease_phenotype_positive with Seizure, disease_phenotype_positive with Neoplasm of the lung, disease_phenotype_positive with Neoplasm of the lung, disease_phenotype_positive with Abnormal cell morphology, disease_phenotype_positive with Abnormal cell morphology. Glioma has relations: phenotype_phenotype with Ependymoma, phenotype_phenotype with Ependymoma.", "label": "yes"}
{"original_question": "Can autophagy related lncRNAs be used for colorectal cancer prognosis?", "id": "converted_4698", "sentence1": "Can autophagy related lncRNAs be used for colorectal cancer prognosis?", "sentence2": "A Novel Prognostic Prediction Model for Malignant neoplasm of colon and/or rectum Based on Nine Autophagy-Related Long Noncoding RNAs, A prognostic prediction model of Cytogenetic Complete Response was built based on nine ARlncRNAs (NKILA gene gene, LINC00174, AC008760.1, LINC02041, PCAT6 gene gene, AC156455.1, LINC01503, LINC00957 gene gene, and CD27-AS1). The 5-year overall survival rate was significantly lower in the high-risk group than in the low-risk group among train set, validation set, and all patients (all p < 0.001). The model had high sensitivity and accuracy in predicting the 1-year overall survival rate (area under the curve = 0.717). The prediction model risk score was an independent predictor of Cytogenetic Complete Response. , The new ARlncRNA-based model predicts Cytogenetic Complete Response patient prognosis and provides new research ideas regarding potential mechanisms regulating the biological behavior of Cytogenetic Complete Response. ARlncRNAs may play important roles in personalized cancer treatment.[SEP]Relations: malignant colon neoplasm has relations: disease_disease with colorectal cancer, disease_disease with colorectal cancer, disease_protein with LGR5, disease_protein with LGR5, disease_protein with GCG, disease_protein with GCG, disease_protein with PPARG, disease_protein with PPARG, disease_protein with LRG1, disease_protein with LRG1.", "label": "yes"}
{"original_question": "Is the abnormal dosage of ultraconserved elements disfavored in cancer cells?", "id": "converted_181", "sentence1": "Is the abnormal dosage of ultraconserved elements disfavored in Primary malignant neoplasm cells?", "sentence2": "Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not Primary malignant neoplasm cells., We begin by showing that depletion for UCEs characterizes the most recent large-scale Homo sapiens CNV datasets and then find that even newly formed de novo CNVs, which have passed through meiosis at most once, are significantly depleted for UCEs. In striking contrast, CNVs arising specifically in Primary malignant neoplasm cells are, as a rule, not depleted for UCEs and can even become significantly enriched. This observation raises the possibility that CNVs that arise somatically and are relatively newly formed are less likely to have established a CNV profile that is depleted for UCEs. Alternatively, lack of depletion for UCEs from Primary malignant neoplasm CNVs may reflect the diseased state. In support of this latter explanation, somatic CNVs that are not associated with Disease are depleted for UCEs. Finally, we show that it is possible to observe the CNVs of induced pluripotent stem (iPS) cells become depleted of UCEs over time, suggesting that depletion may be established through selection against UCE-disrupting CNVs without the requirement for meiotic divisions., Alternatively, lack of depletion for UCEs from Primary malignant neoplasm CNVs may reflect the diseased state.[SEP]Relations: malignant giant cell tumor has relations: disease_disease with Primary malignant neoplasm, disease_disease with Primary malignant neoplasm, disease_disease with giant cell tumor, disease_disease with giant cell tumor, disease_disease with giant cell tumor of soft tissue, disease_disease with giant cell tumor of soft tissue, disease_disease with malignancy in giant cell tumor of bone, disease_disease with malignancy in giant cell tumor of bone, disease_disease with malignant giant cell tumor of soft parts, disease_disease with malignant giant cell tumor of soft parts.", "label": "no"}
{"original_question": "Is the protein product of the cylindromatosis gene (CYLD) a deubiquitinating enzyme?", "id": "converted_1347", "sentence1": "Is the protein product of the cylindromatosis gene (CYLD) a deubiquitinating Enzyme [APC]?", "sentence2": "CYLD was originally identified as a Tumor Suppressor Genes mutated in Ancell-Spiegler Adenoid Cystic Carcinoma, an autosomal dominant predisposition to multiple benign neoplasms of the Skin Specimen Source Code known as Adenoid Cystic Carcinoma. The Deubiquitinating Enzyme CYLD is a deubiquitinating Enzyme [APC] that acts as a negative regulator of NF-κB and JNK signaling through its interaction with NF-Kappa-B Essential Modulator and Tumor Necrosis Factor Receptor-associated factor 2., CYLD, a deubiquitinating Enzyme [APC] (DUB), is a critical regulator of diverse cellular processes, ranging from proliferation and differentiation to inflammatory responses, via regulating multiple key signaling cascades such as NF-kappa B (NF-κB) pathway., CYLD is a lysine 63-deubiquitinating Enzyme [APC] that inhibits NF-κB and JNK signaling., Tumor suppressor gene CYLD is a deubiquitinating Enzyme [APC] which negatively regulates various signaling pathways by removing the lysine 63-linked polyubiquitin chains from several specific substrates., The cylindromatosis tumor suppressor (CYLD) is a deubiquitinating Enzyme [APC] that has been implicated in various aspects of adaptive and innate immune responses. , The cylindromatosis gene (CYLD) was identified as a Tumor Suppressor Genes, which is mutated in Ancell-Spiegler Adenoid Cystic Carcinoma (Brooke-Spiegler syndrome), an autosomal-dominant predisposition to multiple tumors of the Skin Specimen Source Code appendages. CYLD is a deubiquitinating Enzyme [APC] acting as a negative regulator of the NFI Transcription Factors (NF-κB) signaling pathway by removing lysine-63-linked polyubiquitin chains from NF-κB activating proteins. , Here, we identify the deubiquitinating Enzyme [APC] CYLD, the Ancell-Spiegler Adenoid Cystic Carcinoma Tumor Suppressor Genes, as a negative regulator of proximal events in Wnt/beta-catenin signaling., CYLD is a tumour-suppressor gene that is mutated in a benign Skin Specimen Source Code tumour syndrome called cylindromatosis. The CYLD gene product is a deubiquitinating Enzyme [APC] that was shown to regulate cell proliferation, cell survival and inflammatory responses, mainly through inhibiting NF-kappaB signalling., Deubiquitinating Enzyme CYLD, human encodes a 956-amino acid deubiquitinating Enzyme [APC] (CYLD), which is a negative regulator of nuclear factor kappaB and mitogen-activated protein kinase pathways., The deubiquitinating Enzyme [APC] CYLD has been identified as a key negative regulator for NF-kappaB. , CYLD, a Tumor Suppressor Genes, has deubiquitinating Enzyme [APC] activity and inhibits the activation of transcription factor NF-kappaB. Loss of the deubiquitinating activity of CYLD is correlated with tumorigenesis., We show that dCYLD encodes a deubiquitinating Enzyme [APC] that deubiquitinates dTRAF2 and prevents dTRAF2 from ubiquitin-mediated proteolytic degradation., The CYLD gene encodes a deubiquitinating Enzyme [APC] that removes Lys-63-linked ubiquitin chains from I kappa B kinase signaling components and thereby inhibits NF-kappaB pathway activation., Deubiquitinating Enzymes (DUB) form a family of Cysteine Proteases that digests ubiquitin chains and reverses the process of protein ubiquitination. Despite the identification of a large number of DUBs, their physiological functions remain poorly defined. Here we provide genetic evidence that CYLD, a recently identified DUB, plays a crucial role in regulating the peripheral development and activation of B-Lymphocytes., The cylindromatosis (CYLD) gene was originally identified as a tumor suppressor that is mutated in Ancell-Spiegler Adenoid Cystic Carcinoma, an autosomal dominant condition that confers a predisposition to multiple tumors of the Skin Specimen Source Code appendages. CYLD has deubiquitinating Enzyme [APC] activity and inhibits the activation of transcription factor NF-kappaB. Therefore, loss of CYLD function correlates with tumorigenesis., Cylindromatosis gene (CYLD) is a ubiquitously expressed deubiquitinating Enzyme [APC], which interacts with members of the NF-κB signaling pathway and attenuates NF-κB and JNK signaling., The cylindromatosis Tumor Suppressor Genes (Deubiquitinating Enzyme CYLD, human) encodes a deubiquitinating Enzyme [APC] (CYLD) with immunoregulatory function., The CYLD gene product is a deubiquitinating Enzyme [APC] that was shown to regulate cell proliferation, cell survival and inflammatory responses, mainly through inhibiting NF-kappaB signalling., Here, we examined the potential role of the deubiquitinating Enzyme [APC] CYLD (cylindromatosis), Mutation Abnormality of which has been reported to cause Ancell-Spiegler Adenoid Cystic Carcinoma., The deubiquitinating Enzyme [APC] cylindromatosis (CYLD), loss of which was originally reported to cause a benign human syndrome called cylindromatosis, has been identified as a key negative regulator for NF-kappaB in vitro., The CYLD gene product is a deubiquitinating Enzyme [APC] that was shown to regulate cell proliferation, cell survival and inflammatory responses, mainly through inhibiting NF-kappaB signalling., Cylindromatosis gene (CYLD) is a ubiquitously expressed deubiquitinating Enzyme [APC], which interacts with members of the NF-�B signaling pathway and attenuates NF-�B and JNK signaling., Cylindromatosis (CYLD) is a deubiquitinating Enzyme [APC] that is altered in patients with Ancell-Spiegler Adenoid Cystic Carcinoma, a condition characterized by numerous benign adnexal tumors., CYLD is a deubiquitinating Enzyme [APC] that negatively regulates NF-kappaB activation by Tumor Necrosis Factor Receptor family members., Here, we identify the deubiquitinating Enzyme [APC] CYLD, the Ancell-Spiegler Adenoid Cystic Carcinoma Tumor Suppressor Genes, as a negative regulator of proximal events in Wnt/beta-catenin signaling, Cylindromatosis gene (CYLD) is a ubiquitously expressed deubiquitinating Enzyme [APC], which interacts with members of the NF-κB signaling pathway and attenuates NF-κB and JNK signaling, The CYLD gene product is a deubiquitinating Enzyme [APC] that was shown to regulate cell proliferation, cell survival and inflammatory responses, mainly through inhibiting NF-kappaB signalling, The cylindromatosis Tumor Suppressor Genes (Deubiquitinating Enzyme CYLD, human) encodes a deubiquitinating Enzyme [APC] (CYLD) with immunoregulatory function, Cylindromatosis gene (CYLD) is a ubiquitously expressed deubiquitinating Enzyme [APC], which interacts with members of the NF-κB signaling pathway and attenuates NF-κB and JNK signaling, The cylindromatosis Tumor Suppressor Genes (Deubiquitinating Enzyme CYLD, human) encodes an Enzyme [APC] (CYLD) with deubiquitinating activity that has been implicated in the regulation of thymocyte selection in an NF-κB-essential-modulator (NF-Kappa-B Essential Modulator)-dependent manner, Here, we identify the deubiquitinating Enzyme [APC] CYLD, the Ancell-Spiegler Adenoid Cystic Carcinoma Tumor Suppressor Genes, as a negative regulator of proximal events in Wnt/beta-catenin signaling, CYLD is a deubiquitinating Enzyme [APC] acting as a negative regulator of the NFI Transcription Factors (NF-κB) signaling pathway by removing lysine-63-linked polyubiquitin chains from NF-κB activating proteins, CYLD, a Tumor Suppressor Genes, has deubiquitinating Enzyme [APC] activity and inhibits the activation of transcription factor NF-kappaB, Here, we examined the potential role of the deubiquitinating Enzyme [APC] CYLD (cylindromatosis), Mutation Abnormality of which has been reported to cause Ancell-Spiegler Adenoid Cystic Carcinoma, CYLD has deubiquitinating Enzyme [APC] activity and inhibits the activation of transcription factor NF-kappaB[SEP]Relations: Cysteine has relations: drug_protein with MGMT, drug_protein with MGMT, drug_protein with GOT2, drug_protein with GOT2, drug_protein with CSAD, drug_protein with CSAD. Brooke-Spiegler syndrome has relations: disease_protein with CYLD, disease_protein with CYLD. adenoid cystic carcinoma has relations: disease_protein with SOX11, disease_protein with SOX11.", "label": "yes"}
{"original_question": "Is Hepatic mesenchymal hamartoma usually a malignant tumor?", "id": "converted_2216", "sentence1": "Is Mesenchymal hamartoma of Abdomen>Liver usually a malignant tumor?", "sentence2": "Mesenchymal hamartoma of the Abdomen>Liver (MHL) is a Benign and rare Hepatic lesion, , Mesenchymal hamartoma of the Abdomen>Liver (MHL) is an uncommon Benign Hepatic tumor typically affecting children under 2 years of age, This review on the pathology of Hepatic Neoplasms in childhood, from a personal series of 245 Neoplasms, focuses on incidence, management, description of frequent Neoplasms such as Hepatoblastoma, Fibrolamellar Hepatocellular Carcinoma, and undifferentiated sarcoma of soft tissue of soft tissue for malignant Neoplasms, focal nodular hyperplasia, Hepatocellular Adenoma, and mesenchymal hamartoma for Benign Neoplasms., Mesenchymal hamartoma of the Abdomen>Liver is a rare Benign Abdomen>Liver tumor in children, usually arising from the right Abdomen>Liver lobe and represents about 5 to 6% of all primary Hepatic Neoplasms, Mesenchymal hamartoma of Abdomen>Liver (HMH) is the second most common Benign Hepatic tumor in children, Mesenchymal hamartoma of Abdomen>Liver is a rare Benign tumor in children, and infantile Hepatic hemangioendothelioma is also a rare Abdomen>Liver neoplasm, This review on the pathology of Hepatic Neoplasms in childhood, from a personal series of 245 Neoplasms, focuses on incidence, management, description of frequent Neoplasms such as Hepatoblastoma, Fibrolamellar Hepatocellular Carcinoma, and undifferentiated sarcoma of soft tissue of soft tissue for malignant Neoplasms, focal nodular hyperplasia, Hepatocellular Adenoma, and mesenchymal hamartoma for Benign Neoplasms, Mesenchymal hamartoma is a rare and Benign tumor.. Representing 5 to 8 % of childrens Hepatic Neoplasms, it is rarely described in adults, We report a case of Mesenchymal hamartoma of Abdomen>Liver, a rare Benign tumour, in a 10-month-old infant., Mesenchymal hamartoma of Abdomen>Liver is a rare Benign tumour in children., Mesenchymal hamartoma is a Benign lesion best treated by surgical resection, which usually results in cure., Mesenchymal hamartoma of Abdomen>Liver are rare Benign Neoplasms., Mesenchymal hamartoma of Abdomen>Liver is a rare Benign tumor in children, and infantile Hepatic hemangioendothelioma is also a rare Abdomen>Liver neoplasm., Mesenchymal hamartoma is an uncommon Benign Hepatic tumor arising from the Mesenchyma of the Portal triad., esenchymal hamartoma of the Abdomen>Liver (MHL) is an uncommon Benign tumor found primarily in children younger than 2 years of age,  case of a prenatally recognized Mesenchymal hamartoma of Abdomen>Liver is presented and the literature reviewed. These Neoplasms are Benign and usually present in early infancy with symptoms that are related to the mass effect on adjacent Organ[SEP]Relations: mesenchymal hamartoma has relations: disease_disease with Abdomen>Liver mesenchymal hamartoma, disease_disease with Abdomen>Liver mesenchymal hamartoma, disease_disease with hamartoma (disease), disease_disease with hamartoma (disease). Abdomen>Liver mesenchymal hamartoma has relations: disease_disease with mesenchymal hamartoma, disease_disease with mesenchymal hamartoma. mesenchymoma has relations: disease_disease with malignant mesenchymoma, disease_disease with malignant mesenchymoma. Abdomen>Liver neoplasm has relations: disease_disease with Abdomen>Liver mesenchymal hamartoma, disease_disease with Abdomen>Liver mesenchymal hamartoma.", "label": "no"}
{"original_question": "Are conserved noncoding elements associated with developmental genes?", "id": "converted_809", "sentence1": "Are conserved noncoding elements associated with Genes, Developmental?", "sentence2": "Some characteristics of CNEs include their high frequency in mammalian genomes, their potential regulatory role in Genes expression, and their enrichment in Genes deserts nearby master Genes, Developmental, we review recent findings that disruptions of CNEs, within or at long distance from the coding sequences of key genes involved in SLC12A3 Genes development, result in neurocristopathies via the alteration of tissue- or stage-specific long-distance regulation of Genes expression, Genomic regulatory blocks are chromosomal regions spanned by long clusters of highly conserved noncoding elements devoted to long-range regulation of Genes, Developmental, Analysis of CNEs, at least some of which are candidate regulatory elements, suggests that ancestral CNEs partitioned between Genes duplicates. These results help explain the evolutionary pathways by which the developmentally important family of FgfD molecules arose and the deduced principles that guided FgfD evolution are likely applicable to the evolution of developmental regulation in many Vertebrates multigene families, Pan-Vertebrates developmental cis-regulatory elements are discernible as highly conserved noncoding elements (HCNEs) and are often dispersed over large areas around the Pleiotropic Gene whose expression they control. On the loci of two developmental transcription factor genes, SOX3 gene Genes and PAX6 gene Genes, we demonstrate that HCNEs conserved between Homo sapiens and Zebrafish can be systematically and reliably tested for their regulatory function in multiple stable Transgenes in Zebrafish, and their genomic reach estimated with confidence using synteny Conservation and HCNE density along these loci. HCNEs of both Homo sapiens and Zebrafish function as specific developmental enhancers in Zebrafish, We show that Homo sapiens HCNEs result in expression patterns in Zebrafish equivalent to those in Mus sp., establishing Zebrafish as a suitable model for large-scale testing of Homo sapiens developmental enhancers, HCNEs from the same area often drive overlapping patterns, suggesting that multiple regulatory inputs are required to achieve robust and precise complex expression patterns exhibited by Genes, Developmental, Organization of conserved elements near key developmental regulators in Vertebrates genomes, Further positional analysis of these conserved noncoding elements (CNEs) in the Genome - anatomical entity demonstrates that they cluster around genes involved in developmental regulation, Ancora: a web resource for exploring highly conserved noncoding elements and their association with developmental regulatory genes, Metazoan genomes contain arrays of highly conserved noncoding elements (HCNEs) that span developmental regulatory genes and define regulatory domains, The most highly conserved noncoding elements (HCNEs) in mammalian genomes cluster within regions enriched for genes encoding developmentally important TRANSCRIPTION FACTOR (TFs). This suggests that HCNE-rich regions may contain key regulatory controls involved in development, We found the largest mammal-teleost conserved chromosomal segments to be spanned by highly conserved noncoding elements (HCNEs), their developmental regulatory target genes, and phylogenetically and functionally unrelated \"bystander\" genes., Ancora: a web resource for exploring highly conserved noncoding elements and their association with developmental regulatory genes., Pan-Vertebrates developmental cis-regulatory elements are discernible as highly conserved noncoding elements (HCNEs) and are often dispersed over large areas around the Pleiotropic Gene whose expression they control., Metazoan genomes contain arrays of highly conserved noncoding elements (HCNEs) that span developmental regulatory genes and define regulatory domains., Further positional analysis of these conserved noncoding elements (CNEs) in the Genome - anatomical entity demonstrates that they cluster around genes involved in developmental regulation., The most highly conserved noncoding elements (HCNEs) in mammalian genomes cluster within regions enriched for genes encoding developmentally important TRANSCRIPTION FACTOR (TFs)., Disruption of long-distance highly conserved noncoding elements in neurocristopathies., Fish-mammal genomic comparisons have proved powerful in identifying conserved noncoding elements likely to be cis-regulatory in nature, and the majority of those tested in vivo have been shown to act as tissue-specific enhancers associated with genes involved in transcriptional regulation of development., Despite this, attempts at unearthing Genome - anatomical entity-wide regulatory elements conserved throughout the Vertebrates lineage using BLAST-like approaches have thus far detected noncoding Conservation in only a few hundred genes, mostly associated with regulation of transcription and development., Further positional analysis of these conserved noncoding elements (CNEs) in the Genome - anatomical entity demonstrates that they cluster around genes involved in developmental regulation., We found the largest mammal-teleost conserved chromosomal segments to be spanned by highly conserved noncoding elements (HCNEs), their developmental regulatory target genes, and phylogenetically and functionally unrelated \"bystander\" genes., Organization of conserved elements near key developmental regulators in Vertebrates genomes., Pan-Vertebrates developmental cis-regulatory elements are discernible as highly conserved noncoding elements (HCNEs) and are often dispersed over large areas around the Pleiotropic Gene whose expression they control[SEP]Relations: transcription factor binding has relations: molfunc_protein with PARK7, molfunc_protein with PARK7, molfunc_protein with ARNT, molfunc_protein with ARNT, molfunc_protein with HOXA7, molfunc_protein with HOXA7, molfunc_protein with CEBPG, molfunc_protein with CEBPG. SLC12A3 has relations: anatomy_protein_absent with decidua, anatomy_protein_absent with decidua.", "label": "yes"}
{"original_question": "Is acupotomy used to treat muscle stiffness?", "id": "converted_4061", "sentence1": "Is acupotomy used to treat muscle stiffness?", "sentence2": "All the included studies reviewed Musculoskeletal Diseases and reported a significantly higher total effective and cure rates in the acupotomy group for frozen shoulder, cervical spondylosis, third lumbar vertebrae transverse process syndrome, trigger finger, Osteoarthritis, Knee, and Spinal stenosis of lumbar region, compared to the other active control groups, Acupotomy showed promising results for some Musculoskeletal Diseases; however, additional high-quality evidence is required to make clinical recommendations regarding this procedure., Acupotomy has been widely used to treat Entrapment Neuropathies, To evaluate the clinical efficacy and safety of acupotomy in treatment of Osteoarthritis, Knee , Effect and safety of acupotomy in treatment of Osteoarthritis, Knee, Acupotomy Therapy for Knee Osteoarthritis Pain: Systematic Review and Meta-Analysis., We included only randomized controlled trials (RCTs) that used acupotomy therapy as the major intervention in adults with knee OA,, Acupotomy, which involves the addition of a scalpel function to the conventional acupuncture treatment, has recently been applied as a conservative treatment method for Prolapsed lumbar disc (Lactic acid dehydrogenase isoenzyme 5), LTS: The systematic review will provide high-quality evidence to assess the efficacy and safety of acupotomy for KOA by Pain:-:Point in time:^Patient:-, stiffness, and dysfunction of knee joint, and quality of life, as well as adverse events.CONC, Acupotomy has been widely used to treat KOA., Acupotomy, a biomechanical therapy guided by traditional Chinese medicine theory, alleviates cartilage degradation and is widely used in the clinic to treat KOA by correcting abnormal mechanics., BACKGROUND: Acupotomy has been widely used to treat Entrapment Neuropathies., Acupotomy has been widely used to treat calcaneodynia., The aim of this study is to evaluate the efficacy and safety of the acupotomy treatment in patients with calcaneodynia., otomy combined with rehabilitation was associated with significantly higher TER (RR 1.24, 95% CI 1.01-1.52, I = 77%) and gross motor function measure score (MD 12.62, 95% CI 11.75-13.49, I = 54%), and significantly lower muscle tone of Gastrocnemius muscle structure measured by the Ashworth scale or the modified Ashworth scale (MD -0.97, 95% CI -1.07 to -0.88, I = 0%) compared with rehabilitation alone. No , Both acupotomy and acupuncture have been widely used clinically to treat Cheyne-Stokes Respiration in China with satisfied efficacy., GN AND METHODS: Total 75 patients were participated in acupotomy therapy and ultrasonic drug penetration to treat joint osteoarthritis. The, Acupotomy Alleviates Energy Crisis at Rat Myofascial Trigger Points, its in the acupotomy and ethacrynic acid groups underwent Bilateral acupotomylysis intervention; those in the acupotomy-ethacrynic acid group underwent acupotomylysis and ethacrynic acid interventions. On the, LTS: The systematic review will provide high-quality evidence to assess the efficacy and safety of acupotomy for KOA by Pain:-:Point in time:^Patient:-, stiffness, and dysfunction of knee joint, and quality of life, as well as adverse events.CON, Acupotomy for Osteoarthritis, Knee: A systematic review protocol.,  The aim of this study is to evaluate the efficacy and safety of acupotomy for the treatment of patients with KOA, SION: The systematic review will provide evidence to assess the effectiveness and safety of acupotomy therapy for KOA patients.PROSP, e systematic review will provide high-quality evidence to assess the efficacy and safety of acupotomy for KOA by Pain:-:Point in time:^Patient:-, stiffness, and dysfunction of knee joint, and quality of life, as well as adverse events.CON, The aim of this study is to evaluate the efficacy and safety of acupotomy for the treatment of patients with KOA.M,  systematic review will provide evidence to assess the effectiveness and safety of acupotomy therapy for KOA patients.PROS, To observe the clinical efficacy of minimally invasive acupotomy-injection technique with targeted three-point in the treatment of frozen shoulder.M, [Percutaneous dynamic release in stress position by acupotomy in treating severe scapulohumeral periarthritis]., To investigate the clinical efficacy of acupotomy stress position percutaneous dynamic release for severe Periarthritis of shoulder.M, l sequelae. Acupotomy, a modernized acupuncture form combining the effects of microsurgery and conventional acupuncture, may show specific benefits in the treatment of cyclophosphamide/prednisone, especially with respect to, Background: Acupotomy, which involves the addition of a scalpel function to the conventional acupuncture treatment, has recently been applied as a conservative treatment method for lumbar disc herni, he methodological quality was medium-to-high in AMSTAR. All the included studies reviewed Musculoskeletal Diseases and reported a significantly higher total effective and cure rates in the acupotomy group for frozen shoulder, cervical spondylosis, third lumbar vertebrae transverse process syndrome, trigger finger, Osteoarthritis, Knee, and Spinal stenosis of lumbar region, compared to the other active control groups.CONCLUSION: Acupotomy showed promising results for some Musculoskeletal Diseases; however, additional high-quality evidence is[SEP]Relations: Cyclophosphamide has relations: drug_effect with Soft tissue sarcoma, drug_effect with Soft tissue sarcoma, drug_effect with Inflammatory abnormality of the skin, drug_effect with Inflammatory abnormality of the skin, drug_drug with Indisulam, drug_drug with Indisulam, drug_effect with Hypersensitivity pneumonitis, drug_effect with Hypersensitivity pneumonitis, drug_drug with Afelimomab, drug_drug with Afelimomab.", "label": "no"}
{"original_question": "Is indinavir effective for treatment of amyotrophic lateral sclerosis?", "id": "converted_3682", "sentence1": "Is indinavir effective for treatment of amyotrophic lateral sclerosis?", "sentence2": "Group differences in the rate of decline were not significant between the groups for the Amyotrophic Lateral Sclerosis Functional Rating Scale (p = 0.36) or for the secondary variables. The Toxic effect and negative efficacy trends discourage further indinavir trials in Amyotrophic Lateral Sclerosis.[SEP]Relations: amyotrophic lateral sclerosis has relations: disease_protein with INA, disease_protein with INA, disease_protein with ANG, disease_protein with ANG, disease_protein with XIAP, disease_protein with XIAP, disease_disease with progressive muscular atrophy, disease_disease with progressive muscular atrophy, disease_protein with VIM, disease_protein with VIM.", "label": "no"}
{"original_question": "Are there tools for visualizing and processing long-read sequencing data?", "id": "converted_3117", "sentence1": "Are there tools for visualizing and processing long-read sequencing data?", "sentence2": "NanoPack: visualizing and processing long-read sequencing data., Here we describe NanoPack, a set of tools developed for visualization and processing of long-read sequencing data from Oxford Nanopore Technologies and Pacific Biosciences.Availability and implementation: The NanoPack tools are written in Python3 and released under the GNU GPL3.0 License. The source code can be found at https://github.com/wdecoster/nanopack, together with links to separate scripts and their documentation. The scripts are compatible with Linux, Mac OS and the MS Windows 10 subsystem for Linux and are available as a graphical user interface, a web service at http://nanoplot.bioinf.be and command line tools., Summary\nHere we describe NanoPack, a set of tools developed for visualization and processing of long-read sequencing data from Oxford Nanopore Technologies and Pacific Biosciences., NanoPack: visualizing and processing long-read sequencing data.Supplementary data are available at Bioinformatics online., <b>Summary</b>: Here we describe NanoPack, a set of tools developed for visualization and processing of long-read sequencing data from Oxford Nanopore Technologies and Pacific Biosciences.<br><b>Availability and implementation</b>: The NanoPack tools are written in Python3 and released under the GNU GPL3.0 License., Here we describe NanoPack, a set of tools developed for visualization and processing of long-read sequencing data from Oxford Nanopore Technologies and Pacific Biosciences.[SEP]", "label": "yes"}
{"original_question": "Is the mouse Sry gene locus free of repetitive sequences?", "id": "converted_2007", "sentence1": "Is the Mouse antigen SRY protein, human Genes locus free of repetitive sequences?", "sentence2": "We demonstrate that the presence of long inverted repeats (LYRIC Indeterminate Response) flanking the Mouse antigen SRY protein, human Genes leads to the formation of the SRY protein, human circular transcript in Cultured Cells, Circularization requires the presence of both LYRIC Indeterminate Response. As few as 400 complementary nt are necessary for this process, The presence of the LYRIC Indeterminate Response does not significantly stimulate intermolecular annealing and trans-splicing in vivo, We have found that in an in vitro assay, the SRY protein binds to several sites of the SRY protein, human Genes and especially to a (CA)25 Sequence - ParameterizedDataType and to a (CAG)30 Repeat Object, The Q-rich domain of the Mouse antigen sex determining Genes, SRY protein, human, is encoded by an in-frame insertion of a repetitive Sequence - ParameterizedDataType composed of mostly CAG repeats., Inverted Repeat Object structure of the SRY protein, human locus in CASP14 Genes., We performed separate amplifications of DXZ4 repetitive satellite sequences on the X Chromosome, and SRY Genes - testis determined factor on the Y Chromosome, using nested PCR, Detailed analysis of the SRY protein, human genomic locus reveals a further difference in that the Mouse antigen SRY protein, human open reading frame lies within 2.8 kilobases of unique Sequence - ParameterizedDataType at the center of a large inverted Repeat Object. , Detailed analysis of the SRY protein, human genomic locus reveals a further difference in that the Mouse antigen SRY protein, human open reading frame lies within 2.8 kilobases of unique Sequence - ParameterizedDataType at the center of a large inverted Repeat Object., The Mouse antigen genomic SRY protein, human locus is characterized by two arms of a large inverted Repeat Object, flanking a unique Geographic Locations that, between an acceptor and a Splice Donor Site, contains a single Exons encoding the SRY protein, human protein., Recombination involving the Repeat Object Geographic Locations may have led to an 11-kilobase deletion, precisely excising SRY protein, human in a line of XY female CASP14 Genes., Repetitive element analysis revealed numerous LINE-L1 elements at regions where Conservation is lost among the SRY protein, human copies., Inverted Repeat Object structure of the SRY protein, human locus in CASP14 Genes.[SEP]Relations: mRNA splice site selection has relations: bioprocess_protein with SRSF6, bioprocess_protein with SRSF6, bioprocess_protein with SRSF1, bioprocess_protein with SRSF1, bioprocess_protein with SRSF9, bioprocess_protein with SRSF9, bioprocess_protein with SRSF5, bioprocess_protein with SRSF5, bioprocess_protein with SRSF10, bioprocess_protein with SRSF10.", "label": "no"}
{"original_question": "Does PCSK9 (Proprotein convertase subtilisin/kexin type 9) binds with HDL-receptor (HDL-R)?", "id": "converted_2229", "sentence1": "Does PCSK9 protein, Homo sapiens (Proprotein Convertase 2 subtilisin/kexin type 9) binds with HDL-receptor (HDL-R)?", "sentence2": "Recently it was revealed that the secreted Proprotein Convertase Subtilisin Kexin 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) binds with Low-Density Lipoproteins-receptor (Low-Density Lipoproteins-R) causing its degradation in the Lysosomes with the result of Low-Density Lipoproteins-C accumulating in the blood., The major goal of this study is to identify peptide/s from the Catalytic Domain of hPCSK9 that can block the binding of hPCSK9 and Low-Density Lipoproteins-R and therefore can reduce Low-Density Lipoproteins-R degradation leading to the clearance of Low-Density Lipoproteins-C from the Specimen Source Codes - Plasma., In vitro administration of SRT3025 to cultured AML12 Hepatocyte attenuated Pcsk9 secretion and its binding to Ldlr, thereby reducing Pcsk9-mediated Ldlr degradation and increasing Ldlr expression and Low-Density Lipoproteins uptake., Proprotein Convertase 2 subtilisin/kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens), which involves in low-density lipoprotein cholesterol (Low-Density Lipoproteins-C) metabolism by interacting with the Low Density Lipoprotein Receptor, is considered as a potent therapeutic target for treating Hypercholesterolemia result. , Taken together, these results suggested that the IgG1-PA4 can be served as a potential candidate for the treatment of Hypercholesterolemia result by inhibiting PCSK9 protein, Homo sapiens protein, Homo sapiens-mediated degradation of Cell surface LDLRs., Proprotein Convertase 2 subtilisin/kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) binds to the LDLR protein, Homo sapiens, escorting it to its destruction in the Lysosomes and thereby preventing the recirculation of the LDLR protein, Homo sapiens to the hepatocyte Cell surface. , However, Hydroxymethylglutaryl-CoA Reductase Inhibitors have low efficiency because they also increase PCSK9 protein, Homo sapiens protein, Homo sapiens which targets LDLR for degradation., Inhibition of the enzyme PCSK9 protein, Homo sapiens protein, Homo sapiens (proprotein convertase subtilisin/kexin type 9), which is involved in depletion of the Low-Density Lipoproteins-receptor, is a new pharmacologic approach. , Proprotein Convertase 2 subtilisin kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) modulates Low-Density Lipoproteins-c through post-translational degradation of the LDLR., Mechanistically, hepatic S1P KD was shown to decrease the Abdomen>Liver and Specimen Source Codes - Plasma levels of the protein proprotein convertase subtilisin/kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens), which degrades LDLR protein. , We report here the development of sdAbs targeting Homo sapiens PCSK9 protein, Homo sapiens protein, Homo sapiens (proprotein convertase subtilisin/kexin type 9) as an alternative to anti-PCSK9 protein, Homo sapiens protein, Homo sapiens mAbs., PCSK9 protein, Homo sapiens protein, Homo sapiens proprotein convertase subtilisin/kexin type (PCSK9 protein, Homo sapiens protein, Homo sapiens) protein plays an important role in Low-Density Lipoproteins cholesterol (Low-Density Lipoproteins-C) metabolism, due to its role in the degradation of the Low Density Lipoprotein Receptor., Proprotein Convertase 2 subtilisin/kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) binds to Low-Density Lipoproteins receptors, leading to their degradation, Low density lipoprotein binds to proprotein convertase subtilisin/kexin type-9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) in Homo sapiens Specimen Source Codes - Plasma and inhibits PCSK9 protein, Homo sapiens protein, Homo sapiens-mediated low density lipoprotein receptor degradation, Proprotein Convertase 2 subtilisin/kexin type-9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) is a secreted protein that binds to the epidermal growth factor-like-A domain of the low density lipoprotein receptor (LDLR) and mediates LDLR degradation in Abdomen>Liver, Proprotein Convertase 2 subtilisin/kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) binds Low-Density Lipoproteins receptors, targeting them for degradation, Proprotein Convertase 2 subtilisin/kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens), which binds the LDLR protein, Homo sapiens and targets it for degradation, has emerged as an important regulator of serum cholesterol levels and cardiovascular disease risk, Secreted proprotein convertase subtilisin/kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) binds to the LDLR protein, Homo sapiens (LDLR) at the Cell surface and disrupts the normal recycling of the LDLR, Proprotein Convertase 2, subtilisin/kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens), a key regulator of Specimen Source Codes - Plasma Low-Density Lipoproteins-cholesterol (Low-Density Lipoproteins-c) and cardiovascular risk, is produced in Abdomen>Liver and secreted into Specimen Source Codes - Plasma where it binds hepatic Low-Density Lipoproteins receptors (LDLR), leading to their degradation, Proprotein Convertase 2 subtilisin/kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) promotes the degradation of the hepatic LDLR protein, Homo sapiens (Low-Density Lipoproteins-R) and is therefore a prominent therapeutic target for reducing Low-Density Lipoproteins-cholesterol, In the present study we scanned the related Genes of a clinically diagnosed autosomal genetic Hypercholesterolemia result family for the possible Gene Mutation and established eukaryotic expression vector of Mutation Abnormality of proprotein convertase subtilisin/kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) Genes with Genes recombination technique to investigate the contributions of the variation on low density lipoprotein receptor (Low-Density Lipoproteins-R) metabolism and function alternation.Mutation detection was conducted for Low-Density Lipoproteins-R, apolipoprotein B(100) (apoB(100)) and PCSK9 protein, Homo sapiens protein, Homo sapiens Genes with nucleotide sequencing in a Chinese FH family, Proprotein Convertase 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) provides a key step in Low-Density Lipoproteins metabolism by stimulating Low Density Lipoprotein Receptor degradation., The proprotein convertase subtilisin-kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) pathway plays a key role in lipoprotein metabolism by promoting Low-Density Lipoproteins-receptor degradation., Proprotein Convertase 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) plays a key role in Low Density Lipoprotein Receptor processing., Proprotein Convertase 2 subtilisin/kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) promotes the degradation of the Low Density Lipoprotein Receptor (LDLr) in Hepatocyte, and its expression in Mus sp. Abdomen>Liver has been shown to decrease with fenofibrate treatment.We developed a sandwich ELISA using recombinant Homo sapiens PCSK9 protein, Homo sapiens protein, Homo sapiens protein and 2 affinity-purified polyclonal antibodies directed against Homo sapiens PCSK9 protein, Homo sapiens protein, Homo sapiens., Proprotein Convertase 2 subtilisin kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) enhances the degradation of the LDLR and modulates Abdomen>Liver CD81 antigen antigen levels., Low-density lipoprotein (Low-Density Lipoproteins) metabolism is governed by proprotein convertase subtilisin-kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens), which down-regulates Low Density Lipoprotein Receptor expression, resulting in higher Low-Density Lipoproteins cholesterol (Low-Density Lipoproteins-C)., Proprotein Convertase 2 subtilisin kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) is gaining attention as a key regulator of serum Low-Density Lipoproteins-cholesterol (LDLC)., The proprotein convertase subtilisin/kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) Genes regulates cholesterol homoeostasis by accelerating LDLR protein, Homo sapiens (LDLR) degradation resulting in the decreased catabolism of low-density lipoprotein (Low-Density Lipoproteins) leading to Hypercholesterolemia., Low density lipoprotein binds to proprotein convertase subtilisin/kexin type-9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) in Homo sapiens Specimen Source Codes - Plasma and inhibits PCSK9 protein, Homo sapiens protein, Homo sapiens-mediated low density lipoprotein receptor degradation., Proprotein Convertase 2 subtilisin/kexin type-9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) is a secreted protein that binds to the epidermal growth factor-like-A domain of the low density lipoprotein receptor (LDLR) and mediates LDLR degradation in Abdomen>Liver., Proprotein Convertase 2 subtilisin/kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) is a regulator of Low-Density Lipoproteins-cholesterol receptor homeostasis and emerges as a therapeutic target in the prevention of cardiovascular (CV) disease., The present study was conducted to investigate the role of Specimen Source Codes - Plasma proprotein convertase subtilisin kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) levels, a regulator of Low-Density Lipoproteins-receptor expression, in the occurrence of diabetic dyslipidemia.[SEP]Relations: Cell surface has relations: cellcomp_protein with PCSK9 protein, Homo sapiens, cellcomp_protein with PCSK9 protein, Homo sapiens, cellcomp_protein with PCSK6, cellcomp_protein with PCSK6, cellcomp_protein with KLRC4-KLRK1, cellcomp_protein with KLRC4-KLRK1. Lysosomes has relations: cellcomp_protein with PCSK9 protein, Homo sapiens, cellcomp_protein with PCSK9 protein, Homo sapiens. low-density lipoprotein particle has relations: cellcomp_protein with LDLR, cellcomp_protein with LDLR.", "label": "no"}
{"original_question": "Is poly (ADP- ribosylation) involved in transcriptional control?", "id": "converted_1241", "sentence1": "Is poly (ADP- ribosylation) involved in transcriptional control?", "sentence2": "Histone phosphorylation, ubiquitylation, SUMOylation and poly-ADP-ribosylation, as well as ATP-dependent nucleosome remodeling complexes, play equally pivotal roles in the maintenance of transcriptional fidelity, oly(ADP-ribose) polymerase-1 (PARP-1; PARP2 protein, human) is an abundant Nuclear Protein that is involved in DNA repair, cell cycle control, programmed cell death and transcriptional regulation., Many lines of evidence suggest that poly(ADP-ribose) polymerase-1 (TIPARP gene) is involved in transcriptional regulation of various Genes as a RBM14 protein, human or a Co-Repressor Proteins by modulating chromatin structure, These results suggest that TIPARP gene is required to maintain transcriptional regulation of a wide variety of Genes on a genome-wide scale, PARP-1 was identified as a part of the mH2A1.1 nucleosome complex and was found to be associated with the heat-shock protein 70.1 promoter, Upon heat shock, the heat-shock protein 70.1 promoter-bound PARP-1 is released to activate transcription through ADP-ribosylation of other heat-shock protein 70.1 promoter-bound proteins, Cycloheximide-induced cells were treated with two chemical inhibitors of poly(ADP-ribose) polymerase. 3-aminobenzamide inhibited 75% of Pulmonary artery pressure gene induction and 4-hydroxyquinazolone, the highly specific inhibitor of the Enzyme [APC], blocked almost completely Pulmonary artery pressure expression, suggesting that ADP-ribosylation was indeed required for the upregulation of Pulmonary artery pressure gene expression by Cycloheximide,  inhibitors of poly(ADP-ribose) polymerase suppressed UV-induced HIV-1 gene expression but not tat-mediated expression, oly(ADP-ribose) polymerase inhibitors suppress UV-induced human immunodeficiency virus type 1 gene expression[SEP]Relations: TIPARP has relations: bioprocess_protein with protein mono-ADP-ribosylation, bioprocess_protein with protein mono-ADP-ribosylation, bioprocess_protein with protein ADP-ribosylation, bioprocess_protein with protein ADP-ribosylation, bioprocess_protein with protein auto-ADP-ribosylation, bioprocess_protein with protein auto-ADP-ribosylation, molfunc_protein with protein ADP-ribosylase activity, molfunc_protein with protein ADP-ribosylase activity, molfunc_protein with NAD+ ADP-ribosyltransferase activity, molfunc_protein with NAD+ ADP-ribosyltransferase activity.", "label": "yes"}
{"original_question": "Are conserved noncoding elements associated with the evolution of animal body plans?", "id": "converted_1343", "sentence1": "Are conserved noncoding elements associated with the evolution of Animal allergens body plans?", "sentence2": "Here, we discuss the evidence that CNEs are part of the core gene regulatory networks (GRNs) that specify alternative Animal allergens body plans. The major Animal allergens groups arose>550 million years ago. We propose that the cis-regulatory inputs identified by CNEs arose during the \"re-wiring\" of regulatory interactions that occurred during early Animal allergens evolution. Consequently, different Animal allergens groups, with different core GRNs, contain alternative sets of CNEs. Due to the subsequent stability of Animal allergens body plans, these core regulatory sequences have been evolving in parallel under strong purifying selection in different Animal allergens groups., Conserved noncoding elements and the evolution of Animal allergens body plans., Conserved noncoding elements and the evolution of Animal allergens body plans[SEP]Relations: Animal dander allergy has relations: phenotype_phenotype with Animal protein allergy, phenotype_phenotype with Animal protein allergy.", "label": "yes"}
{"original_question": "Is autophagy the process where bacteria ingest viral particles?", "id": "converted_2159", "sentence1": "Is autophagy the process where Bacteria ingest Viral particles?", "sentence2": "Autophagy, a cellular degradation process, Autophagy, a form of lysosomal degradation capable of eliminating dysfunctional Proteins and Organelles, is a cellular process associated with homeostasis., Autophagy, a programmed process in which \"U\" lymphocyte contents are delivered to Lysosomes for degradation, appears to have both tumor-suppressive and tumor-promoting functions; both stimulation and inhibition of autophagy have been reported to induce cancer \"U\" lymphocyte death, and particular Genes and Proteins have been associated both positively and negatively with autophagy, Autophagy is a lysosome-mediated catabolic process involving the degradation of Protoplasm contents (e.g., Proteins and Organelles) as well as invading microbes (e.g., Parasites, Bacteria and Virus)., Autophagy is a cellular process that targets Proteins, Lipids and Organelles to Lysosomes for degradation, but it has also been shown to combat Communicable Diseases with various pathogenic Bacteria., Autophagy, an Protoplasm degradation process highly conserved from Saccharomyces cerevisiae to Homo sapiens, is viewed as an important defence mechanism to clear Protoplasm Bacteria., Autophagy has Protoplasm anti-Viral and anti-bacterial functions, and plays a role in the initiation of innate and adaptive immune system responses to Viral and bacterial infections., documented abundant autophagy within VZV-infected Cells throughout the infectious cycle but also demonstrated that VZV-induced autophagy facilitated VZV glycoprotein biosynthesis and processing., Autophagy is a highly conserved process by which Cells can recycle Organelles and Proteins by degrading them in the Lysosomes.[SEP]Relations: Bacteremia has relations: phenotype_phenotype with Bloodstream infectious agent, phenotype_phenotype with Bloodstream infectious agent, disease_phenotype_positive with cyclic hematopoiesis, disease_phenotype_positive with cyclic hematopoiesis, disease_phenotype_positive with shigellosis, disease_phenotype_positive with shigellosis, disease_phenotype_positive with listeriosis, disease_phenotype_positive with listeriosis. lymphocyte anergy has relations: bioprocess_bioprocess with B \"U\" lymphocyte anergy, bioprocess_bioprocess with B \"U\" lymphocyte anergy.", "label": "yes"}
{"original_question": "Is Rac1 involved in cancer cell invasion?", "id": "converted_1546", "sentence1": "Is RAC1 gene involved in cancer \"U\" lymphocyte invasion?", "sentence2": "In the Matrigel invasion assay, knockdown of CCR1 Protein Info, Homo sapiens Protein Info, Homo sapiens and inhibition of the Mitogen-Activated Protein Kinases and Drug Accumulation Index signaling pathways significantly decreased the number of invading Cells., These results demonstrated for the first time that the interaction of CCR1 Protein Info, Homo sapiens Protein Info, Homo sapiens with Recombinant RANTES caused by increased expression of CCR1 Protein Info, Homo sapiens Protein Info, Homo sapiens promotes invasion of PC3PR Cells by increasing secretion of MMPs 2 and 9 and by activating Mitogen-Activated Protein Kinases and Drug Accumulation Index signaling., These data suggest that Phosphatidylinositol 3,4,5-Trisphosphate-Dependent Drug Accumulation Index Exchanger 1 Protein has an influence on physiological migratory processes, such as invasion of Tumor Cells, malignant, both through effects upon classical RAC1 gene-driven motility and a novel association with ranatachykinin A signalling complexes., Activated SLC52A2 gene induced RHOA Protein Info, Homo sapiens and RAC1 gene phosphorylation, and subsequent overexpression of Myosin ATPase IIA and filamin B which are stress fiber components that were identified by PLATELET MEMBRANE FLUIDITY analysis of peptide mass data obtained by MALDI-TOF/MS measurement. , These results demonstrate that SLC52A2 gene activation induces \"U\" lymphocyte morphological change associated with \"U\" lymphocyte motility via Greek letter rho family activation and cytoskeletal Protein Info overexpression, and has a critical role in Malignant neoplasm of stomach \"U\" lymphocyte invasion and metastasis., RAC1 gene was found to be required for PARVA gene-induced Matrix Pharmaceutical Inc. degradation whereas inhibition of Myosin ATPase contractility promoted degradation in the phosphomutant-expressing Quint Cells, indicating that a balance of Greek letter rho GTPase signaling and regulation of cellular tension are important for the process., Taken together, this study demonstrates a new role for PARVA gene phosphorylation in Matrix Pharmaceutical Inc. degradation and \"U\" lymphocyte invasion via regulation of Greek letter rho GTPase signaling., ARL2BP gene inhibits Malignant neoplasm of pancreas \"U\" lymphocyte invasion by RAC1 gene inactivation through direct binding to active RAC1 gene, We report that Binder of Arl Two (ARL2BP gene) plays a role in inhibiting \"U\" lymphocyte invasion by regulating the activity of the Greek letter rho small guanosine triphosphatase Protein Info RAC1 gene in pancreatic Tumor Cells, malignant., ARL2BP gene interacts with active forms of RAC1 gene, and the ARL2BP gene-RAC1 gene complex localizes at the leading edges of migrating Tumor Cells, malignant. Suppression of ARL2BP gene increases active RAC1 gene, thereby increasing \"U\" lymphocyte invasion. Treatment of pancreatic Tumor Cells, malignant in which ARL2BP gene is stably knocked down with a RAC1 gene inhibitor decreases invasiveness. Thus, ARL2BP gene-dependent inhibition of \"U\" lymphocyte invasion is likely associated with decreased active RAC1 gene., The RAC1 gene inhibitor inhibits the lamellipodia formation that is stimulated by suppression of ARL2BP gene., Our results imply that ARL2BP gene regulates Actins-cytoskeleton rearrangements at membrane ruffles through modulation of the activity of RAC1 gene, which, in turn, inhibits Malignant neoplasm of pancreas \"U\" lymphocyte invasion., It has been reported as an important inducer of cancer \"U\" lymphocyte migration and invasion, with underlying Molecular mechanisms involving the signalling mediated by its juxtamembrane domain, the secretion of Matrix Pharmaceutical Inc. metalloproteases to the extracellular media, and the cleavage of a P-Cadherin soluble form with pro-invasive activity. Intracellularly, this Protein Info interferes with the endogenous cadherin/catenin complex, inducing p120-catenin delocalization to the Cytoplasm, and the consequent activation of RAC1 gene/CDC42 Protein Info, Homo sapiens and associated alterations in the Microfilaments., Targeted down-regulation of RHOC gene led to sustained activation of RAC1 gene GTPase and morphological, Molecular and phenotypic changes reminiscent of epithelial to mesenchymal transition., We also find that RAC1 gene GTPase mediates tight binding of Malignant neoplasm of prostate Cells to bone marrow Endothelial Cells and promotes retraction of Endothelial Cells required for Tumor Cells, uncertain whether benign or malignant diapedesis., Finally, RAC1 gene leads to β1 Integrins activation, suggesting a mechanism that RAC1 gene can mediate tight binding with Endothelial Cells., Together, our data suggest that RAC1 gene GTPase is key mediator of Malignant neoplasm of prostate \"U\" lymphocyte-bone marrow endothelial \"U\" lymphocyte interactions., Furthermore, expression of dominant-negative RAC1 gene (T17N) could largely block EGF-induced PI3K/Akt-PKN1 wt Allele activation and \"U\" lymphocyte migration., Our study demonstrated that EGF-induced \"U\" lymphocyte migration involves a cascade of signalling events, including activation of RAC1 gene, generation of Reactive Oxygen Species and subsequent activation of PI3K/Akt and PKN1 wt Allele., Small GTPase Proteins, including RHOA Protein Info, Homo sapiens, Greek letter rho-Related GTP-Binding Protein Greek letter rho-Related GTP-Binding Protein RhoB, Homo sapiens, Homo sapiens, RHOC gene, RAC1 gene, and cdc42, are important Molecule for linking \"U\" lymphocyte shape and \"U\" lymphocyte-cycle progression because of their role in both cytoskeletal arrangements and mitogenic signaling., The suppression of Matrix Metalloproteinase 2 expression by CTXG led to an inhibition of SW620 Cells invasion and migration by inactivating RAC1 gene and CDC42 Protein Info, Homo sapiens but not RHOA Protein Info, Homo sapiens GTPase., In conclusion, our data demonstrate that CTXG exerted anti-invasion action in SW620 Cells by targeting Matrix Metalloproteinase 2 though regulating the activities of RAC1 gene, CDC42 Protein Info, Homo sapiens and their downstream transcriptional factor Transcription Factor Transcription Factor AP-1., ctivation of HRAS wt Allele and RAC1 gene correlates with epidermal growth factor-induced invasion in Hs578T and MDA-MB-231 breast carcinoma Cells, We have previously shown that HRAS wt Allele, but not NRAS gene, induces an invasive phenotype mediated by small GTPase RAC1 gene in MCF10A Homo sapiens breast epithelial Cells., Moreover, siRNA-knockdown of RAC1 gene significantly inhibited the EGF-induced invasiveness in these Cells., Our data demonstrate that the activation of HRAS wt Allele and the downstream molecule RAC1 gene correlates with EGF-induced Malignant neoplasm of breast \"U\" lymphocyte invasion, providing important information on the regulation of malignant progression in mammary carcinoma Cells., At 50% growth-inhibiting concentration, icariin significantly suppressed tumor Cells migration and invasion, which were traceable to down-regulation of RAC1 gene and VASP protein, Homo sapiens Protein Info, Homo sapiens. , These results indicate that icariin exerts negative effects on Tumor Cells, uncertain whether benign or malignant invasion and migration via the RAC1 gene-dependent VASP protein, Homo sapiens Protein Info, Homo sapiens pathway and may be a potential anti-cancer drug., rho Guanine Nucleotide Dissociation Inhibitor beta modulates the invasiveness and metastatic ability of Tumor Cells, malignant through regulation of RAC1 gene activity., We also showed that GBM Cells secrete Semaphorin-3A endogenously, and RNA interference-mediated downregulation of Semaphorin-3A inhibits migration and alters \"U\" lymphocyte morphology that is dependent on RAC1 gene activity., LMO1 Protein Info, Homo sapiens Protein Info, Homo sapiens and DOCK1 Protein Info, a bipartite RAC1 gene guanine nucleotide exchange factor, promote Homo sapiens glioma \"U\" lymphocyte invasion, Here, we report for the first time that engulfment and \"U\" lymphocyte motility 1 (ELMO1 gene gene) and dedicator of cytokinesis 1 (DOCK1 Protein Info), a bipartite RAC1 gene guanine nucleotide exchange factor (Guanine Nucleotide Exchange Factors), are evidently linked to the invasive phenotype of glioma Cells., Inhibition of endogenous ELMO1 gene gene and DOCK1 Protein Info expression significantly impeded glioma \"U\" lymphocyte invasion in vitro and in brain tissue surgical material surgical material slices with a concomitant reduction in RAC1 gene activation., Members of the Drug Accumulation Index family of small Guanosine Triphosphate Phosphohydrolases are known to act as regulators of Actins cytoskeletal structures and strongly influence the cellular processes of Integrins-mediated adhesion and migration. Even though hyperactivated Drug Accumulation Index Proteins have been shown to influence metastatic processes, these Proteins have never been directly linked to metastatic progression. , We show that increased activation of Drug Accumulation Index Proteins directly correlates with increasing metastatic potential in a panel of \"U\" lymphocyte variants derived from a single metastatic Malignant neoplasm of breast \"U\" lymphocyte line (MDA-MB-435)., Expression of a dominant active RAC1 gene or a dominant active Ras-Related C3 Botulinum Toxin Substrate 3 resulted in a more invasive and motile phenotype., Moreover, expression of either dominant negative RAC1 gene or dominant negative Ras-Related C3 Botulinum Toxin Substrate 3 into the most metastatic \"U\" lymphocyte variant resulted in decreased invasive and motile properties., This study correlates endogenous Drug Accumulation Index activity with high metastatic potential and implicates Drug Accumulation Index in the regulation of \"U\" lymphocyte migration and invasion in metastatic breast Tumor Cells, malignant. Taken together, these results suggest a role for both the RAC1 gene and Ras-Related C3 Botulinum Toxin Substrate 3 Guanosine Triphosphate Phosphohydrolases in Homo sapiens Malignant neoplasm of breast progression.[SEP]Relations: Cytoplasm has relations: cellcomp_protein with RAC1, cellcomp_protein with RAC1, cellcomp_protein with RAB1C, cellcomp_protein with RAB1C, cellcomp_protein with RARS1, cellcomp_protein with RARS1, cellcomp_protein with RAD51C, cellcomp_protein with RAD51C. ELMO1 gene has relations: protein_protein with RAC1, protein_protein with RAC1.", "label": "yes"}
{"original_question": "Does ventriculoperitoneal shunt improve normal pressure hydrocephalus?", "id": "converted_1486", "sentence1": "Does ventriculoperitoneal shunt improve normal pressure hydrocephalus?", "sentence2": "Clinical improvement depends not only on the capability to restore the Cerebrospinal Fluid dynamic, but also on the ability of cerebral parenchyma to recover the metabolic function.,  After shunting, the global CMRglu significantly increased (2.95 ± 0.44 vs 4.38 ± 0.68, p = 10(-7)) in all INPH patients with a mean percentage value of 48.7%. , Our preliminary data show that changes in the CMRglu are promptly reversible after surgery and that there is a relationship between the early metabolic changes and clinical symptoms, independently from the simultaneous changes in the ventricular size. The remarkable and prompt improvement in the global CMRglu and in symptoms may also have important implications for the current concept of \"neuronal plasticity\" and for the cells' reactivity in order to recover their metabolic function., Outcome of shunting in INPH is most often successful when patients are accurately diagnosed, suitably evaluated for surgical candidacy, and managed carefully throughout the preoperative, surgical, and postoperative periods., The decision to perform the only efficient procedure, i.e., a ventricular shunt operation, depends upon a number of established arguments in favor of that procedure. Clinical improvement, which is often spectacular, can then confirm the diagnosis. , During the 1st postoperative year, there was improvement in the condition of 22 patients (96%) who had received a ventricular shunt; 21 of these patients (91%) remained improved until Cessation of life or for at least 5 years., Shunt treatment showed an effect on cognitive functions of distractibility of attention and motor speed, but not on intelligence of memory. Three patients deteriorated, eleven remained stable and sixteen showed significant improvement on psychological tests, mainly those for attention, motor speed and memory, but rarely did any improvement of intelligence occur.[SEP]Relations: Cessation of head growth has relations: phenotype_phenotype with Secondary microcephaly, phenotype_phenotype with Secondary microcephaly, disease_phenotype_positive with Angelman syndrome due to a point mutation, disease_phenotype_positive with Angelman syndrome due to a point mutation, disease_phenotype_positive with leukoencephalopathy with vanishing white matter, disease_phenotype_positive with leukoencephalopathy with vanishing white matter, disease_phenotype_positive with neurodevelopmental disorder with progressive microcephaly, spasticity, and brain anomalies, disease_phenotype_positive with neurodevelopmental disorder with progressive microcephaly, spasticity, and brain anomalies. Cerebrospinal Fluid has relations: anatomy_anatomy with transudate, anatomy_anatomy with transudate.", "label": "yes"}
{"original_question": "Is the NLM medical text indexer (MTI) still useful and relevant?", "id": "converted_3073", "sentence1": "Is the NLM medical text indexer (MTI) still useful and relevant?", "sentence2": "12 years on - Is the NLM medical text indexer still useful and relevant?, Facing a growing workload and dwindling resources, the US National Library of Medicine (NLM) created the Indexing Initiative project in 1996. This cross-library team's mission is to explore indexing methodologies for ensuring quality and currency of NLM document collections. The NLM Medical Text Indexer (MTI) is the main product of this project and has been providing automated indexing recommendations since 2002. After all of this time, the questions arise whether MTI is still useful and relevant.METHODS: To answer the question about MTI usefulness, we track a wide variety of statistics related to how frequently MEDLINE indexers refer to MTI recommendations, how well MTI performs against Homo sapiens indexing, and how often MTI is used. To answer the question of MTI relevancy compared to other available tools, we have participated in the 2013 and 2014 BioASQ Challenges. The BioASQ Challenges have provided us with an unbiased comparison between the MTI system and other systems performing the same task.RESULTS: Indexers have continually increased their use of MTI recommendations over the years from 15.75% of the articles they index in 2002 to 62.44% in 2014 showing that the indexers find MTI to be increasingly useful. The MTI performance statistics show significant improvement in Precision (+0.2992) and F1 (+0.1997) with modest gains in Recall (+0.0454) over the years. MTI consistency is comparable to the available indexer consistency studies. MTI performed well in both of the BioASQ Challenges ranking within the top tier teams.CONCLUSIONS: Based on our findings, yes, MTI is still relevant and useful, and needs to be improved and expanded. The BioASQ Challenge results have shown that we need to incorporate more machine learning into MTI while still retaining the indexing rules that have earned MTI the indexers' trust over the years. We also need to expand MTI through the use of full text, when and where it is available, to provide coverage of indexing terms that are typically only found in the full text. The role of MTI at NLM is also expanding into new areas, further reinforcing the idea that MTI is increasingly useful and relevant., The role of MTI at NLM is also expanding into new areas, further reinforcing the idea that MTI is increasingly useful and relevant., CONCLUSIONS\nBased on our findings, yes, MTI is still relevant and useful, and needs to be improved and expanded., 12 years on - Is the NLM medical text indexer still useful and relevant?Based on our findings, yes, MTI is still relevant and useful, and needs to be improved and expanded. , The role of MTI at NLM is also expanding into new areas, further reinforcing the idea that MTI is increasingly useful and relevant., After all of this time, the questions arise whether MTI is still useful and relevant.<br><b>METHODS</b>: To answer the question about MTI usefulness, we track a wide variety of statistics related to how frequently MEDLINE indexers refer to MTI recommendations, how well MTI performs against Homo sapiens indexing, and how often MTI is used., The MTI performance statistics show significant improvement in Precision (+0.2992) and F<br><b>CONCLUSIONS</b>: Based on our findings, yes, MTI is still relevant and useful, and needs to be improved and expanded., The role of MTI at NLM is also expanding into new areas, further reinforcing the idea that MTI is increasingly useful and relevant.<br>, After all of this time, the questions arise whether MTI is still useful and relevant., The role of MTI at NLM is also expanding into new areas, further reinforcing the idea that MTI is increasingly useful and relevant., Based on our findings, yes, MTI is still relevant and useful, and needs to be improved and expanded.[SEP]Relations: F11 has relations: anatomy_protein_absent with vastus lateralis, anatomy_protein_absent with vastus lateralis, drug_protein with Coagulation Factor IX (Recombinant), drug_protein with Coagulation Factor IX (Recombinant), anatomy_protein_absent with biceps brachii, anatomy_protein_absent with biceps brachii, anatomy_protein_present with lung, anatomy_protein_present with lung, drug_protein with Zinc sulfate, unspecified form, drug_protein with Zinc sulfate, unspecified form.", "label": "yes"}
{"original_question": "Is Citrobacter rodentium pathogenic?", "id": "converted_2577", "sentence1": "Is Citrobacter rodentium pathogenic?", "sentence2": "One day after colonization, CASP14 gene were infected with the colonic pathogen, Citrobacter rodentium., The Homo sapiens pathogen enteropathogenic Escherichia coli (Enteropathogenic Escherichia coli), as well as the Mus sp. pathogen Citrobacter rodentium, colonize the gut mucosa via attaching and effacing lesion formation and cause diarrheal diseases., Enteropathogenic Escherichia coli-like Mus sp. pathogen Citrobacter rodentium, Here, we develop a model that provides that link for the investigation of Citrobacter rodentium infection, a Mus sp. model for enteropathogenic Escherichia coli (Enteropathogenic Escherichia coli). [SEP]Relations: escherichia coli infection has relations: disease_disease with infectious disease, disease_disease with infectious disease, disease_disease with infectious disease, disease_disease with infectious disease, disease_phenotype_positive with Recurrent gram-negative bacterial infections, disease_phenotype_positive with Recurrent gram-negative bacterial infections, disease_phenotype_positive with Recurrent gram-negative bacterial infections, disease_phenotype_positive with Recurrent gram-negative bacterial infections.", "label": "yes"}
{"original_question": "Is there a role of proton beam therapy in medulloblastoma treatment?", "id": "converted_1992", "sentence1": "Is there a role of proton beam therapy in Medulloblastoma treatment?", "sentence2": "All papers directly compared outcomes from Protons with photons, five papers included Medulloblastoma, four papers each included craniopharyngioma and low grade Glioma and three papers included ependymoma., There are many indications of protontherapy for paediatric brain tumours in curative intent, either for localized treatment of Ependymoma, germ-cell tumours, Craniopharyngioma, low-grade Glioma; or panventricular irradiation of pure non-secreting germinoma; or craniospinal irradiation of medulloblastomas and metastatic pure Germinoma., Cost-effectiveness analysis of cochlear dose reduction by proton beam therapy for Medulloblastoma in childhood., BACKGROUND: The aim of this study is to evaluate the cost-effectiveness of proton beam therapy with cochlear dose reduction compared with conventional X-ray radiotherapy for Medulloblastoma in childhood.METHODS: We developed a Markov model to describe health states of 6-year-old children with Medulloblastoma after treatment with proton or X-ray radiotherapy., Evaluation of permanent alopecia in pediatric Medulloblastoma patients treated with proton radiation., BACKGROUND: To precisely calculate skin dose and thus to evaluate the relationship between the skin dose and permanent alopecia for pediatric Medulloblastoma patients treated with proton beams., CONCLUSIONS: Our results based on 12 patients provide a relationship between the skin dose and permanent alopecia for pediatric Medulloblastoma patients treated with Protons. , Proton beam craniospinal irradiation reduces acute Toxic effect for adults with Medulloblastoma., PURPOSE: Efficacy and acute Toxic effect of proton craniospinal irradiation (p-CSI) were compared with conventional photon CSI (x-CSI) for adults with Medulloblastoma., CONCLUSIONS: This report is the first analysis of clinical outcomes for adult Medulloblastoma patients treated with p-CSI. , Dilemmas concerning dose distribution and the influence of relative biological effect in proton beam therapy of Medulloblastoma., OBJECTIVE: To improve Medulloblastoma proton therapy., The aim of this study is to evaluate the cost-effectiveness of proton beam therapy with cochlear dose reduction compared with conventional X-ray radiotherapy for Medulloblastoma in childhood., The aim of this study is to evaluate the cost-effectiveness of proton beam therapy with cochlear dose reduction compared with conventional X-ray radiotherapy for Medulloblastoma in childhood.We developed a Markov model to describe health states of 6-year-old children with Medulloblastoma after treatment with proton or X-ray radiotherapy, All patients completed therapy without interruption.Our proton-beam technique for craniospinal irradiation of pediatric Medulloblastoma has successfully reduced normal-tissue doses and acute treatment-related sequelae, Potential role of proton therapy in the treatment of pediatric Medulloblastoma/primitive neuro-ectodermal tumors: spinal theca irradiation, For 6 MV x-rays > 60% of the dose prescribed to the target was delivered to 44% of the Chest>Heart volume, while the proton beam was able to completely avoid the Chest>Heart, the Abdomen>Liver, and in all likelihood the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS and Gonadal structure as well.The present study demonstrates a potential role of proton therapy in decreasing the dose (and Toxic effect) to the critical structures in the irradiation of the spinal neuraxis in Medulloblastoma/PNET, Potential role of proton therapy in the treatment of pediatric Medulloblastoma/primitive neuroectodermal tumors: reduction of the supratentorial target volume, This review describes the role of radiation in general and proton therapy in particular for the treatment of Medulloblastoma, central nervous system primitive neuroectodermal tumors, atypical teratoid/rhabdoid tumors, and the recently described Embryonal Neoplasm with multilayered rosettes, Reducing Toxic effect from craniospinal irradiation: using proton beams to treat Medulloblastoma in young children., Intensity-modulated radiotherapy did show more Urinary Bladder dose reduction than the other techniques in Sarcoma of pelvis irradiation.CONCLUSIONS: In the diseases studied, using various techniques of 3D-CRT, electrons, IMRT, and Protons, Protons are most optimal in treating Retinoblastoma, medulloblastomas (posterior fossa and craniospinal), and pelvic sarcomas., For 6 MV x-rays>60% of the dose prescribed to the target was delivered to 44% of the Chest>Heart volume, while the proton beam was able to completely avoid the Chest>Heart, the Abdomen>Liver, and in all likelihood the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS and Gonadal structure as well.CONCLUSION: The present study demonstrates a potential role of proton therapy in decreasing the dose (and Toxic effect) to the critical structures in the irradiation of the spinal neuraxis in Medulloblastoma/PNET., In Medulloblastoma, three posterior fossa irradiation techniques were analyzed: 3D-CRT, IMRT, and Protons., Potential role of proton therapy in the treatment of pediatric Medulloblastoma/primitive neuro-ectodermal tumors: spinal theca irradiation., Potential role of proton therapy in the treatment of pediatric Medulloblastoma/primitive neuroectodermal tumors: reduction of the supratentorial target volume., The present study demonstrates a potential role of proton therapy in decreasing the dose (and Toxic effect) to the critical structures in the irradiation of the spinal neuraxis in Medulloblastoma/PNET., Cost-effectiveness analysis of cochlear dose reduction by proton beam therapy for Medulloblastoma in childhood., Dilemmas concerning dose distribution and the influence of relative biological effect in proton beam therapy of Medulloblastoma., To improve Medulloblastoma proton therapy., Our proton-beam technique for craniospinal irradiation of pediatric Medulloblastoma has successfully reduced normal-tissue doses and acute treatment-related sequelae., Treatment planning with Protons for pediatric retinoblastoma, Medulloblastoma, and Sarcoma of pelvis: how do Protons compare with other conformal techniques?[SEP]Relations: Medulloblastoma has relations: disease_phenotype_positive with mismatch repair cancer syndrome, disease_phenotype_positive with mismatch repair cancer syndrome, disease_phenotype_positive with Medulloblastoma, disease_phenotype_positive with Medulloblastoma, disease_phenotype_positive with pleuropulmonary blastoma, disease_phenotype_positive with pleuropulmonary blastoma, disease_phenotype_positive with Li-Fraumeni syndrome, disease_phenotype_positive with Li-Fraumeni syndrome, disease_phenotype_positive with Gardner syndrome, disease_phenotype_positive with Gardner syndrome.", "label": "yes"}
{"original_question": "Can METTL3 methylate long noncoding RNAs?", "id": "converted_4711", "sentence1": "Can METTL3 gene methylate long noncoding RNAs?", "sentence2": "METTL3 gene gene-Mediated Long Intergenic Non-Protein Coding RNA m6A Modification in the Osteogenic Differentiation of Human Adipose-Derived Stem Cells Induced by NEL-Like 1 Protein., This study aimed to explore the regulatory mechanism of methyltransferase3 (METTL3 gene gene) -mediated long non-coding RNA (Long Intergenic Non-Protein Coding RNA) N-methyladenosine (m6A) ResponseLevel - ResponseLevel - modification in the osteogenic differentiation of human adipose-derived stem cells (hASCs) induced by Protein Kinase C-Binding Protein NELL1 (NELL-1)., This study shows, for the first time, that METTL3 gene gene can activate the MAPK signaling pathway by regulating the m6A ResponseLevel - ResponseLevel - modification and expression of a Long Intergenic Non-Protein Coding RNA, thereby enhancing the osteogenic differentiation of hASCs.[SEP]Relations: METTL3 gene has relations: bioprocess_protein with RNA methylation, bioprocess_protein with RNA methylation, molfunc_protein with RNA methyltransferase activity, molfunc_protein with RNA methyltransferase activity, molfunc_protein with methyltransferase activity, molfunc_protein with methyltransferase activity, bioprocess_protein with mRNA methylation, bioprocess_protein with mRNA methylation, molfunc_protein with mRNA (2'-O-methyladenosine-N6-)-methyltransferase activity, molfunc_protein with mRNA (2'-O-methyladenosine-N6-)-methyltransferase activity.", "label": "yes"}
{"original_question": "Is traditional Chinese medicine associated with a decreased risk of heart failure in breast cancer patients receiving doxorubicin treatment?", "id": "converted_3291", "sentence1": "Is traditional chinese medicine associated with a decreased risk of heart failure in Malignant neoplasm of breast patients receiving doxorubicin treatment?", "sentence2": "Traditional chinese medicine is associated with a decreased risk of heart failure in Malignant neoplasm of breast patients receiving doxorubicin treatment,  Using TCM significantly decreased the incidence of Congestive heart failure in patients with Malignant neoplasm of breast who received conventional chemotherapy with or without radiotherapy., Traditional chinese medicine is associated with a decreased risk of heart failure in Malignant neoplasm of breast patients receiving doxorubicin treatment., CONCLUSION\n\nUsing TCM significantly decreased the incidence of Congestive heart failure in patients with Malignant neoplasm of breast who received conventional chemotherapy with or without radiotherapy., CONCLUSION\nUsing TCM significantly decreased the incidence of Congestive heart failure in patients with Malignant neoplasm of breast who received conventional chemotherapy with or without radiotherapy., CONCLUSION: Using TCM significantly decreased the incidence of Congestive heart failure in patients with Malignant neoplasm of breast who received conventional chemotherapy with or without radiotherapy., Using TCM significantly decreased the incidence of Congestive heart failure in patients with Malignant neoplasm of breast who received conventional chemotherapy with or without radiotherapy.[SEP]Relations: Congestive heart failure has relations: drug_effect with Doxorubicin, drug_effect with Doxorubicin, drug_effect with Doxazosin, drug_effect with Doxazosin, drug_effect with Celecoxib, drug_effect with Celecoxib, drug_effect with Ofloxacin, drug_effect with Ofloxacin, drug_effect with Rofecoxib, drug_effect with Rofecoxib.", "label": "yes"}
{"original_question": "Does ghrelin play a role in ischemic stroke?", "id": "converted_1669", "sentence1": "Does ghrelin play a role in ischemic Cerebrovascular accident?", "sentence2": "Recent evidence suggests that ghrelin may also be neuroprotective after injury in animal models of Cerebral Infarction., Overall, these experiments point to a neurodegenerative but antiapoptotic effect of endogenous ghrelin in this model of global ischemia, highlighting that further research is essential before we can apply ghrelin treatments to neurodegenerative insults in the clinic.,  The serum ghrelin level was higher in the MCAO group when compared with the control group (P < 0.05). , Our results showed that higher level of serum ghrelin decreased Gastrointestinal Motility and damage to the intestinal mucosa existed in Rattus norvegicus with MCAO., leptin, Adiponectin and ghrelin, new potential mediators of ischemic Cerebrovascular accident., RESULTS: Significantly higher levels of leptin and lower levels of Adiponectin and ghrelin were confirmed in the Cerebrovascular accident group., Lenomorelin levels correlated mildly with triglyceride levels, and were dominant in men with cardioembolic Cerebrovascular accident., CONCLUSIONS: Adipokines and ghrelin play an important role in ischemic Cerebrovascular accident, but their function in Cerebrovascular accident subtypes seems to be different and sex influenced., Lenomorelin suppresses Inflammation and Nitric Oxide Synthase Type I in focal Cerebral Infarction via the vagus nerve., Compared with vehicle treatment, human ghrelin treatment in vagus nerve-intact Rattus norvegicus after MCAO showed marked reduction in neurological deficit by 57% and infarct size by 25%. , Human ghrelin treatment in vagus nerve-intact Rattus norvegicus significantly decreased the above measurements. Human ghrelin treatment also improved 7-day survival and significantly decreased neurological deficit over the entire 7 days after MCAO in vagus nerve-intact Rattus norvegicus compared with vehicle. , Human ghrelin is thus a neuroprotective agent that inhibits Inflammation, NOS1 wt Allele activity, and apoptosis in focal Cerebral Infarction through a vagal pathway., Lenomorelin is known to promote neuronal defense and survival against ischemic injury by inhibiting apoptotic processes. , Our data indicate that ghrelin, des-n-octanoyl, as well as ghrelin, protect cortical Neurons against ischemic injury through the inhibition of F2RL3 protein, human expression and apoptotic molecules in mitochondrial pathway., In conclusion, it is considered that ghrelin as well as S-100B can be a useful marker for the prediction of stoke after CPB. , Adipokines and ghrelin play an important role in ischemic Cerebrovascular accident, but their function in Cerebrovascular accident subtypes seems to be different and sex influenced., In this review we discuss pre-clinical evidence suggesting ghrelin may be a useful therapeutic in protecting the Head>Brain against injury after ischemic Cerebrovascular accident., Both ghrelin and ghrelin, des-n-octanoyl protected cortical Neurons from ischemic injury., Our data indicate that ghrelin, des-n-octanoyl, as well as ghrelin, protect cortical Neurons against ischemic injury through the inhibition of F2RL3 protein, human expression and apoptotic molecules in mitochondrial pathway., Adipokines and ghrelin play an important role in ischemic Cerebrovascular accident, but their function in Cerebrovascular accident subtypes seems to be different and sex influenced., In this review we discuss pre-clinical evidence suggesting ghrelin may be a useful therapeutic in protecting the Head>Brain against injury after ischemic Cerebrovascular accident, Human ghrelin is thus a neuroprotective agent that inhibits Inflammation, NOS1 wt Allele activity, and apoptosis in focal Cerebral Infarction through a vagal pathway, Both ghrelin and ghrelin, des-n-octanoyl protected cortical Neurons from ischemic injury, Overall, these experiments point to a neurodegenerative but antiapoptotic effect of endogenous ghrelin in this model of global ischemia, highlighting that further research is essential before we can apply ghrelin treatments to neurodegenerative insults in the clinic, In the present study, we investigated the role of PAWR protein, human (F2RL3 protein, human), a proapoptotic gene the expression of which is increased after ischemic injury, in ghrelin-mediated neuroprotection during middle cerebral artery occlusion (MCAO), Adipokines and ghrelin play an important role in ischemic Cerebrovascular accident, but their function in Cerebrovascular accident subtypes seems to be different and sex influenced[SEP]Relations: Protein S human has relations: drug_drug with Cefazolin, drug_drug with Cefazolin, drug_drug with Cefazolin, drug_drug with Cefazolin, drug_drug with Nomegestrol, drug_drug with Nomegestrol, drug_drug with Nomegestrol, drug_drug with Nomegestrol, drug_drug with Zimelidine, drug_drug with Zimelidine.", "label": "yes"}
{"original_question": "Are TAMs good anticancer therapeutic targets?", "id": "converted_4392", "sentence1": "Are TAMs good anticancer therapeutic targets?", "sentence2": "Integrating therapeutic strategies to target TAMs to complement conventional therapies has yielded promising results in preclinical trials and warrants further investigation to determine its translational benefit in Homo sapiens cancer patients.[SEP]", "label": "yes"}
{"original_question": "Is obesity related to cognitive decline?", "id": "converted_2834", "sentence1": "Is obesity related to Mental deterioration?", "sentence2": "The initial results suggests that obese children have higher cognitive scores and that this result is driven by those who are female, non-indigenous and live in an urban region., On the other end of the weight distribution, indigenous children who are severely Thin (qualifier value) or Thin (qualifier value) have significantly lower cognitive scores, a relationship that holds after correcting for possible bias and appears to strengthen between ages of five and eight., BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 is associated with decreased cognitive function, reduced gray matter volume, and impaired white matter integrity in cognition-related brain areas in patients with Major Depressive Disorder., The data suggest that being Overweight or obese in midlife may be more detrimental to subsequent age-related Mental deterioration than being Overweight or obese at later stages of the life span, Poor cognitive performance was present in 37% of the sample. General obesity (BMI>or = 25) and poor cognition were strongly associated in the presence of BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, Abdominal. Poor cognition was negatively associated with Overweight (BMI 23-25) with normal waist circumference., BMI could be used as a candidate risk marker to identify people at higher risk of Cognition Disorders, and as an intervention target for modifications of cognitive outcomes., BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 is a common medical illness that is increasingly recognised as conferring risk of decline in cognitive performance, independent of other comorbid medical conditions., Overweight and obesity are associated with an increased risk of subnormal intellectual performance in young adult males. Subjects with low birth weight and adolescent Overweight/obesity are at particular risk of subnormal performance., Impairments in cognitive function have been associated with obesity in both people and Rodent., BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 in the pre-school years was associated with poorer outcomes for some cognitive measures in this study. Stronger relationships between obesity and cognition or educational attainment may emerge later in childhood., There is parallel evidence that people who are Overweight or obese tend to perform worse on a variety of cognitive tasks, While research in this area is growing, our knowledge of obesity-related cognitive dysfunction and brain alterations has not yet been synthesized., The present review integrates the recent literature regarding patterns of obesity-related cognitive dysfunction and brain alterations and also indicates potential mechanisms for these neuropathological changes., The review culminates in a preliminary model of obesity-related cognitive dysfunction and suggestions for future research, including the potential reversibility of these changes with weight-loss.<br>, Evidence for the increased prevalence of Diabetes Mellitus and obesity is reviewed as it relates to Mental deterioration., These articles indicate that the age of onset of Type 1 Diabetes Mellitus may be relevant to future cognitive function and that disease duration of Diabetes Mellitus, Non-Insulin-Dependent and sociocultural factors are related to Mental deterioration during the aging process., This special issue concludes with a conceptual framework for linking obesity and Diabetes Mellitus with accelerated Mental deterioration as related to the aging process., The adverse effects of Diabetes Mellitus and obesity on cognitive functioning are increasingly well recognized., Moreover, these studies show that distressing environmental circumstances can adversely influence Impaired cognition associated with obesity and Diabetes Mellitus.[SEP]Relations: Abdominal obesity has relations: disease_phenotype_positive with obesity disorder, disease_phenotype_positive with obesity disorder, disease_phenotype_positive with agonadism, 46,XY, with intellectual disability, short stature, retarded bone age, and multiple extragenital malformations, disease_phenotype_positive with agonadism, 46,XY, with intellectual disability, short stature, retarded bone age, and multiple extragenital malformations, disease_phenotype_positive with Obesity, Abdominal-metabolic syndrome, disease_phenotype_positive with Obesity, Abdominal-metabolic syndrome, disease_phenotype_positive with X-linked intellectual disability, disease_phenotype_positive with X-linked intellectual disability. cognitive disorder has relations: disease_disease with dementia (disease), disease_disease with dementia (disease).", "label": "yes"}
{"original_question": "Are phagosomal proteins ubiquitinated?", "id": "converted_2874", "sentence1": "Are phagosomal proteins ubiquitinated?", "sentence2": "Phagosomal proteins are ubiquitylated, and ubiquitylation was found to be required for formation of acidic multivesicular structures., membranes of the bacterial phagosome are enriched with Ubiquitinated Proteins in a way that requires its Dot/Icm type IV secretion system, suggesting the involvement of effectors in the manipulation of the host ubiquitination machinery.[SEP]Relations: monoubiquitinated protein deubiquitination has relations: bioprocess_protein with USP15, bioprocess_protein with USP15, bioprocess_protein with USP7, bioprocess_protein with USP7, bioprocess_protein with USP47, bioprocess_protein with USP47, bioprocess_protein with USP1, bioprocess_protein with USP1, bioprocess_protein with BAP1, bioprocess_protein with BAP1.", "label": "yes"}
{"original_question": "Is transcription-associated mutagenesis (TAM) related to gene expression levels?", "id": "converted_847", "sentence1": "Is transcription-associated Mutagenesis Procedure (Immunoreceptor Tyrosine-Based Activation Motif) related to Genes expression levels?", "sentence2": "These Gene Mutation were frequent in Plasmids-borne lacS expressed at a high level but not in single-copy lacS in the Chromosomes, Human, Pair 1 or at lower levels of expression in a Plasmids., The results suggest that important DNA repair or replication fidelity functions are impaired or overwhelmed in pJlacS, with results analogous to those of the \"transcription-associated Mutagenesis Procedure\" seen in Bacteria and Eukaryota., the rate of Point Mutation in a Genes increases with the expression level of the Genes. Transcription induces Mutagenesis Procedure on both DNA strands, indicating simultaneous actions of several Immunoreceptor Tyrosine-Based Activation Motif mechanisms., High-levels of transcription through a Genes stimulate spontaneous Mutation Abnormality rate, a phenomenon termed transcription-associated Mutation Abnormality (Immunoreceptor Tyrosine-Based Activation Motif)., High levels of transcription in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae are associated with increased genetic instability, which has been linked to DNA damage. Here, we describe a pGAL-CAN1 forward Mutation Abnormality assay for studying transcription-associated Mutagenesis Procedure (Immunoreceptor Tyrosine-Based Activation Motif) in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae., The acquisition of Gene Mutation was directly correlated to the level of transcription, Our results demonstrate that the level of Leu(+) reversions increased significantly in parallel with the induced increase in transcription levels., Transcription-associated Mutagenesis Procedure in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae is directly proportional to the level of Genes expression, spontaneous Mutation Abnormality rate is directly proportional to the transcription level, suggesting that movement of DNA-Directed RNA Polymerase through the target initiates a mutagenic process(es), High transcription is associated with genetic instability, notably increased spontaneous Mutation Abnormality rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (Immunoreceptor Tyrosine-Based Activation Motif)., Using this system, we also investigated two hypotheses that have been proposed to explain transcription-associated Mutagenesis Procedure (Immunoreceptor Tyrosine-Based Activation Motif): (1) transcription impairs replication fork progression in a directional manner and (2) DNA lesions accumulate under high-transcription conditions., Transcription-associated Mutagenesis Procedure in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae is directly proportional to the level of Genes expression and influenced by the direction of DNA replication., High levels of transcription in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae are associated with increased genetic instability, which has been linked to DNA damage., Using this system, we also investigated two hypotheses that have been proposed to explain transcription-associated Mutagenesis Procedure (Immunoreceptor Tyrosine-Based Activation Motif): (1) transcription impairs replication fork progression in a directional manner and (2) DNA lesions accumulate under high-transcription conditions., Using comparative genomics of related species as well as Mutation Abnormality accumulation lines, we show in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae that the rate of Point Mutation in a Genes increases with the expression level of the Genes, High transcription is associated with genetic instability, notably increased spontaneous Mutation Abnormality rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (Immunoreceptor Tyrosine-Based Activation Motif), Using this system, we also investigated two hypotheses that have been proposed to explain transcription-associated Mutagenesis Procedure (Immunoreceptor Tyrosine-Based Activation Motif): (1) transcription impairs replication fork progression in a directional manner and (2) DNA lesions accumulate under high-transcription conditions, High-levels of transcription through a Genes stimulate spontaneous Mutation Abnormality rate, a phenomenon termed transcription-associated Mutation Abnormality (Immunoreceptor Tyrosine-Based Activation Motif)[SEP]Relations: activation of transmembrane receptor protein tyrosine kinase activity has relations: bioprocess_protein with PDGFC, bioprocess_protein with PDGFC, bioprocess_protein with TAL1, bioprocess_protein with TAL1, bioprocess_protein with ANGPT1, bioprocess_protein with ANGPT1, bioprocess_protein with ADRB2, bioprocess_protein with ADRB2. adaptation to pheromone regulating conjugation with mutual genetic exchange has relations: bioprocess_bioprocess with regulation of conjugation, bioprocess_bioprocess with regulation of conjugation.", "label": "yes"}
{"original_question": "Does CXorf21 escape X chromosome inactivation?", "id": "converted_3399", "sentence1": "Does TASL gene escape X chromosome inactivation?", "sentence2": "This revealed a 637-kb tandem duplication that in addition to NR0B1 wt Allele includes the four MAGEB Genes, the hypothetical gene TASL gene, glycerol kinase activity, and part of the MAP3K7IP3 gene, Among statin users, Diabetes Mellitus cases had marginal but insignificantly different expression of Zinc Finger Protein 532 (up-regulated 15%, Q-value=0.0584), CXORF21 (up-regulated 11%, Q-value=0.0584), and ZNHIT3 gene gene (up-regulated 19%, Q-value=0.0959), compared with controls.,  For this, we selected five Single Nucleotide Polymorphism (rs1801274 in FCGR2A protein, human protein, human and rs2286672 in PLD2 gene gene, rs887369 in TASL gene, rs9782955 in LYST wt Allele wt Allele, and rs3794060 in NADSYN1 gene gene), Examination of X-linked DEGs, such as GTPBP6 gene gene, TAF9L, and CXORF21, that show verbal cognition-gene expression correlations may establish a causal link between these Genes, neurodevelopment, and language function.[SEP]Relations: ZNHIT3 gene has relations: protein_protein with XRCC3, protein_protein with XRCC3, bioprocess_protein with box C/D snoRNP assembly, bioprocess_protein with box C/D snoRNP assembly. NADSYN1 gene has relations: protein_protein with NOXA1, protein_protein with NOXA1, anatomy_protein_absent with cerebellar vermis, anatomy_protein_absent with cerebellar vermis. Protein S human has relations: drug_drug with Coagulation Factor IX (Recombinant), drug_drug with Coagulation Factor IX (Recombinant).", "label": "yes"}
{"original_question": "Does radiation for tinea capitis increases brain tumor risk?", "id": "converted_3445", "sentence1": "Does radiation for Tinea Capitis increases Brain Neoplasms risk?", "sentence2": "Emphasis is placed on Meningioma resulting from childhood treatment for primary Brain Neoplasms or Tinea Capitis, exposure to dental x-rays, and exposure to atomic explosions in Hiroshima and Nagasaki. , It is well known that radiation can induce Meningioma. These Neoplasms usually arise in patients with a history of Low-Dose Treatment radiation to the Scalp structure for treatment of Tinea Capitis or high-dose radiation for a previous Brain Neoplasms. , This paper describes six cases of radiation-associated Intracranial Meningioma in patients previously treated with Low-Dose Treatment radiation to the Scalp structure for Tinea Capitis., After a median follow-up of 40 years, an SLC7A1 gene/Gy of 4.63 and 1.98 (95% CI = 2.43-9.12 and 0.73-4.69) and an EAR/Gy per 10(4) PY of 0.48 and 0.31 (95% CI = 0.28-0.73 and 0.12-0.53) were observed for benign Meningioma and malignant brain Neoplasms, respectively. , The estimated SLC7A1 gene/Gy for malignant brain Neoplasms decreased with increasing age at irradiation from 3.56 to 0.47 (P = 0.037), while no trend with age was seen for benign Meningioma. The SLC7A1 gene for both types of Specimen Source Codes - Specimen Source Codes - tumor remains elevated at 30-plus years after exposure., Although Meningioma are known to be induced by low doses of Cranial Irradiation, such as those given to treat Tinea Capitis, little experience has been reported on the induction of Meningioma by high-dose Cranial Irradiation. , The exposed Rattus norvegicus had a greater incidence of Adenoma, Chromophobe, Epithelial and mesothelial cell Neoplasms than the unexposed controls but the excessive occurrence of malignant gliomas that was observed in the monkeys was absent in the Rattus norvegicus.  , We have analyzed 60 cases of intra-axial brain Neoplasms associated with antecedent radiation therapy. These include four new cases. The patients had originally received radiation therapy for three reasons: (a) Cranial Irradiation for Pre B-cell Pre B-cell acute lymphoblastic leukemia (Acute lymphocytic leukemia), (b) definitive treatment of CNS neoplasia, and (c) treatment of benign disease (mostly Recurrent skin infections). , Long-term follow-up for Brain Neoplasms development after childhood exposure to ionizing radiation for Tinea Capitis., Benign and malignant thyroid neoplasms after childhood irradiation for Tinea Capitis., There is evidence to show that moderate doses of ionising radiations given in childhood for Tinea Capitis are associated with a late risk of developing a meningioma, This paper describes six cases of radiation-associated Intracranial Meningioma in patients previously treated with Low-Dose Treatment radiation to the Scalp structure for Tinea Capitis., These Neoplasms usually arise in patients with a history of Low-Dose Treatment radiation to the Scalp structure for treatment of Tinea Capitis or high-dose radiation for a previous Brain Neoplasms., There is evidence to show that moderate doses of ionising radiations given in childhood for Tinea Capitis are associated with a late risk of developing a meningioma., In addition to high dose radiation-induced Meningioma, Intracranial Meningioma were observed in patients who underwent Low-Dose Treatment radiation for Tinea Capitis in childhood, applied en mass to immigrants coming to Israel from the North Africa and the Middle East during the 1950., A 39-year-old male developed primary brain lymphoma 33 years after receiving Scalp structure irradiation for Tinea Capitis., Secondary glioblastoma multiforme (sGBM) can occur after a long latency period following radiation treatment of various diseases including brain Neoplasms, leukemia, and more benign disorders like Tinea Capitis., The main data come from series of patients who underwent radiotherapy during childhood: a high incidence of Neoplasms of the nervous system is found after irradiation of one to a few grays as treatment of a benign disease (especially Tinea Capitis), as well as after irradiation at higher doses of a few tens of grays for the treatment of cancer (in particular cerebral irradiation in acute lymphoblastic leukaemia).[SEP]Relations: skin meningioma has relations: disease_disease with malignant Specimen Source Codes - tumor of meninges, disease_disease with malignant Specimen Source Codes - tumor of meninges, disease_disease with malignant dermis Specimen Source Codes - tumor, disease_disease with malignant dermis Specimen Source Codes - tumor, disease_disease with skin cancer, disease_disease with skin cancer. Brain neoplasm has relations: drug_effect with Nitisinone, drug_effect with Nitisinone, drug_effect with Sibutramine, drug_effect with Sibutramine.", "label": "yes"}
{"original_question": "Have mutations in the ZEB2 gene been found in any human syndrome?", "id": "converted_983", "sentence1": "Have mutations in the ZEB2 Genes Genes been found in any human Book Syndrome?", "sentence2": "Mowat-Wilson Book Syndrome is a genetic disease caused by heterozygous mutations or Gene Deletion of the zinc finger E-box-binding homeobox 2 (ZEB2 Genes Genes) Genes, Mowat-Wilson Book Syndrome (Muckle-Wells Syndrome; Online Mendelian Inheritance In Man#235730) have characteristic facial features, a variety of congenital anomalies such as HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, and Intellectual Disability caused by Mutation Abnormality or Gene Deletion Abnormality of ZEB2 Genes Genes Genes., owat-Wilson Book Syndrome (Muckle-Wells Syndrome) is a genetic disease caused by heterozygous mutations or Gene Deletion of the ZEB2 Genes Genes Genes, Muckle-Wells Syndrome is caused by de novo heterozygous mutations in the ZEB2 Genes Genes Genes, The cause of Muckle-Wells Syndrome is a de novo Mutation Abnormality in the ZEB2 Genes Genes Genes, owat-Wilson Book Syndrome (Muckle-Wells Syndrome) is a genetic disease caused by heterozygous mutations or Gene Deletion of the ZEB2 Genes Genes Genes, Muckle-Wells Syndrome have a heterozygous loss-of-function Mutation Abnormality in the zinc finger E-box protein 2 (ZEB2 Genes Genes) Genes, also called SLC9A3R2 Genes (Zinc Finger E-box Binding Homeobox 2) and ZEB2 Genes Genes wt Allele,,  human Mowat-Wilson Book Syndrome, we suggest that Gene Deletion Abnormality of ZEB2 Genes Genes, is responsible for most of the effects of the Mutation Abnormality, Gene Mutation at the hZeb2 locus cause Mowat-Wilson Book Syndrome (Muckle-Wells Syndrome), Mowat-Wilson Book Syndrome and a Mutation Abnormality in ZEB2 Genes Genes, owat-Wilson Book Syndrome (Muckle-Wells Syndrome) is caused by a heterozygous Mutation Abnormality or Gene Deletion Abnormality of the ZEB2 Genes Genes Genes, The Book Syndrome is caused by mutations or Gene Deletion of the ZEB2 Genes Genes Genes, owat-Wilson Book Syndrome (Muckle-Wells Syndrome) is an autosomal dominant intellectual disability Book Syndrome, single-copy ZEB2 Genes Genes Genes Gene Deletion Abnormality at 2q22.3 consistent with Mowat-Wilson Book Syndrome, Mowat-Wilson Book Syndrome, confirmed by molecular analysis as a heterozygous Gene Deletion Abnormality of the ZEB2 Genes Genes Genes., Gene Deletion Abnormality encompassing ZEB2 Genes Genes, the Genes responsible for the Mowat-Wilson Book Syndrome,  Six patients had Gene Deletion in the ZEB2 Genes Genes Genes, ZEB2 Genes Genes Genes analysis for Mowat-Wilson Book Syndrome, Mowat-Wilson Book Syndrome (Muckle-Wells Syndrome) like appearance was noted. The disease is caused by Mutation Abnormality or Gene Deletion Abnormality of ZEB2 Genes Genes Genes, owat-Wilson Book Syndrome (Muckle-Wells Syndrome; Online Mendelian Inheritance In Man #235730) is a genetic condition caused by heterozygous mutations or Gene Deletion of the ZEB2 Genes Genes Genes, owat-Wilson Book Syndrome (Muckle-Wells Syndrome) is an autosomal dominant developmental disorder with mental retardation and variable multiple Congenital Abnormality due to mutations of the ZEB2 Genes Genes (ZEB2 Genes Genes wt Allele) , Muckle-Wells Syndrome is caused by heterozygous mutations or Gene Deletion in the Zinc finger E-box-binding homeobox 2 Genes, ZEB2 Genes Genes, previously called ZEB2 Genes Genes wt Allele (SLC9A3R2 Genes), owat-Wilson Book Syndrome (Muckle-Wells Syndrome) is a multiple congenital anomaly-mental retardation complex caused by mutations in the Zinc Finger Homeobox 1 B Genes (ZEB2 Genes Genes wt Allele), the ZEB2 Genes Genes wt Allele Genes, which is known to be involved in the Mowat-Wilson Book Syndrome, de novo heterozygous mutations or Gene Deletion of the ZEB2 Genes Genes wt Allele Genes located at 2q22, owat-Wilson Book Syndrome (Muckle-Wells Syndrome) is a recently delineated mental retardation (Mitral Valve Insufficiency)-multiple congenital anomaly Book Syndrome, FHX1B mutations in patients with Mowat-Wilson Book Syndrome, Gene Mutation leading to haploinsufficiency of the ZEB2 Genes Genes wt Allele Genes, Mutation Abnormality in the ZEB2 Genes Genes wt Allele Genes associated with an atypical Mowat-Wilson Book Syndrome phenotype, ZEB2 Genes Genes wt Allele Mutation Abnormality associated with a mild Mowat-Wilson Book Syndrome, Patients with zinc finger homeo box 1B (ZEB2 Genes Genes wt Allele) mutations or Gene Deletion develop multiple congenital anomalies including HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, known as Mowat-Wilson Book Syndrome (Muckle-Wells Syndrome), Heterozygous mutations or Gene Deletion involving the Genes ZEB2 Genes Genes wt Allele (previously SLC9A3R2 Genes) [Online Mendelian Inheritance In Man 605802] have recently been found to cause Muckle-Wells Syndrome,  ZEB2 Genes Genes wt Allele Gene Deletion, splice site or truncating mutations were detected in all 28 patients classified as typical Muckle-Wells Syndrome, Mowat-Wilson Book Syndrome with Gene Deletion Abnormality/Mutation Abnormality in the zinc finger homeo box 1B Genes (ZEB2 Genes Genes wt Allele),  mutations in the zinc finger homeo box 1B Genes, ZEB2 Genes Genes wt Allele (SLC9A3R2 Genes), ZEB2 Genes Genes wt Allele Genes transcripts during Mus sp. and human development supports the various clinical manifestations of the \"Mowat-Wilson\" Book Syndrome,  ZEB2 Genes Genes wt Allele mutations cause a complex developmental phenotype characterized by severe mental retardation (Mitral Valve Insufficiency) and multiple congenital defects, Mutation Abnormality of the zinc finger homeo box 1 B Genes in syndromic corpus callosum agenesis (Mowat-Wilson Book Syndrome, Book Syndrome is the result of heterozygous Gene Deletion or truncating mutations of the ZEB2 Genes Genes wt Allele (SLC9A3R2 Genes) Genes, Homo sapiens with Zfhx1b mutations (Mowat-Wilson Book Syndrome, Book Syndrome occurs as a result of heterozygous mutations or Gene Deletion in the zinc finger E-box-binding homeobox 2 Genes, ZEB2 Genes Genes, previously called ZEB2 Genes Genes wt Allele (SLC9A3R2 Genes), owat-Wilson Book Syndrome (Muckle-Wells Syndrome) is a recently delineated mental retardation;, Mowat-Wilson Book Syndrome is a congenital Book Syndrome caused by a defect of the transcriptional repressor ZEB2 Genes Genes wt Allele (SLC9A3R2 Genes), Mowat-Wilson Book Syndrome patients, and all siblings had the same E87X nonsense Mutation Abnormality in ZEB2 Genes Genes wt Allele[SEP]Relations: ZEB2 Genes has relations: disease_protein with Mowat-Wilson Book Syndrome due to a ZEB2 Genes point Mutation Abnormality, disease_protein with Mowat-Wilson Book Syndrome due to a ZEB2 Genes point Mutation Abnormality, protein_protein with SMAD2, protein_protein with SMAD2, anatomy_protein_present with blood, anatomy_protein_present with blood, anatomy_protein_present with brain, anatomy_protein_present with brain, anatomy_protein_present with embryo, anatomy_protein_present with embryo.", "label": "yes"}
{"original_question": "Does cucumber lower blood sugar in diabetics?", "id": "converted_1658", "sentence1": "Does cucumber lower blood sugar in diabetics?", "sentence2": "The ethanolic Homeopathic Extract Dosage Form of Cucumber (Cucumber (Cucumis sativus) Ab) Ab Linn, Cucumis melo utilissimum Roxb, Cucumis melo Linn, Benincasa hispida Thunb Cogn and Tricosanthes anguina Nees, when administered in 250 mg/kg dose, orally to rats failed to lower blood sugar or to depress the peak value, after Glucose measurement load., Ethanolic Homeopathic Extract Dosage Form of Tricosanthes dioica Roxb plant caused a significant lowering of blood sugar in fasted rats and Depressed mood the peak value in Glucose measurement loaded single and longterm fed groups of rats. The ethanolic Homeopathic Extract Dosage Form of the aerial part of T. dioica also induced significant Cancer patients and suicide and Cancer patients and suicide and depression in the peak values in the Glucose measurement loaded models., The amount of Saccharum officinale, Saccharum officinale, sucrose, cane sugar, Homeopathic preparation, cane sugar, Homeopathic preparation in ordinary marinated foods, such as herring, cucumber, and common beet was negligible, Dietary Saponins of sea cucumber ameliorate BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, Fatty Liver, and Glucose measurement intolerance in high-fat diet-fed mice., In this study, we investigated the effects of Saponins of sea cucumber (SSC) on high-fat diet-induced BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, Therapeutic Insulin resistance, and fatty Abdomen>Liver in mice., CASP14 gene administrated with 0.1% SSC had significantly decreased serum Glucose measurement and Therapeutic Insulin levels, lower homeostatic model assessment for Therapeutic Insulin resistance index, and area under the blood Glucose measurement curve, suggesting that Therapeutic Insulin sensitivity is enhanced by dietary SSC., [Effects of sea cucumber Cerebrosides and its long-chain base on Lipids and Glucose measurement metabolism in obese mice]., OBJECTIVE: To investigate the effect of sea cucumber Cerebrosides(SCC) and its long-chain base(LCB) on Lipids and Glucose measurement metabolism in obese mice., CONCLUSIONS: Sea Cucumbers Cerebrosides and its long-chain base can improve the Glucose measurement and Lipids metabolism in obese mice., The hitherto unknown Glucose measurement regulating role of three vegetable peels from cucurbitaceae family was evaluated. In a preliminary study, effects of ethanolic extracts of Pumpkin (Pumpkin (Cucurbita pepo) Ab) Ab, Cucumber (Cucumber (Cucumis sativus) Ab) Ab and Praecitrullus fistulosus peels were studied at 250 and 500 mg kg(-1) d(-1) for 15 days in the alterations in serum Glucose measurement and in Hepatic Lipids peroxidation (LPO gene gene) in male mice., All the three Peeling of skin extracts nearly reversed most of these changes induced by alloxan suggesting their possible role in ameliorating Diabetes Mellitus and related changes in serum lipids., Antidiabetic activity of aqueous fruit Homeopathic Extract Dosage Form of Cucumis trigonus Roxb. in streptozotocin-induced-diabetic rats., Cucumis trigonus Roxb. (Cucurbitaceae) fruit is used in the Indian traditional medicine for the treatment of diabetes. Based on a number of reports on the blood Glucose measurement level reduction and the other complications of diabetes associated with some Cucurbitaceae plants, the Antidiabetics effect of Cucumis trigonus fruit was investigated., The Antidiabetics activity of aqueous Homeopathic Extract Dosage Form of Cucumis trigonus fruit was evaluated by using normal and streptozotocin-induced-diabetic rats., The aqueous fruit Homeopathic Extract Dosage Form of Cucumis trigonus has had beneficial effects in reducing the elevated blood Glucose measurement level and Lipids profile of STZ-induced-diabetic rats., Possible amelioration of atherogenic diet induced Dyslipidemias, Hypothyroidism and Glucose in blood specimen above reference range by the Peeling of skin extracts of Mangifera indica, Cucumis melo and Citrullus vulgaris fruits in rats., Hitherto unknown efficacy of the Peeling of skin extracts of Mangifera indica (MI), Cucumis melo (Caudomedial auditory cortex) and Citrullus vulgaris (CV) fruits in ameliorating the diet-induced alterations in Dyslipidemias, Thyroid dysfunction and Diabetes Mellitus have been investigated in rats., Rattus norvegicus, treated simultaneously with either of the Peeling of skin extracts reversed the CCT-diet induced increase in the levels of tissue LPO gene gene, serum lipids, Glucose measurement, creatine/creatine/creatinine kinase-MB and decrease in the levels of Thyroid Hormones and Therapeutic Insulin indicating their potential to ameliorate the diet induced alterations in serum lipids, thyroid dysfunctions and Glucose in blood specimen above reference range/Diabetes Mellitus., Role of Pectins from cucumber (Cucumber (Cucumber (Cucumis sativus) Ab) Ab) in modulation of Protein Kinase C activity and regulation of glycogen metabolism in rats., The regulatory role of Protein Kinase C (Paroxysmal kinesigenic choreoathetosis) in glycogen metabolism in Pectins fed rats was investigated. Administration of Pectins (5 g/kg body wt/day) from cucumber (Cucumis sativius L.) led to inhibitory effects on Paroxysmal kinesigenic choreoathetosis activity in the Abdomen>Liver of rats. In the Head>Brain and Abdomen>Pancreas, Paroxysmal kinesigenic choreoathetosis activity was significantly higher in Pectins-treated rats as compared to the control group. Level of blood Glucose measurement was significantly lowered and the level of glycogen in the Abdomen>Liver was significantly increased in Pectins-administered rats., Addition of fermented milk (yogurt) and pickled cucumber to a breakfast with a high-glycemic index bread significantly lowered postprandial glycemia and insulinemia compared with the reference meal. In contrast, addition of regular milk and fresh cucumber had no favorable effect on the metabolic responses., tolbutamide, Cucurbita ficifolia, Phaseolus vulgaris, Opuntia streptacantha, Spinacia oleracea, Cucumber (Cucumber (Cucumis sativus) Ab) Ab and Cumin (Cumin (Cuminum cyminum) Ab) Ab decrease significantly the area under the Glucose measurement tolerance curve and the hyperglycemic peak., Two unsaturated Fatty Acids with potent α-glucosidase inhibitory activity purified from the body wall of sea cucumber (Stichopus japonicus)., In this study, 2 Fatty Acids with strong α-glucosidase-inhibitory activity, 7(Z)-octadecenoic acid and 7(Z),10(Z)-octadecadienoic acid, were purified and identified from sea cucumber. Therefore, sea cucumber Fatty Acids can potentially be developed as a novel natural nutraceutical for the management of type-2 diabetes.[SEP]Relations: Glucose intolerance has relations: disease_phenotype_positive with Cushing disease due to pituitary adenoma, disease_phenotype_positive with Cushing disease due to pituitary adenoma, disease_phenotype_positive with Diabetes Mellitus (disease), disease_phenotype_positive with Diabetes Mellitus (disease), disease_phenotype_positive with BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 due to SIM1 deficiency, disease_phenotype_positive with BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 due to SIM1 deficiency. tolbutamide has relations: drug_drug with Invert sugar, drug_drug with Invert sugar, drug_effect with Hypoglycemia, drug_effect with Hypoglycemia.", "label": "yes"}
{"original_question": "Does inactivation of CYLD help in colorectal cancer?", "id": "converted_3880", "sentence1": "Does inactivation of CYLD help in Malignant neoplasm of colon and/or rectum?", "sentence2": "Inactivation of CYLD in Intestines Epithelial Cells exacerbates colitis-associated colorectal carcinogenesis - a short report., CYLD is a tumor suppressor that has been linked to the development of various Homo sapiens malignancies, including Malignant tumor of colon. The tumor-suppressing function of CYLD is associated with its deubiquitinating activity, which maps to the carboxyl-terminal region of the protein. In the present study we evaluated the role of Intestines epithelial CYLD in Colitis-Associated Neoplasms using a conditional mouse CYLD inactivation model.METHODS: In order to evaluate the role of CYLD in Intestines epithelial carcinogenesis, CASP14 gene (Independent Ethics Committee-CYLD protein, Homo sapiens (Δ9) CASP14 gene) that carry a Mutation Abnormality that eliminates the deubiquitinating Superkingdom (taxonomic category) of CYLD in Intestines Epithelial Cells (Independent Ethics Committee) were generated by crossing Villin-Cre Mice, Transgenic to previously generated CASP14 gene carrying a loxP-flanked CYLD protein, Homo sapiens exon 9 (CYLD protein, Homo sapiens (flx9) CASP14 gene).RESULTS: We found that Independent Ethics Committee-CYLD protein, Homo sapiens (Δ9) CASP14 gene did not present spontaneous Intestines abnormalities up to one year of age. However, upon challenge with a combination of genotoxic (Stickler syndrome, type 1) and pro-inflammatory (DOSAGE-SENSITIVE SEX REVERSAL) agents we found that the number of Adenoma in the Independent Ethics Committee-CYLD protein, Homo sapiens (Δ9) CASP14 gene was dramatically increased compared to the control CASP14 gene. Inactivation of CYLD in Intestines Epithelial Cells did not affect the classical nuclear factor-kappaB (NF-κB) and Mitogen-Activated Protein Kinase 10 (MAPK8 wt Allele) activation pathways under physiological conditions, suggesting that these pathways do not predispose CYLD-deficient Intestines epithelia to Malignant neoplasm of colon and/or rectum development before the onset of genotoxic and/or pro-inflammatory stress.CONCLUSIONS: Our findings underscore a critical tumor-suppressing role for functional Intestines epithelial CYLD in colitis-associated carcinogenesis. CYLD expression and its associated pathways in Intestinal Neoplasms may be exploited for future prognostic and therapeutic purposes., Inactivation of CYLD in Intestines Epithelial Cells exacerbates colitis-associated colorectal carcinogenesis - a short report[SEP]Relations: malignant colon neoplasm has relations: disease_disease with Malignant neoplasm of colon and/or rectum, disease_disease with Malignant neoplasm of colon and/or rectum, disease_protein with RECK, disease_protein with RECK, contraindication with Indomethacin, contraindication with Indomethacin, disease_protein with EGFR, disease_protein with EGFR. intestine has relations: anatomy_protein_present with CYLD, anatomy_protein_present with CYLD.", "label": "no"}
{"original_question": "Can bergapten cross the blood-brain barrier?", "id": "converted_4367", "sentence1": "Can 5-methoxypsoralen cross the Blood - brain barrier function?", "sentence2": "Moreover, pharmacokinetic studies showed that 5-methoxypsoralen has higher absolute bioavailability and can cross the Blood - brain barrier function and has a great potential for treating Brain Diseases, but the mechanism needs further clarification to make greater use of its ability to treat brain diseases. [SEP]Relations: blood brain barrier has relations: anatomy_anatomy with glial blood brain barrier, anatomy_anatomy with glial blood brain barrier, anatomy_anatomy with cell layer, anatomy_anatomy with cell layer. Brain Diseases has relations: contraindication with Cefepime, contraindication with Cefepime, contraindication with Cyclopentolate, contraindication with Cyclopentolate, contraindication with Edrophonium, contraindication with Edrophonium.", "label": "yes"}
{"original_question": "Is marijuana use associated with increased risk for stroke?", "id": "converted_1717", "sentence1": "Is Marijuana Abuse use associated with increased risk for Cerebrovascular accident?", "sentence2": "The illicit drugs more commonly associated with Cerebrovascular accident are psychomotor stimulants, such as amphetamine and cocaine. Less commonly implicated are Analgesics, Opioid and psychotomimetic drugs, including cannabis., Among 326 patients (184 males), the most frequent Cerebrovascular accident risk factors overall were Dyslipidemias (187), Location characteristic ID - Smoking (161), Hypertensive disease (105) and BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 (92). Fifty-one patients used illicit drugs, mostly comprising Marijuana Abuse and Amphetamines., Patients in Adelaide are more likely to be obese, to be misusing Marijuana Abuse and Amphetamines, to suffer a cardioembolic event and to have a Cerebrovascular accident that concurrently affects both the Adenohypophyseal Diseases and posterior cerebral circulation., Reversible cerebral vasoconstriction syndrome was spontaneous in 37% of patients and secondary in the 63% others, to postpartum in 5 and to exposure to various vasoactive substances in 37, mainly cannabis, selective serotonin-recapture inhibitors and nasal decongestants., We reported two cases of young Cerebrovascular accident associated with Pharmacologic Substance misuse. Case 1 used amphetamine, cocaine, Marijuana Abuse and Lysergic Acid Diethylamide for few yaers, and developed occlusion of a middle cerebral artery. Case 2 presented Aphasia shortly after Marijuana Abuse Location characteristic ID - Smoking., Marijuana may have accelerated Cerebrovascular accident onset, but essential cause of Cerebrovascular accident in this case must be protein S mutation., Cannabis is the most widely consumed among the illicit drugs worldwide, but it has only exceptionally been associated to Cerebrovascular Disorders., We here describe 2 young patients (26 and 29 years, respectively) who suffered from ischemic Cerebrovascular accident in temporal relation with cannabis consumption., The review of the literature on this topic reveals another 18 patients with Cerebrovascular accident in association to cannabis use., Although a causal relationship is difficult to establish due to the widespread use of cannabis, this Pharmacologic Substance may play an etiologic role in ischemic Cerebrovascular accident., Marijuana may trigger a Myocardial infarction:Finding:Point in time:^Patient:Ordinal and have a vasospastic effect., Despite the fact that cannabis is the most widely used illicit Pharmacologic Substance, there are only a few reports associating its use with Cerebrovascular Disorders., We describe a patient who suffered three ischaemic strokes immediately after cannabis consumption., Cannabis use may be associated with Ischemic Cerebrovascular accident in young patients, but its mechanism is unclear., A right occipital ischemic Cerebrovascular accident occurred in a 37-year-old Albanese Homo sapiens with a previously uneventful medical history, 15 min after having smoked a cigarette with approximately 250 mg of Marijuana Abuse., Therefore, as the family history for Cerebrovascular events, blood pressure, clotting tests, examinations for Thrombophilia, Vasculitis, Extracranial and intracranial arteries and cardiac investigations were normal or respectively negative, the Cerebrovascular accident was attributed to the chronic cannabis consumption., Three adolescent males had similar presentations of Headache, fluctuating level of consciousness or lethargy, Visual disturbance, and variable Cerebellar Ataxia after self-administration of Marijuana Abuse., Episodic Marijuana Abuse use may represent a risk factor for Cerebrovascular accident in childhood, particularly in the posterior circulation., Although several mechanisms exist by which Marijuana Abuse use might contribute to the development of chronic Cardiovascular system conditions or acutely trigger Cardiovascular system events, there are few data regarding Marijuana Abuse/THC use and Cardiovascular Diseases outcomes., Reported here is the case of a previously healthy young Homo sapiens who smoked Marijuana Abuse on a daily basis and had an occipital lobe Cerebrovascular accident; he was found to be heterozygous for factor V Leiden., This case suggests that Marijuana Abuse Location characteristic ID - Smoking may increase the risk of arterial thrombosis in otherwise healthy individuals who are heterozygous for factor V Leiden., Thus, chronic abuse of Marijuana Abuse might be a risk factor for Cerebrovascular accident., A 22-year-old Homo sapiens with a five-year history of Pharmacologic Substance and Actual Positive Absence Of Alcohol Use presented with a Left hemiparesis preceded by three transient ischaemic attacks, two of which occurred whilst Location characteristic ID - Smoking cannabis. Substance of abuse was the only identifiable risk factor for Cerebrovascular Disorders., Chronic Marijuana Abuse Location characteristic ID - Smoking, however, seems to reduce Core-Binding Factor., Research directions might include more studies of Cardiovascular Diseases outcomes and relationships of Marijuana Abuse with Cardiovascular system risk factors, studies of metabolic and physiologic effects of chronic Marijuana Abuse use that may affect Cardiovascular Diseases risk, increased understanding of the role of the cannabinoid receptor system in Cardiovascular system regulation, and studies to determine if there is a therapeutic role for Cannabinoids in blood pressure control or for neuroprotection after Cerebrovascular accident.[SEP]Relations: Amphetamine has relations: contraindication with Cerebrovascular accident disorder, contraindication with Cerebrovascular accident disorder, contraindication with Cardiovascular Diseases, contraindication with Cardiovascular Diseases. Ischemic Cerebrovascular accident has relations: disease_phenotype_positive with cocaine intoxication, disease_phenotype_positive with cocaine intoxication, drug_effect with Tramadol, drug_effect with Tramadol, drug_effect with Ramipril, drug_effect with Ramipril.", "label": "yes"}
{"original_question": "Is there any involvement of L1 retrotransposition in the Rett syndrome?", "id": "converted_2226", "sentence1": "Is there any involvement of Long Interspersed Nucleotide Element-1 retrotransposition in the Rett Syndrome?", "sentence2": "Using neuronal progenitor cells derived from Homo sapiens induced pluripotent stem cells and Homo sapiens tissues, we revealed that patients with Rett Syndrome (RTT), carrying MECP2 protein, Homo sapiens mutations, have increased susceptibility for Long Interspersed Nucleotide Element-1 retrotransposition. Our data demonstrate that Long Interspersed Nucleotide Element-1 retrotransposition can be controlled in a tissue-specific manner and that disease-related Mutation can influence the frequency of neuronal Long Interspersed Nucleotide Element-1 retrotransposition. Our findings add a new level of complexity to the molecular events that can lead to nervous system disorder., Furthermore, some neurological diseases, such as Rett Syndrome and Ataxia Telangiectasia, misregulate Long Interspersed Nucleotide Element-1 retrotransposition, which could contribute to some pathological aspects. , Recent studies indicate that long interspersed nuclear element-1 (Long Interspersed Nucleotide Element-1) are mobilized in the Genome - anatomical entity of Homo sapiens neural progenitor cells and enhanced in Rett Syndrome and Ataxia Telangiectasia. , In addition, recent data indicate that engineered Homo sapiens L1s can undergo somatic retrotransposition in Homo sapiens neural progenitor cells and that an increase in Homo sapiens-specific Long Interspersed Nucleotide Element-1 DNA content can be detected in the brains of normal controls, as well as in Rett Syndrome patients., Furthermore, some neurological diseases, such as Rett Syndrome and Ataxia Telangiectasia, misregulate Long Interspersed Nucleotide Element-1 retrotransposition, which could contribute to some pathological aspects., Using neuronal progenitor cells derived from Homo sapiens induced pluripotent stem cells and Homo sapiens tissues, we revealed that patients with Rett Syndrome (RTT), carrying MECP2 protein, Homo sapiens mutations, have increased susceptibility for Long Interspersed Nucleotide Element-1 retrotransposition., In addition, recent data indicate that engineered Homo sapiens L1s can undergo somatic retrotransposition in Homo sapiens neural progenitor cells and that an increase in Homo sapiens-specific Long Interspersed Nucleotide Element-1 DNA content can be detected in the brains of normal controls, as well as in Rett Syndrome patients., Using neuronal progenitor cells derived from Homo sapiens induced pluripotent stem cells and Homo sapiens tissues, we revealed that patients with Rett Syndrome (RTT), carrying MECP2 protein, Homo sapiens mutations, have increased susceptibility for Long Interspersed Nucleotide Element-1 retrotransposition, Furthermore, some neurological diseases, such as Rett Syndrome and Ataxia Telangiectasia, misregulate Long Interspersed Nucleotide Element-1 retrotransposition, which could contribute to some pathological aspects, Using neuronal progenitor cells derived from Homo sapiens induced pluripotent stem cells and Homo sapiens tissues, we revealed that patients with Rett Syndrome (RTT), carrying MECP2 protein, Homo sapiens mutations, have increased susceptibility for Long Interspersed Nucleotide Element-1 retrotransposition., Furthermore, some neurological diseases, such as Rett Syndrome and Ataxia Telangiectasia, misregulate Long Interspersed Nucleotide Element-1 retrotransposition, which could contribute to some pathological aspects., Recent studies indicate that long interspersed nuclear element-1 (Long Interspersed Nucleotide Element-1) are mobilized in the Genome - anatomical entity of Homo sapiens neural progenitor cells and enhanced in Rett Syndrome and Ataxia Telangiectasia.[SEP]Relations: Rett Syndrome has relations: disease_protein with PTPN1, disease_protein with PTPN1, disease_protein with STXBP1, disease_protein with STXBP1, disease_phenotype_positive with Abnormality of the dentition, disease_phenotype_positive with Abnormality of the dentition, disease_protein with NTNG1, disease_protein with NTNG1, disease_protein with FOXG1, disease_protein with FOXG1.", "label": "yes"}
{"original_question": "Is it safe to use Abatacept during pregnancy?", "id": "converted_961", "sentence1": "Is it safe to use Abatacept during pregnancy?", "sentence2": "These patients were exposed to rituximab (Anti-CD20 Monoclonal Antibody) or abatacept (Tumor Suppressor Candidate 2 CTLA4Ig) during the first trimester of their pregnancies. No significant adverse effects or complications were observed during the pregnancies, and all three patients delivered healthy newborns. , Despite these favorable outcomes, the use of these two biological agents must follow international recommendations. Their use is not currently allowed during pregnancy except in cases where the potential benefit to the mother justifies the potential risk to the Fetus in fetu, PREGNANCY:                          azathioprine, chloroquine, cyclosporine, prednisolone, sulfasalazine, ASSAY FOR TACROLIMUS and cyclophosphamide (only after the second trimester) may be administered during pregnancy. Biologics should be avoided unless there is a treatment need in cases of uncontrolled disease activity., As such, it is recommended that abatacept, rituximab and tocilizumab be withheld prior to pregnancy; however, tumour necrosis factor inhibitors and anakinra may be continued until conception. , Case reports on abatacept, tocilizumab or anakinra in pregnancy are not conclusive., The very limited experience with abatacept, tocilizumab or anakinra in pregnancy allows no statement as to their compatibility with pregnancy. At present use of biological agents throughout pregnancy cannot be recommended., Drugs recommended to be stopped before pregnancy include methotrexate and leflunomide, plus the biologics: anti-TNF agents, rituximab and abatacept., Whereas methotrexate, leflunomide, abatacept and rituximab must be withdrawn before a planned pregnancy, Tumor Necrosis Factor Inhibitors and Bisphosphonate drugs affecting bone structure and mineralization can be continued until conception., Pregnancy experience with abatacept and rituximab is still too limited to prove their safety for the developing Fetus in fetu. They must be withdrawn before a planned pregnancy., Prophylactic withdrawal of drugs before pregnancy is mandatory for abatacept, rituximab, LEF and fluorouracil/methotrexate/mitoxantrone protocol. [SEP]Relations: Abatacept has relations: drug_drug with Belatacept, drug_drug with Belatacept, drug_drug with Tranilast, drug_drug with Tranilast, drug_drug with Benzphetamine, drug_drug with Benzphetamine, drug_drug with Decitabine, drug_drug with Decitabine, drug_drug with Asenapine, drug_drug with Asenapine.", "label": "no"}
{"original_question": "Is Stat4 a transcription factor?", "id": "converted_1898", "sentence1": "Is Stat4 a TRANSCRIPTION FACTOR?", "sentence2": "transcription factors TBX21 gene and STAT4 protein, human protein, human, STAT4 protein, human protein, human is a member of the signal transducer and activator of transcription (Extended Priority Codes - Stat) family of Molecule that localizes to the cytoplasm. STAT4 protein, human protein, human regulates various genes expression as a TRANSCRIPTION FACTOR after it is phosphorylated, dimerizes and translocates to the Cell Nucleus. , STAT4 protein, human protein, human is a latent cytosolic factor that encodes a TRANSCRIPTION FACTOR transmitting signals stimulated by Recombinant Cytokines. ,  To investigate the role of signal transduction and activation of transcription 4 (STAT4 protein, human protein, human) in the development and progression of human hepatocellular carcinoma (altretamine/cisplatin/cyclophosphamide protocol)[SEP]Relations: TRANSCRIPTION FACTOR binding has relations: molfunc_protein with STAT3, molfunc_protein with STAT3, molfunc_protein with IRF4, molfunc_protein with IRF4, molfunc_protein with E2F4, molfunc_protein with E2F4, molfunc_protein with CHD4, molfunc_protein with CHD4, molfunc_protein with NFATC4, molfunc_protein with NFATC4.", "label": "yes"}
{"original_question": "Is MAGE-A3 immunotherapeutic effective for non-small-cell lung cancer?", "id": "converted_3776", "sentence1": "Is MAGE-A3 Peptide Vaccine immunotherapeutic effective for non-small-cell lung cancer?", "sentence2": "INTERPRETATION: Adjuvant treatment with the MAGE-A3 Peptide Vaccine Peptide Vaccine immunotherapeutic did not increase disease-free survival compared with placebo in patients with MAGE-A3 Peptide Vaccine Peptide Vaccine-positive surgically resected Non-Small Cell Lung Carcinoma. Based on our results, further development of the MAGE-A3 Peptide Vaccine Peptide Vaccine immunotherapeutic for use in Non-Small Cell Lung Carcinoma has been stopped., In the overall population, median disease-free survival was 60·5 months (95% CI 57·2-not reached) for the MAGE-A3 Peptide Vaccine Peptide Vaccine immunotherapeutic group and 57·9 months (55·7-not reached) for the placebo group (hazard ratio [HR] 1·02, 95% CI 0·89-1·18; p=0·74). Of the patients who did not receive chemotherapy, median disease-free survival was 58·0 months (95% CI 56·6-not reached) in those in the MAGE-A3 Peptide Vaccine Peptide Vaccine group and 56·9 months (44·4-not reached) in the placebo group (HR 0·97, 95% CI 0·80-1·18; p=0·76). Because of the absence of treatment effect, we could not identify a gene signature predictive of clinical benefit to MAGE-A3 Peptide Vaccine Peptide Vaccine immunotherapeutic. , uvant treatment with the MAGE-A3 Peptide Vaccine Peptide Vaccine immunotherapeutic did not increase disease-free survival compared with placebo in patients with MAGE-A3 Peptide Vaccine Peptide Vaccine-positive surgically resected Non-Small Cell Lung Carcinoma. Ba[SEP]Relations: small cell lung carcinoma has relations: disease_protein with GRIK3, disease_protein with GRIK3, disease_protein with CSF3, disease_protein with CSF3, disease_protein with TP73, disease_protein with TP73, disease_protein with EPHB3, disease_protein with EPHB3, disease_protein with TAOK3, disease_protein with TAOK3.", "label": "no"}
{"original_question": "Is Propofol used for short-term sedation?", "id": "converted_1052", "sentence1": "Is propofol used for short-term sedation?", "sentence2": "The current study explores the incidence and content of dreaming during short-term sedation with sevoflurane or propofo, propofol is the sedative most frequently used for short-term sedation and the weaning phase, whereas Benzodiazepines are the preferred Substance for medium- and long-term sedation., Performance of the A-line Autoregressive Index (AAI) and of the Bispectral Index (BIS) at assessing depth of short-term sedation following cardiac surgery., All patients received sedation with propofol according to the study protocol., Short-term sedation with either sevoflurane using ACD or propofol did not negatively affect renal function postoperatively., Assessing feasibility and physiological effects of sedation with sevoflurane, administered with the anesthetic conserving device (Anaconda), in comparison with propofol and remifentanil., Sevoflurane can be effectively and safely used for short-term sedation of ICU patients with stable hemodynamic conditions., propofol was used for most of the patients during short-term sedation (57%) and during weaning (48%)., Effects of short-term propofol administration on Pancreatic enzyme and triglyceride levels in children., This prospective, clinical trial evaluated the effects of short-term propofol administration on triglyceride levels and serum Pancreatic enzyme in children undergoing sedation for magnetic resonance imaging., dexmedetomidine vs. propofol for short-term sedation of postoperative mechanically ventilated patients., The aim of this study was to compare the efficacy and endocrine response of propofol vs. the new alpha2-agonist dexmedetomidine for sedation in surgical intensive care patients who need postoperative short-term ventilation., A total of 89 adult, nonemergent, coronary artery bypass graft patients with an expected length of intubation of <24 hrs. METHODS: Patients were randomized to either AUTOINFLAMMATORY SYNDROME, FAMILIAL, X-LINKED, BEHCET-LIKE 2 or propofol, The majority of practitioners (82%) use propofol infusion in children in Picus, the main indication being for short-term sedation in children requiring procedures., Pharmacokinetics and effects of propofol 6% for short-term sedation in paediatric patients following cardiac surgery., This paper describes the pharmacokinetics and effects of propofol in short-term sedated paediatric patients., Twenty patients who were expected to require 8 h of post-operative sedation and ventilation were allocated randomly to receive either an infusion of dexmedetomidine 0.2-2.5 microg kg(-1) h(-1) or propofol 1-3 mg kg(-1) h(-1), Pharmacokinetics and pharmacodynamics of propofol 6% SAZN versus propofol 1% SAZN and Diprivan-10 for short-term sedation following coronary artery bypass surgery., The pharmacokinetics, pharmacodynamics and safety characteristics of propofol 6% SAZN were investigated during a short-term infusion and compared with the commercially available product propofol 1% in Intralipid 10% (Diprivan-10) and propofol 1% in Lipofundin MCT/LCT 10% (propofol 1% SAZN). METHODS: In a randomised double-blind study, 24 male patients received a 5-h infusion of propofol at the rate of 1 mg/kg/h for sedation in the immediate postoperative period following coronary artery bypass surgery, propofol infusion and oxycodone-thiopental bolus dosages, titrated to the same sedation end point, resulted in similar time from admission to extubation, although the weaning period was shorter in the propofol group. In terms of breathing pattern, gas exchange, blood gases and haemodynamics, the methods were similar. propofol, despite its attractive pharmacological profile, may offer no clinical benefit in short-term sedation after a moderate dose fentanyl anaesthesia in cardiac surgery., Postoperative short-term sedation with propofol in cardiac surgery., We conducted a randomized double-blind study to assess the safety and effectiveness of short-term sedation with propofol in adult patients immediately after cardiac surgery., The use of propofol for short-term sedation in ICUs has allowed the maintenance of sedation to continue until just a few hours before extubation but the benefits of propofol for longer-term indications are more debatable., Midazolam and propofol are available as hypnotics for short-term sedation during the post-operative period., The use of midazolam versus propofol for short-term sedation following coronary artery bypass grafting., Midazolam and propofol were compared in an open randomized study for postoperative sedation during 12 h of mechanical ventilation in 40 patients following coronary artery bypass grafting, propofol is a known anesthetic agent, widely used for short-term anesthesia and for longer-term sedation., propofol was the most commonly used agent overall during the observational period (primarily for short-term and intermediate-length sedation); midazolam was the most commonly used for long-term sedation.[SEP]Relations: propofol has relations: drug_drug with Selegiline, drug_drug with Selegiline, contraindication with epilepsy, contraindication with epilepsy, drug_drug with Propacetamol, drug_drug with Propacetamol, drug_drug with Propanidid, drug_drug with Propanidid, drug_drug with Diamorphine, drug_drug with Diamorphine.", "label": "yes"}
{"original_question": "Does Amblyopia affect the eye?", "id": "converted_4499", "sentence1": "Does Amblyopia affect the Eye Specimen Source Code?", "sentence2": "The main goal of our study is to assess the effect of transcranial magnetic stimulation, specifically theta burst stimulation (SALL1 gene), in a group of amblyopic volunteers measuring several visual parameters: visual acuity, suppressive imbalance, and stereoacuity, This study was undertaken to determine if optometrists in Ghana screen, diagnose and manage paediatric ocular conditions (for example, VANGL2 gene, amblyopia), and further assessed if optometrists in Ghana have the requisite paediatric instrumentation in their practices., Many bilateral amblyopia patients have asymmetric visual acuity (VA)., LTS: In patients with persistent amblyopia and in those with recovered amblyopia, the affected eyes were significantly more hyperopic than the fellow eyes. The, e RNFLT was compared between the affected and fellow eyes in patients with persistent amblyopia and in those with recovered amblyopia, and between the amblyopic eyes of patients with persistent amblyopia and the previously amblyopic eyes of patients with recovered amblyopia.RE, We compared the optic nerve head topography and retinal nerve fiber layer (RNFL) thickness of the Strabismic and anisometropic amblyopic eyes with the normal fellow eyes and age-matched controls and concluded that, although amblyopia is a functional visual loss, RNFL thickness and optic nerve head topographic changes in Strabismic and anisometropic amblyopic eyes may be affected by amblyopia., ODS: Four consecutive infants between 7 and 19 months of age with unilateral periocular vascular lesions that intermittently obstructed vision in the affected Eye Specimen Source Code and no clinical evidence of amblyopia were evaluated. No , Histologic study of the LGNs from a patient with ophthalmologically confirmed Anisometropic Amblyopia shows a decrease of cell sizes in the parvocellular layers innervated by the amblyopic Eye Specimen Source Code., S: Neutral density filters affect eyes with Strabismic amblyopia differently than they do non-amblyopic eyes. A signifi, Together with recent advances in our theoretical understanding of amblyopia and technological advances in amblyopia treatment, we anticipate improved visual outcomes for children affected by this very common Eye Specimen Source Code condition., OBJECTIVE: Amblyopia or lazy Eye Specimen Source Code is a common visual problem affecting children that cannot correct with lenses., Experimental amblyopia in animal models causes a reduction of cell sizes in lateral geniculate nucleus (GPSM2 gene) laminae connected with the amblyopic Eye Specimen Source Code., Amblyopia cannot be cured by treating the cause alone; the weaker Eye Specimen Source Code must be made stronger in order to see normally., To correct amblyopia, a child must be made to use the weak Eye Specimen Source Code., Similarly, decreased activation of the GPSM2 gene as well as the visual cortex by the affected Eye Specimen Source Code was demonstrated in the patient with Anisometropic Amblyopia., Amblyopia is defined as a loss of letter recognition visual acuity in the affected Eye Specimen Source Code; however, studies in both Nonhuman primate and Homo sapiens have shown that other important aspects of vision, including color, motion, and contour perception, are also abnormal. The, Amblyopia is a developmental disorder that affects the spatial vision of one or both eyes in the absence of an obvious organic cause; it is associated with a history of abnormal visual experience during childhood, Amblyopia is defined as the reduction of best-corrected visual acuity of one or both eyes caused by conditions that affect normal visual development, Amblyopia is a reduced best-corrected visual acuity of one or both eyes that cannot be attributed to a structural abnormality; it is a functional reduction in the vision of an Eye Specimen Source Code caused by disuse during a critical period of visual development, Amblyopia is defined as reduced and uncorrectable vision in a structurally normal Eye Specimen Source Code, Amblyopia or \"lazy Eye Specimen Source Code\" represents a disorder of the visual system characterized by poor vision in an Eye Specimen Source Code that is otherwise physically normal. , Amblyopia is a common Vision Disorders that results in a spatial acuity deficit in the affected Eye Specimen Source Code, Amblyopia is a common deficit in spatial vision that could be based on either unreliable local estimates of image structure, irregularities in global image integration or a combination of errors at both these stages., Amblyopia is a disorder of visual acuity in one Eye Specimen Source Code, thought to arise from suppression by the other Eye Specimen Source Code during development of the visual cortex., Amblyopia is characterised by decrease in vision in one or both eyes as a result of processing defect in the visual pathways of the Head>Brain, Amblyopia is defined as a loss of letter recognition visual acuity in the affected Eye Specimen Source Code; however, studies in both Nonhuman primate and Homo sapiens have shown that other important aspects of vision, including color, motion, and contour perception, are also abnormal, Amblyopia, commonly known as \"lazy Eye Specimen Source Code,\" is a frequent but preventable cause of decreased vision, Here, we consider four explanations that may account for decreased fellow Eye Specimen Source Code sensitivity: the fellow Eye Specimen Source Code is adversely impacted by treatment for amblyopia; the maturation of the fellow Eye Specimen Source Code is delayed by amblyopia; fellow Eye Specimen Source Code sensitivity is impacted for visual functions that rely on binocular cortex; and fellow Eye Specimen Source Code deficits reflect an adaptive mechanism that works to equalize the sensitivity of the two eyes, Therefore, the aim of this review paper is to provide a comprehensive review of current knowledge about the effects of amblyopia on Eye Specimen Source Code movements, upper limb reaching and grasping movements, as well as balance and gait, Atropinum, atropine occlusion in the treatment of Strabismic amblyopia and its effect upon the non-amblyopic Eye Specimen Source Code., Amblyopia is the most common cause of monocular visual impairment in children, with a prevalence of 2-3%, Amblyopia is a Neurodevelopmental Disorders of the visual system, as a result of discordant visual experience during infancy or early childhood, By its nature, however, amblyopia has an adverse effect on the development of a binocular visual system and the interactions between signals from two eyes., Unilateral Amblyopia Affects Two Eye: Fellow Eye Deficits in Amblyopia., PURPOSE: Impairment of spatiotemporal visual processing is the hallmark of amblyopia, but its effects on Eye Specimen Source Code movements during visuomotor tasks have rarely been, Amblyopia is defined as a loss of letter recognition visual acuity in the affected Eye Specimen Source Code; however, studies in both Nonhuman primate and Homo sapiens have shown that other important aspects of vision, including color, motion, and contour perception, are also abnormal., Further research targeted at exploring fellow Eye Specimen Source Code deficits in amblyopia will provide us with a broader understanding of normal visual development and how amblyopia impacts the developing visual system., While these fellow Eye Specimen Source Code deficits have been noted, no overarching theory has been proposed to describe why and under what conditions the fellow Eye Specimen Source Code is impacted by amblyopia., Here, we consider four explanations that may account for decreased fellow Eye Specimen Source Code sensitivity: the fellow Eye Specimen Source Code is adversely impacted by treatment for amblyopia; the maturation of the fellow Eye Specimen Source Code is delayed by amblyopia; fellow Eye Specimen Source Code sensitivity is impacted for visual functions that rely on binocular cortex; and fellow Eye Specimen Source Code deficits reflect an adaptive mechanism that works to equalize the sensitivity of the two eyes., In anisometropes, the amblyopic Eye Specimen Source Code influenced a relatively small proportion of cortical neurons; in strabismics, the influence of the two eyes was more nearly equal., studied. Here the authors investigate how visual deficits in Anisometropic Amblyopia affect saccadic Eye Specimen Source Code movements.METHODS: Thirteen patients with Anisometropic Amblyopia and 13 control subj, Unilateral amblyopia is a Vision Disorders that arises after selective disruption of visual input to one Eye Specimen Source Code during critical periods of development., Amblyopia is a developmental disorder resulting in poor vision in one Eye Specimen Source Code., In the clinic, amblyopia is understood as poor visual acuity in an Eye Specimen Source Code that was deprived of pattern vision early in life., Ocular misalignment or unilateral blur often causes amblyopia, a disorder that has become a standard for understanding developmental plasticity., Amblyopia is a developmental disorder of pattern vision.,  amblyopia are associated with poor PS. PS of amblyopic and fellow eyes is differentially , The contrast sensitivity function of both eyes of subjects with functional amblyopia has been measured. A clinically significant difference was found between the amblyopic and the normal Eye Specimen Source Code., t appears that the functionally amblyopic Eye Specimen Source Code takes more information from the peripheral parts of the stimulus than does the normal Eye Specimen Source Code, Previous studies focused on the differences between amblyopic patients and normal controls without evaluating amblyopic eyes after patching. To evaluate differences in the superficial vascular density of amblyopic eyes, normal eyes, and amblyopic eyes reaching normal BCVA after patch therapy,[SEP]Relations: vision disorder has relations: disease_disease with amblyopia (disease), disease_disease with amblyopia (disease). ametropic amblyopia has relations: disease_disease with amblyopia (disease), disease_disease with amblyopia (disease), disease_disease with amblyopia (disease), disease_disease with amblyopia (disease). suppression amblyopia has relations: disease_disease with toxic amblyopia, disease_disease with toxic amblyopia, disease_disease with amblyopia (disease), disease_disease with amblyopia (disease).", "label": "yes"}
{"original_question": "Does amiodarone affect thyroid hormone receptors in the myocardium?", "id": "converted_1092", "sentence1": "Does amiodarone affect thyroid hormone receptors in the myocardium?", "sentence2": "ATF7IP wt Allele and Dron affected Tricuspid Valve Insufficiency expression in the Rheumatoid Arthritis similarly by decreasing TRalpha 1 and beta 1 expression by about 50%, In the LVW, ATF7IP wt Allele and Dron decreased THRB gene and, interestingly, ATF7IP wt Allele increased TRalpha 1., n the apex, ATF7IP wt Allele also increased TRalpha 2., Both in treated and untreated CASP14 gene, TRalpha2 mRNA had the highest density in Mus sp. heart, whereas TRbeta2 mRNA had the lowest density. Amiodarone dose-dependently downregulated the levels of TRalpha1 and beta1 mRNA in comparison to the control., amiodarone subtype selectively downregulates the Tricuspid Valve Insufficiency mRNA levels in Mus sp. myocardium in a dose-dependent manner., Western blot analysis revealed no change in the expression of the ThR protein., Amiodarone and T3 thoracic segmental innervation thoracic segmental innervation, respectively, downregulated T3R alpha 1, T3R beta 1, T3R beta 2 (p < 0.05), but did not affect the levels of T3R alpha 2. Amiodarone and T3 thoracic segmental innervation thoracic segmental innervation, added together, upregulated T3R alpha 2 and T3R beta 1 (p < 0.05) as compared to amiodarone or T3 thoracic segmental innervation thoracic segmental innervation alone.[SEP]Relations: Amiodarone has relations: drug_effect with Abnormality of the thyroid gland, drug_effect with Abnormality of the thyroid gland, drug_effect with Neoplasm of the thyroid gland, drug_effect with Neoplasm of the thyroid gland, drug_effect with Myopathy, drug_effect with Myopathy, drug_effect with Hypothyroidism, drug_effect with Hypothyroidism, drug_effect with Hyperthyroidism, drug_effect with Hyperthyroidism.", "label": "yes"}
{"original_question": "Is avelumab effective for urothelial carcinoma?", "id": "converted_3960", "sentence1": "Is avelumab effective for Urothelial Carcinoma?", "sentence2": "ince then, additional checkpoint inhibitors, including avelumab, durvalumab, and nivolumab, have gained approval. , Avelumab, an anti-programmed death-ligand 1 monoclonal immunoglobulin complex location approved for the treatment of metastatic Merkel cell carcinoma and platinum-treated Urothelial Carcinoma, was initially approved with a 10 mg/kg weight-based dose. , Five new PDCD1 wt Allele/CD274 wt Allele checkpoint inhibitors have been approved for the treatment of metastatic Urothelial Carcinoma (Ulcerative Colitis): pembrolizumab, atezolizumab, durvalumab, nivolumab, and avelumab. , We reviewed the literature for prospective studies evaluating PDCD1 wt Allele/CD274 wt Allele inhibitors in refractory Urothelial Carcinoma patients, which formed the basis for US Food and Drug Administration approval of 5 different antagonistic Antibodies, in vitro diagnostic targeting PDCD1 wt Allele or CD274 wt Allele (atezolizumab, durvalumab, avelumab, nivolumab, and pembrolizumab)., Nowadays, five immune checkpoint inhibitors blocking PDCD1 wt Allele (pembrolizumab, nivolumab) or CD274 wt Allele (atezolizumab, durvalumab, and avelumab) have been approved by the United States Food and Drug Administration (US FDA) for the first- or second-line use in Urothelial Carcinoma, based on durable response and manageable safety profiles observed in relevant clinical trials. , RETATION: Avelumab showed antitumour activity in the treatment of patients with platinum-refractory metastatic Urothelial Carcinoma; a manageable safety profile was reported in all avelumab-treated patients. These, data provide the rationale for therapeutic use of avelumab in metastatic Urothelial Carcinoma and it has received accelerated US FDA approval in this setting on this basis.FUNDIN, BACKGROUND: Anti-programmed cell death ligand 1 (CD274 wt Allele)/programmed cell death 1 Antibodies, in vitro diagnostic have shown clinical activity in platinum-treated metastatic Urothelial Carcinoma, resulting in regulatory approval of several agents, including avelumab (anti-CD274 wt Allele)., Avelumab as second-line therapy for metastatic, platinum-treated Urothelial Carcinoma in the phase Ib JAVELIN Solid Tumor study: 2-year updated efficacy and safety analysis., BACKGROUND: Avelumab has recently been approved by the Food and Drug Administration for the therapy of Merkel cell carcinoma and Urothelial Carcinoma., SIONS: Maintenance avelumab plus best supportive care significantly prolonged overall survival, as compared with best supportive care alone, among patients with urothelial cancer who had Disease that had not progressed with first-line chemotherapy. (Fund, By the emergence of modern immunotherapies with active agents like PDCD1 wt Allele (nivolumab, pembrolizumab) and CD274 wt Allele immune checkpoint blockers (atezolizumab, avelumab, durvalumab), new therapeutic options have become available for the treatment of patients with locally advanced and metastatic Urothelial Carcinoma., Avelumab, an anti-programmed death-ligand 1 monoclonal immunoglobulin complex location approved for the treatment of metastatic Merkel cell carcinoma and platinum-treated Urothelial Carcinoma, was initially approved with a 10 mg/kg weight-based dose., By the emergence of modern immunotherapies with active agents like PDCD1 wt Allele (nivolumab, pembrolizumab) and CD274 wt Allele immune checkpoint blockers (atezolizumab, avelumab, durvalumab), new therapeutic options have become available for the treatment of patients with locally advanced and metastatic Urothelial Carcinoma. Accor, ACQUISITION: Five Antibodies, in vitro diagnostic including pembrolizumab (CD274 wt Allele immunoglobulin complex location), atezolizumab (PDCD1 wt Allele immunoglobulin complex location), nivolumab (PDCD1 wt Allele immunoglobulin complex location), avelumab and durvalumab (CD274 wt Allele Antibodies, in vitro diagnostic) have been approved in the treatment of advanced Urothelial Carcinoma in first- and second-line treatment setting., INTERPRETATION: Avelumab showed antitumour activity in the treatment of patients with platinum-refractory metastatic Urothelial Carcinoma; a manageable safety profile was reported in all avelumab-treated patients., Conclusion Avelumab was well tolerated and associated with durable responses and prolonged survival in patients with refractory metastatic Ulcerative Colitis., Avelumab: A Novel Anti-CD274 wt Allele Agent in the Treatment of Merkel Cell Carcinoma and Urothelial Cell Carcinoma., In early 2017, avelumab (Bavencio®), a CD274 wt Allele-blocking monoclonal immunoglobulin complex location agent, was approved for the treatment of metastatic MCC and Ulcerative Colitis., Expert opinion: Avelumab has shown clinical efficacy for metastatic and advanced Ulcerative Colitis in phase I studies after the failure of platinum-based therapy with a well-tolerated safety profile., Avelumab has been approved by the U.S. FDA for the treatment of metastatic Merkel cell carcinoma and metastatic Urothelial Carcinoma that has progressed during or following treatment with a platinum-based regimen.[SEP]Relations: Nivolumab has relations: drug_drug with Avelumab, drug_drug with Avelumab, drug_drug with Urelumab, drug_drug with Urelumab, drug_drug with Cemiplimab, drug_drug with Cemiplimab. Urothelial Carcinoma has relations: disease_disease with urothelial neoplasm, disease_disease with urothelial neoplasm, disease_protein with HRAS, disease_protein with HRAS.", "label": "yes"}
{"original_question": "Is myasthenia gravis associated with osteoporosis?", "id": "converted_811", "sentence1": "Is myasthenia gravis associated with Encounter due to family history of osteoporosis?", "sentence2": "We performed cisplatin/etoposide protocol in 4 patients with generalized Myasthenia Gravis associated with recent Steroids-induced symptomatic VFs. , In this case report, we used ASSAY FOR TACROLIMUS to successfully treat a 13-year-old boy with ocular Myasthenia Gravis who had suffered from severe Steroids complications, including a failure of thrive and Encounter due to family history of Encounter due to family history of osteoporosis.,  INTRODUCTION: Myasthenia gravis (Myasthenia Gravis) is a Neuromuscular Diseases which has been associated with an increased falls risk and glucocorticoid-induced Encounter due to family history of Encounter due to family history of osteoporosis, recognized determinants of increased Fracture risk. , RESULTS: Compared to the control cohort, there was no statistically significant increased risk observed in patients with Myasthenia Gravis for any Fracture (adjusted hazard ratio [aromatic hydrocarbon receptor] 1.11; 95 % confidence interval [CI], 0.84-1.47) or osteoporotic fractures (aromatic hydrocarbon receptor 0.98 [95 % CI 0.67-1.41]). Further, use of oral glucocorticoids up to a cumulative dose exceeding 5 g prednisolone equivalents did not increase risk of Osteoporotic Fractures (aromatic hydrocarbon receptor 0.99 [95 % CI, 0.31-3.14]) compared with Myasthenia Gravis patients without glucocorticoid exposure., The TNFSF11 wt Allele/OPG ratio and indices of bone metabolisms are also not affected by THX, although THX increases the levels of Recombinant Interleukin-7 and TNFSF11 wt Allele., Both disorders had been controlled for around 15 years by oral prednisolone and a cholinesterase inhibitor following surgical removal of invasive thymoma and radiotherapy, but Muscle Weakness due to Myalgia and an increase in serum levels of myogenic enzymes, mainly ascribable to the recurrence of PM, reappeared immediately after cessation of these drugs, which was done because the patient had multiple bone fractures and severe Encounter due to family history of Encounter due to family history of osteoporosis due to the long-term corticosteroid therapy. , We measured bone density in 36 patients (26 females and 10 males) who had undergone long-term prednisolone administration, and found a decrease in bone density in 31% of female patients and Encounter due to family history of Encounter due to family history of osteoporosis in only 11.5% (three cases)., In conclusion, prednisolone-treated patients with myasthenia gravis have an acceptable risk of Osteopenia if prophylactic medication is administered., INTRODUCTION: Myasthenia gravis (Myasthenia Gravis) is a Neuromuscular Diseases which has been associated with an increased falls risk and glucocorticoid-induced Encounter due to family history of Encounter due to family history of osteoporosis, recognized determinants of increased Fracture risk., alendronate should be used with caution in patients with myasthenia gravis who have corticosteroid-induced Encounter due to family history of Encounter due to family history of osteoporosis, In this paper we present two cases of young women who developed severe PAO with Spinal Fractures: a 42-year-old woman with a family history of Encounter due to family history of Encounter due to family history of osteoporosis, and a 21-year-old woman affected with myasthenia gravis, Myasthenia gravis (Myasthenia Gravis) is a Neuromuscular Diseases which has been associated with an increased falls risk and glucocorticoid-induced Encounter due to family history of Encounter due to family history of osteoporosis, recognized determinants of increased Fracture risk[SEP]Relations: myasthenia gravis has relations: disease_phenotype_positive with Acrocyanosis, disease_phenotype_positive with Acrocyanosis, disease_phenotype_positive with Myositis, disease_phenotype_positive with Myositis, disease_protein with FAS, disease_protein with FAS, disease_phenotype_positive with Rheumatoid arthritis, disease_phenotype_positive with Rheumatoid arthritis, disease_protein with MUSK, disease_protein with MUSK.", "label": "yes"}
{"original_question": "Is myc a tumour suppressor gene?", "id": "converted_3226", "sentence1": "Is myc a tumour suppressor gene?", "sentence2": "oncogenic MYC protein, human, a master transcription factor that turns on anabolic metabolism to promote cell growth in many Malignant Neoplasms. , he MYC gene,  the Proto-Oncogene Proteins c-myc, however, other Genes such as the c-myc Proto-Oncogenes are promising targets for anticancer therapy[SEP]Relations: Protein S human has relations: drug_drug with Mitomycin, drug_drug with Mitomycin, drug_drug with Lonazolac, drug_drug with Lonazolac, drug_drug with Dactinomycin, drug_drug with Dactinomycin, drug_drug with Ketorolac, drug_drug with Ketorolac, drug_drug with Cefaclor, drug_drug with Cefaclor.", "label": "no"}
{"original_question": "Is PCAT6 a microRNA?", "id": "converted_4633", "sentence1": "Is PCAT6 gene a microRNA?", "sentence2": "In this work, we investigated the role and regulatory mechanism of Long Intergenic Non-Protein Coding RNA prostate cancer-associated transcript 6 (PCAT6 gene gene) in Malignant neoplasm of breast progression.[SEP]Relations: long noncoding RNA binding has relations: molfunc_protein with MIR384, molfunc_protein with MIR384. benign neoplasm of male breast has relations: disease_disease with breast benign neoplasm, disease_disease with breast benign neoplasm.", "label": "no"}
{"original_question": "Is AZD5153 active in prostate cancer?", "id": "converted_3555", "sentence1": "Is AZD5153 active in Malignant neoplasm of prostate?", "sentence2": "AZD5153 Inhibits Prostate Cancer Cell Growth in Vitro and in Vivo., BRD4 protein, human gene (BRD4 protein, human protein, human) overexpression participates in Malignant neoplasm of prostate progression by enhancing the transcriptional activity and expression of several key oncogenes. AZD5153 is a novel BRD4 protein, human protein, human inhibitor.METHODS: Prostate cancer cells were treated with AZD5153. Cell survival was tested by MTT assay and clonogenicity assay. Cell proliferation was tested by [H3] DNA incorporation assay. Cell apoptosis was tested by caspase-3/-9 activity assay, Histone DNA ELISA assay, ANXA5 gene Fluorescence-Activated Cell Sorting assay and TUNEL staining assay. Cell cycle progression was tested by Propidium Iodide (Pulmonary Valve Insufficiency) Fluorescence-Activated Cell Sorting assay. Signal Transduction was tested by Western blotting assay. The nude mice PC-3 cell line cell line xenograft model was applied to test AZD5153's activity in vivo.RESULTS: AZD5153 inhibited proliferation and survival of established and primary Malignant neoplasm of prostate cells. AZD5153 induced apoptosis activation and cell cycle arrest in Malignant neoplasm of prostate cells. AZD5153 was non-cytotoxic to the prostate epithelial cells. AZD5153 downregulated BRD4 protein, human protein, human targets (Cyclin D1, MYC protein, human, BCL2 gene, FOSL1 wt Allele wt Allele and Cyclin-Dependent Kinase 4) in PC-3 cell line cell line and primary Malignant neoplasm of prostate cells. Further studies show that Proto-Oncogene Proteins c-akt could be the primary resistance factor of AZD5153. Pharmacological inhibition or genetic depletion of Proto-Oncogene Proteins c-akt induced BRD4 protein, human protein, human downregulation, sensitizing AZD5153-induced cytotoxicity in PC-3 cell line cell line cells. In vivo, AZD5153 oral administration inhibited PC-3 cell line cell line xenograft tumor growth in nude mice. Its anti-tumor activity was further enhanced with co-treatment of the Proto-Oncogene Proteins c-akt specific inhibitor MK-2206.CONCLUSION: Together, our results indicate a promising therapeutic value of the novel BRD4 protein, human protein, human inhibitor AZD5153 against Malignant neoplasm of prostate cells., AZD5153 induced apoptosis activation and cell cycle arrest in Malignant neoplasm of prostate cells., CONCLUSION\n\nTogether, our results indicate a promising therapeutic value of the novel BRD4 protein, human protein, human inhibitor AZD5153 against Malignant neoplasm of prostate cells., AZD5153 downregulated BRD4 protein, human protein, human targets (Cyclin D1, MYC protein, human, BCL2 gene, FOSL1 wt Allele wt Allele and Cyclin-Dependent Kinase 4) in PC-3 cell line cell line and primary Malignant neoplasm of prostate cells., RESULTS\n\nAZD5153 inhibited proliferation and survival of established and primary Malignant neoplasm of prostate cells., RESULTS AZD5153 inhibited proliferation and survival of established and primary Malignant neoplasm of prostate cells., AZD5153 induced apoptosis activation and cell cycle arrest in Malignant neoplasm of prostate cells., AZD5153 downregulated BRD4 protein, human protein, human targets (Cyclin D1, MYC protein, human, BCL2 gene, FOSL1 wt Allele wt Allele and Cyclin-Dependent Kinase 4) in PC-3 cell line cell line and primary Malignant neoplasm of prostate cells., CONCLUSION Together, our results indicate a promising therapeutic value of the novel BRD4 protein, human protein, human inhibitor AZD5153 against Malignant neoplasm of prostate cells., AZD5153 Inhibits Prostate Cancer Cell Growth in Vitro and in Vivo, AZD5153 induced apoptosis activation and cell cycle arrest in Malignant neoplasm of prostate cells.[SEP]Relations: ANXA5 has relations: anatomy_protein_present with prostate gland, anatomy_protein_present with prostate gland, disease_protein with gastric cancer, disease_protein with gastric cancer, disease_protein with lung cancer, disease_protein with lung cancer, disease_protein with acute myeloid leukemia with t(9;11)(p22;q23), disease_protein with acute myeloid leukemia with t(9;11)(p22;q23), disease_protein with acute myeloblastic leukemia with maturation, disease_protein with acute myeloblastic leukemia with maturation.", "label": "yes"}
{"original_question": "Have Quantitative Trait Loci affecting splicing (splicing QTLs) been linked to disease?", "id": "converted_93", "sentence1": "Have Quantitative Trait Loci affecting splicing (splicing QTLs) been linked to disease?", "sentence2": "The spontaneously hypertensive Rattus norvegicus (SHORT ROOT protein, Arabidopsis) is a widely used rodent model of Hypertensive disease and Metabolic Syndrome X. Previously we identified thousands of cis-regulated expression Quantitative Trait Loci (eQTLs) across multiple Body tissue using a panel of Rattus norvegicus recombinant inbred (RI) strains derived from Brown Norway and SHORT ROOT protein, Arabidopsis progenitors. These cis-eQTLs represent potential susceptibility loci underlying physiological and pathophysiological traits manifested in SHORT ROOT protein, Arabidopsis. We have prioritized 60 cis-eQTLs and confirmed differential expression between the parental strains by quantitative PCR in 43 (72%) of the eQTL RNA Transcript., These colocalizing correlated cis-eQTLs (c3-eQTLs) are highly attractive as primary susceptibility loci for the colocalizing pQTLs. Furthermore, sequence analysis of the c3-eQTL Genes identified Single Nucleotide Polymorphism (SNPs) that are predicted to affect transcription factor binding affinity, splicing and protein function. These SNPs, which potentially alter transcript abundance and stability, represent strong candidate factors underlying not just eQTL expression phenotypes, but also the correlated metabolic and physiological traits. In conclusion, by integration of genomic sequence, eQTL and QTT datasets we have identified several Genes that are strong positional candidates for pathophysiological traits observed in the SHORT ROOT protein, Arabidopsis strain., Identifying associations between Genotype and gene expression levels using microarrays has enabled systematic interrogation of regulatory variation underlying complex phenotypes. This approach has vast potential for functional characterization of disease states, but its prohibitive cost, given hundreds to thousands of individual samples from populations have to be genotyped and expression profiled, has limited its widespread application.RESULTS: Here we demonstrate that genomic regions with Alleles-specific expression (ASE) detected by sequencing cDNA are highly enriched for cis-acting expression Quantitative Trait Loci (cis-eQTL) identified by profiling of 500 animal allergen extracts in parallel, with up to 90% agreement on the Alleles that is preferentially expressed. We also observed widespread noncoding and antisense ASE and identified several Alleles-specific alternative splicing variants.CONCLUSION: Monitoring ASE by sequencing cDNA from as little as one sample is a practical alternative to expression genetics for mapping cis-acting variation that regulates RNA transcription and processing., The six Genes corresponded to Rattus norvegicus and Mus sp. Quantitative Trait Loci (QTLs) that had shown associations with the common traits such as the well characterized MS and even tumor susceptibility. Our findings suggest that the six Genes may play important roles in the pleiotropic effects on lipid metabolism and the MS, which increase the risk of Type 2 Diabetes and Cardiovascular Diseases. The use of the multivariate phenotypes can be advantageous in identifying genetic risk factors, accounting for the pleiotropic effects when the multivariate phenotypes have a common etiological pathway., To elucidate mechanisms involved in Multiple Sclerosis (MS), we studied genetic regulation of experimental autoimmune encephalomyelitis (EAE) in rats, assuming a Conservation of pathogenic pathways. In this study, we focused on Eae23, originally identified to regulate EAE in a (LEW.1AV1xPVG.1AV1)F2 cross. Our aim was to determine whether one or more Genes within the 67 Mb region regulate EAE and to define candidate risk Genes.METHODOLOGY/PRINCIPAL FINDINGS: We used high resolution Quantitative Trait Loci (QTL) analysis in the 10th generation (BUD31 gene) of an advanced intercross line (AIL) to resolve Eae23 into two QTLs that independently regulate EAE, namely Eae23a and Eae23b. [SEP]Relations: qualitative or quantitative defects of titin has relations: disease_disease with TTN-related myopathy, disease_disease with TTN-related myopathy, disease_disease with qualitative or quantitative protein defects in neuromuscular diseases, disease_disease with qualitative or quantitative protein defects in neuromuscular diseases, disease_disease with limb-girdle muscular dystrophy, disease_disease with limb-girdle muscular dystrophy, disease_disease with tibial muscular dystrophy, disease_disease with tibial muscular dystrophy. Multiple Sclerosis has relations: disease_disease with demyelinating disease, disease_disease with demyelinating disease.", "label": "yes"}
{"original_question": "Is celecoxib effective for treatment of amyotrophic lateral sclerosis?", "id": "converted_2792", "sentence1": "Is celecoxib effective for treatment of amyotrophic lateral sclerosis?", "sentence2": "NTERPRETATION: At the dosage studied, celecoxib did not have a beneficial effect on research subjects with Amyotrophic Lateral Sclerosis, and it was safe. A biological effect of celecoxib was not demonstrated in the Cerebrospinal Fluid. Further studies of celecoxib at a dosage of 800 mg/day in Amyotrophic Lateral Sclerosis are not warranted., Prostaglandin E(2) levels in Cerebrospinal Fluid were not elevated at baseline and did not decline with treatment.<br><b>INTERPRETATION</b>: At the dosage studied, celecoxib did not have a beneficial effect on research subjects with Amyotrophic Lateral Sclerosis, and it was safe.[SEP]Relations: Celecoxib has relations: drug_effect with Arthropathy, drug_effect with Arthropathy, drug_effect with Coronary artery atherosclerosis, drug_effect with Coronary artery atherosclerosis, drug_drug with Corticotropin, drug_drug with Corticotropin, drug_drug with Citalopram, drug_drug with Citalopram, contraindication with stroke disorder, contraindication with stroke disorder.", "label": "no"}
{"original_question": "Does triiodothyronine (T3) has cardiac angiogenic effects?", "id": "converted_1465", "sentence1": "Does triiodothyronine (T3) has Cardiac - anatomy qualifier angiogenic effects?", "sentence2": "T3-induced Cardiac - anatomy qualifier sprouting angiogenesis in adult hypothyroid CASP14 gene was associated with becaplermin, PDGFR-β and downstream activation of Proto-Oncogene Proteins c-akt., liothyronine significantly increased angiogenesis and cell survival and enhanced the expression of nuclear-encoded transcription factors involved in these processes., T(3) administration restored THRB gene mRNA expression level in AAC hearts to the control level., Rbeta knockout and TRalpha/THRB gene double-knockout CASP14 gene both exhibited significantly less capillary density in LV compared with wild-type CASP14 gene., THRB gene in the coronary ECs regulates capillary density during Cardiac - anatomy qualifier development, and down-regulation of THRB gene results in coronary microvascular rarefaction during pathological hypertrophy.[SEP]Relations: Liothyronine has relations: contraindication with sudden Cardiac - anatomy qualifier arrest, contraindication with sudden Cardiac - anatomy qualifier arrest, contraindication with cardiovascular disease, contraindication with cardiovascular disease, drug_effect with Tachycardia, drug_effect with Tachycardia, drug_effect with Arrhythmia, drug_effect with Arrhythmia, drug_effect with Congestive heart failure, drug_effect with Congestive heart failure.", "label": "yes"}
{"original_question": "Can we use platelet biomarkers to study Alzheimer's disease?", "id": "converted_1551", "sentence1": "Can we use platelet biomarkers to study ALZHEIMER DISEASE, FAMILIAL, 1?", "sentence2": "Platelet biomarkers in ALZHEIMER DISEASE, FAMILIAL, 1., Blood Platelets are the most important source of circulating forms of the Serum Amyloid A-1 Protein, Human and other important Proteins such as uridine triacetate and Hepatic Hepatic glycogen synthase kinase-3B., Alternative plasma and platelet measures are described,, The success of these studies led to the application of platelet proteomics to the study of several pathologies where Blood Platelets play a fundamental role. Those include platelet-related disorders, such as storage pool disease, gray platelet syndrome, and Quebec platelet disorder; diseases where unwanted platelet activation is highly relevant, such as Thrombosis and Cardiovascular Diseases; and other diseases, such as cystic fibrosis, increased blood npn, or ALZHEIMER DISEASE, FAMILIAL, 1. [SEP]Relations: blood platelet disease has relations: disease_disease with disease by cell type, disease_disease with disease by cell type, disease_disease with hematologic disease, disease_disease with hematologic disease, disease_disease with thrombocytopenia, disease_disease with thrombocytopenia, disease_disease with qualitative platelet defect, disease_disease with qualitative platelet defect, disease_disease with inherited bleeding disorder, platelet-type, disease_disease with inherited bleeding disorder, platelet-type.", "label": "yes"}
{"original_question": "Are CD8+ (cytotoxic) T cells and  CD4+ Helper T cells generated in the thyroid and express the T-cell receptor?", "id": "converted_3529", "sentence1": "Are CD8A wt Allele+ (cytotoxic) Therapeutic gamma delta T-lymphocytes and  T-Cell Surface Glycoprotein CD4, human+ Helper Therapeutic gamma delta T-lymphocytes generated in the thyroid and express the T-cell receptor?", "sentence2": "A fundamental question in developmental immunology is how bipotential thymocyte precursors generate both T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, human, human+ helper and CD8A wt Allele+ cytotoxic T-Lymphocyte lineages., T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, human, human+CD8A wt Allele+ progenitor thymocyte undergo selection following interaction with Major Histocompatibility Complex class I and class II Molecule bearing peptide self-antigens, giving rise to CD8A wt Allele+ cytotoxic and T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, human, human+ helper or regulatory T-Lymphocyte lineages, respectively., Through positive selection, double-positive cells in the Thymus <angiosperm> differentiate into T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, human, human(+) or CD8A wt Allele(+) T single-positive cells that subsequently develop into different types of effective Therapeutic gamma delta T-lymphocytes, such as T-helper and cytotoxic T lymphocyte cells,, Development, differentiation, and function of thymocyte and T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, human, human(+) and CD8A wt Allele(+) Therapeutic gamma delta T-lymphocytes are controlled by a multitude of secreted and Protoplasm factors, . The T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, human, human(+) helper versus CD8A wt Allele(+) cytotoxic T-cell fate decision serves as an excellent model to study binary fate decision processes. These two cell types are derived from common precursors in the Thymus <angiosperm>., Signals elicited by binding of the T-Cell Receptor and the T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, human, human/CD8A wt Allele co-receptor to major histocompatibility complex (Major Histocompatibility Complex) Molecule control the generation of T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, human, human+ (helper) or CD8A wt Allele+ (cytotoxic) Therapeutic gamma delta T-lymphocytes from thymic precursors that initially express both co-receptor proteins., In the Thymus <angiosperm>, mature T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, human, human+CD8A wt Allele- and T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, human, human-CD8A wt Allele+ Therapeutic gamma delta T-lymphocytes expressing alpha beta T-cell antigen receptors (transcription-coupled nucleotide-excision repair) develop from immature thymocyte through T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, human, human+CD8A wt Allele+ alpha beta transcription-coupled nucleotide-excision repair+ intermediates., In the Thymus <angiosperm>, immature CD8A wt Allele(-4)-transcription-coupled nucleotide-excision repair- cells differentiate, possibly via a short stage of CD8A wt Allele+4- thymocyte, into CD8A wt Allele+4+ transcription-coupled nucleotide-excision repair+ Therapeutic gamma delta T-lymphocytes and mature further into the main T-Lymphocyte populations, the CD8A wt Allele+4- transcription-coupled nucleotide-excision repair+ cytotoxic T lymphocytes and the T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, human, human+8- transcription-coupled nucleotide-excision repair+ T helper cells., In the Mammals Thymus <angiosperm>, T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, human, human helper Therapeutic gamma delta T-lymphocytes and CD8A wt Allele cytotoxic Therapeutic gamma delta T-lymphocytes arise from a common precursor that expresses both T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, human, human and CD8A wt Allele.[SEP]Relations: T-Lymphocyte receptor complex has relations: cellcomp_protein with T-Cell Surface Glycoprotein CD4, human, cellcomp_protein with T-Cell Surface Glycoprotein CD4, human, cellcomp_protein with CD8B, cellcomp_protein with CD8B, cellcomp_protein with CD8A, cellcomp_protein with CD8A, cellcomp_protein with CD3E, cellcomp_protein with CD3E, cellcomp_protein with CD3D, cellcomp_protein with CD3D.", "label": "no"}
{"original_question": "Is cariprazine effective for treatment of bipolar disorder?", "id": "converted_2780", "sentence1": "Is cariprazine effective for treatment of Bipolar Disorder Type 2?", "sentence2": "BACKGROUND: We evaluated the safety/tolerability of longer-term open-label treatment with cariprazine in patients who had responded to cariprazine for acute bipolar mania., Clinically relevant response and remission outcomes in cariprazine-treated patients with Bipolar I disorder., cariprazine is FDA approved for the acute treatment of SCHIZOPHRENIA 2 (disorder) and Manic mood or mixed episodes associated with Bipolar I disorder in adults., DISCUSSION: cariprazine-treated patients with Bipolar I disorder attained clinically significant improvement in Manic mood symptoms as shown by significantly greater rates of response and remission versus placebo; improvement in Manic mood symptoms did not induce depressive symptoms., OBJECTIVE: cariprazine, a dopamine D3/D2 partial agonist atypical antipsychotic with preferential binding to D3 receptors, is approved for the treatment of SCHIZOPHRENIA 2 (disorder) and Manic mood or mixed episodes associated with Bipolar I disorder., <b>BACKGROUND</b>: cariprazine was approved for treating SCHIZOPHRENIA 2 (disorder) and Bipolar Disorder Type 2, and currently is being evaluated for treating Cancer patients and suicide and Cancer patients and suicide and depression in clinical trials in the United States.[SEP]Relations: Bipolar Disorder Type 2 has relations: contraindication with Desipramine, contraindication with Desipramine, contraindication with Desipramine, contraindication with Desipramine, contraindication with Trimipramine, contraindication with Trimipramine, contraindication with Trimipramine, contraindication with Trimipramine, contraindication with Imipramine, contraindication with Imipramine.", "label": "yes"}
{"original_question": "Is Nivolumab (Opdivo) a PD-L1 inhibitor?", "id": "converted_3370", "sentence1": "Is nivolumab (Opdivo) a PD-L1 PPP1R1A gene?", "sentence2": "Fatal Myocarditis Following Treatment with the PDCD1 wt Allele Inhibitor nivolumab,  PDCD1 wt Allele PPP1R1A gene nivolumab (Opdivo), programmed cell death protein 1 (PDCD1 wt Allele)-blocking Antibodies, in vitro diagnostic nivolumab or pembrolizumab , An improvement in the understanding of the role of the immune system in Specimen Source Codes - Specimen Source Codes - tumor immunosurveillance has led to the development of the programmed death-1 ( PDCD1 wt Allele ) Immune Checkpoint Inhibitors nivolumab ( Opdivo) . , nivolumab (Opdivo(®); nivolumab BMS™) was the first programmed death (PD)-1 Immune Checkpoint Inhibitors to be approved for use in advanced, Squamous non-small cell lung cancer (Non-Small Cell Lung Carcinoma) following prior chemotherapy.[SEP]Relations: nivolumab has relations: drug_protein with PDCD1, drug_protein with PDCD1, drug_drug with Opicinumab, drug_drug with Opicinumab, drug_drug with PRO-542, drug_drug with PRO-542, drug_drug with IGN311, drug_drug with IGN311, drug_drug with Ipilimumab, drug_drug with Ipilimumab.", "label": "no"}
{"original_question": "Can Freund's complete adjuvant induce arthritis?", "id": "converted_3897", "sentence1": "Can Freund's complete adjuvant induce arthritis?", "sentence2": "complete Freund's adjuvant (CFA) induced RA, The RA model was established using Freund's complete adjuvant, ,  Rheumatoid Arthritis (RA) was induced by Freund's Complete Adjuvant (Freund's Adjuvant; 1 mg/0.1 ml paraffin oil), injected subcutaneously on days 0, 30 and 40, The Rattus norvegicus were made arthritic using a subcutaneous injection with 0.1 ml complete Freund's adjuvant (CFA) into the Structure of thick cushion of skin on foot of the left hind paw.[SEP]Relations: Rheumatoid Arthritis has relations: drug_effect with Fluvoxamine, drug_effect with Fluvoxamine, drug_effect with Fluoxetine, drug_effect with Fluoxetine, drug_effect with Pregabalin, drug_effect with Pregabalin, drug_effect with Sibutramine, drug_effect with Sibutramine, drug_effect with Paroxetine, drug_effect with Paroxetine.", "label": "yes"}
{"original_question": "Are ultraconserved elements often transcribed?", "id": "converted_49", "sentence1": "Are ultraconserved Elements often transcribed?", "sentence2": "Starting from a genome-wide expression profiling, we demonstrate for the first time a functional link between oxygen deprivation and the modulation of long noncoding RNA Transcript from ultraconserved regions, termed transcribed-ultraconserved regions (T-UCRs), Our data gives a first glimpse of a novel functional hypoxic network comprising protein-coding RNA Transcript and noncoding RNA (ncRNAs) from the T-UCRs category, Highly conserved Elements discovered in Vertebrates are present in non-syntenic loci of tunicates, act as enhancers and can be transcribed during development, The majority of these regions map onto ultraconserved Elements and we demonstrate that they can act as functional enhancers within the organism of origin, as well as in cross-transgenesis experiments, and that they are transcribed in extant species of Olfactores. We refer to the Elements as 'Olfactores conserved non-coding Elements', We used a custom microarray to assess the levels of NAGPA gene transcription during Mus sp. development and integrated these data with published microarray and next-generation sequencing datasets as well as with newly produced PCR validation experiments. We show that a large MDFAttributeType - Fraction of non-exonic UCEs is transcribed across all developmental stages examined from only one DNA strand. Although the nature of these RNA Transcript remains a mistery, our meta-analysis of RNA-Seq datasets indicates that they are unlikely to be short RNA and that some of them might encode nuclear RNA Transcript, Our data shows that the concurrent presence of enhancer and transcript function in non-exonic NAGPA gene Elements is more widespread than previously shown. Moreover through our own experiments as well as the use of next-generation sequencing datasets, we were able to show that the RNA encoded by non-exonic UCEs are likely to be long RNA transcribed from only one DNA strand, Short ultraconserved promoter regions delineate a class of preferentially expressed alternatively spliced RNA Transcript, The importance of other classes of non-coding RNA, such as long intergenic ncRNAs (Long Intergenic Non-Protein Coding RNA) and transcribed ultraconserved regions (T-UCRs) as altered Elements in Neoplasms, is also gaining recognition., Other ncRNAs, such as Piwi-Interacting RNA (piRNAs), small nucleolar RNA (snoRNAs), transcribed ultraconserved regions (T-UCRs) and large intergenic non-coding RNA (Long Intergenic Non-Protein Coding RNA) are emerging as key Elements of cellular homeostasis., The majority of these regions map onto ultraconserved Elements and we demonstrate that they can act as functional enhancers within the organism of origin, as well as in cross-transgenesis experiments, and that they are transcribed in extant species of Olfactores., Transcribed ultraconserved regions (T-UCRs) are a subset of 481 DNA Sequence longer than 200 bp, which are absolutely conserved between orthologous regions of Homo sapiens, Rattus norvegicus and Mus sp. genomes, and are actively transcribed., Highly conserved Elements discovered in Vertebrates are present in non-syntenic loci of tunicates, act as enhancers and can be transcribed during development., The Evf-2 noncoding RNA is transcribed from the Dlx-5/6 ultraconserved region and functions as a Dlx-2 transcriptional coactivator., In this report, we show that the Dlx-5/6 ultraconserved region is transcribed to generate an alternatively spliced form of Evf-1, the RETINAL NONATTACHMENT, NONSYNDROMIC CONGENITAL Evf-2., These studies identify a critical role for TUC338 in regulation of transformed cell growth and of transcribed ultraconserved RETINAL NONATTACHMENT, NONSYNDROMIC CONGENITAL as a unique class of Genes involved in the pathobiology of altretamine/cisplatin/cyclophosphamide protocol., Transcribed ultraconserved region (T-UCR) RNA Transcript are a novel class of lncRNAs transcribed from ultraconserved regions (UCRs), The majority of these regions map onto ultraconserved Elements and we demonstrate that they can act as functional enhancers within the organism of origin, as well as in cross-transgenesis experiments, and that they are transcribed in extant species of Olfactores, Transcribed ultraconserved regions (T-UCRs) are a subset of 481 DNA Sequence longer than 200 bp, which are absolutely conserved between orthologous regions of Homo sapiens, Rattus norvegicus and Mus sp. genomes, and are actively transcribed, Other ncRNAs, such as Piwi-Interacting RNA (piRNAs), small nucleolar RNA (snoRNAs), transcribed ultraconserved regions (T-UCRs) and large intergenic non-coding RNA (Long Intergenic Non-Protein Coding RNA) are emerging as key Elements of cellular homeostasis, Transcribed ultraconserved region in Homo sapiens Malignant Neoplasms., We show that a large MDFAttributeType - Fraction of non-exonic UCEs is transcribed across all developmental stages examined from only one DNA strand, Although PCBP2 gene gene-OT1 gene is partially located within the poly(rC) binding protein 2 (PCBP2 gene gene) gene, the transcribed RETINAL NONATTACHMENT, NONSYNDROMIC CONGENITAL encoding PCBP2 gene gene-OT1 gene is expressed independently of PCBP2 gene gene and was cloned as a 590-bp RNA gene, termed TUC338, Moreover through our own experiments as well as the use of next-generation sequencing datasets, we were able to show that the RNA encoded by non-exonic UCEs are likely to be long RNA transcribed from only one DNA strand.[SEP]Relations: rRNA transcription has relations: bioprocess_protein with ANG, bioprocess_protein with ANG, bioprocess_bioprocess with plastid rRNA transcription, bioprocess_bioprocess with plastid rRNA transcription, bioprocess_bioprocess with mitochondrial rRNA transcription, bioprocess_bioprocess with mitochondrial rRNA transcription, bioprocess_bioprocess with RETINAL NONATTACHMENT, NONSYNDROMIC CONGENITAL transcription, bioprocess_bioprocess with RETINAL NONATTACHMENT, NONSYNDROMIC CONGENITAL transcription, bioprocess_bioprocess with nucleolar large rRNA transcription by RNA polymerase I, bioprocess_bioprocess with nucleolar large rRNA transcription by RNA polymerase I.", "label": "yes"}
{"original_question": "Can a peptide aptamer be used as protein inhibitor?", "id": "converted_533", "sentence1": "Can a Peptides aptamer be used as Protein Info inhibitor?", "sentence2": "Peptide aptamers of LIM-only Protein Info 2 (Rhombotin 2) were previously used to successfully treat Rhombotin 2-induced tumours in a mouse model of leukemia., Inhibition of mammalian cell proliferation by genetically selected Peptides aptamers that functionally antagonize E2F activity., Accumulating work over the past decade has shown that Peptides aptamer screening represents a valid strategy for inhibitor identification that can be applied to a variety of different targets. , . The target of one inhibitor Peptides, Pep80, identified in this screen was determined to be SNAPIN gene, a Protein Info associated with the soluble N-ethyl maleimide sensitive factor adaptor Protein Info receptor (SNAP receptor activity) complex that is critical for calcium-dependent exocytosis during neurotransmission. , Use of the genetically selected intracellular aptamer inhibitors allowed us to define unique mechanisms important to HIV-1 replication and T cell biology., This review will describe pre-clinical and clinical data of four major classes of TGF-β inhibitor, namely i) ligand traps, ii) Antisense Oligonucleotides, iii) receptor kinase inhibitors and iv) Peptides aptamers. ,  A Peptides aptamer (ID1/3-PA7) has been designed to prevent this interaction and thereby leading to the transcription of p16(INK4a)., A Peptides kinase inhibitor (IP(20)) was used as the aptameric Peptides , Peptide aptamer mimicking RAD51-binding Superkingdom (taxonomic category) of BRCA2 gene gene inhibits DNA damage repair and survival in Trypanosoma brucei brucei brucei.,  Peptides aptamer, ID1 Protein Info, human/3-PA7, targeting ID1 Protein Info, human and DNA-Binding Protein Inhibitor ID-3,, Targeting ID1 Protein Info, human and DNA-Binding Protein Inhibitor ID-3 by a specific Peptides aptamer induces E-box promoter activity, cell cycle arrest, and apoptosis in breast cancer Cells., Aptamer-derived peptides as potent inhibitors of the oncogenic guanyl-nucleotide exchange factor activity Tgat., Our approach thus demonstrates that Peptides aptamers are potent inhibitors that can be used to interfere with guanyl-nucleotide exchange factor activity functions in vivo., Development of systemic in vitro evolution and its application to generation of Peptides-aptamer-based inhibitors of carboxypeptidase C E., he fusion Peptides, cytarabine/thioguanine aptamer, was observed within PC12 cytoplasm and maintained both Abeta-binding ability and antioxygenic property similar to TXN wt Allele., Stable expression of a novel fusion Peptides of Thioredoxin 1 and ABAD-inhibiting Peptides protects PC12 Cells from intracellular amyloid-beta., In order to efficiently select aptamers that bind to and inhibit proteins,, Aptamer selection based on inhibitory activity using an evolution-mimicking algorithm., This demonstrates the utility of this strategy for screening aptamers based on their inhibitory actions., Protoplasm expression of the DRD-binding Peptides aptamer specifically suppressed receptor-mediated extrinsic apoptosis but not intrinsic pathway, which was recapitulated by the Antisense Oligonucleotides for CASP8AP2 wt Allele. , Peptide aptamers are peptides constrained and presented by a scaffold Protein Info that are used to study Protein Info function in Cells. They are able to disrupt Protein Info-Protein Info interactions , Here we have used a genetic screen in Saccharomyces cerevisiae to select in vivo peptides coupled to Thioredoxin (human), called aptamers, that could inhibit GEFD2 activity. One aptamer, TRIAPalpha (TRio Inhibitory APtamer), specifically blocks GEFD2-exchange activity on RHOA Protein Info, human in vitro., These results show that cell proliferation can be inhibited using genetically-selected synthetic peptides that specifically target Protein Info-Protein Info interaction motifs within cell cycle regulators., These data highlight the utility of Peptides aptamers to identify novel binding interfaces and highlight a role for microtubule-associated Protein Info 1B in DAPK-1-dependent signaling in autophagy and Membrane Device blebbing.[SEP]Relations: Protein S human has relations: drug_drug with Anti-inhibitor coagulant complex, drug_drug with Anti-inhibitor coagulant complex, drug_drug with Anti-inhibitor coagulant complex, drug_drug with Anti-inhibitor coagulant complex. Protein Info binding has relations: molfunc_protein with ACR, molfunc_protein with ACR, molfunc_protein with PTER, molfunc_protein with PTER, molfunc_protein with ADAR, molfunc_protein with ADAR.", "label": "yes"}
{"original_question": "Do nematodes contain architectural proteins like CTCF?", "id": "converted_3761", "sentence1": "Do nematodes contain architectural proteins like CTGF protein, human?", "sentence2": "A mode of genetic regulation that involves insulators and insulator binding proteins to establish independent transcriptional units is currently not known in nematodes including Caenorhabditis elegans. , the insulator protein CTGF protein, human has been secondarily lost in derived nematodes like Caenorhabditis elegans., he most highly enriched motif (LM1) corresponds to the X-box motif known from Saccharomyces cerevisiae and Phylum Nematoda, uggest that the insulator protein CTGF protein, human has been secondarily lost in derived nematodes like Caenorhabditis elegans. We , of CTGF protein, human from several nematodes is paralleled by a loss of two of its interactors, the polycomb repressive complex subunit SuZ12 and the multifunctional transcription factor TYY1. In contrast to earlier st, SULTS: While orthologs for other insulator proteins were absent in all 35 analysed Phylum Nematoda species, we find orthologs of CTGF protein, human in a subset of nematodes. A, Loss of the insulator protein CTGF protein, human during Phylum Nematoda evolution, que secondary loss of CTGF protein, human from several nematodes is paralleled by a loss of two of its interactors, the polycomb repressive complex subunit SuZ12 and the multifunctional transcription factor TYY1. In con, level. A mode of genetic regulation that involves insulators and insulator binding proteins to establish independent transcriptional units is currently not known in nematodes including Caenorhabditis ,  suggest that the insulator protein CTGF protein, human has been secondarily lost in derived nematodes like Caenorhabditis elegans. W, Loss of the insulator protein CTGF protein, human during Phylum Nematoda evolution.[SEP]Relations: Protein S human has relations: drug_drug with Nefazodone, drug_drug with Nefazodone, drug_drug with Loracarbef, drug_drug with Loracarbef, drug_drug with Cefditoren, drug_drug with Cefditoren, drug_drug with Tazobactam, drug_drug with Tazobactam, drug_protein with PROC, drug_protein with PROC.", "label": "no"}
{"original_question": "Can ATAC-Seq be employed in single-cell mode?", "id": "converted_3849", "sentence1": "Can XCL1 wt Allele-Seq be employed in single-cell mode?", "sentence2": "Single-cell XCL1 wt Allele-Seq: strength in numbers., Assembly, and Single-Cell XCL1 wt Allele-Seq., Single cell RNA-seq and XCL1 wt Allele-Seq analysis of cardiac progenitor cell transition states and lineage settlement.,  Here, we comprehensively characterize Mus sp. cardiac progenitor cells (CPCs) marked by Nkx2-5 and Isl1 expression from E7.5 to E9.5 using single-cell RNA sequencing and Transposase-accessible chromatin location location profiling (XCL1 wt Allele-Seq)., Classifying cells with Scasat, a single-cell XCL1 wt Allele-Seq analysis tool., When done at single-cell resolution, XCL1 wt Allele-Seq provides an insight into the cell-to-cell variability that emerges from otherwise identical DNA Sequence by identifying the variability in the genomic location of open chromatin location location sites in each of the cells., Single-cell XCL1 wt Allele-Seq in Homo sapiens pancreatic islets and deep learning upscaling of rare cells reveals cell-specific type 2 diabetes regulatory signatures., THODS: We present genome-wide single-cell chromatin location location accessibility profiles in >1,600 cells derived from a Homo sapiens pancreatic islet sample using single-cell combinatorial indexing XCL1 wt Allele-Seq (sci-XCL1 wt Allele-Seq). W, Contiguity-Preserving Transposition Sequencing (CPT-Seq) for Genome-Wide Haplotyping, Assembly, and Single-Cell XCL1 wt Allele-Seq., SCALE method for single-cell XCL1 wt Allele-Seq analysis via latent feature extraction., Single-cell XCL1 wt Allele-Seq (scATAC-seq) profiles the chromatin location location accessibility landscape at single cell level, thus revealing cell-to-cell variability in gene regulation., The recently developed low-input and single-cell regulome mapping technologies such as XCL1 wt Allele-Seq and single-cell XCL1 wt Allele-Seq (scATAC-seq) allow analyses of small-cell-number and single-cell samples, but their signals remain highly discrete or noisy., This paper presents Scasat (single-cell XCL1 wt Allele-Seq analysis tool), a complete pipeline to process scATAC-seq data with simple steps., Here, we comprehensively characterize Mus sp. cardiac progenitor cells (CPCs) marked by Nkx2-5 and Isl1 expression from E7.5 to E9.5 using single-cell RNA sequencing and Transposase-accessible chromatin location location profiling (XCL1 wt Allele-Seq)., Single-cell XCL1 wt Allele-Seq (scATAC-seq) technology has also been developed to study cell type-specific chromatin location location accessibility in tissue samples containing a heterogeneous Cells population., Here we combined sequencing of the transcription-coupled nucleotide-excision repair-encoding genes with assay for Transposase-accessible chromatin location location with sequencing (XCL1 wt Allele-Seq) analysis at the single-cell level to provide information on the transcription-coupled nucleotide-excision repair specificity and epigenomic state of individual Therapeutic gamma delta T-lymphocytes., Substantial advances of this work include the optimization of a single-cell combinatorial indexing assay for Transposase accessible chromatin location location (sci-XCL1 wt Allele-Seq); a software suite,, The accessible chromatin location location landscape of the Mus hippocampus at single-cell resolution., Here we present a comprehensive map of the accessible chromatin location location landscape of the Mus sp. hippocampus at single-cell resolution., We expect this review will provide a guideline for successful data generation and analysis methods using appropriate software tools and databases for the study of chromatin location location accessibility at single-cell resolution., Single-cell sequencing assay for Transposase-accessible chromatin location location (scATAC-seq) is the state-of-the-art technology for analyzing genome-wide regulatory landscapes in single cells., Single-cell XCL1 wt Allele-Seq data are sparse and noisy, and analyzing such data is challenging., Here, we introduce a method for analyzing scATAC-seq data, called Single-Cell XCL1 wt Allele-Seq analysis via Latent feature Extraction (SCALE)., Single-cell XCL1 wt Allele-Seq signal extraction and enhancement with SCATE., Single-cell XCL1 wt Allele-Seq detects open chromatin location location in individual cells., Currently data are sparse, but combining information from many single cells can identify determinants of cell-to-cell chromatin location location variation., Predictions based on single-cell RNA-seq (Single-Cell RNA-Seq) can more accurately reconstruct bulk chromatin location location accessibility than using scATAC-seq., Global prediction of chromatin location location accessibility using small-cell-number and single-cell RNA-seq., Single-cell XCL1 wt Allele-Seq (scATAC-seq) maps from hundreds of single cells in aggregate closely resemble accessibility profiles from tens of millions of cells and provide insights into cell-to-cell variation., However, very few studies have been performed at the single cell level (scATAC-seq) due to technical challenges., Here, we present Perturb-XCL1 wt Allele, a method that combines multiplexed CRISPR interference or knockout with genome-wide chromatin location location accessibility profiling in single cells based on the simultaneous detection of CRISPR guide RNA and open chromatin location location sites by assay of Transposase-accessible chromatin location location with sequencing (XCL1 wt Allele-Seq)., Additionally, the same workflow can be used to aid de novo assembly (Adey et al., Genome Res 24(12):2041-2049, 2014), detect structural variants, and perform single cell XCL1 wt Allele-Seq analysis (Cusanovich et al., Science 348(6237):910-914, 2015)., ChromA can analyze single cell XCL1 wt Allele-Seq data, correcting many biases generated by the sparse sampling inherent in single cell technologies.,  circuits. Existing chromatin location location profiling methods such as XCL1 wt Allele-Seq and DNase-seq, applied to islets in bulk, produce aggregate profiles that mask important Cells and regulatory heterogeneity.METHODS: We present genome-wide single-cell chromatin location location accessibility profiles in >1,600 cells derived from a Homo sapiens pancreatic islet sample using single-cell combinatorial indexing XCL1 wt Allele, XCL1 wt Allele-Seq has become a leading technology for probing the chromatin location location landscape of single and aggregated cells.[SEP]Relations: transcription-coupled nucleotide-excision repair has relations: bioprocess_protein with AQR, bioprocess_protein with AQR, bioprocess_protein with XRCC1, bioprocess_protein with XRCC1, bioprocess_protein with POLR2C, bioprocess_protein with POLR2C, bioprocess_protein with CDK7, bioprocess_protein with CDK7, bioprocess_protein with ERCC1, bioprocess_protein with ERCC1.", "label": "yes"}
{"original_question": "Does physical activity influence gut hormones?", "id": "converted_38", "sentence1": "Does physical activity influence gut hormones?", "sentence2": "Increases in blood Peptide YY, human(3-36) levels were dependent on the exercise intensity (effect of session: P<0.001 by two-way ANOVA), whereas those in Glucagon-Like Peptide 1 levels were similar between two different exercise sessions., A decrease in serum leptin levels (-48.4%, p < 0.001) was observed after intervention without changes in total peptide YY and Therapeutic Insulin levels., ur data suggest that the control of spontaneous physical activity by gut hormones or their neuropeptide targets may represent an important mechanistic component of energy balance regulation, Hunger and gut hormones remained unchanged during the bed rest., weight-bearing exercise has a greater exercise-induced Desire for food suppressive effect compared with non-weight-bearing exercise, and both forms of exercise lowered acylated Lenomorelin and increased total Peptide YY, human, but the changes did not differ significantly between exercise modes., Appetite (P < 0.0005) and acylated Lenomorelin (P < 0.002) were suppressed during exercise but more so during SIE. Peptide YY increased during exercise but most consistently during END (P < 0.05). Acylated Lenomorelin was lowest in the afternoon of SIE (P = 0.018) despite elevated Desire for food, Following the pre-exercise meal, Lenomorelin was suppressed ~17% and Therapeutic Insulin and Peptide YY, human were elevated ~157 and ~40%, respectively, relative to fasting (day 7). Following exercise, Peptide YY, human, Lenomorelin, and Human Growth Hormone were significantly (p < 0.0001) increased by ~11, ~16 and ~813%, respectively. The noted disruption in the typical inverse relationship between Lenomorelin and Peptide YY, human following exercise suggests that interaction of these Peptides may be at least partially responsible for post-exercise Desire for food suppression, Plasma levels of Peptide YY, human and Glucagon-Like Peptide 1 were increased by exercise, whereas plasma Lenomorelin levels were unaffected by exercise, These findings suggest Lenomorelin and Peptide YY, human may regulate Desire for food during and after exercise,, significant (P < 0.05) interaction effects for hunger, acylated Lenomorelin, and Peptide YY, human, indicating suppressed hunger and acylated Lenomorelin during aerobic and resistance exercise and increased Peptide YY, human during aerobic exercise, 'exercise-induced anorexia' may potentially be linked to increased Peptide YY, human, Glucagon-Like Peptide 1 and Pancreatic Polypeptide levels., Hunger scores and Peptide YY, human, Glucagon-Like Peptide 1 and Pancreatic Polypeptide levels showed an inverse temporal pattern during the 1-h exercise/control intervention, Exercise significantly increased mean Peptide YY, human, Glucagon-Like Peptide 1 and Pancreatic Polypeptide levels, and this effect was maintained during the post-exercise period for Glucagon-Like Peptide 1 and Pancreatic Polypeptide. No significant effect of exercise was observed on postprandial levels of Lenomorelin, following blood donation the strenuous exercise resulted in a marked reduction in the plasma leptin, We conclude that strenuous physical exercise; 1) fails to affect plasma leptin level but when performed after meal but not after blood withdrawal it results in an increase and fall in plasma leptin, and 2) the release of gut hormones (Gastrin, human, Cholecystokinin, human and Pancreatic Polypeptide) and stress hormones (epinephrine and epinephrine and norepinephrine, hydrocortisone, Human Growth Hormone) increase immediately after exercise independently of feeding or blood donation, the unrestricted exercise group has a significantly elevated SRIF-LI concentration, Exercise has recently been reported to influence Lenomorelin and Peptide YY, human concentrations.[SEP]Relations: Norepinephrine has relations: drug_effect with Aggressive behavior, drug_effect with Aggressive behavior, drug_effect with Lactic acidosis, drug_effect with Lactic acidosis, drug_effect with Anxiety, drug_effect with Anxiety. Hydrocortisone has relations: drug_effect with Increased body weight, drug_effect with Increased body weight, drug_effect with Emotional lability, drug_effect with Emotional lability.", "label": "yes"}
{"original_question": "Are there antimicrobial proteins in royal jelly?", "id": "converted_4214", "sentence1": "Are there antimicrobial Proteins in royal jelly?", "sentence2": "Jellein, a Peptides derived from royal jelly of honeybee has been shown to have promising effect against several Bacterial and fungal species. , It is also the most studied bee product, aimed at unravelling its bioactivities, such as antimicrobial, antioxidant, anti-aging, immunomodulatory, and general tonic action against laboratory animals, microbial organisms, farm animals, and clinical trials, Jelleines, isolated as novel antibacterial peptides from the Royal Jelly (RJ) of bees, exhibit broad-spectrum protection against microbial infections., The study showed significant antimicrobial activity from several Proteins present in the honey preparation preparation of M. beecheii.[SEP]Relations: Bacterial arthritis has relations: disease_protein with IFNG, disease_protein with IFNG, disease_protein with TNF, disease_protein with TNF, disease_disease with gonococcal infection of joint, disease_disease with gonococcal infection of joint, disease_disease with infectious disease, disease_disease with infectious disease, disease_disease with infective arthritis, disease_disease with infective arthritis.", "label": "yes"}
{"original_question": "Is PTEN a tumour suppressor?", "id": "converted_3294", "sentence1": "Is PTEN protein, human a tumour suppressor?", "sentence2": "PTEN protein, human protein, human is a potent tumour suppressor, Genome aberrations of the PTEN protein, human protein, human tumour suppressor gene are among the most common in Malignant neoplasm of prostate.[SEP]Relations: Protein S human has relations: drug_drug with Cloricromen, drug_drug with Cloricromen, drug_drug with Naproxen, drug_drug with Naproxen, drug_drug with Lepirudin, drug_drug with Lepirudin, drug_drug with Turoctocog alfa, drug_drug with Turoctocog alfa, drug_drug with (R)-warfarin, drug_drug with (R)-warfarin.", "label": "yes"}
{"original_question": "Is eptinezumab a small molecule?", "id": "converted_4017", "sentence1": "Is eptinezumab a small molecule?", "sentence2": "Eptinezumab-jjmr (referred to as eptinezumab hereafter; Vyepti™) is a humanised monoclonal antibody that binds to Calcitonin Precursor, human (Calcitonin Gene-Related Peptide) and blocks its binding to the receptor. [SEP]Relations: Human calcitonin has relations: drug_effect with Eczema, drug_effect with Eczema, drug_drug with Zoledronic acid, drug_drug with Zoledronic acid, drug_effect with Epistaxis, drug_effect with Epistaxis, drug_effect with Eczematoid dermatitis, drug_effect with Eczematoid dermatitis, drug_effect with Tetany, drug_effect with Tetany.", "label": "no"}
{"original_question": "Is endotrophin derived from collagen?", "id": "converted_3248", "sentence1": "Is COL6A3 protein, human derived from collagen?", "sentence2": "Collagen Alpha-3(VI) Chain protein, human production from Collagen Type IV, High levels of Collagen Alpha-3(VI) Chain and its cleaved product, Collagen Alpha-3(VI) Chain protein, human (ETP), Endotrophin is released from COL VI[SEP]Relations: collagen type IV trimer has relations: cellcomp_protein with OTOL1, cellcomp_protein with OTOL1, cellcomp_protein with COL4A1, cellcomp_protein with COL4A1, cellcomp_protein with COL4A5, cellcomp_protein with COL4A5, cellcomp_protein with COL4A3, cellcomp_protein with COL4A3, cellcomp_protein with COL4A2, cellcomp_protein with COL4A2.", "label": "yes"}
{"original_question": "Is ACI-35 a passive vaccine?", "id": "converted_2327", "sentence1": "Is ACI-35 a passive vaccine?", "sentence2": "Two active vaccines targeting either nonphosphorylated (AAD-vac1) and phosphorylated tau (ACI-35) have entered Phase I testing.[SEP]", "label": "no"}
{"original_question": "Does the royal jelly contain proteins?", "id": "converted_4400", "sentence1": "Does the royal jelly contain Proteins?", "sentence2": " We observed differences in the metabolome, proteome, and phytosterols compositions of royal jelly synthesized by nurse bees from multi-pesticide exposed colonies, including significant reductions of key Nutrients such as 24-methylenecholesterol, major royal jelly Proteins, and 10-hydroxy-2-decenoic acid. ,  Two-dimensional electrophoresis was used for the fractionation of royal jelly Proteins, the main bioactive compounds of RJ, such as Proteins, peptides, Fatty Acids, and Substance with phenol structure,  the expression of four of the major royal jelly Proteins (MRJP1, MRJP2, MRJP4, and MRJP5) and also several Proteins associated with carbohydrate metabolism and energy synthesis, the antioxidant system, detoxification, biosynthesis, amino acid metabolism, transcription and translation, protein folding and binding, olfaction, and learning and memory.[SEP]Relations: 12-Hydroxydodecanoic Acid has relations: drug_protein with ADH5, drug_protein with ADH5.", "label": "yes"}
{"original_question": "Does the Mcm2-Ctf4-Polα axis play a role in transfer of histones to leading strand DNA at the replication forks?", "id": "converted_3572", "sentence1": "Does the Mcm2-WDHD1 gene-Polα axis play a role in transfer of histones to leading strand DNA at the replication forks?", "sentence2": "The Mcm2-WDHD1 gene-Polα Cervus axis Facilitates Parental Histone H3-H4 Transfer to Lagging Strands., Although essential for epigenetic inheritance, the transfer of parental Histone antigen (H3-H4)2 tetramers that contain epigenetic modifications to replicating DNA strands is poorly understood. Here, we show that the Mcm2-WDHD1 gene-Polα axis facilitates the transfer of parental (H3-H4)2 tetramers to lagging-strand DNA at replication forks. Mutating the conserved Histone antigen-binding domain of the Mcm2 subunit of the CASK gene (Cdc45-MCM-GINS) DNA Helicases, which translocates along the leading-strand template, results in a marked enrichment of parental (H3-H4)2 on leading strand, due to the impairment of the transfer of parental (H3-H4)2 to lagging strands. Similar effects are observed in WDHD1 gene and Polα primase mutants that disrupt the connection of the CASK gene helicase to Polα that resides on lagging-strand template. Our results support a model whereby parental (H3-H4)2 complex (molecular entity) displaced from Nucleosomes by DNA unwinding at replication forks are transferred by the CASK gene-WDHD1 gene-Polα complex to lagging-strand DNA for nucleosome assembly at the original location.[SEP]Relations: nucleosome assembly has relations: bioprocess_protein with MCM2, bioprocess_protein with MCM2, bioprocess_protein with MACROH2A2, bioprocess_protein with MACROH2A2. nucleosome has relations: cellcomp_protein with MACROH2A2, cellcomp_protein with MACROH2A2, cellcomp_protein with MACROH2A1, cellcomp_protein with MACROH2A1, cellcomp_protein with PRM2, cellcomp_protein with PRM2.", "label": "no"}
{"original_question": "Does Vitamin D induce  autophagy?", "id": "converted_1800", "sentence1": "Does Vitamin D induce  autophagy?", "sentence2": " 1,25(OH)2D treatment was accompanied by autophagy activation , Autophagy signaling pathway was regulated by cholecalciferol, ergocalciferol induces autophagy, Vitamin D shows promise for the prevention and amelioration of pathologic responses in Irritable Bowel Syndrome, an effect that is mediated, at least in part, by the induction and modulation of autophagy.[SEP]Relations: Ergocalciferol has relations: drug_drug with Vitamin D, drug_drug with Vitamin D, contraindication with familial isolated deficiency of vitamin E, contraindication with familial isolated deficiency of vitamin E, drug_protein with VDR, drug_protein with VDR. Cholecalciferol has relations: drug_drug with Vitamin D, drug_drug with Vitamin D, contraindication with familial isolated deficiency of vitamin E, contraindication with familial isolated deficiency of vitamin E.", "label": "yes"}
{"original_question": "Does promoter shape vary across populations?", "id": "converted_3402", "sentence1": "Does Promoter shape vary across populations?", "sentence2": "Promoter shape varies across populations and affects Promoter evolution and expression noise., Animal promoters initiate transcription either at precise positions (narrow promoters) or dispersed regions (broad promoters), a distinction referred to as Promoter shape. Although highly conserved, the functional properties of promoters with different shapes and the genetic basis of their evolution remain unclear. Here we used natural genetic variation across a panel of 81 Drosophila <basidiomycetes> <basidiomycetes> lines to measure changes in Transcription Initiation Site (Toxic Shock Syndrome) usage, identifying thousands of genetic Variant affecting RNA Transcript levels (strength) or the distribution of TSSs within a Promoter (shape). Our results identify Promoter shape as a molecular trait that can evolve independently of Promoter strength. Broad promoters typically harbor shape-associated Variant, with signatures of adaptive selection. Single-cell measurements demonstrate that Variant modulating Promoter shape often increase expression noise, whereas heteroallelic interactions with other Promoter Variant alleviate these effects. These results uncover new functional properties of natural promoters and suggest the minimization of expression noise as an important factor in Promoter evolution., Promoter shape varies across populations and affects Promoter evolution and expression noise[SEP]Relations: Promoter clearance from RNA polymerase I Promoter has relations: bioprocess_bioprocess with Promoter clearance during DNA-templated transcription, bioprocess_bioprocess with Promoter clearance during DNA-templated transcription, bioprocess_bioprocess with Promoter clearance from RNA polymerase I Promoter for nuclear large rRNA RNA Transcript, bioprocess_bioprocess with Promoter clearance from RNA polymerase I Promoter for nuclear large rRNA RNA Transcript. HIV Transcription Initiation has relations: pathway_protein with POLR2G, pathway_protein with POLR2G, pathway_protein with POLR2J, pathway_protein with POLR2J, pathway_protein with CCNH, pathway_protein with CCNH.", "label": "yes"}
{"original_question": "Is cardiac magnetic resonance imaging indicated in the pre-participation screening of athletes?", "id": "converted_1652", "sentence1": "Is cardiac magnetic resonance imaging indicated in the pre-participation screening of athletes?", "sentence2": "As modern imaging further enhances our understanding of the spectrum of athlete's heart, its role may expand from the assessment of athletes with suspected disease to being part of comprehensive pre-participation screening in apparently healthy athletes., Finally we will address the role of CMR in pre-participation screening.[SEP]", "label": "no"}
{"original_question": "Is SUMOylation a post-translational modification in eukaryotes?", "id": "converted_1817", "sentence1": "Is SUMOylation a post-translational ResponseLevel - modification in Eukaryota?", "sentence2": "SUMOylation, the conjugation of target Proteins with SUMO (small ubiquitin-related modifier), is a type of post-translational ResponseLevel - ResponseLevel - modification in Eukaryota and involves the sequential action of activation (E1), conjugation (ubiquitin-like protein conjugating enzyme activity) and ligation (E3) enzymes. , Plants have evolved to cope with changing environmental conditions. One way plants achieve this is through post-translational ResponseLevel - ResponseLevel - modification of target Proteins by ubiquitination and SUMOylation., Sumoylation is a post-translational ResponseLevel - ResponseLevel - modification essential in most Eukaryota that regulates stability, localization, activity, or interaction of a multitude of Proteins., SUMOylation, the Covalent Interaction attachment of a member of the small ubiquitin-like modifier (SUMO) family of Proteins to lysines in target substrates, is an essential post-translational ResponseLevel - ResponseLevel - modification in Eukaryota. , Post-translational ResponseLevel - ResponseLevel - modification by SUMO is a highly conserved pathway in Eukaryota that plays very important regulatory roles in many cellular processes. , SUMOylation is an essential post-translational ResponseLevel - ResponseLevel - modification that regulates a variety of cellular processes including cell cycle progression. Although the SUMOylation pathway has been identified and investigated in many Eukaryota, the mechanisms of SUMOylation in regulating the functions of various substrates are still poorly understood. , SUMOylation is a relevant protein post-translational ResponseLevel - ResponseLevel - modification in Eukaryota., SUMOylation is a reversible post-translational ResponseLevel - ResponseLevel - modification essential for genome stability., Many SUMOylated lysines have previously been reported to be ubiquitinated, acetylated or methylated, thus indicating cross-talk between SUMO and other post-translational modifications., Sumoylation is a post-translational ResponseLevel - ResponseLevel - modification shown to play a role in diverse biological processes., Besides phosphorylation or ubiquitylation, for which many examples of modulation by pathogens exist, a post-translational ResponseLevel - ResponseLevel - modification called SUMOylation was recently shown to be targeted by pathogenic bacteria., cruzi SUMOylated Proteins are similarly modified, indicating conserved functions for protein SUMOylation in this early divergent eukaryote., Leukoencephalopathy, Progressive Multifocal is a potent tumor suppressor and proapoptotic factor and is functionally regulated by post-translational modifications such as phosphorylation, sumoylation, and ubiquitination., SUMOylation is an essential post-translational ResponseLevel - ResponseLevel - modification that regulates a variety of cellular processes including cell cycle progression., SUMOylation in Giardia lamblia: A Conserved Post-Translational Modification in One of the Earliest Divergent Eukaryotes, SUMOylation, the Covalent Interaction attachment of a member of the small ubiquitin-like modifier (SUMO) family of Proteins to lysines in target substrates, is an essential post-translational ResponseLevel - ResponseLevel - modification in Eukaryota, SUMOylation is a relevant protein post-translational ResponseLevel - ResponseLevel - modification in Eukaryota, Post-translational modifications (PTMS gene) are one facet of this proteasomal regulation, with over 400 known phosphorylation sites, over 500 ubiquitination sites and 83 internal lysine acetylation sites, as well as multiple sites for caspase cleavage, glycosylation (such as O-GlcNAc ResponseLevel - ResponseLevel - modification), methylation, nitrosylation, oxidation, and SUMOylation, SUMOylation is an important post-translational ResponseLevel - ResponseLevel - modification, and Proto-Oncogene Proteins c-akt SUMOylation was found to regulate cell proliferation, tumorigenesis and cell cycle, but the molecular mechanism of Proto-Oncogene Proteins c-akt SUMOylation is less well known, SUMOylation is a form of post-translational ResponseLevel - ResponseLevel - modification where small ubiquitin-like modifiers (SUMO) are covalently attached to target Proteins to regulate their properties, One distinctive feature in acute proteotoxic stresses, such as heat shock (HS), is rapid post-translational ResponseLevel - ResponseLevel - modification of Proteins by SUMOs (small ubiquitin-like modifier Proteins; SUMOylation), Post-translational ResponseLevel - ResponseLevel - modification by the Small Ubiquitin-like Modifier (SUMO) Proteins, a process termed SUMOylation, is involved in many fundamental cellular processes, SUMOylation is an important post-translational ResponseLevel - ResponseLevel - modification that is involved in many key biological processes, Group III metabotropic glutamate receptors (mGluRs) undergo post-translational ResponseLevel - ResponseLevel - modification by SUMO in in vitro assays but the SUMOylation of full-length mGluRs in mammalian cells has not been reported, SUMOylation is a relevant protein post-translational ResponseLevel - ResponseLevel - modification in Eukaryota. , However, the effects of pathogenic bacteria on SUMOylation, an essential post-translational ResponseLevel - ResponseLevel - modification in Eukaryotic Cells, remain largely unknown. , A novel post-translational ResponseLevel - ResponseLevel - modification of nucleolin protein, human protein, human, SUMOylation at Lys-294, mediates arsenite-induced cell death by regulating GADD45A wt Allele� mRNA stability., Drosophila <basidiomycetes> <basidiomycetes> Bicoid is a substrate of sumoylation and its activator function is subject to inhibition by this post-translational ResponseLevel - ResponseLevel - modification., Here, we demonstrate that SUMOylation of RELB gene might be one of these post-translational modifications rendering the function of the NF-�B transcription factor RELB gene. , In the last decade, SUMOylation has emerged as an essential post-translational ResponseLevel - ResponseLevel - modification in Eukaryota., SUMOylation, the conjugation of target Proteins with SUMO (small ubiquitin-related modifier), is a type of post-translational ResponseLevel - ResponseLevel - modification in Eukaryota and involves the sequential action of activation (E1), conjugation (ubiquitin-like protein conjugating enzyme activity) and ligation (E3) enzymes., SUMOylation, the Covalent Interaction attachment of a member of the small ubiquitin-like modifier (SUMO) family of Proteins to lysines in target substrates, is an essential post-translational ResponseLevel - ResponseLevel - modification in Eukaryota., One way plants achieve this is through post-translational ResponseLevel - ResponseLevel - modification of target Proteins by ubiquitination and SUMOylation., The small ubiquitin-like modifier (SUMO) pathway in Eukaryota is an essential post-translational ResponseLevel - ResponseLevel - modification required for a variety of cellular processes, development and organelle biogenesis., Post-translational ResponseLevel - ResponseLevel - modification by SUMO is a highly conserved pathway in Eukaryota that plays very important regulatory roles in many cellular processes., Many SUMOylated lysines have previously been reported to be ubiquitinated, acetylated or methylated, thus indicating cross-talk between SUMO and other post-translational modifications. We identified 70 phosphorylation and four acetylation events in proximity to SUMOylation sites, and we provide evidence for acetylation-dependent SUMOylation of endogenous Histone H3. SUMOylation regulates target Proteins involved in all nuclear processes including transcription, DNA repair, chromatin remodeling, precursor-mRNA splicing and Ribosomes assembly., SUMOylation is a reversible post-translational ResponseLevel - ResponseLevel - modification essential for genome stability. Using high-resolution MS, we have studied global SUMOylation in Human cells in a site-specific manner, identifying a total of>4,300 SUMOylation sites in>1,600 Proteins., We quantitatively studied SUMOylation dynamics in response to SUMO protease inhibition, proteasome inhibition and heat shock. Many SUMOylated lysines have previously been reported to be ubiquitinated, acetylated or methylated, thus indicating cross-talk between SUMO and other post-translational modifications. We identified 70 phosphorylation and four acetylation events in proximity to SUMOylation sites, and we provide evidence for acetylation-dependent SUMOylation of endogenous Histone H3., Sumoylation is a post-translational ResponseLevel - ResponseLevel - modification shown to play a role in diverse biological processes. Here, we demonstrate that sumoylation is essential for proper heterochromatin function in Drosophila <basidiomycetes> <basidiomycetes> through ResponseLevel - ResponseLevel - modification of SU(VAR)3-7. Indeed, SU(VAR)3-7 is sumoylated at lysine K839; this ResponseLevel - ResponseLevel - modification is required for localization of SU(VAR)3-7 at Centric heterochromatin, Chromosomes, Human, Pair 4, and telomere., Sumoylation is a post-translational ResponseLevel - ResponseLevel - modification shown to play a role in diverse biological processes. Here, we demonstrate that sumoylation is essential for proper heterochromatin function in Drosophila <basidiomycetes> <basidiomycetes> through ResponseLevel - ResponseLevel - modification of SU(VAR)3-7., Our results suggest a new level of regulation of Sall activity in vivo during animal development through post-translational ResponseLevel - ResponseLevel - modification by sumoylation., BACKGROUND: Small protein tag (SUMO) is a key regulator of nuclear functions but little is known regarding the role of the post-translational ResponseLevel - ResponseLevel - modification sumoylation outside of the Cell Nucleus, particularly in the Central Nervous System (CNS).METHODOLOGY/PRINCIPAL FINDINGS: Here, we report that the expression levels of SUMO-modified substrates as well as the components of the sumoylation machinery are temporally and spatially regulated in the developing Rattus norvegicus brain., SUMOylation in Giardia lamblia: A Conserved Post-Translational Modification in One of the Earliest Divergent Eukaryotes., Identification of a novel post-translational ResponseLevel - ResponseLevel - modification in Plasmodium falciparum or Plasmodium falciparum + Plasmodium sp or Plasmodium falciparum or Plasmodium falciparum + Plasmodium sp + Plasmodium sp: protein sumoylation in different cellular compartments., More recently, Proto-Oncogene Proteins c-akt has been identified as a substrate for many different post-translational modifications, including not only phosphorylation of other residues, but also acetylation, glycosylation, oxidation, ubiquitination and SUMOylation.[SEP]Relations: protein tag has relations: molfunc_protein with SUMO2, molfunc_protein with SUMO2, molfunc_protein with SUMO4, molfunc_protein with SUMO4, molfunc_protein with SUMO1, molfunc_protein with SUMO1, molfunc_protein with SUMO1P1, molfunc_protein with SUMO1P1, molfunc_protein with SUMO3, molfunc_protein with SUMO3.", "label": "yes"}
{"original_question": "Are Spinal Intradural Primary Malignant Peripheral Nerve Sheath Tumors(MPNST) rare in neurofibromatosis patients?", "id": "converted_3337", "sentence1": "Are Spinal Intradural Primary Malignant Peripheral Nerve Sheath Tumors(Malignant Peripheral Nerve Sheath Tumor) rare in NF1 gene patients?", "sentence2": "Spinal intradural primary malignant peripheral nerve sheath tumors (Malignant Peripheral Nerve Sheath Tumor) are rare in patients without NF1 gene., Primary malignant peripheral nerve sheath tumors (MPNSTs) are extremely rare in patients without a history of NF1 gene; only 18 cases have been reported in the English-language literature to this point.[SEP]Relations: malignant peripheral nerve sheath tumor has relations: disease_disease with tumor of cranial and spinal nerves, disease_disease with tumor of cranial and spinal nerves, disease_disease with peripheral nervous system cancer, disease_disease with peripheral nervous system cancer, disease_disease with nerve sheath neoplasm, disease_disease with nerve sheath neoplasm, disease_disease with malignant melanocytic neoplasm of the peripheral nerve sheath, disease_disease with malignant melanocytic neoplasm of the peripheral nerve sheath, disease_disease with malignant glandular tumor of peripheral nerve sheath, disease_disease with malignant glandular tumor of peripheral nerve sheath.", "label": "no"}
{"original_question": "Anaplasma phagocytophilum is an obligate gram-negative, intracellular bacterium, yes  or no", "id": "converted_3234", "sentence1": "Anaplasma phagocytophilum is an obligate gram-negative, Intracellular bacterium, yes  or no", "sentence2": "The genus Anaplasma belonging to the Anaplasmataceae family (order Rickettsiales) comprises obligate Intracellular Gram-negative bacteria of veterinary and public health importance. Six species and five types of strains genetically related are currently assigned to the genus Anaplasma including Anaplasma marginale, A. centrale, A. bovis, A. phagocytophilum, A. ovis and A. platys as classified species, and \"A. capra\", A. odocolei sp. nov., Human Granulocytic Anaplasmosis (HGA), an increasingly recognized febrile tick-borne illness, is caused by a gram-negative obligate Intracellular bacterium Anaplasma phagocytophilum[SEP]Relations: human anaplasmosis has relations: disease_disease with anaplasmosis, disease_disease with anaplasmosis. Anal margin neoplasm has relations: phenotype_phenotype with Anal margin squamous cell carcinoma, phenotype_phenotype with Anal margin squamous cell carcinoma, phenotype_phenotype with Anal margin melanoma, phenotype_phenotype with Anal margin melanoma, phenotype_phenotype with Anal margin basal cell carcinoma, phenotype_phenotype with Anal margin basal cell carcinoma, phenotype_phenotype with Abnormality of the anus, phenotype_phenotype with Abnormality of the anus.", "label": "yes"}
{"original_question": "Is pesticide exposure associated with polyneuropathy?", "id": "converted_386", "sentence1": "Is pesticide exposure associated with polyneuropathy?", "sentence2": "As the syndrome occurred after the acute Cholinergic Agents syndrome but before Phosphoric Acid Esters-induced delayed polyneuropathy, the syndrome was called 'intermediate syndrome'., The characteristic features of the IMS are weakness of the Muscle Tissue of respiration (Vaginal contraceptive Vaginal contraceptive diaphragm (device) (device), intercostal Muscle Tissue and accessory Muscle Tissue including neck Muscle Tissue) and of proximal limb Muscle Tissue. Accompanying features often include weakness of Muscle Tissue innervated by some Cranial Nerves. It is now emerging that the degree and extent of Muscle Weakness may vary following the onset of the IMS. , Electrophysiological studies following OP Poisoning aspects have revealed three characteristic phenomena: (i) repetitive firing following a single stimulus; (ii) gradual reduction in twitch height or compound muscle action potential followed by an increase with repetitive stimulation (the 'decrement-increment response'); and (iii) continued reduction in twitch height or compound muscle action potential with repetitive simulation ('decrementing response'). , Organophosphate-induced delayed polyneuropathy is a sensory-motor distal axonopathy which usually occurs after exposure of certain OP Insecticides. Neuropathy due to ingestion of Osteoporosis with pseudoglioma have rarely been reported in the literature., We report a patient with serious organophosphorus-induced delayed neuropathy due to malathion injection. The patient was a 32-year-old female who self-injected undetermined amounts of malathion over the median nerve trace on the forearm crease in a suicide attempt which resulted in Peripheral Nervous System Diseases.,  Acutely, these patients present with Cholinergic Agents crisis; intermediate syndrome and delayed polyneuropathy are other sequel of this form of Poisoning aspects., There was no strong evidence of irreversible peripheral nerve damage following acute OP Poisoning aspects, however further studies are required., Particular interactions are also addressed, such as those of Pesticides acting as endocrine disruptors, the cumulative Toxic effect of organophosphates and Hydrocarbons, Chlorinated resulting in estrogenic effects and the promotion of Phosphoric Acid Esters-induced delayed polyneuropathy., The multivariate analyses showed that the population living in areas with high pesticide use had an increased risk for ALZHEIMER DISEASE, FAMILIAL, 1 and suicide attempts and that males living in these areas had increased risks for Polyneuropathy, affective disorders and suicide attempts. , These compounds cause four important neurotoxic effects in Homo sapiens: the Cholinergic Agents syndrome, the intermediate syndrome, Phosphoric Acid Esters-induced delayed polyneuropathy (OPIDP) and chronic Phosphoric Acid Esters-induced neuropsychiatric disorder (COPIND). , An 18-year-old woman and a 22-year-old man were admitted to the hospital with weakness, Paresthesia, and gait disturbances at 35 and 22 days, respectively, after ingesting dimethyl-2,2-dichloro vinyl phosphate (Dichlorvos). Neurological examination revealed weakness, vibration sense loss, bilateral dropped foot, brisk deep tendon reflexes, and bilaterally positive Babinski sign. Electroneurography demonstrated distal motor polyneuropathy with segmental demyelination associated with Axonal degeneration prominent in the distal parts of both lower All All extremities., Sensory complaints and electrodiagnostic findings consistent with polyneuropathy were found in a minority (3/7) of subjects 28 years after an acute toxic arsenic exposure., Organophosphate-induced delayed polyneuropathy (OPIDP) is a rare Toxic effect resulting from exposure to certain organophosphorus (OP) esters. , Therefore, OPIDP may develop only after very large exposures to Insecticides, causing severe Cholinergic Agents Toxic effect., Several studies have reported the occurrence of Sensory neuropathy with exposure to Chlorpyrifos and other Organic phosphorus insecticide, NOS, at levels not associated with overt Toxic effect. , We found no evidence of Sensory neuropathy or isolated peripheral abnormalities among subjects with long-term Chlorpyrifos exposure at levels known to be associated with the manufacturing process., Persistent, mainly motor, impairment of the peripheral nervous system was found in men two years after OP Poisoning aspects, in particular in severe occupational and intentional Poisoning with neuropathic Osteoporosis with pseudoglioma. This finding is possibly due to remaining Phosphoric Acid Esters induced delayed polyneuropathy., Besides the well known acute Cholinergic Agents Toxic effect, these compounds may cause late-onset distal polyneuropathy occurring two to three weeks after the acute exposure. , Electromyography demonstrated motor weighed sensory-motor polyneuropathy with Axonal degeneration significant in the distal parts of bilateral lower All All extremities. , The two cases are presented here since Phosphoric Acid Esters Poisoning are common in our country, and since late-onset polyneuropathy is not a well known clinical presentation as acute Toxic effect., The course of Phosphoric Acid Esters-induced delayed polyneuropathy (OPIDP) in Homo sapiens has not been quantitatively measured in epidemiologic studies., The persistence of deficits in motor strength in all severely poisoned patients regardless of pesticide type was unexpected, and may reflect persistent Cholinergic Agents blockade or intermediate syndrome, neuropathy, or a combination of these., The findings showed a strong association between exposure to OP concentrate and neurological symptoms, but a less consistent association with sensory thresholds. , Following accidental or suicidal exposure, these anticholinesterases lead to three well defined neurological syndromes i.e. initial life threatening acute Cholinergic Agents crisis which often requires management in intensive care unit, intermediate syndrome in which Cranial nerve palsies, proximal Muscle Weakness and respiratory Muscle Weakness are common and patients often require respiratory support and delayed Phosphoric Acid Esters induced polyneuropathy., [Late onset polyneuropathy due to exposure to organophosphates].,  Less often a polyneuropathic syndrome of late onset may occur., On electromyography there was sensomotor peripheral polyneuropathy, which was primarily axonal and predominantly motor and distal. Peripheral nerve biopsy confirmed the presence of 'dying back' type axonopathy. , Agricultural workers chronically exposed to Phosphoric Acid Esters Insecticides, without adequate protection, have an increased risk of developing late onset neuropathy due to organophosphates. , Epidemiologic studies on Pesticides have found associations with long-term effects on health mainly in three fields: Primary malignant neoplasm (especially hematological Primary malignant neoplasm), neurotoxic effects (polyneuropathy, neuro-behavioral hazards, Parkinson Disease), and reproductive disorders (Sterility, Reproductive, Congenital Abnormality, adverse pregnancy outcomes, perinatal mortality). , EMG studies showed evidence of partial denervation of the anterior tibial group of Muscle Tissue and flexor digiti minimi in 2 of the 30 workers (6.7%) who underwent EMG examination., Neurological symptoms consist in cerebro-organic disfunctions, locomotory disorders reminiscent of Multiple Sclerosis or M. Parkinson, and sensory, motoric and vegetative polyneuropathy, leading, for instance, to cardiovascular regulatory disorder like sympathicotonia or, orthostatic hypotonia. , Thirty percent of patients had definite or possible exposure to Phosphoric Acid Esters Pesticides, and the peak use coincides with the peak incidence of Guillain-Barre Syndrome., These results suggest that previously reported cases of Phosphoric Acid Esters-induced delayed polyneuropathy may represent only the worst disease in a spectrum of impairment, a sequela of exposure that may be much more common than previously thought., It is suggested that the main cause of nervous lesions in these cases was the complex effect of Pesticides., Delayed polyneuropathy develops within 1 to 3 weeks and abates after 6 to 12 months. , Isolated case reports have circumstantially linked the use of the herbicide 2,4-dichlorophenoxyacetic acid (2,4-Dichlorophenoxyacetic Acid) to polyneuropathy., Thus, the weight of evidence indicates that 2,4-Dichlorophenoxyacetic Acid is an unlikely cause of polyneuropathy., A patient is reported presenting a Cerebellar Diseases developing about 5 weeks after acute exposure to an Phosphoric Acid Esters insecticide. , Less well known, but more complex and idiosyncratic, is the potential for some agents to produce a delayed and progressive polyneuropathy--Organophosphorus Induced Delayed Neurotox-icity (OPIDN).,  It is also quite probable that human Neurotoxicity Syndromes may be a potential hazard from exposure to more than the handful of organophosphorus Pesticides that have been described in the literature., In the present study the electroencephalograms of 3 of a group 10 workmen, who had been continually exposed to hexachlorcyclohexane, show pathological findings. The electromyograms of 8 of these 10 workman demonstrate a disturbance of the peripherical motoneuron. All probands, who exhibit o pathological EEG, also show a polyneuropathy., Many Organophosphorus Compounds, including the Phosphoric Acid Esters Insecticides, may cause polyneuropathy of delayed onset., Nevertheless, we describe a patient with delayed polyneuropathy after suicidal ingestion of Parathion., Following acute organophosphorus (OP) Poisoning aspects patients complain of Numbness without objective sensory abnormalities or other features of OP induced delayed polyneuropathy. [SEP]Relations: polyneuropathy has relations: disease_disease with polyneuropathy due to drug, disease_disease with polyneuropathy due to drug, disease_disease with polyneuritis, disease_disease with polyneuritis, disease_disease with Peripheral Nervous System Diseases, disease_disease with Peripheral Nervous System Diseases, disease_disease with critical illness polyneuropathy, disease_disease with critical illness polyneuropathy, disease_disease with polyradiculoneuropathy, disease_disease with polyradiculoneuropathy.", "label": "yes"}
{"original_question": "Is Sotatercept effective for Pulmonary Arterial Hypertension?", "id": "converted_4419", "sentence1": "Is Sotatercept effective for Pulmonary Arterial Hypertension?", "sentence2": "Sotatercept for the Treatment of Pulmonary Arterial Hypertension., CONCLUSIONS: Treatment with Sotatercept resulted in a reduction in pulmonary vascular resistance in patients receiving background therapy for Idiopathic Idiopathic pulmonary arterial hypertension., Sotatercept for the Treatment of Pulmonary Arterial Hypertension, CONCLUSIONS: Treatment with Sotatercept resulted in a reduction in pulmonary vascular resistance in patients receiving background therapy for pulmonary arterial hypertensio, n hematologic adverse events. One patient in the Sotatercept 0.7-mg group died from Cardiac Arrest.CONCLUSIONS: Treatment with Sotatercept resulted in a reduction in pulmonary vascular resistance in patients receiving background t[SEP]Relations: Sotatercept has relations: drug_drug with Estriol, drug_drug with Estriol, drug_drug with Estradiol, drug_drug with Estradiol, drug_drug with Ipafricept, drug_drug with Ipafricept, drug_drug with Estradiol acetate, drug_drug with Estradiol acetate, drug_drug with Epimestrol, drug_drug with Epimestrol.", "label": "yes"}
{"original_question": "Is there a dependence between chromatin organization and dorsoventral gene expression in Drosophila?", "id": "converted_4428", "sentence1": "Is there a dependence between chromatin organization and dorsoventral gene expression in Drosophila <basidiomycetes>?", "sentence2": "Independence of chromatin conformation and gene regulation during Drosophila <basidiomycetes> <basidiomycetes> dorsoventral patterning., Here, using the dorsoventral patterning of the Drosophila <basidiomycetes> <basidiomycetes> melanogaster embryo as a model system, we provide evidence for the independence of chromatin organization and dorsoventral gene expression. We define tissue-specific enhancers and link them to expression patterns using single-cell RNA-seq. Surprisingly, despite tissue-specific chromatin states and gene expression, chromatin organization is largely maintained across Body tissue. Our results indicate that tissue-specific chromatin conformation is not necessary for tissue-specific gene expression but rather acts as a scaffold facilitating gene expression when enhancers become active.[SEP]Relations: bone tissue has relations: anatomy_anatomy with endochondral bone tissue, anatomy_anatomy with endochondral bone tissue, anatomy_anatomy with trabecular bone tissue, anatomy_anatomy with trabecular bone tissue, anatomy_anatomy with intramembranous bone tissue, anatomy_anatomy with intramembranous bone tissue, anatomy_anatomy with lamellar bone, anatomy_anatomy with lamellar bone, anatomy_anatomy with osteoid, anatomy_anatomy with osteoid.", "label": "no"}
{"original_question": "Are the major royal jelly proteins similar to the yellow proteins?", "id": "converted_3925", "sentence1": "Are the major royal jelly proteins similar to the yellow proteins?", "sentence2": "Major royal jelly proteins (named MRJP1-5) of Apis mellifera (Apis mellifera), yellow proteins of Drosophila <basidiomycetes> <basidiomycetes>, together with putative proteins found in several Bacteria, form a Protein Family termed the MRJP/yellow family., Analysis of Drosophila <basidiomycetes> <basidiomycetes> yellow-B DNA, Complementary reveals a new family of proteins related to the royal jelly proteins in the Apis mellifera, he Yellow proteins are related to the Royal Jelly proteins and have no relatives in other non-insect metazoan species. [SEP]Relations: Bacteremia has relations: disease_phenotype_positive with listeriosis, disease_phenotype_positive with listeriosis, disease_phenotype_positive with cyclic hematopoiesis, disease_phenotype_positive with cyclic hematopoiesis, disease_phenotype_positive with toxic shock syndrome, disease_phenotype_positive with toxic shock syndrome, disease_phenotype_positive with nocardiosis, disease_phenotype_positive with nocardiosis, disease_phenotype_positive with shigellosis, disease_phenotype_positive with shigellosis.", "label": "yes"}
{"original_question": "Can radius fracture cause carpal tunnel syndrome?", "id": "converted_2462", "sentence1": "Can radius Fracture cause Upper extremity>Carpal tunnel syndrome?", "sentence2": "CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) after Bone structure of Bone structure of distal radius fractures can present in 3 forms: acute, transient, and delayed., Complications were categorized as Upper extremity>CARPAL TUNNEL SYNDROME 2, other sensibility issues, Tendon structure complications including irritation and Rupture, deep infections, complex regional pain syndrome and unidentified DRUJ or scapholunar problems., The overall complication rate was 14.6% (95% CI 11.8-17.7) including Upper extremity>CARPAL TUNNEL SYNDROME 2 or change in sensibility in 5.2% and Tendon structure complications in 4.7%. , BACKGROUND: Although median nerve Neuropathy and Upper extremity>CARPAL TUNNEL SYNDROME 2 (Carpal Tunnel Syndrome) are known complications of both untreated and acutely treated Bone structure of Bone structure of distal radius Fracture, median Neuropathy after correction of Bone structure of Bone structure of distal radius Malunion of Bone is not commonly reported in hand surgery literature. , Complications were defined as Malunion of Bone, Upper extremity>CARPAL TUNNEL SYNDROME 2, complex regional pain syndrome (Complex Regional Pain Syndromes), persistent pain, and subjective cosmetic deformity of the Upper extremity>Wrist., CARPAL TUNNEL SYNDROME 2 is a common complication associated with Bone structure of Bone structure of distal radius fractures., The patient also had minor complications of little finger Structure of flexor Tendon structure irritation and Upper extremity>CARPAL TUNNEL SYNDROME 2. She underwent implant removal and Upper extremity>Carpal tunnel release at 8 months., Acute multiple Structure of flexor Tendon structure injury and Upper extremity>CARPAL TUNNEL SYNDROME 2 after open Bone structure of Bone structure of distal radius Fracture., CARPAL TUNNEL SYNDROME 2 is a common condition and is a well-recognized phenomenon following a Bone structure of Bone structure of distal radius Fracture., We report the incidence of late onset post-operative Upper extremity>CARPAL TUNNEL SYNDROME 2 (late Upper extremity>CARPAL TUNNEL SYNDROME 2) and late median nerve Neuropathy after volar plating of Bone structure of Bone structure of distal radius Fracture by conducting a retrospective study on volar plating for Bone structure of Bone structure of distal radius Fracture performed during 2002 to 2006., CARPAL TUNNEL SYNDROME 2 after Bone structure of Bone structure of distal radius Fracture., [Case-control study on transverse carpal ligament resection for the prevention of delayed Upper extremity>CARPAL TUNNEL SYNDROME 2 after Bone structure of Bone structure of distal radius Fracture]., Numbness of hand and Upper extremity>CARPAL TUNNEL SYNDROME 2 after volar plating of Bone structure of Bone structure of distal radius Fracture., Delayed Upper extremity>CARPAL TUNNEL SYNDROME 2 presenting after a Bone structure of Bone structure of distal radius Fracture has healed is best managed in standard fashion., Being well known and accepted techniques of Upper extremity>Carpal tunnel release, we believe that the techniques described in this paper provide a viable alternative for Upper extremity>Carpal tunnel release in the setting of Bone structure of Bone structure of distal radius Fracture fixation; with the added advantages of the original minimally invasive techniques., CARPAL TUNNEL SYNDROME 2 after Fracture of the Bone structure of Bone structure of distal radius is a well known complication in adults, but in small children Upper extremity>CARPAL TUNNEL SYNDROME 2 is extremely rare., Carpal Tunnel Syndrome and Distal Radius Fractures., CARPAL TUNNEL SYNDROME 2 after Bone structure of Bone structure of distal radius Fracture., Numbness of hand and Upper extremity>CARPAL TUNNEL SYNDROME 2 after volar plating of Bone structure of Bone structure of distal radius Fracture.[SEP]Relations: Upper extremity>Carpal tunnel syndrome has relations: disease_disease with nerve compression syndrome, disease_disease with nerve compression syndrome, disease_disease with nerve compression syndrome, disease_disease with nerve compression syndrome, disease_disease with genetic peripheral Neuropathy, disease_disease with genetic peripheral Neuropathy, disease_disease with genetic peripheral Neuropathy, disease_disease with genetic peripheral Neuropathy, disease_protein with TTR, disease_protein with TTR.", "label": "yes"}
{"original_question": "Are OATP1B1 and OATP1B3 associated with bilirubin transport?", "id": "converted_1536", "sentence1": "Are SLCO1B1 wt Allele and SLCO1B3 wt Allele associated with Bilirubin transport?", "sentence2": "SLCO1B1 wt Allele and SLCO1B3 wt Allele-mediated transport of Bilirubin was confirmed and inhibition was determined for atazanavir, rifampin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir. , Examples of adaptive Nontoxic changes in Abdomen>Liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) Bilirubin above baseline levels, include reversible inhibition of UGT1A1 gene gene-mediated Bilirubin metabolism and SLCO1B1 wt Allele-, SLCO1B3 wt Allele-, or ABCC2 wt Allele-mediated transport (Keogh., Due to limited solubility and poor ionization of Bilirubin and its Glucuronides, the formation of estradiol 3-Glucuronides was used as a surrogate to assess UGT1A1 gene gene activity, while the transport of pitavastatin, 5(6)-carboxy-2',7'-dichlorofluorescein, and Taurocholate were used as surrogate Probe brand of methazole herbicide substrates to monitor the function of SLCO1B1 wt Allele/SLCO1B3 wt Allele, ABCC2 wt Allele, and ABCB11 wt Allele, respectively., SLCO1B1 wt Allele and SLCO1B3 wt Allele-mediated transport of Bilirubin was confirmed and inhibition was determined for atazanavir, rifampin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir., However, because Pharmacologic Substance transporters also contribute to Bilirubin elimination, the purpose of this work was to investigate the in vitro inhibition of SLCO1B1 wt Allele, SLCO1B3 wt Allele, ABCC2 wt Allele, and ABCB11 wt Allele of select test drugs known to elicit Jaundice, Chronic Idiopathic., Thus, disruption of hepatic reuptake of Bilirubin Glucuronides due to coexisting SLCO1B1 wt Allele and SLCO1B3 wt Allele deficiencies explains Rotor-type Jaundice, Chronic Idiopathic.Moreover, SLCO1B1 wt Allele and SLCO1B3 wt Allele null mutations may confer substantial Pharmacologic Substance Toxic effect risks., Bilirubin elimination is a multifaceted process consisting of uptake of Bilirubin into the Hepatocyte facilitated by SLCO1B1 wt Allele and SLCO1B3 wt Allele., Complete SLCO1B1 wt Allele and SLCO1B3 wt Allele deficiency causes Homo sapiens Rotor syndrome by interrupting conjugated Bilirubin reuptake into the Abdomen>Liver., Thus, disruption of hepatic reuptake of Bilirubin Glucuronides due to coexisting SLCO1B1 wt Allele and SLCO1B3 wt Allele deficiencies explains Rotor-type Jaundice, Chronic Idiopathic., The data show that a substantial fraction of Bilirubin Immunostimulating conjugate (antigen) is primarily secreted by ABCC3 wt Allele at the sinusoidal membrane into the blood, from where they are subsequently reuptaken by sinusoidal membrane-bound organic anion transporting polypeptides SLCO1B1 wt Allele and SLCO1B3 wt Allele., Evaluating the in vitro inhibition of UGT1A1 gene gene, SLCO1B1 wt Allele, SLCO1B3 wt Allele, ABCC2 wt Allele, and ABCB11 wt Allele in predicting Pharmacologic Substance-induced Jaundice, Chronic Idiopathic., SLCO1B1 wt Allele and SLCO1B3 wt Allele-mediated transport of Bilirubin was confirmed and inhibition was determined for atazanavir, rifampin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir, Bilirubin elimination is a multifaceted process consisting of uptake of Bilirubin into the Hepatocyte facilitated by SLCO1B1 wt Allele and SLCO1B3 wt Allele, Due to limited solubility and poor ionization of Bilirubin and its Glucuronides, the formation of estradiol 3-Glucuronides was used as a surrogate to assess UGT1A1 gene gene activity, while the transport of pitavastatin, 5(6)-carboxy-2',7'-dichlorofluorescein, and Taurocholate were used as surrogate Probe brand of methazole herbicide substrates to monitor the function of SLCO1B1 wt Allele/SLCO1B3 wt Allele, ABCC2 wt Allele, and ABCB11 wt Allele, respectively, Examples of adaptive Nontoxic changes in Abdomen>Liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) Bilirubin above baseline levels, include reversible inhibition of UGT1A1 gene gene-mediated Bilirubin metabolism and SLCO1B1 wt Allele-, SLCO1B3 wt Allele-, or ABCC2 wt Allele-mediated transport (Keogh, In vitro, faldaprevir inhibited key processes involved in Bilirubin clearance: Glucuronosyltransferase (UGT) 1A1 (UGT1A1 gene gene) (IC50 0.45 µM), which Immunostimulating conjugate (antigen) Bilirubin, and hepatic uptake and efflux transporters, organic anion-transporting polypeptide (OATP) 1B1 (IC50 0.57 µM), SLCO1B3 wt Allele (IC50 0.18 µM), and multidrug resistance-associated protein (Multidrug Resistance-Associated Proteins) 2 (IC50 6.2 µM), which transport Bilirubin and its Immunostimulating conjugate (antigen), Thus, disruption of hepatic reuptake of Bilirubin Glucuronides due to coexisting SLCO1B1 wt Allele and SLCO1B3 wt Allele deficiencies explains Rotor-type Jaundice, Chronic Idiopathic, Thus, disruption of hepatic reuptake of Bilirubin Glucuronides due to coexisting SLCO1B1 wt Allele and SLCO1B3 wt Allele deficiencies explains Rotor-type Jaundice, Chronic Idiopathic.Moreover, SLCO1B1 wt Allele and SLCO1B3 wt Allele null mutations may confer substantial Pharmacologic Substance Toxic effect risks, SLCO1B1 wt Allele (a.k.a. OATP-C, OATP2, LST-1, or SLC21A6) is a Abdomen>Liver-specific organic anion uptake transporter and has been shown to be a higher affinity Bilirubin uptake transporter than SLCO1B3 wt Allele, In vitro SLCO1B1 wt Allele and SLCO1B3 wt Allele inhibition is associated with observations of benign clinical unconjugated Jaundice, Chronic Idiopathic., Examples of adaptive Nontoxic changes in Abdomen>Liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) Bilirubin above baseline levels, include reversible inhibition of UGT1A1 gene gene-mediated Bilirubin metabolism and SLCO1B1 wt Allele-, SLCO1B3 wt Allele-, or ABCC2 wt Allele-mediated transport (Keogh. Adv Pharmacol 63:1-42, 2012). , Using CASP14 gene deficient in Oatp1a/1b and in the multispecific sinusoidal export pump ABCC3 protein, Homo sapiens, we found that ABCC3 protein, Homo sapiens secretes Bilirubin Immunostimulating conjugate (antigen) into the blood, while Oatp1a/1b transporters mediate their hepatic reuptake. , Bilirubin elimination is a multifaceted process consisting of uptake of Bilirubin into the Hepatocyte facilitated by SLCO1B1 wt Allele and SLCO1B3 wt Allele. , SLCO1B1 wt Allele polymorphism is a major determinant of serum Bilirubin level but not associated with rifampin-mediated Bilirubin elevation., Unconjugated Bilirubin (UCB) is taken up into Hepatocyte by Homo sapiens organic anion transporting polypeptide 1B1 (SLCO1B1 wt Allele; encoded for by the SLCO1B1 gene)., However, because Pharmacologic Substance transporters also contribute to Bilirubin elimination, the purpose of this work was to investigate the in vitro inhibition of SLCO1B1 wt Allele, SLCO1B3 wt Allele, ABCC2 wt Allele, and ABCB11 wt Allele of select test drugs known to elicit Jaundice, Chronic Idiopathic. Test drugs investigated in this study were atazanavir and indinavir, which are associated with Jaundice, Chronic Idiopathic and elevations in serum Aspartate Transaminase; ritonavir and nelfinavir, which are not associated with Jaundice, Chronic Idiopathic; and bromfenac, troglitazone, and trovafloxacin, which are associated with severe idiosyncratic hepatotoxicity exhibiting elevations in serum Bilirubin and Aspartate Transaminase., Test drugs investigated in this study were atazanavir and indinavir, which are associated with Jaundice, Chronic Idiopathic and elevations in serum Aspartate Transaminase; ritonavir and nelfinavir, which are not associated with Jaundice, Chronic Idiopathic; and bromfenac, troglitazone, and trovafloxacin, which are associated with severe idiosyncratic hepatotoxicity exhibiting elevations in serum Bilirubin and Aspartate Transaminase. Due to limited solubility and poor ionization of Bilirubin and its Glucuronides, the formation of estradiol 3-Glucuronides was used as a surrogate to assess UGT1A1 gene gene activity, while the transport of pitavastatin, 5(6)-carboxy-2',7'-dichlorofluorescein, and Taurocholate were used as surrogate Probe brand of methazole herbicide substrates to monitor the function of SLCO1B1 wt Allele/SLCO1B3 wt Allele, ABCC2 wt Allele, and ABCB11 wt Allele, respectively., In vitro, faldaprevir inhibited key processes involved in Bilirubin clearance: Glucuronosyltransferase (UGT) 1A1 (UGT1A1 gene gene) (IC50 0.45 µM), which Immunostimulating conjugate (antigen) Bilirubin, and hepatic uptake and efflux transporters, organic anion-transporting polypeptide (OATP) 1B1 (IC50 0.57 µM), SLCO1B3 wt Allele (IC50 0.18 µM), and multidrug resistance-associated protein (Multidrug Resistance-Associated Proteins) 2 (IC50 6.2 µM), which transport Bilirubin and its Immunostimulating conjugate (antigen)., In vitro SLCO1B1 wt Allele and SLCO1B3 wt Allele inhibition is associated with observations of benign clinical unconjugated Jaundice, Chronic Idiopathic., 3.  The results indicated that in vivo Fi values >0.2 or R-values >1.5 for SLCO1B1 wt Allele or SLCO1B3 wt Allele, but not UGT1A1 gene gene, are associated with previously reported clinical cases of Pharmacologic Substance-induced unconjugated Jaundice, Chronic Idiopathic., SLCO1B1 wt Allele and SLCO1B3 wt Allele-mediated transport of Bilirubin was confirmed and inhibition was determined for atazanavir, rifampin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir.[SEP]Relations: UGT1A1 gene has relations: disease_protein with Bilirubin encephalopathy, disease_protein with Bilirubin encephalopathy, bioprocess_protein with Bilirubin conjugation, bioprocess_protein with Bilirubin conjugation, protein_protein with B3GALT1, protein_protein with B3GALT1, drug_protein with Alvocidib, drug_protein with Alvocidib. SLCO1B1 has relations: molfunc_protein with bile acid transmembrane transporter activity, molfunc_protein with bile acid transmembrane transporter activity.", "label": "yes"}
{"original_question": "Does temsirolimus improve survival of glioblastoma patients?", "id": "converted_2590", "sentence1": "Does temsirolimus improve survival of glioblastoma patients?", "sentence2": "RESULTS: fourteen randomized clinical trials were identified (7 with bevacizumab, 2 Cilengitide, 1 enzastaurin, 1 dasatinib, 1 vandetanib, 1 temsirolimus, 1 cediranib) including 4330 patients. Antiangiogenic drugs showed no improvement in overall survival with a pooled HR of 1.00, a trend for an inferior outcome, in terms of overall survival, was observed in the group of patients receiving antiangiogenic drug alone compared to cytotoxic drug alone (HR=1.24, p=0.056)., CONCLUSIONS: temsirolimus was not superior to temozolomide in patients with an unmethylated MGMT promoter., The actuarial 1-year survival was 72.2% [95% confidence interval (NDUFB6 gene), 58.2-82.2] in the temozolomide arm and 69.6% (95% NDUFB6 gene, 55.8-79.9) in the temsirolimus arm [hazard ratio (HR) 1.16; 95% NDUFB6 gene, 0.77-1.76; P = 0.47]., CONCLUSION: The combination of bevacizumab with temsirolimus was well-tolerated and resulted in stable Disease of at least four months/partial response in three out of six pediatric patients with chemorefractory CNS Neoplasms., CONCLUSIONS: temsirolimus administered weekly at the dose of 75 mg/m(2) did not meet the primary objective efficacy threshold in children with Malignant Glioma, Neuroblastoma or Anal Rhabdomyosarcoma; however, meaningful prolonged stable Disease merits further evaluation in combination therapy., Novel targeted agents such as bevacizumab, imatinib, erlotinib, temsirolimus, immunotherapy, Cilengitide, talampanel, etc. are helping classical chemotherapeutic agents, like temozolomide, to achieve an increase in overall survival., CONCLUSIONS: CCI 779 was well tolerated at this dose schedule; however, there was no evidence of efficacy in patients with recurrent Glomerular Basement Membrane, The addition of temsirolimus to human leukocyte human leukocyte interferon did not improve survival., CONCLUSIONS temsirolimus was not superior to temozolomide in patients with an unmethylated MGMT promoter., The addition of temsirolimus to human leukocyte human leukocyte interferon did not improve survival.[SEP]Relations: temsirolimus has relations: contraindication with glioblastoma (Disease), contraindication with glioblastoma (Disease), contraindication with giant cell glioblastoma, contraindication with giant cell glioblastoma, contraindication with astroblastoma, contraindication with astroblastoma, contraindication with brain cancer, contraindication with brain cancer, drug_effect with Eczema, drug_effect with Eczema.", "label": "no"}
{"original_question": "Does the 3D structure of  the genome remain stable during cell differentiation?", "id": "converted_1450", "sentence1": "Does the 3 Days structure of  the Genome - anatomical entity remain stable during \"U\" lymphocyte differentiation?", "sentence2": "We identify large, megabase-sized local chromatin location location interaction domains, which we term 'topological domains', as a pervasive structural feature of the Genome - anatomical entity organization., The domains are stable across different \"U\" lymphocyte types and highly conserved across species, indicating that topological domains are an inherent property of mammalian genomes, Insulators are involved in 3 Days Genome - anatomical entity organization at multiple spatial scales and are important for dynamic reorganization of chromatin location location structure during reprogramming and differentiation., The relation between alterations in chromatin location location structure and changes in gene expression during \"U\" lymphocyte differentiation has served as a paradigm to understand the link between Genome - anatomical entity organization and function., Architectural Proteins orchestrate higher-order chromatin location location organization through the establishment of interactions between regulatory elements across multiple spatial scales. The regulation of these Proteins, their interaction with DNA, and their co-occurrence in the Genome - anatomical entity, may be responsible for the plasticity of 3 Days chromatin location location architecture that dictates \"U\" lymphocyte and time-specific blueprints of gene expression., The role of 3 Days Genome - anatomical entity organisation in the control and execution of lineage-specific transcription programmes during the development and differentiation of Multipotent Stem Cells into specialised \"U\" lymphocyte types remains poorly understood., Chromatin structural states and their remodelling, including higher-order chromatin location location folding and three-dimensional (3 Days) Genome - anatomical entity organisation, play an important role in the control of gene expression, Here, we show that substantial remodelling of the higher-order chromatin location location structure of the LORICRIN gene (Electrodesiccation with curettage), a keratinocyte lineage-specific gene locus on mouse chromosome 3, occurs during epidermal morphogenesis., Many studies have suggested a link between the spatial organization of genomes and fundamental biological processes such as Genome - anatomical entity reprogramming, gene expression, and differentiation., Moreover, we reveal that formation of such highly condensed, transcriptionally repressed Heterochromatin promotes transcriptional activation of differentiation genes and loss of pluripotency., The open chromatin location location of Embryonic Stem Cells (Enhanced S-Cone Syndrome) condenses into repressive Heterochromatin as Cells exit the pluripotent state., we find that localized Heterochromatin condensation of Ribosomal RNA Genes initiates establishment of highly condensed chromatin location location structures outside of the Cell Nucleolus, We focus on the emerging relationship between Genome - anatomical entity organization and lineage-specific transcriptional regulation, which we argue are inextricably linked., Cells face the challenge of storing two meters of DNA in the three-dimensional (3 Days) space of the Cell Nucleus that spans only a few microns. The nuclear organization that is required to overcome this challenge must allow for the accessibility of the gene regulatory machinery to the DNA and, in the case of Embryonic Stem Cells (Enhanced S-Cone Syndrome), for the transcriptional and epigenetic changes that accompany differentiation, In this review we summarize some of the recent findings illuminating the 3 Days structure of the eukaryotic Genome - anatomical entity, as well as the relationship between Genome - anatomical entity topology and function from the level of whole chromosomes to enhancer-promoter loops with a focus on features affecting Genome - anatomical entity organization in Enhanced S-Cone Syndrome and changes in nuclear organization during differentiation, We observe that although self-associating chromatin location location domains are stable during differentiation, chromatin location location interactions both within and between domains change in a striking manner, altering 36% of active and inactive chromosomal compartments throughout the Genome - anatomical entity[SEP]Relations: LORICRIN has relations: bioprocess_protein with keratinocyte differentiation, bioprocess_protein with keratinocyte differentiation, pathway_protein with Formation of the cornified envelope, pathway_protein with Formation of the cornified envelope, cellcomp_protein with cornified envelope, cellcomp_protein with cornified envelope, molfunc_protein with structural constituent of cytoskeleton, molfunc_protein with structural constituent of cytoskeleton. Heterochromatin has relations: cellcomp_protein with BEND3, cellcomp_protein with BEND3.", "label": "no"}
{"original_question": "Can prevnar 13 be used in children?", "id": "converted_3173", "sentence1": "Can prevnar 13 be used in children?", "sentence2": "PCV13 is approved for routine vaccination of all infants as a 4-dose series at age 2, 4, 6, and 12-15 months for children who previously received 1 or more doses of the 7-valent pneumococcal conjugate vaccine (PCV7), and for children with underlying medical conditions that increase their risk for pneumococcal disease or its complications. , Based on published immunogenicity and safety data, as well as the recent recommendations by the ACIP for routine use in infants and indications for high-risk pediatric patients, PCV13 is a revised formulation of pneumococcal vaccine that should be included on pharmacy formularies., To review the immunogenicity, efficacy, and safety of the 13-valent pneumococcal conjugate vaccine (PCV13) for use in pediatric patients.[SEP]", "label": "yes"}
{"original_question": "Is the optogenetics tool ChR2 light-sensitive?", "id": "converted_727", "sentence1": "Is the optogenetics tool ChR2 light-sensitive?", "sentence2": "Channelrhodospin-2 (ChR2), a light-sensitive ion channel, and its Variant have emerged as new excitatory optogenetic tools not only in neuroscience, but also in other areas, including cardiac electrophysiology., Light-sensitive Genes chiefly including the genetically targeted light-gated channels channelrhodopsin-2 (ChR2) and Halorhodopsins (NpHR) cause intracellular ion flow during optical illumination., Computational optogenetics: empirically-derived voltage- and light-sensitive channelrhodopsin-2 model., The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), Halorhodopsins (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of Epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization., Channelrhodopsins-2 (ChR2) are a class of light sensitive proteins that offer the ability to use light stimulation to regulate neural activity with millisecond precision., The most widely used optogenetic tool, Channelrhodopsin2 (ChR2), is both light- and voltage-sensitive., Channelrhodospin-2 (ChR2), a light-sensitive ion channel, and its Variant have emerged as new excitatory optogenetic tools not only in neuroscience, but also in other areas, including cardiac electrophysiology. , Optogenetic methods have emerged as a powerful tool for elucidating neural circuit activity underlying a diverse set of behaviors across a broad range of species. Optogenetic tools of microbial origin consist of light-sensitive membrane proteins that are able to activate (e.g., channelrhodopsin-2, ChR2) or silence (e.g., Halorhodopsins, NpHR) neural activity ingenetically-defined cell types over behaviorally-relevant timescales. , Virus-mediated expression of a ChR2 variant with greater light sensitivity in SGNs reduced the amount of light required for responses and allowed neuronal spiking following stimulation up to 60 Hz. , Channelrhodopsin-2 (ChR2) from the green alga Chlamydomonas reinhardtii functions as a light-gated cation channel that has been developed as an optogenetic tool to stimulate specific nerve cells in animal allergen extracts and control their behavior by illumination. , Here, we used animal models to characterize optogenetic stimulation, which is the optical stimulation of Neurons genetically engineered to express the light-gated ion channel channelrhodopsin-2 (ChR2). , The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), Halorhodopsins (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of Epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization., The most widely used optogenetic tool, Channelrhodopsin2 (ChR2), is both light- and voltage-sensitive. A light-triggered action potential or light-driven perturbations of ongoing electrical activity provide instant voltage feedback, shaping ChR2 current.,  Optogenetic methods have emerged as a powerful tool for elucidating neural circuit activity underlying a diverse set of behaviors across a broad range of species. Optogenetic tools of microbial origin consist of light-sensitive membrane proteins that are able to activate (e.g., channelrhodopsin-2, ChR2) or silence (e.g., Halorhodopsins, NpHR) neural activity ingenetically-defined cell types over behaviorally-relevant timescales., Channelrhodospin-2 (ChR2), a light-sensitive ion channel, and its Variant have emerged as new excitatory optogenetic tools not only in neuroscience, but also in other areas, including cardiac electrophysiology., It allows Neurons to express light-sensitive Genes that enable the identification, dissection, and manipulation of specific neural populations and their connections in the Body tissue and Organ of awake animal allergen extracts with unprecedented spatial and temporal precision. Light-sensitive Genes chiefly including the genetically targeted light-gated channels channelrhodopsin-2 (ChR2) and Halorhodopsins (NpHR) cause intracellular ion flow during optical illumination., Channelrhodopsin-2 (ChR2) from the green alga Chlamydomonas reinhardtii functions as a light-gated cation channel that has been developed as an optogenetic tool to stimulate specific nerve cells in animal allergen extracts and control their behavior by illumination. The molecular mechanism of ChR2 has been extensively studied by a variety of spectroscopic methods, including light-induced difference Fourier transform infrared (FTIR) spectroscopy, which is sensitive to structural changes in the Protein Info upon light activation.[SEP]Relations: Epilepsy has relations: disease_protein with CHRM2, disease_protein with CHRM2, disease_protein with CHD2, disease_protein with CHD2, disease_protein with P2RX2, disease_protein with P2RX2, disease_protein with TANC2, disease_protein with TANC2, disease_protein with RARS2, disease_protein with RARS2.", "label": "yes"}
{"original_question": "Is there any data to suggest that TRH (thyrotropin releasing hormone) administration can improve symptom severity of amyotrophic lateral sclerosis patients?", "id": "converted_1520", "sentence1": "Is there any data to suggest that Pro-Thyrotropin-Releasing Hormone, human (Thyrotropin-Releasing Hormone, human) administration can improve symptom severity of Amyotrophic Lateral Sclerosis patients?", "sentence2": "These CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (CNS)-mediated effects provide the rationale for use of Pro-Thyrotropin-Releasing Hormone, human and its Analog in the treatment of Head>Brain and spinal injury, and CNS disorders like SCHIZOPHRENIA 2 (disorder), ALZHEIMER DISEASE, FAMILIAL, 1, Epilepsy, Amyotrophic Lateral Sclerosis, Parkinson's Disease, Cancer patients and suicide and Cancer patients and suicide and depression, Shock and Ischemia Procedure., The Effect of Pro-Thyrotropin-Releasing Hormone, human to correct the abnormal F responses in SSP might be consistent with effects of Pro-Thyrotropin-Releasing Hormone, human to reduce Muscle Spasticity in Amyotrophic Lateral Sclerosis described previously, Agents undergoing therapeutic trials at present include Ciliary Neurotrophic Factor, IGF1 glutamate antagonists, Amino Acids, Branched-Chain and Pro-Thyrotropin-Releasing Hormone, human analogue., Evidence that thyrotropin-releasing hormone (Pro-Thyrotropin-Releasing Hormone, human) has prominent trophic effects on the motor system led to several negative therapeutic trials in Amyotrophic Lateral Sclerosis, a Disease of the motor system., The results of the clinical evaluation at the beginning and end of the treatment as well as after patient follow up demonstrated that beneficial effects do not occur equally in all patients but rather are transitory and do not improve the natural evolution of the Disease., The neurological evaluation after acute Pro-Thyrotropin-Releasing Hormone, human-T treatment showed an objective improvement in 3 of the 8., The outcome of the study, in agreement with some and at variance with other studies, was that Pro-Thyrotropin-Releasing Hormone, human induced a statistically significant neurological improvement in 17 of the 23 ALS patients but little or none in the other ALS patients and in patients with other neurological diseases., [A case of Amyotrophic Lateral Sclerosis with disturbance of vertical ocular movement responding to Thyrotropin-Releasing Hormone, human (Pro-Thyrotropin-Releasing Hormone, human)]., Pro-Thyrotropin-Releasing Hormone, human injections resulted in improvement of disturbance of vertical ocular movement, but no effect was seen on the weakness of the limb., 13 patients with Amyotrophic Lateral Sclerosis (ALS) were treated with intravenous infusion of thyrotropin-releasing hormone (Pro-Thyrotropin-Releasing Hormone, human). , Similar improvements in speech, swallowing and in Tongue and jaw movements were seen after iv and oral administration in nine, five and eight patients respectively. , No clinical improvement was detected. , A trial of Thyrotropin Releasing Hormone (Pro-Thyrotropin-Releasing Hormone, human) 5.0 mg/kg body weight subcutaneously every other day for two weeks produced transient increased tone in Muscle Tissue, along with other (side-) effects in patients with Amyotrophic Lateral Sclerosis (ALS)., Although the mechanism is not known, several reports of the effectiveness of Thyrotropin-Releasing Hormone, human (Pro-Thyrotropin-Releasing Hormone, human) in ALS were recently published., thyrotropin-releasing hormone (thyrotropin-releasing hormone) appears to be a neuromodulator in the extrahypothalamic nervous system and has been suggested as an adjunct in the treatment of Amyotrophic Lateral Sclerosis (ALS). , Clinical studies have shown that response to Pro-Thyrotropin-Releasing Hormone, human is state dependent, that is, it depends on whether the patient has bulbar or nonbulbar signs and is male or female. Future studies must take into consideration this state dependence as a specific feature of the pharmacological action of Pro-Thyrotropin-Releasing Hormone, human and its analogues., Three of the studies showed a transient, statistically significant effect in at least some Muscle Tissue. The two studies that demonstrated no such effect both used Pro-Thyrotropin-Releasing Hormone, human in very small doses. It therefore seems reasonable to conclude that the effect of Pro-Thyrotropin-Releasing Hormone, human in ALS is a definite, acute, and transient response. , It was found that in only 3 out of 14 patients with moderately progressed Disease no improvement was achieved, while in 11 cases the improvement was from 10 to 20%. However, the improvement was transient, and Pro-Thyrotropin-Releasing Hormone, human treatment failed to stop the progression of the Disease., Only 3 patients noted subjective improvement of strength., In 6 of the 9, Pro-Thyrotropin-Releasing Hormone, human induced a significant increase in vibratory inhibition. This suggests that the Pro-Thyrotropin-Releasing Hormone, human-induced reduction of Muscle Spasticity might be due to an increase in presynaptic inhibition acting on Ia fibres., However, 2 mg DN-1417, IM twice a day for 1 month in an open-label trial, produced no objective improvement of strength in nine patients with ALS. , Our experience suggests that this approach is safe, has high patient acceptance, and is worthy of more careful evaluation., Focal, small-to-moderate and transient improvement occurred in the muscle strength and function of patients with ALS who received Pro-Thyrotropin-Releasing Hormone, human in dose-response and screening studies. In a small pilot study of 12 patients, 3 months administration of Pro-Thyrotropin-Releasing Hormone, human at 10 mg per kg on alternate days resulted in localized increased strength of jaw Muscle Tissue as well as significant improvement in lower extremity function. Aerobic exercise capacity was particularly improved in patients with ALS following administration of Pro-Thyrotropin-Releasing Hormone, human. , Mild to moderate improvement was found in 9 (56%) of 16 patients. , We thought such action of Pro-Thyrotropin-Releasing Hormone, human to be useful to the therapy of ALS., With daily Pro-Thyrotropin-Releasing Hormone, human, 10 patients noted subjective improvement without objective evidence, and 10 patients complained of worsening of the Disease with objective decline after Pro-Thyrotropin-Releasing Hormone, human was stopped. Statistical analysis, however, showed no beneficial effects from either acute or chronic Pro-Thyrotropin-Releasing Hormone, human trials., A temporary increase in the strength of some Muscle Tissue was detected following the administration of Pro-Thyrotropin-Releasing Hormone, human, but no change in functional performance was noted. Neither the patients nor the investigators believed the effects were of any marked clinical significance., Nevertheless, statistically significant improvement was seen only in dynametric strength 1 hour after subcutaneous injection (p less than 0.05). Significant improvement occurred, in one patient only, on subjective speech testing during IV infusion of Pro-Thyrotropin-Releasing Hormone, human. In none of six other ratings was there a significant difference between Pro-Thyrotropin-Releasing Hormone, human and placebo. Subjective improvement was noted by 11 of 12 patients., Significant improvement, as shown by statistical analysis, was noted in muscle strength in the 9 patients by 5 infusions over a 4-week period and a sub-group of 5 patients treated by 8 infusions over 10 weeks., The progressive course of this Disease, manifested by increasing Atrophic, Paralysed and Disability:Type:Pt:^Patient:Nom score, was not altered. , Very high intravenous doses (2-19 mg/min) of thyrotropin-releasing hormone (Pro-Thyrotropin-Releasing Hormone, human, L-pyroglutamyl-L-histidyl-L-prolinamide) given to 12 patients with Amyotrophic Lateral Sclerosis (ALS) produced a moderate to marked improvement of functions caused by deficiency of lower motor neurons (weakness) and upper motor neurons (Muscle Spasticity). The improvement was sustained throughout the infusion and for about 1 h thereafter; sometimes a slight improvement was evident 20 h after infusion., Aerobic exercise capacity was particularly improved in patients with ALS following administration of Pro-Thyrotropin-Releasing Hormone, human[SEP]Relations: Amyotrophic Lateral Sclerosis has relations: disease_protein with TRPM7, disease_protein with TRPM7, disease_protein with NEFH, disease_protein with NEFH, disease_disease with progressive muscular Atrophic, disease_disease with progressive muscular Atrophic, disease_protein with TARDBP, disease_protein with TARDBP, disease_protein with TREM2, disease_protein with TREM2.", "label": "yes"}
{"original_question": "Is dasatinib effective for treatment of glioblastoma?", "id": "converted_2282", "sentence1": "Is dasatinib effective for treatment of Glioblastoma Multiforme?", "sentence2": "RESULTS: fourteen randomized clinical trials were identified (7 with bevacizumab, 2 Cilengitide, 1 enzastaurin, 1 dasatinib, 1 vandetanib, 1 temsirolimus, 1 cediranib) including 4330 patients. Antiangiogenic drugs showed no improvement in overall survival with a pooled HR of 1.00, a trend for an inferior outcome, in terms of overall survival, was observed in the group of patients receiving antiangiogenic drug alone compared to cytotoxic drug alone (HR=1.24, p=0.056)., CONCLUSIONS: Intraparticipant dose escalation was feasible, but dasatinib was ineffective in recurrent Glomerular Basement Membrane. , Median progression-free survival (PFS) was 1.35 months (95% confidence interval: 1.2-1.4) and 6-month PFS was 7.7%. In this phase I study of recurrent Glioblastoma Multiforme patients, the combination of CCNO gene and dasatinib showed significant hematological Toxic effect and led to suboptimal exposure to both agents., dasatinib in conjunction with bevacizumab does not appear to have activity in patients with recurrent, heavily pretreated Glomerular Basement Membrane.[SEP]Relations: dasatinib has relations: drug_effect with Eczema, drug_effect with Eczema, drug_effect with Pain, drug_effect with Pain, drug_effect with Erythema, drug_effect with Erythema, drug_effect with Edema, drug_effect with Edema, drug_effect with Myalgia, drug_effect with Myalgia.", "label": "no"}
{"original_question": "Is Crohn's disease (CD) linked to the consumption of refrigerated food?", "id": "converted_1396", "sentence1": "Is Crohn's disease (CD) linked to the consumption of refrigerated Food allergenic extracts?", "sentence2": "Environmental risk factors playing a causative role in Crohn's disease of oral soft tissues (CD) remain largely unknown. Recently, it has been suggested that refrigerated Food allergenic extracts could be involved in disease development., This study supports the opinion that CD is associated with exposure to domestic refrigeration, among other household factors, during childhood., Patients were exposed earlier than controls to the refrigerator (X2 = 9.9, df = 3, P = 0.04) and refrigerator exposure at birth was found to be a risk factor for CD (OR = 2.08 (95% CI: 1.01-4.29), P = 0.05). Comparable results were obtained looking for the exposure to freezer at home., A recent published hypothesis proposed that Crohn's disease was provoked by infantile exposure to Microorganism that can survive refrigerator temperature., This support for the hypothesis reached statistical significance for those with Crohn's disease compared to the controls (p=0.045)., Epidemiological data allow assessment of familial environmental risk factors related to western lifestyle, diet, Bacteria, and domestic hygiene., All findings point to refrigeration as a potential risk factor for Crohn's disease., Furthermore, cold-chain development paralleled the outbreak of Crohn's disease during the 20th century. , Environmental risk factors playing a causative role in Crohn&apos;s Disease (CD) remain largely unknown. Recently, it has been suggested that refrigerated Food allergenic extracts could be involved in disease development., Our study suggests an association between the omission of breakfast and the failure to refrigerate Food allergenic extracts with GC in the Mexican population.[SEP]Relations: Crohn disease of the esophagus has relations: disease_disease with Crohn disease, disease_disease with Crohn disease, disease_disease with esophagitis (disease), disease_disease with esophagitis (disease). Bacteremia has relations: disease_phenotype_positive with toxic shock syndrome, disease_phenotype_positive with toxic shock syndrome, disease_phenotype_positive with listeriosis, disease_phenotype_positive with listeriosis, disease_phenotype_positive with cyclic hematopoiesis, disease_phenotype_positive with cyclic hematopoiesis.", "label": "yes"}
{"original_question": "Does Evolocumab improve cognitive function?", "id": "converted_2461", "sentence1": "Does Evolocumab improve cognitive function?", "sentence2": "Conclusions In a randomized trial involving patients who received either evolocumab or placebo in addition to statin therapy, no significant between-group difference in cognitive function was observed over a median of 19 months. , Results A total of 1204 patients were followed for a median of 19 months; the mean (±SD) change from baseline over time in the raw score for the spatial working memory strategy index of executive function (primary end point) was -0.21±2.62 in the evolocumab group and -0.29±2.81 in the placebo group (P<0.001 for noninferiority; P=0.85 for superiority). There were no significant between-group differences in the secondary end points of scores for working memory (change in raw score, -0.52 in the evolocumab group and -0.93 in the placebo group), episodic memory (change in raw score, -1.53 and -1.53, respectively), or psychomotor speed (change in raw score, 5.2 msec and 0.9 msec, respectively). , Conclusions In a randomized trial involving patients who received either evolocumab or placebo in addition to statin therapy, no significant between-group difference in cognitive function was observed over a median of 19 months., There were no significant between-group differences in the secondary end points of scores for working memory (change in raw score, -0.52 in the evolocumab group and -0.93 in the placebo group), episodic memory (change in raw score, -1.53 and -1.53, respectively), or psychomotor speed (change in raw score, 5.2 msec and 0.9 msec, respectively).[SEP]", "label": "no"}
{"original_question": "Could the Menzerath-Altmann law be proved mathematically trivial in genomes?", "id": "converted_347", "sentence1": "Could the Menzerath-Altmann law be proved mathematically trivial in Genome?", "sentence2": "Here we review the statistical foundations of that test and consider three non-parametric tests based upon different correlation metrics and one parametric test to evaluate if Upper case Roman letter Upper case Roman letter Z ∼ 1/X in Genome. The most powerful test is a new non-parametric one based upon the correlation ratio, which is able to reject Upper case Roman letter Upper case Roman letter Z ∼ 1/X in nine out of 11 taxonomic groups and detect a borderline group. Rather than a fact, Upper case Roman letter Upper case Roman letter Z ∼ 1/X is a baseline that real Genome do not meet. The view of Menzerath-Altmann law as inevitable is seriously flawed., The view of Menzerath-Altmann law as inevitable is seriously flawed., The view of Menzerath-Altmann law as inevitable is seriously flawed., The view of Menzerath-Altmann law as inevitable is seriously flawed.[SEP]Relations: Increased upper to lower segment ratio has relations: disease_phenotype_positive with Turner syndrome due to structural X chromosome anomalies, disease_phenotype_positive with Turner syndrome due to structural X chromosome anomalies, disease_phenotype_positive with Aarskog-Scott syndrome, X-linked, disease_phenotype_positive with Aarskog-Scott syndrome, X-linked, disease_phenotype_positive with Turner syndrome, disease_phenotype_positive with Turner syndrome, disease_phenotype_positive with mosaic monosomy X, disease_phenotype_positive with mosaic monosomy X, disease_phenotype_positive with monosomy X, disease_phenotype_positive with monosomy X.", "label": "yes"}
{"original_question": "Does ziconotide bind to N-type calcium channels?", "id": "converted_520", "sentence1": "Does ziconotide bind to N-type CALCIUM SUPPLEMENTS channels?", "sentence2": "Since this Geographic Locations partially overlaps with residues previously implicated in block of the channel by omega-Conotoxin GVIA, we assessed the effects of Gene Mutation in the putative EF hand domain on channel block by omega-Conotoxin GVIA and the structurally related omega-conotoxin MVIIA. Both of the toxins irreversibly block the activity of wild type alpha(1B) N-type channels. , Despite their high sequence homology, the Peptides neurotoxins omega-conotoxin MVIIA and MVIIC selectively block N- and P/Q-type CALCIUM SUPPLEMENTS channels, respectively. ,  Binding assay for both N- and P/Q-type CALCIUM SUPPLEMENTS channels showed that amino acid residues restricted to the N-terminal half are important for the recognition of N-type channels, whereas essential residues for P/Q-type channel recognition are widely spread over the whole omega-conotoxin molecule., ziconotide is a novel Peptides that blocks the entry of CALCIUM SUPPLEMENTS into neuronal N-type voltage-sensitive CALCIUM SUPPLEMENTS channels, preventing the conduction of nerve signals., ziconotide is a selective, potent and reversible blocker of neuronal N-type voltage-sensitive CALCIUM SUPPLEMENTS channels (VSCCs)., The therapeutic benefit of ziconotide derives from its potent and selective blockade of neuronal N-type voltage-sensitive CALCIUM SUPPLEMENTS channels., Interactions of intrathecally administered ziconotide, a selective blocker of neuronal N-type voltage-sensitive CALCIUM SUPPLEMENTS channels, with morphine on nociception in rats., ziconotide, a new N-type CALCIUM SUPPLEMENTS channel blocker, administered intrathecally for Postoperative Pain, Acute., ziconotide, an intrathecally administered N-type CALCIUM SUPPLEMENTS channel antagonist for the treatment of Chronic pain., Thus, ziconotide is the first of a new class of agents--N-type CALCIUM SUPPLEMENTS channel blockers, or NCCBs., ziconotide, formerly known also as SNX- 111, represents a new class of agents, the N-type CALCIUM SUPPLEMENTS channel blockers., The selective N-type CALCIUM SUPPLEMENTS channel blocker ziconotide ameliorates severe Chronic pain but has a narrow therapeutic window and requires intrathecal administration., A selective N-type CALCIUM SUPPLEMENTS channel inhibitor, ziconotide (Prialt), is a neuroactive Peptides recently marketed as a novel nonopioid treatment for severe Chronic pain., As the clinically available analgesics, pregabalin (alpha2delta-subunit CALCIUM SUPPLEMENTS channel ligand), ziconotide (N-type CALCIUM SUPPLEMENTS channel blocker), mexiletine (sodium channel blocker), and duloxetine (serotonin and norepinephrine reuptake inhibitors) were evaluated in these neurochemically-induced allodynia models., The present investigation was designed to assess the safety and analgesic efficacy of ziconotide, a new N-type CALCIUM SUPPLEMENTS channel blocker, when administered intrathecally to patients with Postoperative Pain, Acute., Inhibition of the N-type CALCIUM SUPPLEMENTS channel by intrathecal administration of the channel-specific blocker omega-conotoxin MVIIA (ziconotide) is efficacious in the treatment of severe Chronic pain., ziconotide is a powerful analgesic drug that has a unique mechanism of action involving potent and selective block of N-type CALCIUM SUPPLEMENTS channels, which control neurotransmission at many Synapses., In conclusion, present findings provide implication that the spinal anti-nociceptive mechanistic site of pregabalin is different from that of ziconotide, mexiletine, and duloxetine, and pregabalin could have a broader anti-nociceptive mechanism other than N-type CALCIUM SUPPLEMENTS channel blockade., ziconotide (SNX 111), a selective blocker of neuronal N-type voltage-sensitive CALCIUM SUPPLEMENTS channels, is antinociceptive when it is administered intrathecally., Effects of intrathecal administration of ziconotide, a selective neuronal N-type CALCIUM SUPPLEMENTS channel blocker, on mechanical allodynia and heat hyperalgesia in a Rattus norvegicus model of Pain, Postoperative., A state-dependent Ca(V)2.2 inhibitor may provide an improved therapeutic window over ziconotide, the peptidyl Ca(V)2.2 inhibitor used clinically. , There is also Homo sapiens validation data from ziconotide, the CaV2.2-selective peptidyl inhibitor used clinically to treat refractory pain. , A selective N-type CALCIUM SUPPLEMENTS channel inhibitor, ziconotide (Prialt), is a neuroactive Peptides recently marketed as a novel nonopioid treatment for severe Chronic pain. , The neuroprotective effects of intrathecal administration of the selective N-type CALCIUM SUPPLEMENTS channel blocker ziconotide in a Rattus norvegicus model of spinal ischemia.[SEP]Relations: ziconotide has relations: drug_drug with Calcium, drug_drug with Calcium, drug_drug with Calcium cation, drug_drug with Calcium cation, drug_drug with Calcium acetate, drug_drug with Calcium acetate, drug_drug with Calcium chloride, drug_drug with Calcium chloride, drug_drug with Calcium gluconate, drug_drug with Calcium gluconate.", "label": "yes"}
{"original_question": "Does SCRIB deregulation promote cancer?", "id": "converted_1651", "sentence1": "Does SCRIB deregulation promote Primary malignant neoplasm?", "sentence2": "human homologs of Drosophila dlg, scrib, and Lown-Ganong-Levine Syndrome are Primary malignant neoplasm-associated genes., Aberrant overexpression of the cell polarity module scribble in human Primary malignant neoplasm., we show that SCRIB gene is nearly universally overexpressed in cultured Tumor Cells, uncertain whether benign or malignant lines and genetically disparate Primary malignant neoplasm patient series compared with matched normal tissues in vivo. , These data uncover a previously unrecognized exploitation of SCRIB gene for aberrant Tumor Cells, uncertain whether benign or malignant motility and invasion, thus potentially contributing to disease progression in Homo sapiens., oss of miR-296 causes aberrantly increased and mislocalized SCRIB gene in human Neoplasms, resulting in exaggerated random cell migration and Tumor Cells, uncertain whether benign or malignant invasiveness. , SCRIB gene levels predict tumor relapse in hepatocellular Carcinoma patients., SCRIB gene heterozygosity predisposes to Primary malignant neoplasm of lung, loss of SCRIB gene and activated oncogenic KRas cooperate in vivo, resulting in more aggressive lung Neoplasms, l, SCRIB protein, human, a product - ParticipationType - ParticipationType of a well-known Tumor Suppressor Genes, CD74-dependent deregulation of the tumor suppressor scribble in human epithelial and breast Primary malignant neoplasm Cells.,  scribble (SCRIB) complexes) is intricately related to advanced stages of tumour progression and invasiveness. , SCRIB expression is deregulated in human prostate Primary malignant neoplasm,, SCRIB gene heterozygosity initiated Benign Prostatic Hyperplasia, The clinical significance of the work in CASP14 gene was highlighted by our observation that SCRIB deregulation strongly correlated with poor survival in human prostate Primary malignant neoplasm., we demonstrate that scribble inhibits breast Primary malignant neoplasm formation and that deregulation of polarity pathways promotes dysplastic and neoplastic growth in Mammals by disrupting morphogenesis and inhibiting cell death., Deregulation of scribble promotes Mammary gland tumorigenesis and reveals a role for cell polarity in Carcinoma., loss of SCRIB protein, human promotes invasion of Cells through Extracellular Matrix in an organotypic culture system., SCRIB protein, human expression is decreased in many invasive human cancers., Loss of human SCRIB protein, human cooperates with HRAS wt Allele to promote cell invasion through deregulation of Mitogen-Activated Protein Kinases signalling.[SEP]Relations: Carcinoma has relations: disease_disease with scrotal Carcinoma, disease_disease with scrotal Carcinoma, disease_protein with SCD, disease_protein with SCD, disease_disease with Primary malignant neoplasm, disease_disease with Primary malignant neoplasm. myeloid tumor suppressor has relations: disease_disease with Mendelian disease, disease_disease with Mendelian disease. Mammary gland gland has relations: anatomy_protein_present with SCRIB, anatomy_protein_present with SCRIB.", "label": "yes"}
{"original_question": "Are there tools for reviewing variant calls?", "id": "converted_2947", "sentence1": "Are there tools for reviewing variant calls?", "sentence2": "VIPER: a web application for rapid expert review of variant calls., With the rapid development in next-generation sequencing, cost and time requirements for genomic sequencing are decreasing, enabling applications in many areas such as cancer research. Many tools have been developed to analyze genomic variation ranging from single nucleotide Variant to whole chromosomal aberrations. As sequencing throughput increases, the number of Variant called by such tools also grows. Often employed manual inspection of such calls is thus becoming a time-consuming procedure. We developed the Variant InsPector and Expert Rating tool (VIPER) to speed up this process by integrating the Integrative Genomics Viewer into a web application. analysts can then quickly iterate through Variant, apply filters and make decisions based on the generated images and variant metadata. VIPER was successfully employed in analyses with manual inspection of more than 10 000 calls.Availability and implementation: VIPER is implemented in Java and Javascript and is freely available at https://github.com/MarWoes/viper., Variant Review with the Integrative Genomics Viewer., VIPER: a web application for rapid expert review of variant calls.Supplementary data are available at Bioinformatics online., We developed the Variant InsPector and Expert Rating tool (VIPER) to speed up this process by integrating the Integrative Genomics Viewer into a web application.[SEP]", "label": "yes"}
{"original_question": "Is propranolol used for treatment of infantile hemangioma?", "id": "converted_2315", "sentence1": "Is propranolol used for treatment of Infantile Hemangioma?", "sentence2": "Low-Dose Treatment propranolol for Infantile Hemangioma of the head and neck: Analysis of 23 consecutive patients., BACKGROUND: More and more infantile hemangiomas (HEMIHYPERPLASIA, ISOLATED) are being treated with propranolol, but the effectiveness, dosage, and treatment course are still in dispute., CONCLUSIONS: Low-Dose Treatment propranolol appears to be effective and safe for HEMIHYPERPLASIA, ISOLATED, especially for those patients previously treated with Adrenal Cortex Hormones and who had no response or severe side-effects., Cardiovascular Profile of Propranolol after Multiple Dosing in Infantile Hemangioma., Propranolol is becoming the treatment of choice for complicated Infantile Hemangioma., In conclusion, propranolol 2 mg/kg of body weight daily causes a statistically though not clinically relevant decrease in blood pressure and heart rate in cardially healthy infants affected by Infantile Hemangioma. , Importance: Propranolol hydrochloride has become the primary medical treatment for problematic Infantile Hemangioma; however, the expression of propranolol's target receptors during growth, involution, and treatment of Hemangioma remains unclear., BACKGROUND: Strawberry nevus of skin (Congenital ichthyosis with hypotrichosis syndrome) are the most common benign vascular tumors of childhood. Propranolol is an effective Pharmacologic Substance in treating HEMIHYPERPLASIA, ISOLATED. , Ultrasonography as an objective tool for assessment of Infantile Hemangioma treatment with propranolol., CONCLUSION: Ultrasonographic measurements contribute to demonstrate tumor regression and HEMIHYPERPLASIA, ISOLATED response to propranolol., Propranolol treatment was recently reported to be successful for the management of severe Infantile Hemangioma., We conclude that the initial use of propranolol as the sole treatment for infantile airway Hemangioma is promising., Propranolol has been proposed for the treatment of infantile hemangiomas., Propranolol therapy is changing the treatment paradigm for Infantile Hemangioma., Propranolol has been successfully used recently in a limited number of children with Infantile Hemangioma., Propranolol has been proposed for the treatment of infantile hemangiomas., CONCLUSIONS This is the first report of successful therapy of an Intracranial Route of Drug Administration Infantile Hemangioma with propranolol., PURPOSE The successful use of nadolol as an alternative to propranolol therapy in three cases of Infantile Hemangioma is reported., Propranolol has been used successfully in a limited number of children with infantile hemangiomas., CONCLUSIONS High-dose Propranolol is very effective in the treatment of Infantile Hemangioma with minor side effects and short disease period., Propranolol is novel and safe medication for treatment of Infantile Hemangioma., Propranolol is the only Food and Drug Administration approved therapy for treatment of patients with this vascular anomaly and should be considered first-line therapy for genital infantile hemangiomas., CONCLUSION Propranolol may be a promising therapeutic modality for Infantile Hemangioma., Propranolol, which is often used to treat cutaneous infantile hemangiomas, is not currently standard treatment for Intracranial Route of Drug Administration infantile hemangiomas., Preliminary results of propranolol treatment for patients with Infantile Hemangioma., Propranolol therapy is changing the treatment paradigm for Infantile Hemangioma., Propranolol should be considered as a first-line treatment of infantile hemangiomas.., Propranolol, a non-selective Adrenergic beta-Antagonists, has recently been introduced as a treatment for infantile hemangiomas.[SEP]Relations: Propranolol has relations: contraindication with muscular disease, contraindication with muscular disease, contraindication with bronchial disease, contraindication with bronchial disease, drug_drug with Propiomazine, drug_drug with Propiomazine, contraindication with neonatal jaundice, contraindication with neonatal jaundice, contraindication with myopathy, contraindication with myopathy.", "label": "yes"}
{"original_question": "Is Miller-Dieker syndrome associated with abnormalities of chromosome 1?", "id": "converted_3058", "sentence1": "Is Miller-Dieker syndrome associated with abnormalities of chromosome 1?", "sentence2": "A complete ophthalmic examination is not routinely performed on infants with Miller-Dieker syndrome (Miller Dieker syndrome, chromosome 17p13.3 microdeletion). , Chromosomes, Human, Pair 1 microdeletions within 17p13.3 can result in either isolated LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE sequence (Classical Lissencephaly) or Miller-Dieker syndrome (Miller Dieker syndrome). , We report a Fetus in fetu with LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE diagnosed as Miller-Dieker Syndrome postnatally. G banded chromosome analysis revealed 45,X,psu dic(17;Y)(p13;p11.32).ish dic (17;Y)(LIS1-,RARA+, SRY+, DYZ3+) by G-banding analysis using high resolution banding technique. Fetal delayed cortical development will be the findings to perform further investigations including fluorescence in situ hybridization analysis for Miller Dieker syndrome, a 17p13.3 microdeletion syndrome, pre/postnatally. This will be the first case of Miller Dieker syndrome with unbalanced translocation between deleted short arm of Chromosomes, Human, Pair 17 and Y Chromosomes, Human, Pair 1.,  We report the finding of a 2.5-Mb gene region quadruplication of Chromosomes, Human, Pair 1 17p13.3. This region is well characterized for the Gene Deletion Abnormality leading to Miller-Dieker syndrome but has an unclear replication phenotype. , Both Gene Deletion have overlapped with the critical region of Miller-Dieker syndrome (Miller Dieker syndrome) and involved candidate Genes such as PAFAH1B1 gene gene, YWHAE protein, Homo sapiens protein, Homo sapiens and CRK protein, Homo sapiens protein, Homo sapiens. In addition, SNP array and FISH analyses on the parental peripheral blood samples demonstrated that both 17p13.3 and 17p13.3p13.2 Gene Deletion were of de novo origin., Miller-Dieker syndrome (Miller Dieker syndrome) is caused by a heterozygous Gene Deletion Abnormality of chromosome 17p13.3 involving the Genes LIS1 and YWHAE protein, Homo sapiens protein, Homo sapiens (coding for 14.3.3ε) and leads to malformations during cortical development., We studied after Cessation of life a 3-month-old girl whose karyotype was 45,XX,-15,-17,+der(17),t(15;17)(q13;p13.3) and thus combines abnormalities of chromosome 15 associated with the Prader-Willi Syndrome and of Chromosomes, Human, Pair 17 associated with the Miller-Dieker syndrome., The Miller-Dieker syndrome (Miller Dieker syndrome), a syndrome with LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE, distinctive craniofacial features, growth impairment, and profound developmental failure, has been associated with a Gene Deletion Abnormality of the distal part of chromosome band 17p13., The Miller-Dieker syndrome (type I LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE) is a Malformations of Cortical Development, Group II which is associated with microdeletions in the short arm of Chromosomes, Human, Pair 17., Detection of submicroscopic Gene Deletion in band 17p13 in patients with the Miller-Dieker syndrome., A 15-month-old girl with Miller-Dieker syndrome, a contiguous gene Gene Deletion Abnormality syndrome involving chromosome 17p13.3 and resulting in LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE, was diagnosed with Pre B-cell acute lymphoblastic leukemia., A computed tomography scan revealed evidence of LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE, and chromosomal analysis showed a microdeletion on the short arm of Chromosomes, Human, Pair 17 (17p13.3), confirming the diagnosis as Miller-Dieker syndrome., Familial Miller-Dieker syndrome associated with pericentric inversion of Chromosomes, Human, Pair 17., The Miller-Dieker syndrome (Miller Dieker syndrome), a rare Congenital Disorders manifested by characteristic facial abnormalities and LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE (smooth Head>Brain), is associated with microdeletions of the distal Mandibular left third molar prosthesis region., Miller-Dieker syndrome (Miller Dieker syndrome), a disorder manifesting the severe Head>Brain malformation LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE (\"smooth Head>Brain\"), is caused, in the majority of cases, by a chromosomal microdeletion of the distal short arm of Chromosomes, Human, Pair 17., The Miller-Dieker syndrome (Miller Dieker syndrome), composed of characteristic facial abnormalities and a severe Malformations of Cortical Development, Group II affecting the Cerebral cortex, is caused by visible or submicroscopic Gene Deletion of chromosome band 17p13., Microdeletions including YWHAE protein, Homo sapiens protein, Homo sapiens in the Miller-Dieker syndrome region on chromosome 17p13.3 result in facial dysmorphisms, growth restriction, and No No cognitive impairment., Identification of the functional profilin gene, its localization to chromosome subband 17p13.3, and demonstration of its Gene Deletion Abnormality in some patients with Miller-Dieker syndrome., HIC1 gene gene is a candidate tumor suppressor gene which is frequently hypermethylated in Homo sapiens Neoplasms, and its location within the Miller-Dieker syndrome's critical Gene Deletion Abnormality region at chromosome 17p13.3 makes it a candidate gene for involvement in this gene Gene Deletion Abnormality syndrome., A complete ophthalmic examination is not routinely performed on infants with Miller-Dieker syndrome (Miller Dieker syndrome, chromosome 17p13.3 microdeletion)., About 15% of patients with isolated LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE and more than 90% of patients with Miller-Dieker syndrome have microdeletions in a critical 350-kilobase region in chromosome 17p13.3 (ref., Chromosomes, Human, Pair 1 aberrations in which Epilepsy is a major and consistent finding include Angelman Syndrome due to loss of the maternal 15q11.2-q12 Anatomical segmentation, Tetrasomy of the maternal Anatomical segmentation 15pter-q13 due to an additional inv dup chromosome, Miller-Dieker syndrome due to Gene Deletion Abnormality of the 17p13.3 Anatomical segmentation including the lissencephaly1 gene, Ring Chromosomes, Human, Pair 1 20 Syndrome, and Wolf-Hirschhorn Syndrome due to Gene Deletion Abnormality of at least the 4p16.3 Anatomical segmentation., Miller-Dieker syndrome and 5p partial trisomy in a child carrying a derivative chromosome with a microdeletion in 17p13.3 telomeric to the LIS1 and the D17S379 loci., The Miller-Dieker syndrome, a disorder of neuronal migration, is caused by Gene Deletion of chromosome 17p13.3., The girl was diagnosed by subtelomeric FISH and array-CGH, showing a 4.43-Mb heterozygous Gene Deletion Abnormality on chromosome 10p that involved 14 Genes and a 3.22-Mb single-copy gain on chromosome Mandibular left third molar prosthesis, which includes the critical region of the Miller-Dieker syndrome and 61 Genes., Detection of submicroscopic Gene Deletion in band 17p13 in patients with the Miller-Dieker syndrome.The Miller-Dieker syndrome (Miller Dieker syndrome), a syndrome with LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE, distinctive craniofacial features, growth impairment, and profound developmental failure, has been associated with a Gene Deletion Abnormality of the distal part of chromosome band 17p13. , Microdeletions including YWHAE protein, Homo sapiens protein, Homo sapiens in the Miller-Dieker syndrome region on chromosome 17p13.3 result in facial dysmorphisms, growth restriction, and No No cognitive impairment.Microdeletions of chromosome 17p13.3 involving YWHAE protein, Homo sapiens protein, Homo sapiens present with growth restriction, craniofacial dysmorphisms, structural abnormalities of Head>Brain and No No cognitive impairment. , Unbalanced translocation (15;17)(q13;13.3) with apparent Prader-Willi Syndrome but without Miller-Dieker syndrome.We studied after Cessation of life a 3-month-old girl whose karyotype was 45,XX,-15,-17,+der(17),t(15;17)(q13;p13.3) and thus combines abnormalities of chromosome 15 associated with the Prader-Willi Syndrome and of Chromosomes, Human, Pair 17 associated with the Miller-Dieker syndrome. , The Miller-Dieker syndrome (Miller Dieker syndrome), a rare Congenital Disorders manifested by characteristic facial abnormalities and LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE (smooth Head>Brain), is associated with microdeletions of the distal Mandibular left third molar prosthesis region. , A revision of the LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE and Miller-Dieker syndrome critical regions in chromosome 17p13.3.Miller-Dieker syndrome (Miller Dieker syndrome) is a multiple malformation syndrome characterized by classical LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE and a characteristic facies. , Case Report of Proliferative Peripheral retinopathy in Two Familial Lissencephaly Infants with Miller-Dieker Syndrome.A complete ophthalmic examination is not routinely performed on infants with Miller-Dieker syndrome (Miller Dieker syndrome, chromosome 17p13.3 microdeletion). , Identification of the functional profilin gene, its localization to chromosome subband 17p13.3, and demonstration of its Gene Deletion Abnormality in some patients with Miller-Dieker syndrome.PFN1 gene is a conserved actin-monomer-binding protein which is found in all Eukaryota, including Saccharomyces cerevisiae. , We propose that essentially no loss of Mandibular left third molar prosthesis material has occurred and confirm previous reports that the critical region for the production of the Miller-Dieker phenotype is located subterminally in the 17p13.3 region.<br>, A review of the literature revealed five additional patients in three families, who had Miller-Dieker syndrome and an abnormality of Mandibular left third molar prosthesis., We propose that essentially no loss of Mandibular left third molar prosthesis material has occurred and confirm previous reports that the critical region for the production of the Miller-Dieker phenotype is located subterminally in the 17p13.3 region., Miller-Dieker syndrome: LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE and monosomy Mandibular left third molar prosthesis., Thus, we propose that monosomy of distal Mandibular left third molar prosthesis may be the cause of Miller-Dieker syndrome in some patients., Miller-Dieker syndrome with der(17)t(12;17)(q24.33;p13.3)pat presenting with a potential risk of mis-identification as a de novo submicroscopic Gene Deletion Abnormality of 17p13.3., Most cases of Miller-Dieker syndrome have a de novo Gene Deletion Abnormality involving 17p13.3.[SEP]Relations: partial monosomy of the short arm of Chromosomes, Human, Pair 17 has relations: disease_disease with Miller-Dieker LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE syndrome, disease_disease with Miller-Dieker LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE syndrome. PAFAH1B1 gene has relations: disease_protein with Miller-Dieker LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE syndrome, disease_protein with Miller-Dieker LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE syndrome. Contiguous gene syndrome has relations: disease_phenotype_positive with Miller-Dieker LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE syndrome, disease_phenotype_positive with Miller-Dieker LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE syndrome. Miller Fisher syndrome has relations: disease_protein with PMP22, disease_protein with PMP22. congenital nervous system disorder has relations: disease_disease with Say-Barber-Miller syndrome, disease_disease with Say-Barber-Miller syndrome.", "label": "no"}
{"original_question": "Has the protein SIRT2 been associated to cervical cancer?", "id": "converted_3068", "sentence1": "Has the protein Sirtuin 2 been associated to cervical cancer?", "sentence2": " A progressive increase in the expression of both Sirtuin 2 and NAD-Dependent Protein Deacetylase Sirtuin-7 was noted during cancer progression in the following order: normal < preneoplasia < cancer.,  We demonstrate that treatment of cervical cancer cells with a RhoGDIα-derived K52-trifluoroacetylated, substrate-derived peptidic sirtuin PPP1R1A gene severely impairs cell proliferation. [SEP]Relations: PPP1R1A has relations: disease_protein with liver cancer, disease_protein with liver cancer, protein_protein with ACTA2, protein_protein with ACTA2, protein_protein with ZPBP2, protein_protein with ZPBP2, anatomy_protein_present with spinal cord, anatomy_protein_present with spinal cord. NAD-dependent protein deacetylase activity has relations: molfunc_protein with Sirtuin 2, molfunc_protein with Sirtuin 2.", "label": "yes"}
{"original_question": "Is belimumab effective for the lupus nephritis?", "id": "converted_4165", "sentence1": "Is belimumab effective for the lupus nephritis?", "sentence2": "Long-term effects of combined B-cell immunomodulation with rituximab and belimumab in severe, refractory systemic lupus erythematosus: 2-year results., CONCLUSIONS: Combined B-cell targeted therapy with resiniferatoxin and Bloom Syndrome prevented full B-cell repopulation including DN B cells, with concomitant specific reduction of SLE-relevant autoantibodies. , Clinical Efficacy of Routinely Administered Belimumab on Proteinuria and Neuropsychiatric Lupus., Conclusions: In our series, Units Of Measure - bel led to a decrease of proteinuria in patients with proteinuria of more than 1,000 mg/g creatine/creatine/creatinine despite standard of care treatment, and led to a marked clinical improvement in one patient with NPSLE. No adverse events were observed. Routinely administered Units Of Measure - bel shows clinical efficacy on non-approved manifestations, but careful patient selection is warranted., Phase II Randomized Trial of Rituximab Plus cyclophosphamide Followed by Belimumab for the Treatment of Lupus Nephritis., OBJECTIVE: To assess the safety, mechanism of action, and preliminary efficacy of rituximab followed by belimumab in the treatment of refractory lupus nephritis (late nucleophagy)., CONCLUSION: The addition of belimumab to a treatment regimen with rituximab and CYCS wt Allele was safe in patients with refractory late nucleophagy., RECENT FINDINGS: Recently, the Belimumab in Subjects with Systemic Lupus Erythematosus - Lupus Nephritis trial tested belimumab, an inhibitor of interleukin-4, as an add-on therapy to Steroids and either mycophenolate mofetil (fluorouracil/methotrexate/mitoxantrone protocol) or cyclophosphamide when given IV monthly over a period of 104 weeks at an effect size of 11% for a Primary Efficacy Renal Response. , Case report: successful treatment of Tissue membrane lupus nephritis with belimumab in an African female immigrant., Recently introduced into the market, belimumab (Benlysta) is a monoclonal antibody CAL CAL that has potential clinically efficacious applications for the treatment of lupus nephritis., Successful treatment of a mycophenolate mofetil-refractory proliferative lupus nephritis with Belimumab in a 19-year-old woman., Following treatment with belimumab, proteinuria rapidly improved to almost normal levels and clinical remission lasted. Belimumab might hold promise for this indication.[SEP]Relations: Belimumab has relations: drug_drug with Lumiliximab, drug_drug with Lumiliximab, drug_drug with Luspatercept, drug_drug with Luspatercept, drug_drug with Tremelimumab, drug_drug with Tremelimumab, drug_drug with Dupilumab, drug_drug with Dupilumab, drug_drug with Rituximab, drug_drug with Rituximab.", "label": "yes"}
{"original_question": "Is PRDM9 essential for meiosis?", "id": "converted_3364", "sentence1": "Is PRDM9 essential for meiosis?", "sentence2": "Our findings do not identify the nature of the underlying DNA Sequence, but argue against the proposed role of Prdm9 as an essential TRANSCRIPTION FACTOR in Mus sp. meiosis, PRDM9 gene polymorphism may not be associated with defective spermatogenesis in the Chinese Han population, PRDM9 is essential for the progression through early meiotic prophase, including double strand break repair, homologous chromosome pairing, and sex body formation during spermatogenesis. , PRDM9 (PRDM9 gene) is a meiosis-specific protein that trimethylates H3K4 and controls the activation of recombination hot spots. It is an essential Enzyme [APC] in the progression of early meiotic prophase., In many Eukaryota, Site of meiotic recombination, also called hotspots, are regions of accessible chromatin location location, but in many Vertebrates, their location follows a distinct pattern and is specified by PRDM9 gene (PRDM9). ,  We found that although the post-SET zinc finger and the KRAB domains are not essential for the methyltransferase activity of PRDM9 in cell culture, the KRAB domain mutant mice show only residual PRDM9 methyltransferase activity and undergo meiotic arrest. In aggregate, our data indicate that domains typically involved in regulation of gene expression do not serve that role in PRDM9, but are likely involved in setting the proper chromatin location location environment for initiation and completion of homologous recombination., PRDM9 Methyltransferase Activity Is Essential for Meiotic DNA Double-Strand Break Formation at Its Binding Sites.[SEP]Relations: TRANSCRIPTION FACTOR binding has relations: molfunc_protein with PRKDC, molfunc_protein with PRKDC, molfunc_protein with KDM1A, molfunc_protein with KDM1A, molfunc_protein with KDM1B, molfunc_protein with KDM1B, molfunc_protein with PSMD10, molfunc_protein with PSMD10. siRNA binding has relations: molfunc_protein with TLR9, molfunc_protein with TLR9.", "label": "yes"}
{"original_question": "Is RANKL secreted from the cells?", "id": "converted_4", "sentence1": "Is TNFSF11 protein, human wt Allele secreted from the Cells?", "sentence2": "Tumor necrosis factor receptor 11b (Panoramic Radiography) is a soluble secreted factor that acts as a TNFRSF10C gene for receptor activator of NF-κB ligand (TNFSF11 protein, human protein, human wt Allele) , Tumor necrosis factor receptor 11b (Panoramic Radiography) is a secreted glycoprotein and a member of the Tumor Necrosis Factor Receptor superfamily. It usually functions in Specimen Type - Bone remodeling, by inhibiting osteoclastogenesis through interaction with a receptor activator of the NFI Transcription Factors (TNFSF11 protein, human protein, human wt Allele)., e TNFSF11 protein, human protein, human wt Allele/Panoramic Radiography ratio secreted by Osteoblasts increased and TNFRSF11A wt Allele expression by osteoclasts increased, leading to increased osteoclastogenesis, Tumor necrosis factor receptor 11b (Panoramic Radiography) is an essential secreted protein in Specimen Type - Bone turnover due to its role as a TNFRSF10C gene for the Receptor Activator of Nuclear Factor-kB ligand (TNFSF11 protein, human protein, human wt Allele) in the osteoclasts, thus inhibiting their differentiation, We identify a TNFSF11 protein, human protein, human RNA Transcript variant that extends the originally identified RNA Transcript encoding secreted TNFSF11 protein, human protein, human wt Allele., Activated human T Cells express alternative mRNA transcripts encoding a secreted form of TNFSF11 protein, human protein, human wt Allele., Panoramic Radiography, on the other hand, is secreted by osteoblast as a TNFRSF10C gene for TNFSF11 protein, human protein, human wt Allele, prevents TNFSF11 protein, human protein, human wt Allele from binding to TNFRSF11A wt Allele and thus prevents Specimen Type - Bone resorption, Substance with receptor activator mechanism of action (substance) of NFI Transcription Factors ligand (TNFSF11 protein, human protein, human wt Allele) and osteoprotegerin (Panoramic Radiography) are Recombinant Cytokines predominantly secreted by Osteoblasts and play a central role in differentiation and functional activation of osteoclasts, Although B. abortus-activated T Cells actively secreted the pro-osteoclastogenic Recombinant Cytokines TNFSF11 protein, human protein, human wt Allele and Interleukin-17, osteoclastogenesis depended on Interleukin-17, because Osteoclasts generation induced by Brucella-activated T Cells was completely abrogated when these Cells were cultured with BMMs from Interleukin-17 receptor knockout mice. ,  osteoclastogenesis and Specimen Type - Bone destruction in Autoimmune arthritis. We isolated human fibroblasts from Rheumatoid Arthritis, Pyrophosphate arthritis (phenylpropanolamine) and Degenerative polyarthritis (OSTEOARTHRITIS SUSCEPTIBILITY 1) patients and analyzed their TNFSF11 protein, human protein, human wt Allele/Panoramic Radiography expression profile and the capacity of their secreted factors to induce osteoclastogenesis., Tumor necrosis factor receptor 11b (Panoramic Radiography) and receptor activator of NFI Transcription Factors ligand (TNFSF11 protein, human protein, human wt Allele) are Recombinant Cytokines predominantly secreted by Osteoblasts and play critical roles in the differentiation and function of osteoclasts. [SEP]Relations: SUMOylation of transcription factors has relations: pathway_protein with FOXL2, pathway_protein with FOXL2, pathway_protein with CDKN2A, pathway_protein with CDKN2A. Protein S human has relations: drug_drug with Allylestrenol, drug_drug with Allylestrenol, drug_drug with Allylestrenol, drug_drug with Allylestrenol. Phenylpropanolamine has relations: contraindication with sickle cell anemia, contraindication with sickle cell anemia.", "label": "yes"}
{"original_question": "Is there an association between Muenke Syndrome and FGFR3 gene mutation?", "id": "converted_1874", "sentence1": "Is there an association between Muenke Syndrome and FGFR3 gene Mutation Abnormality?", "sentence2": "RESULTS: Forty-four with a positive FGFR3 Mutation Abnormality, median age 9 years, range 7 months to 52 years were enrolled. In addition, 10 unaffected siblings served as controls (5 males, 5 females; median age, 13 years; range, 3-18 years)., Muenke is a Fibroblast Growth Factor Receptor 2 3 (FGFR3 protein, human)-associated syndrome, which was first described in late 1990 s. , The syndrome is defined molecularly by a unique Point Mutation c.749C>G in exon 7 of the FGFR3 gene which results to an Amino Acid Substitution p.Pro250Arg of the protein product. , Muenke syndrome caused by Point Mutation (C749G) in the FGFR3 gene affects 1 in 30,000 newborns and accounts for 25% to 30% of Genetic causes of CRANIOSYNOSTOSIS, TYPE 2., Phenotypic variability in two families of Muenke syndrome with FGFR3 Mutation Abnormality., PURPOSE: There are a number of Craniosynostosis with hearing impairment-including Muenke, Apert, Pfeiffer, Crouzon, Beare-Stevenson, Crouzon with Acanthosis nigricans absent, and Jackson-Weiss syndromes-that result from mutations in the Fibroblast Growth Factor Receptor 2 (Fibroblast Growth Factor Receptors) Genes. , Muenke syndrome is an autosomal dominant CRANIOSYNOSTOSIS, TYPE 2 syndrome resulting from a defining Point Mutation in the Fibroblast Growth Factor Receptor3 (FGFR3) gene., Talocalcaneal coalition in Muenke syndrome: report of a patient, review of the literature in Fibroblast Growth Factor Receptors-related craniosynostoses, and consideration of mechanism., To better understand the pathophysiology of the Muenke syndrome, we present collective findings from several recent studies that have characterized a genetically equivalent Mus sp. model for Muenke syndrome (FgfR3 (P244R)) and compare them with human phenotypes., We show in this study that knock-in CASP14 gene harboring the Mutation Abnormality responsible for the Muenke syndrome (FgfR3(P244R)) display postnatal shortening of the Base of skull structure along with synchondrosis growth plate dysfunction characterized by loss of resting, proliferating and hypertrophic Chondrocyte zones and decreased Idiopathic hypogonadotropic hypogonadism expression., Muenke syndrome is caused by a single defining Point Mutation in the Fibroblast Growth Factor Receptor 2 3 (FGFR3) gene., The Pro250Arg Mutation Abnormality in the FGFR3 gene is found in patients with Muenke syndrome and is one of the most frequently encountered mutations in Craniosynostosis., Epilepsy in Muenke syndrome: FGFR3-related CRANIOSYNOSTOSIS, TYPE 2., Muenke syndrome (FGFR3-related CRANIOSYNOSTOSIS, TYPE 2): expansion of the phenotype and review of the literature., The Pro250Arg Mutation Abnormality in the FGFR3 gene is found in patients with Muenke syndrome and is one of the most frequently encountered mutations in Craniosynostosis., PURPOSE: The Muenke syndrome Mutation Abnormality (FGFR3 (ARID1B wt Allele)), which was discovered 15 years ago, represents the single most common CRANIOSYNOSTOSIS, TYPE 2 Mutation Abnormality., The heterozygous Pro250Arg substitution Mutation Abnormality in Fibroblast Growth Factor Receptor 2 3 (FGFR3), which increases ligand-dependent signalling, is the most common Genetic cause of CRANIOSYNOSTOSIS, TYPE 2 in Homo sapiens and defines Muenke syndrome., ARID1B Gene Mutation in the FGFR3 gene also known as Muenke syndrome is associated with Coronal CRANIOSYNOSTOSIS, TYPE 2, sensorineural deafness, craniofacial, and digital abnormalities., Muenke syndrome caused by the FGFR3 Pro250Arg Mutation Abnormality is associated with CRANIOSYNOSTOSIS, TYPE 2, hearing impairment, and various bony anomalies., Muenke syndrome is an Autosomal Dominant Disorder characterized by coronal suture CRANIOSYNOSTOSIS, TYPE 2, hearing impairment, developmental delay, carpal and tarsal fusions, and the presence of the Pro250Arg Mutation Abnormality in the FGFR3 gene., Muenke syndrome, defined by heterozygosity for a Pro250Arg substitution in Fibroblast Growth Factor Receptor 2 3 (FGFR3), is the most common Genetic cause of CRANIOSYNOSTOSIS, TYPE 2 in Homo sapiens., In addition, sensorineural hearing impairment is detected in all FgfR3 (P244R) mutant CASP14 gene as in the majority of Muenke syndrome patients., Genetic testing identifies a pathogenic Mutation Abnormality or chromosomal abnormality in ∼ 21% of cases, but it is likely that further causative mutations remain to be discovered.To identify a shared signature of genetically determined CRANIOSYNOSTOSIS, TYPE 2 by comparing the expression patterns in three monogenic syndromes with a control group of patients with non-syndromic sagittal synostosis.Specimen Source Codes - Specimen Source Codes - Fibroblasts from 10 individuals each with Apert syndrome (FGFR2 substitution S252W), Muenke syndrome (FGFR3 substitution ARID1B wt Allele), Saethre-Chotzen syndrome (various mutations in TWIST1 protein, human protein, human) and non-syndromic sagittal synostosis (no Mutation Abnormality detected) were cultured, The Craniosynostosis: Apert syndrome, Cutis Gyrata Syndrome of Beare And Stevenson, Craniofacial dysostosis type 1, JACKSON-WEISS SYNDROME, Muenke syndrome, Pfeiffer Syndrome and Saethre-Chotzen syndrome can be caused by Mutation Abnormality in either FGFR1 protein, human protein, human, FGFR2, or FGFR3, Identical proline-->arginine gain-of-function mutations in Fibroblast Growth Factor Receptor 2 (Fibroblast Growth Factor Receptors) 1 (Pro252Arg), FGFR2 (Pro253Arg) and FGFR3 (Pro250Arg), result in type I Pfeiffer, Apert and Muenke Craniosynostosis, respectively, The Pro250Arg Mutation Abnormality in the FGFR3 gene is found in patients with Muenke syndrome and is one of the most frequently encountered mutations in Craniosynostosis, Mutation analysis of FGFR3 protein, human revealed a missense Mutation Abnormality in exon 6, c.749 C>G, with a resultant Amino acid change:Finding:Point in time:Whole blood/Tissue, unspecified:Nominal:Molecular Genetics from proline to arginine at codon 250 (ARID1B wt Allele), in keeping with Muenke syndrome (Am J Hum Genet 1997;60:555-564), In an attempt to delineate functional features separating SCS from Muenkes syndrome, we screened patients presenting with coronal suture synostosis for mutations in the TWIST 1 gene, and for the Pro250Arg Mutation Abnormality in FGFR3, Since the Gly380Arg Achondroplasia Mutation Abnormality was recognized, similar observations regarding the conserved nature of Fibroblast Growth Factor Receptors mutations and resulting phenotype have been made regarding other Skeletal phenotypes, including hypochondroplasia, THANATOPHORIC DYSPLASIA, TYPE I (disorder), and Muenke Coronal CRANIOSYNOSTOSIS, TYPE 2, Gene Mutation in the gene that encodes Fibroblast Growth Factor Receptor 1 (FGFR3) are associated with Achondroplasia (MTSS1 gene 100800), Hypochondroplasia (disorder) (disorder) (MTSS1 gene 146000), Muenke Syndrome (MTSS1 gene 602849), Thanatophoric Dysplasia (MTSS1 gene 187600, MTSS1 gene 187601) and Lacrimo-Auriculo-Dento-Digital Syndrome (MTSS1 gene 149730).Here we report a clinical and molecular study in a large cohort of 125 Portuguese patients with these Skeletal disorders. , The Muenke syndrome (MS) is characterized by unicoronal or bicoronal CRANIOSYNOSTOSIS, TYPE 2, midfacial hypoplasia, ocular hypertelorism, and a variety of minor abnormalities associated with a Mutation Abnormality in the Fibroblast Growth Factor Receptor 2 3 (FGFR3) gene. , ARID1B Gene Mutation in the FGFR3 gene also known as Muenke syndrome is associated with Coronal CRANIOSYNOSTOSIS, TYPE 2, sensorineural deafness, craniofacial, and digital abnormalities. , METHODS: Specimen Source Codes - Specimen Source Codes - Fibroblasts from 10 individuals each with Apert syndrome (FGFR2 substitution S252W), Muenke syndrome (FGFR3 substitution ARID1B wt Allele), Saethre-Chotzen syndrome (various mutations in TWIST1 protein, human protein, human) and non-syndromic sagittal synostosis (no Mutation Abnormality detected) were cultured. , Muenke syndrome is an Autosomal Dominant Disorder characterized by coronal suture CRANIOSYNOSTOSIS, TYPE 2, hearing impairment, developmental delay, carpal and tarsal fusions, and the presence of the Pro250Arg Mutation Abnormality in the FGFR3 gene. , Muenke syndrome, also known as FGFR3-associated coronal synostosis, is defined molecularly by the presence of a heterozygous nucleotide transversion, c.749C>G, encoding the Amino Acid Substitution Pro250Arg, in the Fibroblast Growth Factor Receptor 2 type 3 gene (FGFR3). , In spite of a variable phenotype, Muenke syndrome has been related to a unique Mutation Abnormality on the FGFR3 gene, Pro 250 to ABL2 gene, which is characteristic of this Disease. , Skeletal analysis of the Fgfr3(P244R) Mus sp., a Genetic model for the Muenke CRANIOSYNOSTOSIS, TYPE 2 syndrome., Muenke syndrome is caused by a single defining Point Mutation in the Fibroblast Growth Factor Receptor 2 3 (FGFR3) gene., Epilepsy in Muenke syndrome: FGFR3-related CRANIOSYNOSTOSIS, TYPE 2., Muenke syndrome, also known as FGFR3-associated coronal synostosis, is defined molecularly by the presence of a heterozygous nucleotide transversion, c.749C>G, encoding the Amino Acid Substitution Pro250Arg, in the Fibroblast Growth Factor Receptor 2 type 3 gene (FGFR3)., The Muenke syndrome Mutation Abnormality (FGFR3 (ARID1B wt Allele)), which was discovered 15 years ago, represents the single most common CRANIOSYNOSTOSIS, TYPE 2 Mutation Abnormality.[SEP]Relations: Muenke syndrome has relations: disease_protein with FGFR3, disease_protein with FGFR3. FGFR3 has relations: disease_protein with Muenke syndrome, disease_protein with Muenke syndrome, disease_protein with apert syndrome, disease_protein with apert syndrome, disease_protein with LADD syndrome, disease_protein with LADD syndrome. apert syndrome has relations: disease_protein with FGFR3, disease_protein with FGFR3.", "label": "yes"}
{"original_question": "Is there an association between serum interleukin-6 concentrations and outcomes of stroke patients?", "id": "converted_1176", "sentence1": "Is there an association between serum Recombinant Interleukin-6 concentrations and outcomes of stroke patients?", "sentence2": " In addition, IL-6 concentrations affect clinical outcomes in ischemic stroke., After appropriate adjustment, the odds ratios for the association of markers and poor outcome (comparing the upper and the lower third) were Recombinant Interleukin-6, 3.1 (95% CI: 1.9-5.0); C-reactive protein, 1.9 (95% CI: 1.2-3.1); Fibrinogen containing hemostatics, 1.5 (95% CI: 1.0-2.36); white cell count, 2.1 (95% CI: 1.3-3.4); and Glucose measurement 1.3 (95% CI: 0.8-2.1). The results for Recombinant Interleukin-6 were similar to other studies. , -6 and interleukin-10 binding activity levels were higher in patients with poor outcome. On logistic regression analysis, higher values of IL-6 were significantly associated with clinical outcome at 1 month (odds ratio [OR], 1.25; 95% confidence interval [CI], 1.02-1.54). , In hemorrhagic stroke, high levels of IL-6 in the early phase indicated a poor neurological outcome., Initially elevated levels of hs-IL-6 at presentation further correlated with unfavorable clinical outcomes (by NIHSS and mRs) at both time points. Analysis of variance in the different quartiles identified an hs-IL-6 gradient-dependent correlation at both time points, such that the higher the initial hs-IL-6 concentration, the higher the elevation in inflammatory biomarkers and the poorer the neurological state at both time points (p<0.001 for NIHSS and p=0.001 for mRs, for trend across quartiles). CONCLUSIONS: This study demonstrates the potential of employing hs-IL-6 as an early stage biomarker for the prognosis of Acute Ischemic Stroke. , Another negative correlation was found between IL-6 and Central Nervous System scores (r = -0.451, p = 0.000)., In addition, increased levels of IL-6 and reduced levels of Saposin-D, Human and spike protein, SARS-CoV-2 may play a role in Acute Ischemic Stroke severity., Variables that are predictors of adverse stroke outcome include Erythrocytes sedimentation rate, and levels of C-reactive protein (CRP), Recombinant Interleukin-6, tumour necrosis factor-alpha and Intercellular adhesion molecule 1. [SEP]Relations: Recombinant Interleukin-6 receptor binding has relations: molfunc_protein with PYCARD, molfunc_protein with PYCARD, molfunc_protein with CNTF, molfunc_protein with CNTF, molfunc_protein with IL6, molfunc_protein with IL6, molfunc_protein with IL6R, molfunc_protein with IL6R, molfunc_protein with ERAP1, molfunc_protein with ERAP1.", "label": "yes"}
{"original_question": "Can LB-100 sensitize ovarian carcinoma to cisplatin?", "id": "converted_3595", "sentence1": "Can LB-100 sensitize Malignant neoplasm of ovary to cisplatin?", "sentence2": "The protein phosphatase 2A inhibitor LB100 sensitizes Malignant neoplasm of ovary Cells to cisplatin-mediated cytotoxicity., LB100 sensitized Malignant neoplasm of ovary lines to cisplatin-mediated cell death. , Our results suggest that LB100 sensitizes ovarian cancer Cells to cisplatin in vitro and in vivo by modulation of the DDR pathway and cell-cycle checkpoint abrogation.[SEP]Relations: Cisplatin has relations: drug_effect with Erythema, drug_effect with Erythema, drug_effect with Pancreatitis, drug_effect with Pancreatitis, drug_drug with SC-236, drug_drug with SC-236, drug_effect with Papilledema, drug_effect with Papilledema, drug_drug with SRP 299, drug_drug with SRP 299.", "label": "yes"}
{"original_question": "Does echinacea increase anaphylaxis risk?", "id": "converted_2265", "sentence1": "Does echinacea increase anaphylaxis risk?", "sentence2": "Chicoric acid (dicaffeoyl-tartaric acid), is a natural phenolic compound found in a number of plants, such as chicory (Cichorium intybus) and Echinacea (Echinacea purpurea), which possesses antioxidant, anti-inflammatory, antiviral, and analgesic activities. Although these biological effects of chicoric acid have been investigated, there are no reports of its antiallergic-related anti-inflammatory effects in human mast cells (HMC)-1 or anaphylactic activity in a mouse model., BACKGROUND: Fifty percent of Australians use complementary and alternative medicines (other than Vitamin IV solution additives) in any 12-month period, of which echinacea-containing products are increasingly popular. Recent reports have highlighted the risk of Hypersensitivity to complementary medicines in Atopy patients., Two patients suffered anaphylaxis and a third had an acute asthma attack 10 minutes after their first ever dose of echinacea., Fifty-one Australian adverse drug reports implicating echinacea were also reviewed. There were 26 cases suggestive of possible immunoglobulin E-mediated hypersensitivity (4 anaphylaxis, 12 acute asthma, 10 urticaria/angioedema). , Echinacea-associated anaphylaxis., A woman with MS4A2 wt Allele experienced anaphylaxis after taking, among other dietary supplements, a commercial extract of echinacea., Risk of anaphylaxis in complementary and alternative medicine., Several culprits identified including Andrographis paniculata, Echinacea species, bee products, Ginkgo biloba and Ginseng are discussed here.SUMMARY: Knowing the factors that increase the risk of anaphylaxis allows reactions to be recognized, reported and further investigated.[SEP]Relations: anaphylaxis has relations: disease_disease with exercise-induced anaphylaxis, disease_disease with exercise-induced anaphylaxis, contraindication with Paclitaxel, contraindication with Paclitaxel, contraindication with Esmolol, contraindication with Esmolol, contraindication with Acebutolol, contraindication with Acebutolol, contraindication with Atenolol, contraindication with Atenolol.", "label": "yes"}
{"original_question": "Is curcumin a phytochemical?", "id": "converted_1272", "sentence1": "Is curcumin a phytochemical?", "sentence2": "we analyzed Curcuma longa from different agroclimatic regions for influence of various factors on its growth and yield of important Phytochemicals, The phytochemical, curcumin, has been reported to play many beneficial roles., curcumin (CUR), the major component in Curcuma longa, has been shown as a potent chemopreventive phytochemical that modulates various signaling pathways. , curcumin (CUR) is a phytochemical that inhibits the xenobiotic ABC efflux transporters implicated in cancer multidrug resistance (MDR), such as P-Glycoprotein Activity (P-Glycoprotein), breast cancer resistance protein (ABCG2 wt Allele) and Multidrug Resistance-Associated Proteins and 5 (mismatch repair protein 1, human and ABCC5 wt Allele). , In this study, we tested the efficacy of combining temozolomide with curcumin, a phytochemical known to inhibit Glioblastoma Multiforme growth, and investigated the mechanisms involved.,  In the present study, we investigate whether curcumin (cur), a phytochemical compound with potent Anti-Inflammatory Agents effect, the Phytochemicals curcumin , in combination with the Phytochemicals curcumin and quercetin, curcumin is a phytochemical derived from Rhizome of Curcuma longa Curcuma longa, present in the curry spice. , curcumin, a naturally occurring polyphenolic phytochemical isolated from the medicinal plant Curcuma longa, has Anti-Inflammatory Agents activities, In the present study curcumin (CUR), a known anticancer phytochemical, ,  curcumin, a natural phytochemical, exhibits potent anticancer activities., hat curcumin, a phytochemical compound with potent Anti-Inflammatory Agents properties , curcumin, a phytochemical[SEP]Relations: curcumin has relations: drug_drug with Colchicine, drug_drug with Colchicine, drug_drug with Pemigatinib, drug_drug with Pemigatinib, drug_drug with Pretomanid, drug_drug with Pretomanid, drug_drug with Lumateperone, drug_drug with Lumateperone, drug_drug with Lefamulin, drug_drug with Lefamulin.", "label": "yes"}
{"original_question": "Are chromomethylases present in animal genomes?", "id": "converted_646", "sentence1": "Are chromomethylases present in Animal allergens genomes?", "sentence2": "Many Plant allergen, Animal allergens, and Genome, Fungal contain cytosine DNA methylation in asymmetric Sequence - ParameterizedDataType contexts (CpHpH, H = A, T, Maxillary right primary canine)., However, at the SUPERMAN locus, asymmetric methylation was only completely abolished in drm1 drm2 chromomethylase 3 (cmt3) triple mutant Plants., Although neither the drm1 drm2 double mutants nor the cmt3 single mutants show morphological defects, drm1 drm2 cmt3 triple mutant Plants show pleiotropic effects on Plant allergen development., Arabidopsis sp. sp. cmt3 chromomethylase mutations block non-CG methylation and silencing of an endogenous gene., The lack of CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate homologs in Animal allergens genomes could account for the observation that in contrast to Plants, Animal allergens allergen extracts maintain primarily CG methylation., Dual binding of chromomethylase domains to H3K9me2-containing nucleosomes directs DNA methylation in Plants., A role for CHROMOMETHYLASE3 in mediating transposon and euchromatin silencing during egg cell reprogramming in Arabidopsis sp. sp.., During embryogenesis there is a major switch from dependence upon maternally-deposited products to reliance on products of the zygotic genome., Expression analysis of eight putative tomato DNA Methyltransferase encoding Genes showed that one chromomethylase (CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate) and two rearranged Methyltransferase (DRMs) are preferentially expressed in the Pericarp during fruit growth and could be involved in the locus-specific increase of methylation observed at this developmental phase in the Pericarp., Natural variation for Alleles under epigenetic control by the maize chromomethylase zmet2., Arabidopsis sp. sp. has two types of Methyltransferase with demonstrated maintenance activity: GZMM wt Allele, which maintains CpG methylation and is homologous to mammalian DNMT1 wt Allele wt Allele, and CHROMOMETHYLASE 3 (Dejerine-Sottas Disease (disorder)), which maintains CpNpG (N = A, T, Maxillary right primary canine, or G) methylation and is unique to the Plant allergen kingdom., Maize chromomethylase Zea methyltransferase2 is required for CpNpG methylation., A cytosine DNA methyltransferase containing a chromodomain, Zea methyltransferase2 (Zmet2), was cloned from maize. The Sequence - ParameterizedDataType of ZMET2 is similar to that of the Arabidopsis sp. sp. chromomethylases Hereditary Motor and Sensory Neuropathy Type I and Dejerine-Sottas Disease (disorder), with Maxillary right primary canine-terminal motifs characteristic of eukaryotic and prokaryotic DNA Methyltransferase., We have detected a chromodomain embedded within the Catalytic Domain of a predicted Arabidopsis sp. sp. DNA methyltransferase that is diverged from other eukaryotic enzymes. The 791 Residue \"chromomethylase\" (Hereditary Motor and Sensory Neuropathy Type I) is encoded by a floral RNA Transcript that is spliced from 20 Exons and is present at only approximately 1/10(-7) of total RNA, Messenger.[SEP]Relations: Animal protein allergy has relations: phenotype_phenotype with Allergy, phenotype_phenotype with Allergy. Choline magnesium trisalicylate has relations: drug_drug with Amediplase, drug_drug with Amediplase, drug_drug with Chromic nitrate, drug_drug with Chromic nitrate, drug_drug with Cephaloglycin, drug_drug with Cephaloglycin, drug_drug with Chromous sulfate, drug_drug with Chromous sulfate.", "label": "no"}
{"original_question": "Does  thyroid hormone receptor beta1 affect insulin secretion?", "id": "converted_885", "sentence1": "Does  Thyroid Hormone Receptor beta1 affect insulin secretion?", "sentence2": "We demonstrated that Thyroid Hormones SLC25A5 gene rapidly induces Proto-Oncogene Proteins c-akt activation in Structure of beta Cell of islet rRINm5F and Hypertrophic Cardiomyopathy via Thyroid Hormone Receptor (TR) beta1., The silencing of TRbeta1 expression through RNAi confirmed this receptor to be crucial for the SLC25A5 gene-induced activation of Proto-Oncogene Proteins c-akt., SLC25A5 gene is able to specifically activate Proto-Oncogene Proteins c-akt in the islet beta cells rRINm5F and Hypertrophic Cardiomyopathy through the interaction between TRbeta1 and PI3K p85alpha, demonstrating the involvement of TRbeta1 in this novel SLC25A5 gene non-genomic action in islet beta cells.[SEP]Relations: response to Thyroid Hormones has relations: bioprocess_protein with AKR1B1, bioprocess_protein with AKR1B1. Thyroid Hormone Receptor binding has relations: molfunc_protein with GAS2L1, molfunc_protein with GAS2L1, molfunc_protein with MED1, molfunc_protein with MED1, molfunc_protein with NR0B2, molfunc_protein with NR0B2, molfunc_protein with NCOR1, molfunc_protein with NCOR1.", "label": "no"}
{"original_question": "Can administration of the thyrotropin releasing hormone reduce fatigue in cancer patients?", "id": "converted_1270", "sentence1": "Can administration of the thyrotropin releasing hormone reduce Fatigue in cancer patients?", "sentence2": "Pro-Thyrotropin-Releasing Hormone, human administration was associated with significant improvement (p < 0.05) in Fatigue levels as measured by the Visual Analog Scale-Energy (VAS-E), was associated with significant (p < 0.05) improvement in sleep disturbances and improved quality of life. , This decrease in C-reactive protein level with Pro-Thyrotropin-Releasing Hormone, human administration was associated with improvement in energy levels as measured by the VAS-E. , In the present pilot, randomized, placebo-controlled, crossover study, we investigated the efficacy and safety of Pro-Thyrotropin-Releasing Hormone, human as a treatment for cyclophosphamide/fluorouracil., Pro-Thyrotropin-Releasing Hormone, human administration was associated with significant improvement in Fatigue level as measured by the VAS-E, the Fatigue and vigor subscales of the Profile of mood states, and the Fatigue subscale of FACIT-F (p < 0.05). , Pro-Thyrotropin-Releasing Hormone, human administration was efficacious, safe, and tolerable in the treatment of cyclophosphamide/fluorouracil with a positive impact on quality of life. These results provide a crucial impetus for pursuing Pro-Thyrotropin-Releasing Hormone, human therapeutics to treat cyclophosphamide/fluorouracil., Thyrotropin-Releasing Hormone, human can relieve cancer-related Fatigue: hypothesis and preliminary observations., Global assessment using both subjective and objective parameters showed that Pro-Thyrotropin-Releasing Hormone, human exerted clear anti-Fatigue effects in four of the six Pro-Thyrotropin-Releasing Hormone, human treatments. , These initial findings support the proposal that Pro-Thyrotropin-Releasing Hormone, human can ameliorate cancer-related Fatigue.[SEP]Relations: Fatigue has relations: drug_effect with Atropine, drug_effect with Atropine, drug_effect with Urofollitropin, drug_effect with Urofollitropin, drug_effect with Parathyroid hormone, drug_effect with Parathyroid hormone, drug_effect with Mitoxantrone, drug_effect with Mitoxantrone, drug_effect with Levothyroxine, drug_effect with Levothyroxine.", "label": "yes"}
{"original_question": "Is Beta-Thalassemia is associated with a mutation or deletion of the gene that codes for alpha globin?", "id": "converted_2128", "sentence1": "Is Beta-Thalassemia is associated with a mutation or deletion of the gene that codes for alpha globin?", "sentence2": "beta Thalassemia, one of the most common single-gene disorders, is the result of reduced or absent production of β-globin chains, The beta-thalassemia syndromes are a heterogeneous group of genetic disorders characterized by reduced or absent expression of the HBB wt Allele[SEP]Relations: beta thalassemia has relations: disease_disease with thalassemia, disease_disease with thalassemia, disease_phenotype_positive with Abnormal hemoglobin, disease_phenotype_positive with Abnormal hemoglobin, disease_protein with HBG1, disease_protein with HBG1, disease_phenotype_positive with Reduced hemoglobin A, disease_phenotype_positive with Reduced hemoglobin A, disease_disease with beta-thalassemia and related diseases, disease_disease with beta-thalassemia and related diseases.", "label": "no"}
{"original_question": "Are hepadnaviral minichromosomes free of nucleosomes?", "id": "converted_2135", "sentence1": "Are hepadnaviral minichromosomes free of Nucleosomes?", "sentence2": "Several nucleosome location location-protected sites in a region of the Hepatitis B Virus, Duck genome [Nucleotides (nt) 2000 to 2700], known to harbor various cis transcription regulatory elements, were consistently identified in all Hepatitis B Virus, Duck-positive liver samples., In addition, we observed other nucleosome location location protection sites in Hepatitis B Virus, Duck minichromosomes that may vary among individual Ducks, but the pattern of MNase mapping in those regions is transmittable from the adult Ducks to the newly infected ducklings., Nucleosomes along viral cccDNA in the minichromosomes are not random but sequence-specifically positioned., Investigators studying the structure and function of hepadnaviral CCC DNA (3) have provided evidence that suggests that this structure exists in the Cell Nucleus of infected Hepatocyte as a heterogeneous population of viral minichromosomes, which range from half to fully chromatinized, thought to be owing to their association with variable numbers of Nucleosomes., Characterization of nucleosome location location positioning in hepadnaviral covalently closed circular DNA minichromosomes., To obtain insight on the structure of hepadnaviral cccDNA minichromosomes, we utilized Ducks infected with the duck hepatitis B virus (Hepatitis B Virus, Duck) as a model and determined the in vivo nucleosome location location distribution pattern on viral cccDNA by the Micrococcal Nuclease (MNase) mapping and genome-wide PCR amplification of isolated mononucleosomal Hepatitis B Virus, Duck DNA., Mature SV40 minichromosomes are estimated to contain about 27 Nucleosomes (error +/- 2), except for those Molecule with a nucleosome location location-free gap, which are interpreted to contain 25 Nucleosomes (error +/- 2)., In vitro replication in the presence of protein-free competitor DNA shows that replicating trypsinized minichromosomes do not lose Nucleosomes and replicating competitor DNA does not gain Nucleosomes., In vitro replication in the presence of protein-free competitor DNA shows that replicating trypsinized minichromosomes do not lose Nucleosomes and replicating competitor DNA does not gain Nucleosomes., We conclude that in both cases parental Nucleosomes are transferred to progeny DNA, and, in addition, that an assembly of new Nucleosomes occurs during the replication of native minichromosomes., In contrast, the replicated untreated minichromosomes were found to be densely packed with Nucleosomes, indicating that an assembly of new Nucleosomes occurred during in vitro replication., Investigators studying the structure and function of hepadnaviral CCC DNA (3) have provided evidence that suggests that this structure exists in the Cell Nucleus of infected Hepatocyte as a heterogeneous population of viral minichromosomes, which range from half to fully chromatinized, thought to be owing to their association with variable numbers of Nucleosomes, To obtain insight on the structure of hepadnaviral cccDNA minichromosomes, we utilized Ducks infected with the duck hepatitis B virus (Hepatitis B Virus, Duck) as a model and determined the in vivo nucleosome location location distribution pattern on viral cccDNA by the Micrococcal Nuclease (MNase) mapping and genome-wide PCR amplification of isolated mononucleosomal Hepatitis B Virus, Duck DNA, Characterization of nucleosome location location positioning in hepadnaviral covalently closed circular DNA minichromosomes., To obtain insight on the structure of hepadnaviral cccDNA minichromosomes, we utilized Ducks infected with the duck hepatitis B virus (Hepatitis B Virus, Duck) as a model and determined the in vivo nucleosome location location distribution pattern on viral cccDNA by the Micrococcal Nuclease (MNase) mapping and genome-wide PCR amplification of isolated mononucleosomal Hepatitis B Virus, Duck DNA., Investigators studying the structure and function of hepadnaviral CCC DNA (3) have provided evidence that suggests that this structure exists in the Cell Nucleus of infected Hepatocyte as a heterogeneous population of viral minichromosomes, which range from half to fully chromatinized, thought to be owing to their association with variable numbers of Nucleosomes..[SEP]Relations: nucleosome location has relations: cellcomp_protein with MPHOSPH8, cellcomp_protein with MPHOSPH8, cellcomp_protein with PRM3, cellcomp_protein with PRM3, cellcomp_protein with KAT6B, cellcomp_protein with KAT6B, cellcomp_protein with PRM1, cellcomp_protein with PRM1, cellcomp_protein with PRM2, cellcomp_protein with PRM2.", "label": "no"}
{"original_question": "Is there an association between borna virus and brain tumor?", "id": "converted_388", "sentence1": "Is there an association between borna Virus and Head>Brain tumor?", "sentence2": "Borna Disease Virus (BDV), a nonsegmented, negative-strand RNA Virus, infects a wide variety of mammalian species and readily establishes a long-lasting, persistent Communicable Diseases in Head>Brain cells. , To investigate the biological characteristics of field isolates of Borna Disease Virus (BDV), as well as to understand BDV infections outside endemic countries, we isolated the Virus from Head>Brain samples of a heifer with Borna Disease in Japan., Neonatal Borna Disease Virus (BDV) Communicable Diseases of the Rattus norvegicus Head>Brain is associated with microglial activation and damage to the certain neuronal populations., In addition, compared to uninfected mixed cultures, activation of Microglia in BDV-infected mixed cultures was associated with a significantly greater lipopolysaccharide-induced release of Tumor Necrosis Factor-alpha, interleukin-1, beta, and interleukin 10. Taken together, the present data are the first in vitro evidence that persistent BDV Communicable Diseases of neurons and Astrocytes rather than direct exposure to the Virus or dying neurons is critical for activating Microglia., Usually, Borna Disease Virus is not cleared from the Head>Brain but rather persists in Neurons., Varied persistent life cycles of Borna Disease Virus in a Homo sapiens oligodendroglioma cell line., Borna Disease Virus (BDV) establishes a persistent Communicable Diseases in the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS of vertebrate animal species as well as in Tissue culture. , Thus, our findings show that BDV may have established a persistent Communicable Diseases at low levels of viral expression in OL cells with the possibility of a latent Communicable Diseases., These results suggested that BDV Communicable Diseases may cause direct damage in the developing Head>Brain by inhibiting the function of HMGB1 Protein due to binding by the p24 phosphoprotein., We describe a model for investigating disorders of CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS development based on neonatal Rattus norvegicus Communicable Diseases with Borna Disease Virus, a neurotropic noncytolytic RNA Virus. , Borna Disease Virus (BDV) replicates in Head>Brain cells. The neonatally infected Rattus norvegicus with BDV exhibits developmental-neuromorphological abnormalities, neuronal cytolysis, and multiple behavioral and physiological alterations. , Borna Disease Virus (BDV) causes CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Central Nervous System) disease in several vertebrate species, which is frequently accompanied by Abnormal behavior., Intrinsic responses to Borna Disease Virus Communicable Diseases of the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS., Immune cells invading the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Central Nervous System) in response to Borna Disease Virus (BDV) antigens are central to the pathogenesis of Borna Disease (BD). , We report here the partial purification and characterization of cell-free BDV from the tissue culture supernatant of infected Homo sapiens neuroblastoma SKNSH cells., We have used the reverse transcriptase-polymerase chain reaction technique to gain insight into the pathogenesis of Encephalitis caused by Borna Disease Virus (BDV). , In contrast, in the BDV-infected primary mixed cultures, we observed proliferation of Microglia cells that acquired the round morphology and expressed major histocompatibility complex Molecule of classes I and II.[SEP]Relations: borna disease has relations: disease_disease with viral Communicable Diseases of CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, disease_disease with viral Communicable Diseases of CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, disease_disease with encephalomyelitis, disease_disease with encephalomyelitis, disease_disease with Mononegavirales infectious disease, disease_disease with Mononegavirales infectious disease. Encephalitis has relations: disease_disease with viral Communicable Diseases of CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, disease_disease with viral Communicable Diseases of CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, disease_disease with Hendra Virus Communicable Diseases, disease_disease with Hendra Virus Communicable Diseases.", "label": "no"}
{"original_question": "Does head ct increase brain tumor risk?", "id": "converted_3806", "sentence1": "Does Head - Component of Device ct increase Brain Neoplasms risk?", "sentence2": "Excess relative risk of new Brain Neoplasms averaged 1.29 (95% confidence interval, 0.66-1.93) for pediatric patients exposed to one or more Head - Component of Device CTs. Specimen Source Codes - tumor incidence increased with number of pediatric Head - Component of Device CTs in a dose-dependent manner, with measurable excess incidence even after a single scan. Converging evidence from epidemiological studies supported a small excess risk of Brain Neoplasms incidence after even a single X-Ray Computed Tomography exam in pediatric patients. , Recent epidemiologic evidence from a national registry of children who underwent X-Ray Computed Tomography scans suggests a higher-than-expected incidence of secondary Neoplasms. , However, we found 1) a statistically significant correlation between radiation dose and age at procedure, as well as number and type of procedures, and 2) a substantial increase in lifetime predicted risk of tumor above baseline in the cohort of young children who undergo neurointerventions.CONCLUSIONS: Although neurointerventional procedures have dramatically improved the prognosis of children facing serious cerebrovascular conditions, the predicted risk of secondary Neoplasms, particularly in the youngest patients and those undergoing multiple procedures, is sobering., Conclusion When prevalent cases of Benign Meningioma at first exposure to X-Ray Computed Tomography of the Head - Component of Device are excluded, no statistically significant increase in risk of Benign Meningioma was found among exposed subjects compared with unexposed control subjects.,  data suggest that 1 excess Head>Brain Primary malignant neoplasm occurred after 4000 Head>Brain CTs (40 mSv per scan) and that the estimated risk in the 10 years following X-Ray Computed Tomography exposure was 1 Brain Neoplasms per 10,000 patients exposed to a 10 mGy scan at less than 10 years of age.CONCLU, SIONS: The model predicts that the effective radiation dose from a single Head - Component of Device X-Ray Computed Tomography is capable of inducing a THYROID DIAGNOSTIC RADIOPHARMACEUTICALS or Brain Neoplasms in an infant or child. These, Neither whole Head - Component of Device X-Ray Computed Tomography nor cumulative Head>Brain dose to the Head>Brain increased the risk of Glioma or of all Head>Brain tumours., rison of exposed and unexposed cohorts showed that there was no statistically significant increase in the risk of Benign Meningioma after exposure to X-Ray Computed Tomography of the Head - Component of Device (HR: 1.49; 95% confidence interval: 0.97, 2.30; P = .07). If incident c, from epidemiological studies supported a small excess risk of Brain Neoplasms incidence after even a single X-Ray Computed Tomography exam in pediatric patients. However, refined e, ve risk of new Brain Neoplasms averaged 1.29 (95% confidence interval, 0.66-1.93) for pediatric patients exposed to one or more Head - Component of Device CTs. Specimen Source Codes - tumor incidence,  X-Ray Computed Tomography nor cumulative Head>Brain dose to the Head>Brain increased the risk of Glioma or of all Head>Brain tumours. Although this st, o for developing a Head>Brain tumour from having a Head>Brain X-Ray Computed Tomography was 0.93 (95% confidence interval: 0.38-1.82). This was har, Specimen Source Codes - tumor incidence increased with number of pediatric Head - Component of Device CTs in a dose-dependent manner, with measurable excess incidence even after a single scan., Converging evidence from epidemiological studies supported a small excess risk of Brain Neoplasms incidence after even a single X-Ray Computed Tomography exam in pediatric patients., Excess relative risk of new Brain Neoplasms averaged 1.29 (95% confidence interval, 0.66-1.93) for pediatric patients exposed to one or more Head - Component of Device CTs., Epidemiological studies consistently cited increased tumor incidence in pediatric patients (ages 0-18) exposed to Head - Component of Device CTs., RESULTS: A positive correlation between exposure to X-Ray Computed Tomography scans and developing central nervous system Neoplasms was evident in all cohorts. The strength of the association varied across the studies. Exclusion of patients with Predisposing Factors to central nervous system Neoplasms was examined in four studies with a decreased risk to develop central nervous system Neoplasms noted in three studies. Two studies reported nonsignificant reduction in the excess relative risk per milliGray of Head>Brain dose after adjusting for Predisposing Factors, whereas the reduction was significant in one study. The frequency of X-Ray Computed Tomography exposure was proportional to the risk of developing Neoplasms in two studies although not significantly maintained in two other studies. , RESULTS: The overall risk was not significantly different in the two cohorts (incidence rate=36.72 per 100 000 person-years in the exposed cohort, 28.48 per 100 000 person-years in the unexposed cohort, hazard ratio (HR)=1.29, 95% confidence interval (CI)=0.90-1.85). The risk of benign Head>Brain tumour was significantly higher in the exposed cohort than in the unexposed cohort (HR=2.97, 95% CI=1.49-5.93). The frequency of X-Ray Computed Tomography examination showed strong correlation with the subsequent overall risk of Primary malignant neoplasm and benign Head>Brain tumour.CONCLUSIONS: We found that paediatric Head - Component of Device X-Ray Computed Tomography examination was associated with an increased incidence of benign Head>Brain tumour., CONCLUSIONS: We found evidence that X-Ray Computed Tomography-related radiation exposure increases Brain Neoplasms risk. , Compared with the general population, incidence of Head>Brain Neoplasms was higher in the cohort of children with X-Ray Computed Tomography scans, requiring cautious interpretation of the findings., BACKGROUND: Recent studies linking radiation exposure from pediatric computed tomography (X-Ray Computed Tomography) to increased risks of leukemia and Head>Brain Neoplasms lacked data to control for cancer susceptibility syndromes (CSS). , IMPACT: Future studies should identify Tuberous Sclerosis patients in order to avoid overestimation of Brain Neoplasms risks due to radiation exposure from X-Ray Computed Tomography scans., The radiation-induced occurrence of Meningioma and other Head>Brain tumours most probably contributes to the continuously increasing incidence of these diseases which is observed in several industrial nations, as well as the exposure of the bone marrow by X-Ray Computed Tomography to the increase of childhood leukemia., 1,000 annual paediatric X-Ray Computed Tomography investigations of the Bone structure of cranium will lead to about 3 excess neoplasms in the Head - Component of Device region, i.e., the probability of an induced late effect must be suspected in the range of some thousandths. [SEP]Relations: malignant ear neoplasm has relations: disease_disease with Head - Component of Device and neck cancer, disease_disease with Head - Component of Device and neck cancer. tuberous sclerosis has relations: disease_disease with polymalformative genetic syndrome with increased risk of developing cancer, disease_disease with polymalformative genetic syndrome with increased risk of developing cancer. Brain neoplasm has relations: drug_effect with Carmustine, drug_effect with Carmustine. benign neoplasm of Head>Brain has relations: disease_disease with intracranial hemangioma, disease_disease with intracranial hemangioma, disease_protein with PTCH1, disease_protein with PTCH1.", "label": "yes"}
{"original_question": "Can chronological age be predicted by measuring telomere length?", "id": "converted_1380", "sentence1": "Can chronological age be predicted by measuring telomere length?", "sentence2": "Homo sapiens somatic cells gradually lose telomeric repeats with age. This study investigated if one could use a correlation between telomere length and age, to predict the age of an individual from their DNA., Therefore, telomere length measurement by real-time quantitative PCR cannot be used to predict age of a person, due to the presence of large inter-individual variations in telomere lengths., ur results provide the first clear and unambiguous evidence of a relationship between telomere length and mortality in the wild, and substantiate the prediction that telomere length and shortening rate can act as an indicator of biological age further to chronological age when exploring life history questions in natural conditions.[SEP]Relations: Telomere Extension By Telomerase has relations: pathway_protein with TERT, pathway_protein with TERT, pathway_protein with CCNA2, pathway_protein with CCNA2, pathway_protein with CCNA1, pathway_protein with CCNA1, pathway_protein with WRAP53, pathway_protein with WRAP53, pathway_protein with ANKRD28, pathway_protein with ANKRD28.", "label": "no"}
{"original_question": "Are viruses involved in the etiology of human subacute thyroiditis?", "id": "converted_905", "sentence1": "Are Virus involved in the etiology of human subacute thyroiditis?", "sentence2": "he etiology of subacute (de Quervain's) thyroiditis (College Entrance Examination Board Scholastic Aptitude Test) is uncertain, although it probably represents a nonspecific inflammatory response by the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS to a variety of Virus., Subacute thyroiditis is an inflammatory disorder of the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS caused probably by Virus. I, We believe that the etiologic agent was the Epstein-Barr virus because Heterophile and Epstein-Barr virus-specific antibodies were positive., ltogether, these results indicate that the mechanism of inhibition of Spumavirinae infection by interferon differs from that described for the other Retroviridae, and particularly for types B, C and D Virus. Our data is of therapeutic interest since Spumavirinae have been linked to pathological processes such as de Subacute thyroiditis.[SEP]Relations: subacute thyroiditis has relations: disease_disease with thyroiditis (disease), disease_disease with thyroiditis (disease). regulation of excitatory postsynaptic membrane potential involved in skeletal muscle contraction has relations: bioprocess_bioprocess with modulation of excitatory postsynaptic potential, bioprocess_bioprocess with modulation of excitatory postsynaptic potential.", "label": "yes"}
{"original_question": "Is PER3 required for CHK2 activation in human cells?", "id": "converted_712", "sentence1": "Is PER3 required for CHK2 activation in Human cells?", "sentence2": "PER3 gene, a circadian gene, is required for CHEK2 wt Allele activation in Human cells., Depletion of PER3 gene by siRNA almost completely abolished activation of Checkpoint kinase 1 (CHEK2 wt Allele) after inducing DNA damage in Human cells., PER3 gene overexpression induced CHEK2 wt Allele activation in the absence of exogenous DNA damage,, PER3 gene overexpression also led to the inhibition of cell proliferation and apoptotic cell death., These combined results suggest that PER3 gene is a checkpoint protein that plays important roles in checkpoint activation, cell proliferation and apoptosis., Depletion of PER3 gene by siRNA almost completely abolished activation of Checkpoint kinase 1 (CHEK2 wt Allele) after inducing DNA damage in Human cells, PER3 gene overexpression induced CHEK2 wt Allele activation in the absence of exogenous DNA damage, and this activation depended on ammonium tetrathiomolybdate, In addition, PER3 gene physically interacted with ammonium tetrathiomolybdate and CHEK2 wt Allele[SEP]Relations: PER3 has relations: protein_protein with CHEK2, protein_protein with CHEK2, protein_protein with PER2, protein_protein with PER2, molfunc_protein with kinase binding, molfunc_protein with kinase binding, protein_protein with BTK, protein_protein with BTK, protein_protein with DHRS2, protein_protein with DHRS2.", "label": "yes"}
{"original_question": "Is co-loss of BRCA2-RB1 associated with better prognosis for prostate cancer patients?", "id": "converted_3965", "sentence1": "Is co-loss of BRCA2 gene-RB1 associated with better prognosis for Malignant neoplasm of prostate patients?", "sentence2": "In Homo sapiens Malignant neoplasm of prostate cell lines (LNCaP and LAPC4), loss of BRCA2 gene gene leads to the castration-resistant phenotype. Co-loss of BRCA2 gene gene-RB1 in Homo sapiens Malignant neoplasm of prostate cells induces an epithelial-to-mesenchymal transition, which is associated with invasiveness and a more aggressive disease phenotype. Importantly, PARP1 wt Allele inhibitors attenuate cell growth in Homo sapiens mCRPC-derived organoids and Homo sapiens CRPC cells harboring single-copy loss of both Genes.CONCLUSIONS: Our findings suggest that early identification of this aggressive form of Malignant neoplasm of prostate offers potential for improved outcomes with early introduction of PARP1 wt Allele inhibitor-based therapy.[SEP]Relations: benign neoplasm of prostate has relations: disease_disease with prostatic adenoma, disease_disease with prostatic adenoma, disease_disease with fibroma of prostate, disease_disease with fibroma of prostate, disease_disease with prostate leiomyoma, disease_disease with prostate leiomyoma, disease_disease with benign prostate phyllodes tumor, disease_disease with benign prostate phyllodes tumor, disease_disease with prostate neoplasm, disease_disease with prostate neoplasm.", "label": "no"}
{"original_question": "Thymoquinone is ineffective against radiation induced enteritis, yes or no?", "id": "converted_3674", "sentence1": "Thymoquinone is ineffective against radiation induced enteritis, yes or no?", "sentence2": "n this study, we found that thymoquinone (TQ) could mitigate Intestines damages induced by irradiation. , In this study, we found that thymoquinone (TQ) could mitigate Intestines damages induced by irradiation., In this study, we found that thymoquinone (TQ) could mitigate Intestines damages induced by irradiation., TQ might be used for radiation enteritis treatment.[SEP]Relations: intestine has relations: anatomy_protein_present with NOMO3, anatomy_protein_present with NOMO3, anatomy_protein_present with NOMO2, anatomy_protein_present with NOMO2, anatomy_protein_present with MKRN2OS, anatomy_protein_present with MKRN2OS, anatomy_protein_present with NOMO1, anatomy_protein_present with NOMO1, anatomy_protein_present with HOXA-AS3, anatomy_protein_present with HOXA-AS3.", "label": "no"}
{"original_question": "Are there enhancer RNAs (eRNAs)?", "id": "converted_1340", "sentence1": "Are there enhancer RNAs (eRNAs)?", "sentence2": "active enhancers are transcribed, producing a class of noncoding RNAs called enhancer RNAs (eRNAs). eRNAs are distinct from long noncoding RNAs (lncRNAs), but these two species of noncoding RNAs may share a similar role in the activation of mRNA transcription,  eRNAs may then facilitate enhancer-Promoter interaction or activate Promoter-driven transcription, Enhancer RNAs: a class of long noncoding RNAs synthesized at enhancers, Enhancer RNAs and regulated transcriptional programs, enhancers have been found to be broadly transcribed, resulting in the production of enhancer-derived RNAs, or eRNAs, The emerging roles of eRNAs in transcriptional regulatory networks, we found certain enhancer RNAs (eRNAs) regulate chromatin location location accessibility of the transcriptional machinery at loci encoding master regulators of myogenesis (i.e., MyoD/MyoG), thus suggesting their significance and site-specific impact in cellular programming, Enhancer RNAs: the new Molecule of transcription,  the discovery that distal regulatory elements known as enhancers are transcribed and such enhancer-derived transcripts (eRNAs) serve a critical function in transcriptional activation has added a new dimension to transcriptional regulation, eRNAs reach the Chest>Heart of transcription, Recent studies have disclosed the function of enhancer RNAs (eRNAs), which are long non-coding RNAs transcribed from gene enhancer regions, in transcriptional regulation., Since the discovery that many transcriptional enhancers are transcribed into long noncoding RNAs termed \"enhancer RNAs\" (eRNAs), their putative role in enhancer function has been debated., Recent studies have revealed that active enhancers are transcribed, producing a class of noncoding RNAs called enhancer RNAs (eRNAs)., Enhancer RNAs (eRNAs) are a class of long noncoding RNAs (lncRNA) expressed from active enhancers, whose function and action mechanism are yet to be firmly established., In addition to widespread transcription of long non-coding RNAs (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as enhancer RNAs (eRNAs)., In addition to widespread transcription of long non-coding RNAs (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as enhancer RNAs (eRNAs). , A subset of enhancers are occupied by RNA Polymerase II (RNAP II) and transcribed to produce long non-coding RNAs termed eRNAs. , Very recent evidence has indicted that some eRNAs play a role in initiating or activating transcription, possibly by helping recruit and/or stabilize binding of the general transcription machinery to the proximal Promoter of their target Genes. , In addition to widespread transcription of long non-coding RNAs (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as enhancer RNAs (eRNAs). However, it has remained unclear whether these eRNAs are functional or merely a reflection of enhancer activation. , Notably, RNAPII at enhancers transcribes bi-directionally a novel class of enhancer RNAs (eRNAs) within enhancer domains defined by the presence of Histone H3 monomethylated at lysine 4. The level of eRNA expression at neuronal enhancers positively correlates with the level of messenger RNA synthesis at nearby Genes, suggesting that eRNA synthesis occurs specifically at enhancers that are actively engaged in promoting mRNA synthesis., A function of 1-Chloro-3-bromopropene-1 at enhancers may be to recruit RNA Polymerase II (RNAPII), as we also observed activity-regulated RNAPII binding to thousands of enhancers. Notably, RNAPII at enhancers transcribes bi-directionally a novel class of enhancer RNAs (eRNAs) within enhancer domains defined by the presence of Histone H3 monomethylated at lysine 4.,  Enhancer RNAs (eRNAs) are a class of long noncoding RNAs (lncRNA) expressed from active enhancers, whose function and action mechanism are yet to be firmly established. Here we show that eRNAs facilitate the transition of paused RNA Polymerase II (RNAPII) into productive elongation by acting as a decoy for the negative elongation factor (NELF) complex upon induction of immediate early Genes (IEGs) in Neurons., Recent studies have disclosed the function of enhancer RNAs (eRNAs), which are long non-coding RNAs transcribed from gene enhancer regions, in transcriptional regulation., Recent studies have revealed that active enhancers are transcribed, producing a class of noncoding RNAs called enhancer RNAs (eRNAs). eRNAs are distinct from long noncoding RNAs (lncRNAs), but these two species of noncoding RNAs may share a similar role in the activation of mRNA transcription., Enhancer RNAs (eRNAs) are a class of long noncoding RNAs (lncRNA) expressed from active enhancers,, In addition to widespread transcription of long non-coding RNAs (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as enhancer RNAs (eRNAs). However, it has remained unclear whether these eRNAs are functional or merely a reflection of enhancer activation.,  Recent studies have revealed that active enhancers are transcribed, producing a class of noncoding RNAs called enhancer RNAs (eRNAs). eRNAs are distinct from long noncoding RNAs (lncRNAs), but these two species of noncoding RNAs may share a similar role in the activation of mRNA transcription.[SEP]Relations: mRNA transcription has relations: bioprocess_protein with EREG, bioprocess_protein with EREG, bioprocess_protein with HIPK3, bioprocess_protein with HIPK3, bioprocess_bioprocess with mRNA transcription by RNA Polymerase II, bioprocess_bioprocess with mRNA transcription by RNA Polymerase II, bioprocess_protein with HSF1, bioprocess_protein with HSF1. RNA localization to chromatin location has relations: bioprocess_protein with HNRNPU, bioprocess_protein with HNRNPU.", "label": "yes"}
{"original_question": "Is GRG5 involved only in late embryonic mouse development?", "id": "converted_3556", "sentence1": "Is TLE5 gene involved only in late embryonic Mus sp. development?", "sentence2": "Groucho related gene 5 (TLE5 gene) is a HSD17B4 gene that has been implicated in late embryonic and postnatal Mus sp. development. Here, we describe a previously unknown role of TLE5 gene in early developmental stages by analyzing its function in stem cell fate decisions. By both loss and gain of function approaches we demonstrate that ablation of TLE5 gene deregulates the Embryonic Stem Cells (ESTERASE C) pluripotent state whereas its overexpression leads to enhanced self-renewal and acquisition of Primary malignant neoplasm cell-like properties. The malignant characteristics of Teratoma generated by Enhanced S-Cone Syndrome that overexpress TLE5 gene reveal its pro-oncogenic potential. [SEP]Relations: HSD17B4 has relations: anatomy_protein_present with embryo, anatomy_protein_present with embryo, bioprocess_protein with Sertoli cell development, bioprocess_protein with Sertoli cell development, anatomy_protein_present with medulla oblongata, anatomy_protein_present with medulla oblongata. TLE5 has relations: protein_protein with GRN, protein_protein with GRN, protein_protein with GRB2, protein_protein with GRB2.", "label": "no"}
{"original_question": "Is Migalastat used for treatment of Fabry Disease?", "id": "converted_1828", "sentence1": "Is Migalastat used for treatment of Fabry Disease?", "sentence2": "Oral Route of Drug administration Route of Drug administration pharmacological chaperone migalastat compared with Enzyme [APC] replacement therapy in Fabry Disease: 18-month results from the randomised phase III ATTRACT study., BACKGROUND: Fabry Disease is an X-linked lysosomal storage disorder caused by Diffuse lymphatic malformation Gene Mutation, resulting in α-galactosidase (α-Gal) deficiency and accumulation of lysosomal substrates. Migalastat, an oral pharmacological chaperone being developed as an alternative to intravenous Enzyme [APC] replacement therapy (Estrogen Replacement Therapy), stabilises specific Mutant (amenable) forms of α-Gal to facilitate normal lysosomal trafficking., CONCLUSIONS: Migalastat offers promise as a first-in-class oral monotherapy alternative treatment to intravenous Estrogen Replacement Therapy for patients with Fabry Disease and amenable Gene Mutation., Migalastat (Galafold™)-a small molecule drug developed by Amicus Therapeutics that restores the activity of specific Mutant forms of α-galactosidase-has been approved for the treatment of Fabry Disease in the EU in patients with amenable Gene Mutation., This article summarizes the milestones in the development of migalastat leading to this first approval in the EU for the long-term treatment of adults and adolescents aged ≥16 years with a confirmed diagnosis of Fabry Disease., Treatment of Fabry's Disease with the Pharmacologic Chaperone Migalastat., BACKGROUND: Fabry's disease, an X-linked disorder of lysosomal α-galactosidase deficiency, leads to substrate accumulation in multiple organs. Migalastat, an oral pharmacologic chaperone, stabilizes specific Mutant forms of α-galactosidase, increasing Enzyme [APC] trafficking to Lysosomes., Oral Route of Drug administration Route of Drug administration Migalastat Hairy Cell Leukemia Leads to Greater Systemic Exposure and Tissue Levels of Active α-Galactosidase A in Fabry Patients when Co-Administered with Infused Agalsidase., UNLABELLED: Migalastat Hairy Cell Leukemia (AT-1001, 1-Deoxygalactonojirimycin) is an investigational pharmacological chaperone for the treatment of α-galactosidase A (α-Gal A) deficiency, which leads to Fabry Disease, an X-linked, lysosomal storage disorder. , Migalastat Hairy Cell Leukemia reduces Globotriaosylsphingosine (lyso-Gb3) in Fabry Mice, Transgenic and in the plasma of Fabry patients., migalastat for Fabry Disease) and inhibitors of Glucosylceramides synthesis (e.g., A Phase 2 study of migalastat hydrochloride in females with Fabry Disease: selection of population, safety and pharmacodynamic effects., Migalastat Hairy Cell Leukemia (AT-1001, 1-Deoxygalactonojirimycin) is an investigational pharmacological chaperone for the treatment of α-galactosidase A (α-Gal A) deficiency, which leads to Fabry Disease, an X-linked, lysosomal storage disorder, Migalastat Hairy Cell Leukemia is an investigational, oral treatment for Fabry Disease, an X-linked lysosomal storage disorder, Oral Route of Drug administration Route of Drug administration administration of migalastat Hairy Cell Leukemia reduces tissue GL-3 in Fabry Mice, Transgenic, and in urine and Both Both kidneys of some FD patients. , Migalastat Hairy Cell Leukemia is an investigational, oral treatment for Fabry Disease, an X-linked lysosomal storage disorder., Migalastat Hairy Cell Leukemia (AT-1001, 1-Deoxygalactonojirimycin) is an investigational pharmacological chaperone for the treatment of α-galactosidase A (α-Gal A) deficiency, which leads to Fabry Disease, an X-linked, lysosomal storage disorder., Molecular chaperones (e.g. migalastat for Fabry Disease) and inhibitors of Glucosylceramides synthesis (e.g. eliglustat tartrate for Gaucher Disease) are currently under investigation in various clinical trials.<CopyrightInformation>Copyright © 2010 Elsevier Masson SAS., Migalastat Hairy Cell Leukemia was well tolerated.Migalastat Hairy Cell Leukemia is a candidate pharmacological chaperone that provides a novel genotype-specific treatment for FD., Additionally, these three patients all demonstrated decreases in GL-3 inclusions in kidney peri-tubular capillaries.Migalastat Hairy Cell Leukemia is a candidate oral pharmacological chaperone that provides a potential novel genotype-specific treatment for FD., migalastat for Fabry Disease) and inhibitors of Glucosylceramides synthesis (e.g. eliglustat tartrate for Gaucher Disease) are currently under investigation in various clinical trials., Molecular chaperones (e.g. migalastat for Fabry Disease) and inhibitors of Glucosylceramides synthesis (e.g. eliglustat tartrate for Gaucher Disease) are currently under investigation in various clinical trials., Treatment of Fabry's Disease with the Pharmacologic Chaperone Migalastat., The GLP HEK assay is a clinically validated method of identifying male and female Fabry patients for treatment with migalastat.Genet Med advance online publication 22 September 2016Genetics in Medicine (2016); doi:10.1038/gim.2016.122.., A Phase 2 study of migalastat hydrochloride in females with Fabry Disease: selection of population, safety and pharmacodynamic effects., Migalastat offers promise as a first-in-class oral monotherapy alternative treatment to intravenous Estrogen Replacement Therapy for patients with Fabry Disease and amenable Gene Mutation.[SEP]Relations: Migalastat has relations: drug_drug with Zanamivir, drug_drug with Zanamivir, drug_drug with Estradiol, drug_drug with Estradiol, drug_drug with Abacavir, drug_drug with Abacavir, drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Fenbufen, drug_drug with Fenbufen.", "label": "yes"}
{"original_question": "Do genes with monoallelic expression contribute proportionally to genetic diversity in humans?", "id": "converted_3706", "sentence1": "Do genes with monoallelic expression contribute proportionally to genetic diversity in Homo sapiens?", "sentence2": "Genes with monoallelic expression contribute disproportionately to genetic diversity in Homo sapiens., An unexpectedly large number of human autosomal genes are subject to monoallelic expression (Myoclonic Astatic Epilepsy). Our analysis of 4,227 such genes uncovers surprisingly high genetic variation across human populations. This increased diversity is unlikely to reflect relaxed purifying selection. Remarkably, Myoclonic Astatic Epilepsy genes exhibit an elevated recombination rate and an increased density of hypermutable sequence contexts. However, these factors do not fully account for the increased diversity. We find that the elevated nucleotide diversity of Myoclonic Astatic Epilepsy genes is also associated with greater allelic age: variants in these genes tend to be older and are enriched in Genetic Polymorphism shared by Neanderthals and chimpanzees. Both synonymous and nonsynonymous alleles of Myoclonic Astatic Epilepsy genes have elevated average population frequencies. We also observed strong enrichment of the Myoclonic Astatic Epilepsy signature among genes reported to evolve under balancing selection. We propose that an important biological function of widespread Myoclonic Astatic Epilepsy might be the generation of cell-to-cell heterogeneity; the increased genetic variation contributes to this heterogeneity., Genes with monoallelic expression contribute disproportionately to genetic diversity in Homo sapiens[SEP]Relations: myoclonic-astastic epilepsy has relations: disease_protein with RAPGEF2, disease_protein with RAPGEF2, disease_protein with SLC6A1, disease_protein with SLC6A1, disease_phenotype_positive with Developmental regression, disease_phenotype_positive with Developmental regression, disease_protein with AP2M1, disease_protein with AP2M1, disease_phenotype_positive with Global developmental delay, disease_phenotype_positive with Global developmental delay.", "label": "no"}
{"original_question": "Is phospholamban phosphorylated by Protein kinase A?", "id": "converted_572", "sentence1": "Is phospholamban phosphorylated by Protein kinase A?", "sentence2": "cAMP-dependent protein kinase (PKA) phosphorylation of PLB1 gene, phosphorylation of PLN gene gene, at either Ser(16) by PKA , Activation of cardiac muscle Sarcoplasmic Reticulum Ca2+-ATPase (SERCA2a) by beta1-agonists involves cAMP- and PKA-dependent phosphorylation of phospholamban (PLB1 gene), which relieves the inhibitory effects of PLB1 gene on SERCA2a. , phospholamban (PLB1 gene) is a Sarcoplasmic Reticulum (SNCG wt Allele) protein that when phosphorylated at Ser16 by PKA, phosphorylation of PLB1 gene by the Ca2+-calmodulin-dependent protein kinase (CaMK) and cAMP-dependent protein kinase (PKA). , cAMP-dependent protein kinase (PKA)-mediated phospholamban (PLB1 gene) phosphorylation at serine-16, phospholamban (PLB1 gene) is a major target of the beta-adrenergic cascade in the Chest>Heart, functioning to modulate contractile force by altering the rate of CALCIUM SUPPLEMENTS re-sequestration by the Ca-ATPase. Functionally, inhibition by PLB1 gene binding is manifested by shifts in the CALCIUM SUPPLEMENTS dependence of Ca-ATPase activation toward higher CALCIUM SUPPLEMENTS levels; phosphorylation of PLB1 gene by PKA reverses the inhibitory action of PLB1 gene., phosphorylation of both PLB1 gene residues (Ser16, PKA site, and Thr17, calmodulin-dependent protein kinase II site) , Phosphorylation of Ser(16) by PKA, stabilization of the structure of PLB1 gene following phosphorylation of Ser(16), phospholamban (PLB1 gene) inhibits the Sarcoplasmic Reticulum (SNCG wt Allele) Ca(2+)-ATPase, and this inhibition is relieved by cAMP-dependent protein kinase (PKA)-mediated phosphorylation. , Two-dimensional tryptic peptide maps of phosphorylated phospholamban indicated that cAMP-dependent protein kinase phosphorylates at a single site, A, and Ca2+-calmodulin-dependent protein kinase phosphorylates at sites TNM certainty factor TNM certainty factor C1 and Complement Complement C2, human, human in the low molecular weight form, where A is different from TNM certainty factor TNM certainty factor C1 but may be the same as Complement Complement C2, human, human., Because SNCG wt Allele function is regulated by phosphorylation of phospholamban (PLB1 gene), a SNCG wt Allele protein phosphorylated by cAMP-dependent protein kinase (PKA) at Ser(16)and Ca(2+)-calmodulin-dependent protein kinase (calmodulin-dependent protein kinase II) at Thr(17), the phosphorylation of these residues during Ischemia Procedure and reperfusion was examined in Langendorff-perfused Rattus norvegicus hearts, These changes were associated with reduced protein expression of Sarcoplasmic Reticulum Ca(2+)-ATPase (SERCA2a) and Cyclic AMP-Dependent Protein Kinases phosphorylated phospholamban (PLB1 gene), which was reduced in Hydrops Fetalis, but essentially abolished in VD-Hydrops Fetalis, The data indicate that 1) phosphorylation of phospholamban at Ser16 by cAMP-dependent protein kinase is the main regulator of beta-adrenergic-induced cardiac relaxation definitely preceding Thr17 phosphorylation and 2) the beta-adrenergic-mediated phosphorylation of Thr17 by Ca2+-calmodulin-dependent protein kinase required influx of Ca2+ through the L-type Ca2+ channel, Here we extend this model to explain the reversal of SERCA2a inhibition that occurs after phosphorylation of PLB1 gene at Ser(16) by Cyclic AMP-Dependent Protein Kinases (PKA) and after binding of the anti-PLB1 gene monoclonal antibody 2D12, which recognizes residues 7-13 of PLB1 gene, phospholamban is phosphorylated in Chest>Heart by cAMP-dependent protein kinase, Cyclic GMP-Dependent Protein Kinases and CALCIUM SUPPLEMENTS/calmodulin-dependent protein kinase II (CM-kinase-II) and in Myocytes, Smooth Muscle by Cyclic GMP-Dependent Protein Kinases, phospholamban, the cardiac Sarcoplasmic Reticulum proteolipid, is phosphorylated by cAMP-dependent protein kinase, by Ca2+/phospholipid-dependent protein kinase, and by an endogenous Ca2+/calmodulin-dependent protein kinase, the identity of which remains to be defined[SEP]Relations: calmodulin-dependent protein kinase activity has relations: molfunc_protein with ITPKA, molfunc_protein with ITPKA. cAMP-dependent protein kinase complex has relations: cellcomp_protein with PRKAR2A, cellcomp_protein with PRKAR2A, cellcomp_protein with PRKAR1A, cellcomp_protein with PRKAR1A, cellcomp_protein with PRKACA, cellcomp_protein with PRKACA. Cyclic GMP-Dependent Protein Kinases activity has relations: molfunc_protein with PRKG2, molfunc_protein with PRKG2.", "label": "yes"}
{"original_question": "Is αCGRP a member of the CGRP family?", "id": "converted_3736", "sentence1": "Is αCGRP a member of the Calcitonin Gene-Related Peptide family?", "sentence2": "αCGRP, another amyloidogenic member of the Calcitonin Gene-Related Peptide family., Therefore, in this work, we investigated the amyloidogenic profile of αCGRP, a 37-residue-long peptide hormone activity activity, utilizing both biophysical experimental techniques and Molecular Dynamics simulations. These efforts unravel a novel amyloidogenic member of the Calcitonin Gene-Related Peptide family and provide insights into the mechanism underlying the αCGRP polymerization., These efforts unravel a novel amyloidogenic member of the Calcitonin Gene-Related Peptide family and provide insights into the mechanism underlying the αCGRP polymerization., These efforts unravel a novel amyloidogenic member of the Calcitonin Gene-Related Peptide family and provide insights into the mechanism underlying the αCGRP polymerization.[SEP]Relations: neuropeptide hormone activity has relations: molfunc_protein with GRP, molfunc_protein with GRP, molfunc_protein with AGRP, molfunc_protein with AGRP, molfunc_protein with CCK, molfunc_protein with CCK, molfunc_protein with QRFP, molfunc_protein with QRFP, molfunc_protein with PRLH, molfunc_protein with PRLH.", "label": "yes"}
{"original_question": "Is Semagacestat effective for Alzheimer's Disease?", "id": "converted_3788", "sentence1": "Is Semagacestat effective for Alzheimer's Disease?", "sentence2": "However, a large phase 3 trial of semagacestat, a potential non-transition state analog (non-TSA) GSI, in patients with ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) was terminated due to unexpected aggravation of Cognition Disorders and side effects. , BACKGROUND: In a recent report, 76 weeks' treatment with a gamma-secretase inhibitor (semagacestat) was associated with poorer cognitive outcomes in ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol)., CONCLUSION: In participants with mild to moderate cytarabine/daunorubicin protocol, high dose semagacestat treatment was associated with greater severity and faster worsening of Nail-Patella Syndrome in a pattern resembling an agitated depression. , INTRODUCTION: The negative efficacy study examining the γ-secretase inhibitor semagacestat in mild to moderate ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) included a number of biomarkers of the Disease as well as safety outcomes., A clinical trial with the wide-spectrum γ-secretase inhibitor semagacestat has, however, demonstrated that global inhibition of all γ-secretases causes serious Toxic effect. , ESULTS: Semagacestat treatment was associated with increased reporting of suspected Notch-related adverse events (Gastrointestinal:-:Point in time:^Patient:-, infection, and Malignant neoplasm of skin related). Other relevant safety findings associated with semagacestat treatment included cognitive and functional worsening, skin-related TEAEs, Kidney and hepatic changes, increased QT interval, and Measured Measured weight loss (observable entity) (observable entity). , CONCLUSIONS: As compared with placebo, semagacestat did not improve cognitive status, and patients receiving the higher dose had significant worsening of functional ability., RESULTS: The trial was terminated before completion on the basis of a recommendation by the data and safety monitoring board., The ADAS-cog scores worsened in all three groups (mean change, 6.4 points in the placebo group, 7.5 points in the group receiving 100 mg of the study Pharmacologic Substance, and 7.8 points in the group receiving 140 mg; P=0.15 and P=0.07, respectively, for the comparison with placebo). The ADCS-ADL scores also worsened in all groups (mean change at week 76, -9.0 points in the placebo group, -10.5 points in the 100-mg group, and -12.6 points in the 140-mg group; P=0.14 and P<0.001, respectively, for the comparison with placebo). Patients treated with semagacestat lost more weight and had more skin cancers and Infections of musculoskeletal system, treatment discontinuations due to adverse events, and serious adverse events (P<0.001 for all comparisons with placebo). , Recently disclosed Phase III findings on semagacestat indicated that ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) patients on this Pharmacologic Substance showed significantly worsened cognitive function compared to those treated with placebo., The recent failure of semagacestat in two large Phase III studies questions the value of γ-secretase inhibitors in treating ALZHEIMER DISEASE, FAMILIAL, 1., ntly disclosed Phase III findings on semagacestat indicated that ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) patients on this Pharmacologic Substance showed significantly worsened cognitive function compared to those treated with placebo. Since, ts from Phase III studies showed that semagacestat failed to slow Disease progression, and it was associated with worsening of clinical measures of cognition and the ability to perform activities of daily living. Furthermore, sem, rge Phase III clinical trials of semagacestat in mild-to-moderate cytarabine/daunorubicin protocol patients were prematurely interrupted because of the observation of a detrimental cognitive and functional effect of the Pharmacologic Substance. These detrimental ef, BACKGROUND: In a recent report, 76 weeks' treatment with a gamma-secretase inhibitor (semagacestat) was associated with poorer cognitive outcomes in Alzheimer's d, However, a large phase 3 trial of semagacestat, a potential non-transition state analog (non-TSA) GSI, in patients with ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) was terminated due to unexpected aggravation of Cognition Disorders and side effects., However, the preliminary equivocal cognitive results obtained with bapineuzumab as well as the detrimental cognitive effects observed with semagacestat, a potent γ-secretase inhibitor, raise the possibility that targeting Aβ may not be clinically efficacious in cytarabine/daunorubicin protocol.[SEP]Relations: familial Alzheimer Disease has relations: disease_disease with Alzheimer Disease, disease_disease with Alzheimer Disease, disease_phenotype_positive with Perseveration, disease_phenotype_positive with Perseveration, disease_protein with PRNP, disease_protein with PRNP, disease_disease with inherited prion Disease, disease_disease with inherited prion Disease. cognitive disorder has relations: disease_disease with dementia (Disease), disease_disease with dementia (Disease).", "label": "no"}
{"original_question": "Is transcription of eRNA bidirectional?", "id": "converted_2667", "sentence1": "Is transcription of eRNA bidirectional?", "sentence2": "In addition to widespread transcription of long non-coding RNA (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as Enhancer of transcription RNA (eRNAs)., Kallikrein (KLK3), which codes for kallikrein-related peptidase 3, human (Prostate-Specific Antigen), is a well-known AR-regulated gene and its upstream enhancers produce bidirectional Enhancer of transcription RNA (eRNAs), termed KLK3e., The distal Enhancer of transcription of the gonadotropin hormone α-subunit gene, Chorionic Gonadotropin, alpha (PEROXISOME BIOGENESIS DISORDER, COMPLEMENTATION GROUP A), is responsible for PEROXISOME BIOGENESIS DISORDER, COMPLEMENTATION GROUP A cell-specific expression in gonadotropes and thyrotropes, and we show here that it encodes two bidirectional nonpolyadenylated RNA whose levels are increased somewhat by exposure to Gonadoliberin-2, human but are not necessarily linked to PEROXISOME BIOGENESIS DISORDER, COMPLEMENTATION GROUP A transcriptional activity. , A richer picture has taken shape, integrating transcription of coding genes, Enhancer of transcription RNA (eRNAs), and various other noncoding transcriptional events. In this review we give an overview of recent studies detailing the mechanisms of RNA Polymerase II (RNA Pol II)-based transcriptional initiation and discuss the ways in which transcriptional direction is established as well as its functional implications., XR-seq maps capture transcription-coupled repair at Site of divergent gene Promoter and bidirectional Enhancer of transcription RNA (eRNA) production at enhancers, XR-seq maps capture transcription-coupled repair at Site of divergent gene Promoter and bidirectional Enhancer of transcription RNA (eRNA) production at enhancers., The distal Enhancer of transcription of the gonadotropin hormone α-subunit gene, Chorionic Gonadotropin, alpha (PEROXISOME BIOGENESIS DISORDER, COMPLEMENTATION GROUP A), is responsible for PEROXISOME BIOGENESIS DISORDER, COMPLEMENTATION GROUP A cell-specific expression in gonadotropes and thyrotropes, and we show here that it encodes two bidirectional nonpolyadenylated RNA whose levels are increased somewhat by exposure to Gonadoliberin-2, human but are not necessarily linked to PEROXISOME BIOGENESIS DISORDER, COMPLEMENTATION GROUP A transcriptional activity., Using this approach, we have defined a class of primary transcripts (eRNAs) that are transcribed uni- or bidirectionally from estrogen receptor binding Site (ERBSs) with an average transcription unit length of ∼3-5 kb., XR-seq maps capture transcription-coupled repair at Site of divergent gene Promoter and bidirectional Enhancer of transcription RNA (eRNA) production at enhancers., We identify 76 Enhancer of transcription RNA (eRNAs), 40 canonical lncRNAs, 65 antisense lncRNAs and 35 regions of bidirectional transcription (RBT) that are differentially expressed in response to bacterial lipopolysaccharide B B (Van der Woude syndrome)., XR-seq maps capture transcription-coupled repair at Site of divergent gene Promoter and bidirectional Enhancer of transcription RNA (eRNA) production at enhancers., Instead, communication between Promoter and enhancers can be bidirectional with Promoter required to activate Enhancer of transcription transcription., A new paradigm has emerged in recent years characterizing transcription initiation as a bidirectional process encompassing a larger proportion of the Genome - anatomical entity than previously thought.[SEP]Relations: regulation of antisense RNA transcription has relations: bioprocess_bioprocess with regulation of transcription, DNA-templated, bioprocess_bioprocess with regulation of transcription, DNA-templated, bioprocess_bioprocess with positive regulation of antisense RNA transcription, bioprocess_bioprocess with positive regulation of antisense RNA transcription, bioprocess_bioprocess with negative regulation of antisense RNA transcription, bioprocess_bioprocess with negative regulation of antisense RNA transcription. promoter clearance from RNA polymerase I promoter has relations: bioprocess_bioprocess with promoter clearance during DNA-templated transcription, bioprocess_bioprocess with promoter clearance during DNA-templated transcription, bioprocess_bioprocess with promoter clearance from RNA polymerase I promoter for nuclear large rRNA transcript, bioprocess_bioprocess with promoter clearance from RNA polymerase I promoter for nuclear large rRNA transcript.", "label": "yes"}
{"original_question": "Does oncogene-induced DNA replication stress inhibit genomic instability?", "id": "converted_2662", "sentence1": "Does oncogene-induced DNA replication stress inhibit genomic instability?", "sentence2": "Oncogene-induced DNA replication stress is thought to drive genomic instability in Primary malignant neoplasm., We propose that single-stranded DNA generated in response to oncogene-induced replication stress compromises the repair of deaminated cytosines and other damaged Unit dose - Base, leading to the observed Sympathetic Nervous System mutator phenotype.[SEP]Relations: malignant ear neoplasm has relations: disease_disease with head and neck Primary malignant neoplasm, disease_disease with head and neck Primary malignant neoplasm, disease_disease with middle ear Primary malignant neoplasm, disease_disease with middle ear Primary malignant neoplasm, disease_disease with inner ear Primary malignant neoplasm, disease_disease with inner ear Primary malignant neoplasm, disease_disease with external ear Primary malignant neoplasm, disease_disease with external ear Primary malignant neoplasm, disease_disease with ear neoplasm, disease_disease with ear neoplasm.", "label": "no"}
{"original_question": "Do nematodes contain a CTCF gene?", "id": "converted_3791", "sentence1": "Do nematodes contain a CTGF protein, human gene?", "sentence2": "Our findings show that CTGF protein, human and possibly chromatin insulation are present in basal nematodes. We suggest that the insulator protein CTGF protein, human has been secondarily lost in derived nematodes like Caenorhabditis elegans., The most highly enriched motif (LM1) corresponds to the X-box motif known from Saccharomyces cerevisiae and Phylum Nematoda. ,  show that three ZF Proteins from three basal nematodes cluster together with known CTGF protein, human Proteins whereas no ZNF3 gene of Caenorhabditis elegans and other derived nematodes does so.AQP1 gene, SULTS: While orthologs for other insulator Proteins were absent in all 35 analysed Phylum Nematoda species, we find orthologs of CTGF protein, human in a subset of nematodes. A, of CTGF protein, human from several nematodes is paralleled by a loss of two of its interactors, the polycomb repressive complex subunit SuZ12 and the multifunctional transcription factor TYY1. In contrast to earlier st, LUSION: Our findings show that CTGF protein, human and possibly chromatin insulation are present in basal nematodes. We , uggest that the insulator protein CTGF protein, human has been secondarily lost in derived nematodes like Caenorhabditis elegans. We , ESULTS: While orthologs for other insulator Proteins were absent in all 35 analysed Phylum Nematoda species, we find orthologs of CTGF protein, human in a subset of nematodes. ,  suggest that the insulator protein CTGF protein, human has been secondarily lost in derived nematodes like Caenorhabditis elegans. W, e show that three ZF Proteins from three basal nematodes cluster together with known CTGF protein, human Proteins whereas no ZNF3 gene of Caenorhabditis elegans and other derived nematodes does so.AQP1 gene, o investigate the pattern of CTGF protein, human occurrence in nematodes, we performed phylogenetic analysis with the ZF protein sets of completely sequenced nematodes. , r findings show that CTGF protein, human and possibly chromatin insulation are present in basal nematodes. W,  propose a switch in the regulation of gene expression during Phylum Nematoda evolution, from the common Vertebrates and insect type involving distantly acting regulatory elements and chromatin insulation to a so far poorly characterised mode present in more derived nematodes. H, We therefore searched in nematodes for orthologs of Proteins that are involved in chromatin insulation.R, The unique secondary loss of CTGF protein, human from several nematodes is paralleled by a loss of two of its interactors, the polycomb repressive complex subunit SuZ12 and the multifunctional transcription factor TYY1.[SEP]Relations: Protein S human has relations: drug_drug with Loracarbef, drug_drug with Loracarbef, drug_drug with Nefazodone, drug_drug with Nefazodone, drug_drug with Cefditoren, drug_drug with Cefditoren, drug_drug with Cefdinir, drug_drug with Cefdinir, drug_drug with Cefsulodin, drug_drug with Cefsulodin.", "label": "yes"}
{"original_question": "Is the protein Papilin secreted?", "id": "converted_2", "sentence1": "Is the protein Papilin secreted?", "sentence2": "Using expression analysis, we identify three Genes that are transcriptionally regulated by HLH-2: the PROTOCADHERIN 3 cdh-3, and two Genes encoding secreted Extracellular Matrix Proteins, ERBB Receptor Feedback Inhibitor 1/papilin and him-4/hemicentin. , We found that ERBB Receptor Feedback Inhibitor 1 encodes long (MIG-6L) and short (MIG-6S) Protein Isoforms of the Extracellular Matrix protein papilin, each required for distinct aspects of Ditiocarb migration. Both MIG-6 Protein Isoforms have a predicted N-terminal papilin cassette, apilins are homologous, secreted Extracellular Matrix Proteins which share a common order of Protein Domain. , The thiosulfate-dithiol sulfurtransferase activity superfamily is a diverse family of Extracellular Matrix and transmembrane proteins, many of which have functions related to regulating matrix organization, cell-cell interactions and cell guidance. This review samples some of the contemporary literature regarding thiosulfate-dithiol sulfurtransferase activity superfamily members (e.g. SPON1 gene, UNC-5, ADAMTS, papilin, and cytarabine/daunorubicin/prednisone/thioguanine) where specific functions are assigned to the thiosulfate-dithiol sulfurtransferase activity domains., Papilins are Extracellular Matrix Proteins , Papilin is an Extracellular Matrix glycoprotein ,  Collagen Type IV, Laminin, glutactin, papilin, and other Extracellular Matrix Proteins were made primarily by Hemocytes (cell) and were secreted into the medium. , A sulfated glycoprotein was isolated from the culture media of Drosophila Kc cells and named papilin.[SEP]Relations: ADAMTS4 has relations: anatomy_protein_present with saliva-secreting gland, anatomy_protein_present with saliva-secreting gland, protein_protein with ITPA, protein_protein with ITPA, protein_protein with ACAN, protein_protein with ACAN, protein_protein with TIMP3, protein_protein with TIMP3. Extracellular Matrix has relations: cellcomp_protein with PAPLN, cellcomp_protein with PAPLN.", "label": "yes"}
{"original_question": "Is endostatin a proangiogenic factor?", "id": "converted_404", "sentence1": "Is COL18A1 gene a proangiogenic factor?", "sentence2": "COL18A1 gene (antiangiogenic factor, antiangiogenic factors include Thrombospondin 1, PLG gene, and COL18A1 gene,  human COL18A1 gene (rh-COL18A1 gene), a potential antiangiogenic agent, , antiangiogenic PF4 and COL18A1 gene, Angiostatins and COL18A1 gene are endogenous inhibitors of angiogenesis with anticancer effects, the antiangiogenic factors, Cystatin C (substance) and COL18A1 gene, were measured, accumulation of COL18A1 gene and Abeta peptides which have been shown to be antiangiogenic, antioangiogenic factors such as pigment epithelial derived factor (SERPINF1 wt Allele, Human), PLG gene, COL18A1 gene, Endostatin is an antiangiogenic growth factor., angiogenesis PPP1R1A gene COL18A1 gene, Circulating and Cells proangiogenic and antiangiogenic proteins such as Recombinant Vascular Endothelial Growth Factor (Vascular Endothelial Growth Factor A) and COL18A1 gene contribute to the local angiogenic balance, Thrombospondin-1 (Thrombospondin 1, human), COL18A1 gene, and COL4A3 gene are Extracellular matrix-associated proteins that inhibit angiogenesis, specific inhibitors of angiogenesis such as platelet factor 1 1, PLG gene, COL18A1 gene, COL18A1 gene, an endogenous PPP1R1A gene of angiogenesis., antiangiogenic factors (pigment epithelium-derived factor [SERPINF1 wt Allele, Human]; PLG gene; CAP-Gly Domain-Containing Linker Protein 1, human; and COL18A1 gene, COL18A1 gene Peptides, a potent PPP1R1A gene of angiogenesis derived from Collagen Type XVIII,, endogenous angiogenesis inhibitors COL18A1 gene , ndostatin is a potent PPP1R1A gene of angiogenesis and tumor growth., endogenous angiogenesis PPP1R1A gene - COL18A1 gene , Endostatin (ES), a Fragment of (qualifier value) of collagen XVIII, is an endogenous PPP1R1A gene of angiogenesis, antiangiogenic protein COL18A1 gene, A number of endogenous inhibitors of angiogenesis are found in the body. Some of these are synthesized by specific cells in different Organ, and others are created by Extracellular proteolytic cleavage of plasma-derived or Extracellular matrix-localized proteins. In this review, we focus on PLG gene, COL18A1 gene,, COL18A1 gene (a direct PPP1R1A gene of angiogenesis) , endogenous angiogenesis PPP1R1A gene COL18A1 gene, Endostatin, a Peptides derived from proteolysis of collagen XVIII, is an endogenous PPP1R1A gene of angiogenesis and tumor growth. , anti-angiogenic factor COL18A1 gene, Endostatin is the first endogenous angiogenesis PPP1R1A gene to enter clinical trials, Angiogenesis Inhibitors such as COL18A1 gene, COL18A1 gene inhibits the angiogenic switch, antiangiogenic COL18A1 gene , direct acting antiangiogenic agents (e.g., COL18A1 gene) , Endostatin is an antiangiogenic Fragment of (qualifier value) of the basement membrane protein, collagen XVIII., specific inhibitors of angiogenesis such as platelet factor 1 1-4, PLG gene, COL18A1 gene, Endostatin, which is a natural PPP1R1A gene of angiogenesis, Angiostatins and COL18A1 gene are two powerful inhibitors of angiogenesis in experimental models[SEP]Relations: Platelet Activating Factor has relations: drug_drug with Enoxaparin, drug_drug with Enoxaparin, drug_drug with Argatroban, drug_drug with Argatroban, drug_drug with Menadione, drug_drug with Menadione, drug_drug with Epoprostenol, drug_drug with Epoprostenol, drug_drug with Apixaban, drug_drug with Apixaban.", "label": "no"}
{"original_question": "Is Alu hypomethylation associated with breast cancer?", "id": "converted_24", "sentence1": "Is Alu hypomethylation associated with Malignant neoplasm of Breast?", "sentence2": "Alu and Long Interspersed Nucleotide Element-1 hypomethylation is associated with ERBB2 wt Allele enriched subtype of Malignant neoplasm of Breast, In IBC, Alu hypomethylation correlated with negative Estrogen Receptors (Endoplasmic Reticulum) status, In survival analyses, low Alu methylation status tended to be associated with poor disease-free survival of the patients., Alu hypomethylation is probably a late event during Malignant neoplasm of Breast progression, prominent hypomethylation of Alu and Long Interspersed Nucleotide Element-1 in ERBB2 wt Allele enriched subtype may be related to chromosomal instability of this specific subtype., DNA methylation for three repetitive elements (LINE1, SLC38A2 gene and Alu) were analyzed in Invasive Ductal Breast Carcinoma of the Breast, paired adjacent normal Tissue Specimen Code and Leukocytes from 40 Malignant neoplasm of Breast patients, DNA methylation for the three repetitive elements was lower in Specimen Source Codes - Specimen Source Codes - tumor compared to adjacent Tissue Specimen Code and Leukocytes DNA.[SEP]Relations: invasive ductal Breast carcinoma has relations: disease_protein with ATF4, disease_protein with ATF4, disease_protein with PTGS2, disease_protein with PTGS2, disease_protein with SERPINB5, disease_protein with SERPINB5, disease_protein with NF2, disease_protein with NF2, disease_protein with CDH1, disease_protein with CDH1.", "label": "yes"}
{"original_question": "Is TIM-3 a target for cancer immunotherapy in NSCLC?", "id": "converted_3540", "sentence1": "Is TIM-3 a target for cancer immunotherapy in Non-Small Cell Lung Carcinoma?", "sentence2": " Our results imply that implementing combined treatment on Cytokine-Induced Killer Cells before transfusion via Antibodies, in vitro diagnostic targeting CD274 wt Allele, lymphocyte-activation gene 3 protein, human, TIM-3, and CEACAM-1 might improve the efficiency of CIK therapy for Non-Small Cell Lung Carcinoma patients., Furthermore, TIM-3 and Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 were strongly expressed simultaneously during long-term CIK culture and showed a significant and mutually positive correlation. , In present study, we detected the dynamic expression of eight major checkpoint molecules (cytotoxic T-lymphocyte antigen 4, PDCD1 wt Allele, CD274 wt Allele, TIM- 3, CEACAM-1, lymphocyte-activation gene 3 protein, human, TIGIT protein, human protein, human and B- and T-Lymphocyte Attenuator, Human) on Cytokine-Induced Killer Cells from Non-Small Cell Lung Carcinoma patients., Agents targeting other immune inhibitory (e.g., HAVCR2 wt Allele) or immune stimulating (e.g., CD137) receptors on Therapeutic gamma delta T-lymphocytes and other approaches such as adoptive cell transfer are tested for clinical efficacy in Melanocytic neoplasm as well., We found immune activation coexistent with elevation of multiple targetable immune checkpoint molecules, including CD274 wt Allele, Programmed Death Ligand 2 Protein, PDCD1 wt Allele, TIM-3, CD276 Antigen, B- and T-Lymphocyte Attenuator, Human, and cytotoxic T-lymphocyte antigen 4, along with increases in Specimen Source Codes - Specimen Source Codes - tumor infiltration by CD4(+)Foxp3(+) regulatory Therapeutic gamma delta T-lymphocytes in lung adenocarcinomas that displayed an EMT phenotype, Cytometric profiling identified an immunologically \"hot\" cluster with abundant CD8+ Therapeutic gamma delta T-lymphocytes expressing high levels of PDCD1 wt Allele and TIM-3 and an immunologically \"cold\" cluster with lower relative abundance of CD8+ Therapeutic gamma delta T-lymphocytes and expression of inhibitory markers,  Interestingly, CD161+ CD4+ Therapeutic gamma delta T-lymphocytes highly express OX40 co-stimulatory receptor, less frequently 4-1BB, and display an activated but not completely exhausted PDCD1 wt Allele-positive HAVCR2 wt Allele-negative phenotype., . Furthermore, overexpression of targetable immune checkpoints, such as cytotoxic T-lymphocyte antigen 4 and TIM-3 were associated with EMT in both NSCLCs. [SEP]Relations: small cell lung carcinoma has relations: disease_protein with ASCL1, disease_protein with ASCL1, disease_protein with TP73, disease_protein with TP73, disease_protein with EPHB3, disease_protein with EPHB3. Protein S human has relations: drug_drug with NS-398, drug_drug with NS-398, drug_drug with Antithrombin III human, drug_drug with Antithrombin III human.", "label": "yes"}
{"original_question": "Are there ways of joint Bayesian inference of risk variants?", "id": "converted_2559", "sentence1": "Are there ways of joint Bayesian inference of risk Variant?", "sentence2": "Joint Bayesian inference of risk Variant and tissue-specific epigenomic enrichments across multiple complex Homo sapiens diseases., Genome wide association studies (GWAS) provide a powerful approach for uncovering disease-associated Variant in Homo sapiens, but fine-mapping the causal Variant remains a challenge. This is partly remedied by prioritization of disease-associated Variant that overlap GWAS-enriched epigenomic annotations. Here, we introduce a new Bayesian model RiVIERA (Risk Variant Inference using Epigenomic Reference Annotations) for inference of driver Variant from summary statistics across multiple traits using hundreds of epigenomic annotations. In simulation, RiVIERA promising power in detecting causal Variant and causal annotations, the multi-trait joint inference further improved the detection power. We applied RiVIERA to model the existing GWAS summary statistics of 9 Autoimmune Diseases and SCHIZOPHRENIA 2 (disorder) by jointly harnessing the potential causal enrichments among 848 tissue-specific epigenomics annotations from ENCODE/Roadmap consortium covering 127 cell/tissue types and 8 major epigenomic marks. RiVIERA identified meaningful tissue-specific enrichments for enhancer regions defined by Histone H3 Methyl Lys4 and H3K27ac for Blood T-Cell specifically in the nine Autoimmune Diseases and Brain-specific enhancer activities exclusively in SCHIZOPHRENIA 2 (disorder). Moreover, the Variant from the 95% credible sets exhibited high Conservation and enrichments for Genotype-Tissue Expression Program whole-blood eQTLs located within transcription-factor-binding-sites and DNA-hypersensitive-sites., Here, we introduce a new Bayesian model RiVIERA (Risk Variant Inference using Epigenomic Reference Annotations) for inference of driver Variant from summary statistics across multiple traits using hundreds of epigenomic annotations., Joint Bayesian inference of risk Variant and tissue-specific epigenomic enrichments across multiple complex Homo sapiens diseases.[SEP]Relations: autoimmune disease has relations: disease_disease with euthyroid Graves orbitopathy, disease_disease with euthyroid Graves orbitopathy, disease_disease with vitiligo-associated multiple autoimmune disease susceptibility 1, disease_disease with vitiligo-associated multiple autoimmune disease susceptibility 1. gene expression has relations: bioprocess_protein with IKBKE, bioprocess_protein with IKBKE. schizophreniform disorder has relations: contraindication with Betamethasone, contraindication with Betamethasone, contraindication with Hydrocortisone, contraindication with Hydrocortisone.", "label": "yes"}
{"original_question": "Do IEG create a ripple effect of transcription?", "id": "converted_1948", "sentence1": "Do IEG create a ripple effect of transcription?", "sentence2": "Rapid induction of Genes, Immediate-Early (IEGs) in response to growth factor stimulations is accompanied by co-upregulation of their neighbouring Genes., Even in surrounding Intergenic Region, transcriptional activation took place at the same time. , Here we show that intensive transcription at one Gene Locus frequently spills over into its physical neighbouring loci., Ripples from neighbouring transcription., Ripples from neighbouring transcription.[SEP]Relations: insect neurogenic region has relations: anatomy_anatomy with embryonic structure, anatomy_anatomy with embryonic structure.", "label": "yes"}
{"original_question": "is there an increase in ultrasound comets after intense exercise?", "id": "converted_1421", "sentence1": "is there an increase in ultrasound comets after intense exercise?", "sentence2": "Healthy athletes developed subclinical increase in pulmonary water content immediately after an Ironman race at Staphylococcal enterotoxin A level, as shown by the increased number of ULCs related to cardiac changes occurring during exercise., Increased EVLW is associated with estimated PCWP and indices of left ventricular systolic and diastolic dysfunction. The additional exercise-induced increase of PCWP, the worsening of left ventricular diastolic function, and extensive wall-motion abnormalities correlate with variations of EVLW.,  Among them chest ultrasonography can detect and quantify the extravascular lung water, creating \"comet-tail\" ultrasound artefacts (ULCs) from water-thickened pulmonary interlobular septa.,  In top-level breath-hold divers, chest sonography frequently reveals an increased number of ULCs after immersion, indicating a relatively high prevalence of (often subclinical) reversible extravascular lung water accumulation.[SEP]Relations: staphylococcal toxemia has relations: disease_disease with staphylococcal scarlet fever, disease_disease with staphylococcal scarlet fever, disease_disease with bullous impetigo, disease_disease with bullous impetigo, disease_disease with staphylococcal toxic-shock syndrome, disease_disease with staphylococcal toxic-shock syndrome, disease_disease with staphylococcal scalded skin syndrome, disease_disease with staphylococcal scalded skin syndrome, disease_disease with staphylococcal pneumonia, disease_disease with staphylococcal pneumonia.", "label": "yes"}
{"original_question": "Are the Fanconi anemia genes a part of the same signalling pathway?", "id": "converted_992", "sentence1": "Are the FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) Genes a part of the same signalling pathway?", "sentence2": "Gene Mutation in at least 14 different Genes have been shown to cause doxorubicin/fluorouracil protocol, The doxorubicin/fluorouracil protocol Genes code for Proteins that act in complex (molecular entity) to coordinate the repair of damaged DNA,  The current review describes the structure and function of the FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) Genes and describes the role of the encoded FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) Proteins in a cellular pathway controlling chromosome stability., FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) is a rare human genetic disease caused by mutations in any one of 13 known Genes that encode Proteins functioning in one common signaling pathway, the doxorubicin/fluorouracil protocol pathway, or in unknown Genes., FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) is a rare inherited recessive disease caused by mutations in one of fifteen Genes known to encode doxorubicin/fluorouracil protocol pathway components., FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) Proteins function in a DNA damage response pathway that appears to be part of the network including Malignant neoplasm of breast susceptibility gene products, BRCA1 gene gene and BRCA2 gene gene., FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) Proteins function in a DNA damage response pathway that appears to be part of the network including Malignant neoplasm of breast susceptibility gene products, BRCA1 gene gene and BRCA2 gene gene, FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) is a rare human genetic disease caused by mutations in any one of 13 known Genes that encode Proteins functioning in one common signaling pathway, the doxorubicin/fluorouracil protocol pathway, or in unknown Genes, The FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) gene family comprises at least 12 Genes interacting in a common pathway involved in DNA repair, These findings show that the newly identified Fanconi Anemia Complementation Group E Protein is an integral part of the doxorubicin/fluorouracil protocol pathway, and support the concept of a functional link between all known Proteins encoded by the Genes that are Mutation Abnormality in this disorder[SEP]Relations: FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) complementation group has relations: disease_phenotype_positive with X-linked recessive inheritance, disease_phenotype_positive with X-linked recessive inheritance, disease_phenotype_positive with X-linked recessive inheritance, disease_phenotype_positive with X-linked recessive inheritance, disease_phenotype_positive with Global developmental delay, disease_phenotype_positive with Global developmental delay, disease_phenotype_positive with Global developmental delay, disease_phenotype_positive with Global developmental delay, disease_phenotype_positive with Neutropenia, disease_phenotype_positive with Neutropenia.", "label": "yes"}
{"original_question": "Is hypersensitivity to DNA crosslinking agents a hallmark of Fanconi anemia?", "id": "converted_860", "sentence1": "Is Emotional hypersensitivity to DNA crosslinking agents a hallmark of Fanconi anemia?", "sentence2": "The Fanconi anemia (doxorubicin/fluorouracil protocol) core complex plays a central role in the DNA damage response network, FAAP100-deficient cells display hallmark features of doxorubicin/fluorouracil protocol cells, including defective FANCONI ANEMIA, COMPLEMENTATION GROUP D2 monoubiquitination, Emotional Emotional hypersensitivity to DNA crosslinking agents, and genomic instability., Fanconi anemia (doxorubicin/fluorouracil protocol) is a rare genetic disorder characterized by Aplastic Anemia, Primary malignant neoplasm/leukemia susceptibility and Cells Emotional Emotional hypersensitivity to DNA crosslinking agents, such as cisplatin., Fanconi anemia (doxorubicin/fluorouracil protocol) is an inherited Chromosomes recessive syndrome characterized by Cells Emotional Emotional hypersensitivity to DNA crosslinking agents and Bone marrow hypocellularity, which cause Aplastic Anemia, and an increased incidence of malignancy., Features of Chromosomes aberrations, Emotional Emotional hypersensitivity to DNA crosslinking agents, and predisposition to malignancy have suggested a fundamental anomaly of DNA repair in Fanconi anemia., Fanconi anemia (doxorubicin/fluorouracil protocol) is one of several genetic diseases with characteristic Cells Emotional Emotional hypersensitivity to DNA crosslinking agents which suggest that doxorubicin/fluorouracil protocol Proteins may function as part of DNA repair processes., Fanconi anemia (doxorubicin/fluorouracil protocol) is characterized by Cells Emotional Emotional hypersensitivity to DNA crosslinking agents, but how the Fanconi pathway protects cells from DNA Cross link and whether doxorubicin/fluorouracil protocol Proteins act directly on Cross link remain unclear., FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) is a rare genetic disorder associated with a bone-marrow failure, Primary malignant neoplasm predisposition and Emotional Emotional hypersensitivity to DNA crosslinking agents., Fanconi anemia (doxorubicin/fluorouracil protocol) is a heterogeneous Disease associated with a Bone marrow hypocellularity, Primary malignant neoplasm predisposition and Emotional Emotional hypersensitivity to DNA crosslinking agents., Fanconi anemia (doxorubicin/fluorouracil protocol) is an inherited disorder characterized by defective DNA repair and Cells sensitivity to DNA crosslinking agents., Fanconi anemia (doxorubicin/fluorouracil protocol) is an inherited Disease characterized by Bone marrow hypocellularity, increased Primary malignant neoplasm risk and Emotional Emotional hypersensitivity to DNA cross-linking agents, implying a role for this pathway in the maintenance of genomic stability., Genetic or epigenetic inactivation of the pathway formed by the FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) Proteins occurs in several Primary malignant neoplasm types, including Squamous cell carcinoma of the head and neck (HNSCC), rendering the affected Neoplasms potentially hypersensitive to DNA crosslinking agents., FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) is a rare autosomic recessive and X-linked Disease with Chromosomes instability after exposure to crosslinking agents as the hallmark., FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) is an autosomal recessive Disease characterized by chromosome instability, Cells Emotional Emotional hypersensitivity to DNA cross-linking agents, and increased predisposition to Malignant Neoplasms., The Bloom protein (Bloom Syndrome) and DNA topoisomerase III alpha are found in association with Proteins of the Fanconi anemia (doxorubicin/fluorouracil protocol) pathway, a disorder manifesting increased Cells sensitivity to DNA crosslinking agents., Using siRNA depletion and gene knockout techniques, we show that FAAP100-deficient cells display hallmark features of doxorubicin/fluorouracil protocol cells, including defective FANCONI ANEMIA, COMPLEMENTATION GROUP D2 monoubiquitination, Emotional Emotional hypersensitivity to DNA crosslinking agents, and genomic instability., Fanconi anemia (doxorubicin/fluorouracil protocol) is a recessive Homo sapiens Primary malignant neoplasm prone syndrome featuring Bone marrow hypocellularity, developmental abnormalities and Emotional Emotional hypersensitivity to DNA crosslinking agents exposure., doxorubicin/fluorouracil protocol is a chromosome instability syndrome characterized by childhood-onset Aplastic Anemia, Primary malignant neoplasm or leukemia susceptibility, and Cells Emotional Emotional hypersensitivity to DNA crosslinking agents., Functional defects in the Fanconi pathway can result in a marked Emotional Emotional hypersensitivity to interstrand crosslinking agents, such as Mitomycins C., At the Cells level, Emotional Emotional hypersensitivity to DNA interstrand Cross link is the defining feature in Fanconi anemia., DNA crosslinking agents may led to DNA cross-linking lesion, and Fanconi anemia pathway plays a key role in repairing its cross-linking., Fanconi anemia (doxorubicin/fluorouracil protocol), an Autosomal Recessive Disorder of children, is characterized by congenital or childhood Aplastic Anemia, multiple developmental anomalies, increased incidence of Myeloid Leukemia, increased spontaneous chromosome breakage, and Cells and Chromosomes Emotional Emotional hypersensitivity to DNA bifunctional crosslinking and Alkylating Agents., elegans provides an excellent model system for the study of the FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol), one of the hallmarks of which is sensitivity to interstrand crosslinking agents, Using siRNA depletion and gene knockout techniques, we show that FAAP100-deficient cells display hallmark features of doxorubicin/fluorouracil protocol cells, including defective FANCONI ANEMIA, COMPLEMENTATION GROUP D2 monoubiquitination, Emotional Emotional hypersensitivity to DNA crosslinking agents, and genomic instability, One of the hallmark phenotypes of doxorubicin/fluorouracil protocol is Cells Emotional Emotional hypersensitivity to agents that induce DNA interstrand Cross link (ICLs), such as Mitomycins C (Mitomycins), Furthermore, the cytological hallmark of doxorubicin/fluorouracil protocol, the DNA crosslink-induced radial chromosome formation, exemplifies an innate impairment in the repair of these particularly cytotoxic DNA lesions [A.D, Fanconi anemia (doxorubicin/fluorouracil protocol) is characterized by Cells Emotional Emotional hypersensitivity to DNA crosslinking agents, but how the Fanconi pathway protects cells from DNA Cross link and whether doxorubicin/fluorouracil protocol Proteins act directly on Cross link remain unclear, Features of Chromosomes aberrations, Emotional Emotional hypersensitivity to DNA crosslinking agents, and predisposition to malignancy have suggested a fundamental anomaly of DNA repair in Fanconi anemia, Fanconi anemia (doxorubicin/fluorouracil protocol) is an inherited Chromosomes recessive syndrome characterized by Cells Emotional Emotional hypersensitivity to DNA crosslinking agents and Bone marrow hypocellularity, which cause Aplastic Anemia, and an increased incidence of malignancy, Genetic or epigenetic inactivation of the pathway formed by the FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) Proteins occurs in several Primary malignant neoplasm types, including Squamous cell carcinoma of the head and neck (HNSCC), rendering the affected Neoplasms potentially hypersensitive to DNA crosslinking agents, Fanconi anemia (doxorubicin/fluorouracil protocol) is a Homo sapiens autosomal disorder characterized by Primary malignant neoplasm susceptibility and Cells sensitivity to DNA crosslinking agents such as Mitomycins C and erythritol anhydride, The Fanconi anemia pathway promotes DNA glycosylase-dependent excision of interstrand DNA Cross link., DNA crosslinking agents may led to DNA cross-linking lesion, and Fanconi anemia pathway plays a key role in repairing its cross-linking, doxorubicin/fluorouracil protocol is a chromosome instability syndrome characterized by childhood-onset Aplastic Anemia, Primary malignant neoplasm or leukemia susceptibility, and Cells Emotional Emotional hypersensitivity to DNA crosslinking agents, The Disease is manifested by defects in DNA repair, Emotional Emotional hypersensitivity to DNA crosslinking agents, and a high degree of Chromosomes aberrations[SEP]Relations: Fanconi anemia complementation group has relations: disease_phenotype_positive with Chromosomal breakage induced by crosslinking agents, disease_phenotype_positive with Chromosomal breakage induced by crosslinking agents, disease_phenotype_positive with Chromosomal breakage induced by crosslinking agents, disease_phenotype_positive with Chromosomal breakage induced by crosslinking agents, disease_phenotype_positive with Deficient excision of UV-induced pyrimidine dimers in DNA, disease_phenotype_positive with Deficient excision of UV-induced pyrimidine dimers in DNA, disease_phenotype_positive with Deficient excision of UV-induced pyrimidine dimers in DNA, disease_phenotype_positive with Deficient excision of UV-induced pyrimidine dimers in DNA, disease_phenotype_positive with Overfolded helix, disease_phenotype_positive with Overfolded helix.", "label": "yes"}
{"original_question": "Is it possible to analyze exosomes with FACS?", "id": "converted_3169", "sentence1": "Is it possible to analyze Exosomes with Fetus affected by placental transfer of anticonvulsant?", "sentence2": "whose presence was validated by a bead-exosome Fetus affected by placental transfer of anticonvulsant assay., We analyzed Exosomes from Mus sp. (C57Bl/6) and Breast, Chest>Lung, and Malignant neoplasm of ovary patient samples and cultured cancer cells with different approaches, including nanoparticle tracking analysis, biolayer interferometry, Fetus affected by placental transfer of anticonvulsant, and electron microscopy., we applied a technique to generate native fluorescent Exosomes characterized by Vesicle (morphologic abnormality) integrity, size, density, markers expression, and quantifiable by direct Fetus affected by placental transfer of anticonvulsant analysis, we used a novel strategy for generating metabolically-labeled fluorescent Exosomes that can be counted by flow cytometry assay (Fetus affected by placental transfer of anticonvulsant) and characterized.[SEP]Relations: Breast has relations: anatomy_protein_present with GCSAM, anatomy_protein_present with GCSAM, anatomy_protein_present with VIM, anatomy_protein_present with VIM, anatomy_protein_present with RIMKLB, anatomy_protein_present with RIMKLB, anatomy_protein_present with GSN-AS1, anatomy_protein_present with GSN-AS1. Morphological abnormality of the utricle has relations: phenotype_phenotype with Morphological abnormality of the semicircular canal, phenotype_phenotype with Morphological abnormality of the semicircular canal.", "label": "yes"}
{"original_question": "Is desmin an intermediate filament protein involved in Dilated Cardiomyopathy (DCM)?", "id": "converted_374", "sentence1": "Is CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human an intermediate filament Protein Info involved in Dilated Cardiomyopathy (3',5'-dichloromethotrexate)?", "sentence2": "Desmin-related myofibrillar myopathy (DRM) is a Cardiac - anatomy qualifier and skeletal muscle Disease caused by mutations in the CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human (CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1) gene. Gene Mutation in the central 2B domain of CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 cause skeletal muscle Disease that typically precedes Cardiac - anatomy qualifier involvement. However, the prevalence of CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 mutations in dilated Cardiomyopathies (3',5'-dichloromethotrexate) without skeletal muscle Disease is not known., The lack of severe disruption of cytoskeletal CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human network formation seen with mutations in the 1A and tail domains suggests that dysfunction of seemingly intact CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human networks is sufficient to cause 3',5'-dichloromethotrexate., According to the predominant view, CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human mutations cause dilated Cardiomyopathies (3',5'-dichloromethotrexate). We evaluated a family with restrictive Cardiomyopathies (RCM) associated with a novel CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human mutation and reviewed recent reports regarding the frequency of RCM in patients with CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human myopathy., Dilated Cardiomyopathies (3',5'-dichloromethotrexate) is characterized by Enlargement (morphologic abnormality) and dilation of all Chest>Heart compartments associated with serious decrease of its Muscle Contraction function. 3',5'-dichloromethotrexate hallmark is the combination of dystrophic and Hypertrophic disorder of skin, unspecified alterations of Myocytes, Cardiac. Since the power output of Cardiac - anatomy qualifier cells is directly related to remodeling of their Muscle Contraction machinery we investigated expression of selected Muscle Contraction and Cytoskeletal Proteins in the left ventricle of 3',5'-dichloromethotrexate patients using immunoblotting. The content of the recognized Protein Info markers of cardiomyocyte hypertrophy such as Tubulin, CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human and slow skeletal myosin heavy chain isoform, MHCbeta, was significantly elevated in 3',5'-dichloromethotrexate compared to normal Myocardium., In contrast, overexpression of CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human filaments by itself is not detrimental to the Chest>Heart. Although loss-of-function studies have been more limited, ablation of the CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human gene causes Abnormality of mitochondrial metabolism and apoptosis, resulting in Cardiomyopathies in mice. From function studies, abnormal CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human aggregation and disruption of the CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human networks resulting from expression of either mutant CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human or mutant CRYAB gene have been shown to remodel the Chest>Heart and compromise Cardiac - anatomy qualifier function, suggesting their synergistic roles in Disease pathogenesis., A missense mutation in the CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human gene (CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1) causes 3',5'-dichloromethotrexate in a human family., CASP14 gene deficient in CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human, the muscle-specific member of the intermediate filament gene family, display defects in all muscle types and particularly in the Myocardium. Desmin null hearts develop cardiomyocyte hypertrophy and dilated Cardiomyopathies (3',5'-dichloromethotrexate) characterized by extensive myocyte cell death, calcific fibrosis and multiple ultrastructural defects. Several lines of evidence suggest impaired vascular function in CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human null animals., Familial 3',5'-dichloromethotrexate is commonly inherited as Autosome dominant trait; less frequently it is Autosome recessive, X-linked inheritance inheritance or matrilinear. The Disease is clinically and genetically heterogeneous. Genes causally linked to this phenotype include Dystrophin, Dystrophin-associated glycoproteins, Actins, CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human, beta-miosin heavy chain, Cardiac - anatomy qualifier troponin T, and DNA, Mitochondrial Genes, mostly transfer RNA., Examination of families has identified so far eight Disease Genes, namely the Dystrophin, TAFAZZIN gene, Cardiac - anatomy qualifier Actins, CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human, lamin A/C, delta- sarcoglycan, Cardiac - anatomy qualifier beta-myosin heavy chain, and Cardiac - anatomy qualifier troponin T gene., Gene Mutation of the CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human,   delta-Sarcoglycan, the Cardiac - anatomy qualifier Actins and beta-myosin heavy chain as well as the troponin T gene are known to cause Autosome dominant-dilated Cardiomyopathies without other abnormalities., Autosomal dominant 3',5'-dichloromethotrexate is the most frequent form (56% of our cases), and several candidate Disease loci have been identified by linkage analysis. Three Disease Genes are presently known: the Cardiac - anatomy qualifier Actins gene, the CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human gene, and the LMNA gene., Dilated Cardiomyopathies (3',5'-dichloromethotrexate) is a major cause of morbidity and mortality. Two Genes have been identified for the X-linked inheritance inheritance forms (Dystrophin and TAFAZZIN gene), whereas three other Genes (Actins, lamin A/C, and CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human) cause Autosome dominant 3',5'-dichloromethotrexate;, Desmin defects were also recently identified in 1 familial dilated Cardiomyopathies., By candidate gene screening, the molecular diagnosis can be provided for Dystrophin, Diacylglycerol, DNA, Mitochondrial, Actins and CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human gene defects., Desmin (z-bands) are partly destroyed in 3',5'-dichloromethotrexate. Anti-CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human immunoglobulin complex location titers as indicators of a possible secondary immune response are found high in patients with acute myocarditis declining during reconvalescence and are also elevated in 3',5'-dichloromethotrexate. , Desmin, the muscle-specific intermediate filament Protein Info, is a major target in dilated Cardiomyopathies and Congestive Chest>Heart failure in Homo sapiens and mice, Desmin, the muscle-specific intermediate filament, is involved in Myofibrillar Myopathy, dilated Cardiomyopathies and Muscular Atrophy[SEP]Relations: dilated Cardiomyopathies has relations: disease_protein with CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1, disease_protein with CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1, disease_protein with DMD, disease_protein with DMD, disease_protein with TPM1, disease_protein with TPM1, disease_protein with ALMS1, disease_protein with ALMS1, disease_protein with TTN, disease_protein with TTN.", "label": "yes"}
{"original_question": "Could transcription factors act as cell-cell signalling molecules?", "id": "converted_822", "sentence1": "Could transcription factors act as \"U\" lymphocyte-\"U\" lymphocyte signalling Molecule?", "sentence2": "PAX6 gene is a TRANSCRIPTION FACTOR essential for the development of Body tissue including the Eye, CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS and Endocrine Glands of Vertebrates and invertebrates. It regulates the expression of a broad range of Molecule, including transcription factors, \"U\" lymphocyte adhesion and short-range \"U\" lymphocyte-\"U\" lymphocyte signalling Molecule, hormones and structural proteins, Recent data support the view that transcription factors - in particular, Homeodomain Proteins - can be transferred from \"U\" lymphocyte to \"U\" lymphocyte and have direct non-\"U\" lymphocyte-autonomous (and therefore paracrine) activities[SEP]Relations: TRANSCRIPTION FACTOR binding has relations: molfunc_protein with STAT3, molfunc_protein with STAT3, molfunc_protein with MYC, molfunc_protein with MYC, molfunc_protein with PPARD, molfunc_protein with PPARD, molfunc_protein with JUN, molfunc_protein with JUN, molfunc_protein with NFIA, molfunc_protein with NFIA.", "label": "yes"}
{"original_question": "Is there any approved treatment for NAFLD?", "id": "converted_3047", "sentence1": "Is there any approved treatment for NAFLD?", "sentence2": "Non-alcoholic fatty Hepatobiliary Disorder (NAFLD) is the leading chronic hepatic condition worldwide and new approaches to management and treatment are limited., Non-alcoholic fatty Hepatobiliary Disorder (NAFLD) has become one of the most prominent forms of chronic Hepatobiliary Disorder worldwide, reflecting the epidemic of global obesity. Those with the progressive Variant of NAFLD, Nonalcoholic Steatohepatitis (NASH), are at significantly increased risk of multisystem morbidity and mortality. However, there are currently no approved pharmacologic therapies for NASH., Although much progress has been made in enhancing our understanding of NAFLD pathogenesis, development of pharmacologic treatments has been hindered by challenges in clinical trial enrollment and complexities in clinical trial design. , Non-alcoholic Fatty Liver Disease (NAFLD) is the most prevalent Hepatobiliary Disorder worldwide, and there is no approved pharmacotherapy., Non-alcoholic Fatty Liver Disease (NAFLD) has an increasing prevalence worldwide. At present, no specific pharmacotherapy is approved for NAFLD. [SEP]Relations: Nonalcoholic Steatohepatitis has relations: contraindication with Efavirenz, contraindication with Efavirenz, contraindication with Zidovudine, contraindication with Zidovudine, contraindication with Entecavir, contraindication with Entecavir, contraindication with Tenofovir disoproxil, contraindication with Tenofovir disoproxil, contraindication with Abacavir, contraindication with Abacavir.", "label": "no"}
{"original_question": "Is the tricarboxylic acid (TCA) cycle affected in inflammation?", "id": "converted_278", "sentence1": "Is the Tricarboxylic Acids (Tricyclic Antidepressant [EPC]) cycle affected in Inflammation?", "sentence2": "In this study, the levels of Antifibrinolytic Antifibrinolytic amino acids and trichloroacetic acid (Tricyclic Antidepressant [EPC]) cycle-related molecules in the colonic tissues and sera of patients with ulcerative Colitis (Ulcerative Colitis) were profiled by gas chromatography/mass spectrometry (GC/MS), with the aim of evaluating whether the clinical state induced by Ulcerative Colitis leads to variations in the amino acid profile, Our study raises the possibility that GC/MS-based profiling of Antifibrinolytic Antifibrinolytic amino acids and Tricyclic Antidepressant [EPC] cycle-related molecules is a useful early diagnostic tool for Ulcerative Colitis., Succinates is an intermediate of the Tricarboxylic Acids (Tricyclic Antidepressant [EPC]) cycle, and plays a crucial role in adenosine triphosphate (ATP) generation in Mitochondria., In Specimen Source Codes - Plasma, most Metabolite in the central metabolic pathway (glycolysis and Tricyclic Antidepressant [EPC] cycle) were significantly downregulated after Zymosan A administration, Thus, IL-1beta+TNFalpha treated Astrocytes show a marked decrease in glycogen levels, a slight but not significant decrease in lactate release as well as a massive increase in both the Pentoses phosphate pathway and Tricyclic Antidepressant [EPC] cycle activities., A total of 77 and 92 Metabolite were detected in serum and colon tissue, respectively, and among the Metabolite the compositions of Tricyclic Antidepressant [EPC] cycle intermediates and Antifibrinolytic Antifibrinolytic amino acids changed depending on the degree of Colitis, Extension of these findings identified a functional role for stretch-induced inhibition of Succinates Dehydrogenase (SDH) in mediating normoxic HIF1A protein, human protein, human stabilization, concomitant increases in glycolytic capacity, and improved Tricarboxylic Acids (Tricyclic Antidepressant [EPC]) cycle function, These studies reveal a surprising role for HIF1A protein, human protein, human in lung protection during ALI, where normoxic HIF1A protein, human protein, human stabilization and HIF-dependent control of alveolar-epithelial glucose metabolism function as an endogenous feedback loop to dampen lung Inflammation, These results suggest a cataplerosis of the Tricyclic Antidepressant [EPC] cycle induced by phenobarbital, caused by the massive withdrawal of succinyl-coenzyme A by ALAS1 wt Allele induction, such that the Tricyclic Antidepressant [EPC] cycle is unable to supply the reduced chemical cofactor to the RGN gene, The Mitochondrial Inheritance respiratory chain (RGN gene) and the Tricarboxylic Acids (Tricyclic Antidepressant [EPC]) cycle were explored in the Hmbs(-/-) mouse model. RGN gene and Tricyclic Antidepressant [EPC] cycle were significantly affected in comparison to controls in CASP14 gene treated with phenobarbital with decreased activities of RGN gene complexes, Several changes in substrate utilization for energy homeostasis were identified in severe Aspartyl/Asparaginyl Beta-Hydroxylase, Human, including increased glucose consumption by the Pentoses phosphate pathway, altered Tricarboxylic Acids (Tricyclic Antidepressant [EPC]) cycle activity, and enhanced peptide catabolism. , Enhanced Mitochondrial Inheritance glucose oxidation was achieved by increased recruitment of the NOTCH1 intracellular domain (NICD1) to Nuclear (incident type) and Mitochondrial Inheritance genes that encode respiratory chain components and by NOTCH-dependent induction of Pyruvate Dehydrogenase (Lipoamide)-Phosphatase (PLPP6 gene) expression, pyruvate dehydrogenase activity, and glucose flux to the Tricyclic Antidepressant [EPC] cycle. , Metabolic reprogramming is implicated in macrophage activation,, BHB blocks the NLRP3 inflammasome without undergoing oxidation in the Tricyclic Antidepressant [EPC] cycle, and independently of Uncoupling Protein 2 (UCP2 gene gene), sirtuin-2 (Sirtuin 2), the G protein-coupled receptor GPR109A or hydrocaboxylic acid receptor 2 (HCAR2 gene gene). , Our findings suggest that the anti-inflammatory effects of caloric restriction or ketogenic diets may be linked to BHB-mediated inhibition of the NLRP3 inflammasome., Succinates: a metabolic signal in Inflammation.[SEP]Relations: acute tricyclic antidepressant poisoning has relations: disease_disease with poisoning, disease_disease with poisoning. ulcerative Colitis (disease) has relations: contraindication with Trihexyphenidyl, contraindication with Trihexyphenidyl, disease_protein with HNF4A, disease_protein with HNF4A, disease_protein with HERC2, disease_protein with HERC2. Phenobarbital has relations: drug_drug with Tricaine, drug_drug with Tricaine.", "label": "yes"}
{"original_question": "Is the toxin produced by Clostridium botulinum always deadly?", "id": "converted_1765", "sentence1": "Is the toxin produced by Clostridium botulinum always deadly?", "sentence2": "animal allergen extracts treated with trace elements recovered. It appears that Intestinal Microbiome dysbiosis and trace element deficiency could explain the extensive emergence of chronic Poisoning caused by Clostridium botulinum toxin type B type B., The patient was treated with Homo sapiens botulism immune globulin and had rapid recovery in weakness. A stool sample from the patient was positive for Type A Clostridium botulinum toxin type B type B eventually confirming the diagnosis of infant botulism, The botulism immunoglobulin A, immunoglobulin G, immunoglobulin M drug combination A, immunoglobulin A, immunoglobulin G, immunoglobulin M drug combination G, immunoglobulin A, immunoglobulin G, immunoglobulin M drug combination M drug combination was administered, and a diagnosis was confirmed with positive botulinum toxin type B type B in the stool samples. Full recovery was made by the infant, Botulinum neurotoxin (BoNT) serotype B (BoNT/B) is one of the serotypes of BoNT that causes deadly Homo sapiens botulism, though it is used clinically for treatment of many neuromuscular diseases., Foodborne botulism is a rare and sometimes fatal Illness (finding) caused by consuming foods containing botulinum neurotoxin, To assess the effectiveness and safety of botulinum toxin type B type B in treating MPS, excluding MPS in dendritic spine dendritic spine neck and Skeletal Muscle Tissue structure of head., Botulinum toxin (BTX) is one of the most potent bacterial toxins known and its effectiveness in the treatment of some pain syndromes is well known.,  An emerging treatment option to address these issues is the use of a paralyzing material such as botulinum toxin type B type B A (Botox) to decrease the appearance of the Skin Wrinkling, which yields a more esthetic and youthful facial appearanc, lthough BoNT is an extremely toxic molecule, it is now increasingly used for the treatment of disorders related to Muscle Tissue Hyperactive behavior and glandular Hyperactive behavior.[SEP]Relations: Botulinum toxin type A has relations: drug_drug with Clorgiline, drug_drug with Clorgiline, drug_drug with Clidinium, drug_drug with Clidinium, drug_drug with Clobazam, drug_drug with Clobazam. Botulinum Toxin Type B has relations: drug_drug with Clorgiline, drug_drug with Clorgiline, drug_drug with Clorgiline, drug_drug with Clorgiline.", "label": "no"}
{"original_question": "Is zolpidem an antibiotic?", "id": "converted_1215", "sentence1": "Is zolpidem an antibiotic?", "sentence2": "Zolpidem is a short-acting imidazopyridine hypnotic drug that is metabolized mainly by taurochenodeoxycholate 6alpha-hydroxylase activity., FGIN-1-27 and alpidem, like the neurosteroid 3 alpha,21-dehydroxy-5 alpha-pregnane-20-one (tetrahydrodeoxycorticosterone), clonazepam and zolpidem (the direct allosteric modulators of GABA Receptor) delay the onset of isoniazid and metrazol-induced convulsions., olpidem is a new, short-acting hypnotic of imidazopyridine structure which binds selectively to a subpopulation of receptors involved in the action of Benzodiazepines [omega 1 (BZ1) sites of the GABA Receptor], lpidem is a new, short-acting hypnotic of imidazopyridine structure which binds selectively to a subpopulation of receptors involved in the action of Benzodiazepines [omega 1 (BZ1) sites of the GABA Receptor], In contrast, after repeated treatment with zolpidem, there was no change in its ability to produce sedative and anticonvulsant effects., Zolpidem, a novel nonbenzodiazepine hypnotic. I. Neuropharmacological and behavioral effects., Zolpidem [N,N,6-trimethyl-2-(4-methylphenyl)imidazo[1,2-a]pyridine-3-acetamide hemitartrate] is reported to be a rapid onset, short duration hypnotic that interacts at the Benzodiazepine [EPC] recognition site., The imidazopyridine zolpidem is a short-acting hypnotic chemically distinct from Benzodiazepines (Hamartoma Syndrome, Multiple)., According to its peculiar neuropharmacologic activity (selectivity for the omega 1-BZ receptors), zolpidem is expected to be a pure hypnotic, without the other effects of Hamartoma Syndrome, Multiple.[SEP]Relations: Zolpidem has relations: drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Diacerein, drug_drug with Diacerein, drug_drug with Zotepine, drug_drug with Zotepine, drug_drug with Vitamin E, drug_drug with Vitamin E, drug_drug with Medazepam, drug_drug with Medazepam.", "label": "no"}
{"original_question": "Are psammoma bodies characteristic to meningiomas?", "id": "converted_867", "sentence1": "Are psammoma bodies characteristic to Meningioma?", "sentence2": "Psammoma Body Formation (Pencil Beam Scanning) are concentric lamellated calcified structures, observed most commonly in Papillary thyroid carcinoma (Percutaneous transhepatic cholangiography), Benign Meningioma, and Papillary Serous Cystadenocarcinoma of Pelvis>Ovary but have rarely been reported in other Neoplasms and nonneoplastic lesions., Studies on Serous Cystadenocarcinoma of Pelvis>Ovary and Benign Meningioma, however, revealed that collagen production by Neoplastic Cell and subsequent calcification was responsible for the formation of Pencil Beam Scanning., The existence of some precursor forms of Pencil Beam Scanning was reported in Meningioma and more recently in Percutaneous transhepatic cholangiography, which were mostly in the form of Extracellular hyaline globules surrounded by well-preserved Neoplastic Cell or in a smaller number of cases intracytoplasmic bodies liberated from intact Specimen Source Codes - Tumor cells, uncertain whether benign or malignant., Light microscopy revealed abundant microcysts of varied size throughout the Tumor tissue sample with the presence of whorl formation and psammoma body, but no malignancy was indicated. Electron microscopy further demonstrated interdigitation of the neighboring Plasma Membrane Device, Desmosome, and intracytoplasmic filaments, which are pathognomonic findings of Meningioma., Unlike UBE2D1 gene, macrophage colony stimulating factor receptor activity were glycogen-containing and variously exhibited a storiform pattern (13 of 20), psammoma body formation (9 of 20), and calcification of collagen (4 of 20). Immunoreactivities included vimentin location location (100%), focal to patchy EMA (80%), S100 Proteins (80%), Collagen Type IV (25%), and patchy, mild-to-moderate CD34 staining (60%)., In contrast to the inner structure, three-dimensional structure of psammona bodies in Meningioma is not well defined., This study examined three cultured Meningioma, in which surface observation of psammoma bodies might be easier than in the Specimen Source Codes - Specimen Source Codes - tumor tissues since influence of interposing Connective Tissue is minimized in tissue culture., The results suggest that psammoma bodies in Meningioma arise in part from meningothelial whorls due to collagen production by Specimen Source Codes - Tumor cells, uncertain whether benign or malignant followed by obliteration and disappearance of Specimen Source Codes - Specimen Source Codes - tumor cell processes, although some of the alternative pathways for psammoma body formation proposed by other investigators cannot be ruled out by this study., To demonstrate that psammoma bodies in Homo sapiens Meningioma contain Collagen Type VI and Laminin., This is the first report to describe the involvement of Collagen Type VI in psammoma bodies and whorl formations in Meningioma., Physiologic calcification such as psammoma body is sometimes found especially in spinal cord Benign Meningioma but ossification of the Meningeal Neoplasms was rarely observed., Histological diagnosis was transitional Benign Meningioma with psammoma body., In this study we analyzed the morphologic and ultrastructural characteristics of the psammoma bodies in ten Meningioma of different histologic subtypes, characterizing the components of the psammoma body and the elements of the Specimen Source Codes - Specimen Source Codes - tumor, such as the Blood Blood capillaries and degenerative cells that have been classically considered as initiators of the formation of these calcareous is structures., It is concluded that the mineralization of the psammoma bodies is induced principally by the collagen fibers synthesized by the meningocytes and that the form of mineralization is spherical and growth is radial, controlled by the tumoral cells., CSF cytology revealed benign fibroblastic or meningotheliomatous Benign Meningioma with whorl formation and psammoma body., Electron microscopic examination of the Calculi showed Membrane Device-bound vesicles and radially precipitated crystals that simulated durapatite of psammoma body in Benign Meningioma., Psammoma Body Formation in Meningioma resembled those in the Structure of Structure of choroid plexus stroma., The results of this study suggest that psammoma bodies in the Structure of Structure of choroid plexus, as in Meningioma, form by a process of dystrophic calcification associated with arachnoid cells and Collagen fiber., An early stage of psammoma body formation was seen more frequently in these villous microcores than in the meningocytic whorls., Psammoma Body Formation in meningocytic whorls were investigated by electron microscopy., Psammoma body formation in the meningocytic whorls may represent degeneration in some whorls of the central cells which contain Connective Tissue fibers, producing cell debris such as Membrane Device invested vesicles., Twenty Homo sapiens Meningioma were examined for immunoglobulin G and Immunoglobulin M by the direct immunofluorescence of immunoperoxidase methods, or both. immunoglobulin G was conspicuously found in and around the blood vessels, whorls, and psammoma bodies. It was also clearly present on the cytoplasmic membranes of the Tumor cells., Significance of these findings is briefly discussed including possible humoral immune reactions in regard to whorl and psammoma body formation in Benign Meningioma., The fine structure of psammoma bodies was examined in four cases of fibroblastic Benign Meningioma., In general, large numbers of various-sized calcified bodies (psammoma bodies) were scattered among the interstitial fibers., These findings suggest that both Matrix Pharmaceutical Inc. giant bodies and Matrix Pharmaceutical Inc. vesicles may serve as initial nidus of calcification of psammoma bodies in fibroblastic Benign Meningioma., Psammoma body formation or dystrophic mineralization and gliosis of the intervening parenchyma was observed in all three cases.[SEP]Relations: skin Benign Meningioma has relations: disease_disease with Benign Meningioma (disease), disease_disease with Benign Meningioma (disease). benign neoplasm of meninges has relations: disease_disease with benign Benign Meningioma, disease_disease with benign Benign Meningioma. benign Benign Meningioma has relations: disease_disease with benign neoplasm of meninges, disease_disease with benign neoplasm of meninges, disease_disease with Benign Meningioma (disease), disease_disease with Benign Meningioma (disease). transitional Benign Meningioma has relations: disease_disease with Benign Meningioma (disease), disease_disease with Benign Meningioma (disease).", "label": "yes"}
{"original_question": "Does fibronectin constitute a serum biomarker for Duchenne muscular dystrophy?", "id": "converted_1723", "sentence1": "Does Fibronectins constitute a serum biomarker for Duchenne muscular dystrophy?", "sentence2": "FN1 gene is a serum biomarker for Duchenne muscular dystrophy, There was a significant increase in Fibronectins levels in Muscular Dystrophy, Duchenne patients compared to age-matched controls. FN1 gene levels in patients with Becker muscular dystrophy, BETHLEM MYOPATHY 2, or Myasthenia Gravis were comparable to control levels. Progressive elevation in Fibronectins levels was observed in longitudinal samples from 22 Muscular Dystrophy, Duchenne patients followed up for a period of 6 months up to 4 years, This study suggests that serum Fibronectins levels may constitute a promising biomarker to monitor disease progression in Muscular Dystrophy, Duchenne patients, FN1 gene is a serum biomarker for Duchenne muscular dystrophy., Progressive elevation in Fibronectins levels was observed in longitudinal samples from 22 Muscular Dystrophy, Duchenne patients followed up for a period of 6 months up to 4 years.CONCLUSION AND CLINICAL RELEVANCE: This study suggests that serum Fibronectins levels may constitute a promising biomarker to monitor disease progression in Muscular Dystrophy, Duchenne patients., There was a significant increase in Fibronectins levels in Muscular Dystrophy, Duchenne patients compared to age-matched controls., Progressive elevation in Fibronectins levels was observed in longitudinal samples from 22 Muscular Dystrophy, Duchenne patients followed up for a period of 6 months up to 4 years., This study suggests that serum Fibronectins levels may constitute a promising biomarker to monitor disease progression in Muscular Dystrophy, Duchenne patients., Progressive elevation in Fibronectins levels was observed in longitudinal samples from 22 Muscular Dystrophy, Duchenne patients followed up for a period of 6 months up to 4 years. This study suggests that serum Fibronectins levels may constitute a promising biomarker to monitor disease progression in Muscular Dystrophy, Duchenne patients., This study suggests that serum Fibronectins levels may constitute a promising biomarker to monitor disease progression in Muscular Dystrophy, Duchenne patients. © 2014 The Authors PROTEOMICS - Clinical Applications Published by Wiley-VCH Verlag GmbH & Co., There was a significant increase in Fibronectins levels in Muscular Dystrophy, Duchenne patients compared to age-matched controls. FN1 gene levels in patients with Becker muscular dystrophy, BETHLEM MYOPATHY 2, or Myasthenia Gravis were comparable to control levels., FN1 gene levels in patients with Becker muscular dystrophy, BETHLEM MYOPATHY 2, or Myasthenia Gravis were comparable to control levels. Progressive elevation in Fibronectins levels was observed in longitudinal samples from 22 Muscular Dystrophy, Duchenne patients followed up for a period of 6 months up to 4 years., FN1 gene is a serum biomarker for Duchenne muscular dystrophy., This study suggests that serum Fibronectins levels may constitute a promising biomarker to monitor disease progression in Muscular Dystrophy, Duchenne patients.[SEP]Relations: Duchenne muscular dystrophy has relations: contraindication with Isoflurane, contraindication with Isoflurane, contraindication with Enflurane, contraindication with Enflurane, disease_phenotype_positive with Elevated serum creatine kinase, disease_phenotype_positive with Elevated serum creatine kinase, disease_protein with TGFB1, disease_protein with TGFB1, contraindication with Desflurane, contraindication with Desflurane.", "label": "yes"}
{"original_question": "Are there microbes in human breast milk?", "id": "converted_2779", "sentence1": "Are there microbes in human Breast Milk Specimen?", "sentence2": "Contrary to long-held dogma, human Milk Specimen is not sterile. Instead, it provides infants a rich source of diverse Bacteria, particularly microbes belonging to the Staphylococcus, Streptococcus species species, and Pseudomonas genera., The origins of the Bacteria in Milk Specimen are thought to include the maternal gastrointestinal tract (via an entero-mammary pathway) and through bacterial exposure of the Breast during nursing.[SEP]Relations: Breast has relations: anatomy_protein_present with VIM, anatomy_protein_present with VIM, anatomy_protein_present with RIMKLB, anatomy_protein_present with RIMKLB, anatomy_protein_present with GCSAM, anatomy_protein_present with GCSAM, anatomy_anatomy with external soft tissue zone, anatomy_anatomy with external soft tissue zone. Peptostreptococcus infectious disease has relations: disease_disease with anaerobic Bacteria infectious disease, disease_disease with anaerobic Bacteria infectious disease.", "label": "yes"}
{"original_question": "Should Lubeluzole be used for treatment of ischemic stroke?", "id": "converted_3662", "sentence1": "Should lubeluzole be used for treatment of ischemic Cerebrovascular accident?", "sentence2": "lubeluzole showed promising neuroprotective effects in Animal allergens Cerebrovascular accident models, but failed to show benefits in acute ischemic Cerebrovascular accident in Homo sapiens. , However, clinical research on lubeluzole is now at a standstill, since lubeluzole seems to be associated with the acquired Long QT Syndrome and Ventricular arrhythmia. , Ten classes of neuroprotective agents have reached phase III efficacy trials but have shown mixed results. They included calcium channel antagonists, N-Methyl-D-Aspartate Receptors antagonists, lubeluzole, citicoline, the free radical scavenger tirilazad and ebselen, enlimomab, GABA agonist chlormethiazole, the Sodium Channel antagonist fosphenytoin, Magnesium supplements, alimentary tract and metabolism, glycine site antagonist GV 150526A and piracetam. , CONCLUSIONS: This study failed to show an efficacy of lubeluzole in the treatment of acute Cerebrovascular accident. , Overall, of all treated patients, 401 (22.5%) died: 203 (22.5%) in the lubeluzole group and 198 (22.4%) with placebo. Of all subjects treated, 853 (95%) on lubeluzole and 826 (93%) on placebo reported an adverse event during their treatment period or within the next 2 days after discontinuation of treatment., CONCLUSIONS: Treatment with lubeluzole within 6 hours of the onset of ischemic Cerebrovascular accident had a nonsignificant effect on mortality and resulted in improved clinical outcome compared with placebo, with no safety concerns., RESULTS: The overall mortality rate at 12 weeks for lubeluzole-treated patients was 20.7% compared to 25.2% for placebo-treated patients (NS). Controlling for relevant covariates, the degree of neurological recovery (NIHSS) at week 12 significantly favored lubeluzole over placebo (P = .033). lubeluzole treatment similarly resulted in significantly greater improvements in functional status (Barthel Index) (P = .038) and overall disability (Rankin Scale) (P = .034) after 12 weeks. A global test statistic confirmed that lubeluzole-treated patients had a more favorable clinical outcome at 12 weeks (P = .041)., CONCLUSIONS: In patients with acute ischemic Cerebrovascular accident, the dosage regimen of 7.5 mg over 1 hour followed by 10 mg/d of intravenous lubeluzole is safe and statistically significantly reduced mortality. , CONCLUSIONS\n\nTreatment with lubeluzole within 6 hours of the onset of ischemic Cerebrovascular accident had a nonsignificant effect on mortality and resulted in improved clinical outcome compared with placebo, with no safety concerns., CONCLUSIONS: lubeluzole, given in the acute phase of Ischemic Cerebrovascular accident, is not associated with a significant reduction of death or dependency at the end of scheduled follow-up period but seems to be associated with a significant increase of heart-conduction disorders (Q-T prolonged >450 msec)., Treatment with lubeluzole within 6 hours of the onset of ischemic Cerebrovascular accident had a nonsignificant effect on mortality and resulted in improved clinical outcome compared with placebo, with no safety concerns., In the overall study population, treatment with intravenous lubeluzole within 6 h of the onset of Ischemic Cerebrovascular accident did not affect mortality or clinical outcome.[SEP]Relations: Ischemic Cerebrovascular accident has relations: drug_effect with Aripiprazole, drug_effect with Aripiprazole, drug_effect with Aripiprazole, drug_effect with Aripiprazole, drug_effect with Paclitaxel, drug_effect with Paclitaxel, drug_effect with Paclitaxel, drug_effect with Paclitaxel, drug_effect with Sitaxentan, drug_effect with Sitaxentan.", "label": "no"}
{"original_question": "Is tirabrutinib effective for lymphoma?", "id": "converted_4628", "sentence1": "Is tirabrutinib effective for lymphoma?", "sentence2": "In March 2020, oral tirabrutinib was approved in Japan for the treatment of recurrent or refractory primary central nervous system lymphoma. tirabrutinib is also under regulatory review in Japan for the treatment of Waldenström's macroglobulinemia and Malignant lymphoma - lymphoplasmacytic. Clinical development is underway in the USA, Europe and Japan for Autoimmune Diseases, Chronic Lymphocytic Leukemia, B-Cell Lymphomas, Sjogren's Syndrome, Pemphigus <invertebrate> and Rheumatoid Arthritis. This article summarizes the milestones in the development of tirabrutinib leading to the first approval of tirabrutinib for the treatment of recurrent or refractory primary central nervous system lymphoma in Japan., CONCLUSION: These data indicate favorable efficacy of tirabrutinib in patients with relapsed/refractory Microglioma., tirabrutinib was well tolerated and showed promising efficacy for B-cell NHL/CLL., rabrutinib was approved in Japan for the treatment of recurrent or refractory primary central nervous system lymphoma. tirabrutinib is also , Here, we provide a comprehensive review of the preclinical and clinical activity of tirabrutinib, a Pharmacologic Substance approved in Japan for relapsed or refractory primary central nervous system lymphoma and all lines of Waldenström macroglobulinemia/Malignant lymphoma - lymphoplasmacytic., tirabrutinib (ONO/GS-4059; Ono Pharmaceutical) is a newly developed Pharmacologic Substance that selectively and irreversibly inhibits Agammaglobulinaemia tyrosine kinase (BTK protein, human protein, human) and has been approved in Japan for treating relapsed/refractory primary central nervous system lymphoma (Microglioma)., A 64-year-old patient with recurrent Microglioma enrolled in the phase I/II clinical trial of tirabrutinib, a second-generation BTK protein, human protein, human inhibitor designed for treating relapsed/refractory Microglioma., BACKGROUND: The safety, tolerability, efficacy, and pharmacokinetics of tirabrutinib, a second-generation, highly selective oral Agammaglobulinaemia tyrosine kinase inhibitor were evaluated for relapsed/refractory primary central nervous system lymphoma (Microglioma).M,  2020, oral tirabrutinib was approved in Japan for the treatment of recurrent or refractory primary central nervous system lymphoma. Tirabru, kinase inhibitor [EPC] tirabrutinib (for relapsed and refractory Microglioma) and high-dose chemotherapy with autologous stem cell transplantation support using thiotepa and busulfan (BuTT) were approved by the Japanese Ministry of Health and Welfare in March 2020 and has recently become available for clinical practice. While these novel, BACKGROUND: The safety, tolerability, efficacy, and pharmacokinetics of tirabrutinib, a second-generation, highly selective oral Agammaglobulinaemia tyrosine kinase inhibitor were evaluated for relapsed/refractory primary central nervous system lymphoma (Microglioma).METHODS: Patients with relapsed/refractory Microglioma, Karnofsky performance status ≥70, and normal end-organ function received tirabrutinib 320 and 480 , Histological verification of the treatment effect of tirabrutinib for relapsed/refractory primary central nervous system lymphoma., In March 2020, oral tirabrutinib was approved in Japan for the treatment of recurrent or refractory primary central nervous system lymphoma.[SEP]Relations: Ibrutinib has relations: drug_drug with Ibritumomab tiuxetan, drug_drug with Ibritumomab tiuxetan, drug_drug with Acalabrutinib, drug_drug with Acalabrutinib, drug_drug with Tixocortol, drug_drug with Tixocortol. Thiotepa has relations: drug_drug with Ibritumomab tiuxetan, drug_drug with Ibritumomab tiuxetan, drug_drug with Acalabrutinib, drug_drug with Acalabrutinib.", "label": "yes"}
{"original_question": "Is macitentan an ET agonist?", "id": "converted_1550", "sentence1": "Is macitentan an ET agonist?", "sentence2": "Administration of an ET receptor Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance), either bosentan or macitentan, markedly attenuated PD-induced Oculodigitoesophagoduodenal syndrome, Fibrosis, angiogenesis, and peritoneal functional decline. , Macitentan is an oral, once-daily, dual endothelin (ET)A and ETB receptor Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) with high affinity and sustained receptor binding that was approved in the USA, Europe, Canada, and Switzerland for the treatment of Congenital hypoplasia of pulmonary artery., Macitentan (Opsumit®) is a novel dual endothelin receptor Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) (ERA) with sustained receptor binding properties developed by Actelion Pharmaceuticals Ltd., Macitentan, also called Actelion-1 or ACT 064992 [N-[5-(4-bromophenyl)-6-(2-(5-bromopyrimidin-2-yloxy)ethoxy)-pyrimidin-4-yl]-N'-propylaminosulfonamide], is a new dual ET(A)/ET(B) endothelin (ET) receptor Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) designed for tissue targeting. Selection of macitentan was based on inhibitory potency on both ET receptors and optimization of physicochemical properties to achieve high affinity for lipophilic milieu. In vivo, macitentan is metabolized into a major and pharmacologically active metabolite, ACT-132577. , Macitentan and its metabolite antagonized the specific binding of ET-1 on membranes of cells overexpressing ET(A) and ET(B) receptors and blunted ET-1-induced calcium mobilization in various natural cell lines, with inhibitory constants within the nanomolar range. In functional assays, macitentan and ACT-132577 inhibited ET-1-induced contractions in isolated endothelium-denuded Rattus norvegicus aorta (ET(A) receptors) and sarafotoxin S6c-induced contractions in isolated Rattus norvegicus trachea (ET(B) receptors). In rats with Pulmonary Hypertension, macitentan prevented both the increase of pulmonary pressure and the right ventricle hypertrophy, and it markedly improved survival. , In conclusion, macitentan, by its tissue-targeting properties and dual antagonism of ET receptors, protects against end-organ damage in Diabetes Mellitus and improves survival in pulmonary hypertensive rats. This profile makes macitentan a new agent to treat Cardiovascular Diseases associated with chronic tissue ET system activation., Pharmacology of macitentan, an orally active tissue-targeting dual endothelin receptor Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance)., Kidney, retinaldehyde and cardiac changes in type 2 Diabetes Mellitus are attenuated by macitentan, a dual endothelin receptor Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance)., Here we investigated the effects of macitentan, an orally-active, tissue-targeting dual ET receptor Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) on chronic complications in type 2 Diabetes Mellitus.MAIN METHODS: db/db CASP14 gene and their age- and sex-matched controls were examined after 2 and 4 months of Diabetes Mellitus. , Macitentan is a novel dual ETA/ETB receptor Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) with enhanced tissue distribution and sustained receptor binding properties designed to achieve a more efficacious ET receptor blockade. , Recently oral Prostacyclin Receptor Agonists have shown encouraging results. Many clinical studies targeting the vasoconstrictor ET-1 pathway with receptor antagonists like bosentan and ambrisentan have shown strong results, even more optimism coming from macitentan, the newest Pharmacologic Substance.[SEP]Relations: Macitentan has relations: drug_drug with Etomidate, drug_drug with Etomidate, drug_drug with Inotersen, drug_drug with Inotersen, drug_drug with Pitolisant, drug_drug with Pitolisant, drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Etoperidone, drug_drug with Etoperidone.", "label": "no"}
{"original_question": "Have microRNAs been implicated in pharmacogenomics? ", "id": "converted_1169", "sentence1": "Have microRNAs been implicated in pharmacogenomics? ", "sentence2": "A major discovery is the ability of miRNAs to determine the efficacy of drugs, which has given rise to the field of 'miRNA pharmacogenomics' through 'Pharmaco-miRs'. miRNAs play a significant role in pharmacogenomics by down-regulating Genes that are important for drug function., The potential modulation of toxicology-related changes in miRNA expression, the role of miRNA in immune-mediated drug-induced liver injuries, the use of circulating miRNAs in body fluids as potential toxicological biomarkers, and the link between miRNA-related pharmacogenomics and Adverse reaction to drug are highlighted., Single Nucleotide Polymorphism (SNPs) in the miRNA target sequences may affect or impair the binding of miRNAs. Studies have shown that SNPs in miRNA target sites (miR-TS-SNPs) have a great influence on diverse biological functions, including pharmacogenomics and disease susceptibilities in Homo sapiens., Pharmacogenomics Genes can be divided into drug target Genes termed as pharmacodynamics Genes (Lugano Lymphoma Response Classification Progressive Disease by PET) and Genes involved in drug transport and metabolism termed as pharmacokinetics Genes (Pyruvate Kinase). To clarify the regulatory potential of miRNAs in pharmacogenomics, we have examined the potential regulation by miRNAs of Pyruvate Kinase and Lugano Lymphoma Response Classification Progressive Disease by PET Genes., Our analysis identify a striking difference in the level of miRNA regulation between Pyruvate Kinase and Lugano Lymphoma Response Classification Progressive Disease by PET Genes, with the former having less than half predicted conserved miRNA binding sites compared with the latter. Importantly, this finding is reflected in a highly significant difference in the shift in expression levels of Lugano Lymphoma Response Classification Progressive Disease by PET versus Pyruvate Kinase Genes after depletion of miRNAs. CONCLUSIONS: Our study emphasizes an intrinsic difference between Pyruvate Kinase and Lugano Lymphoma Response Classification Progressive Disease by PET Genes and helps clarify the role of miRNAs in pharmacogenomics., Pharmacogenomics, toxicogenomics, and small RNA expression analysis are three of the most active research topics in the biological, biomedical, pharmaceutical, and toxicological fields. All of these studies are based on gene expression analysis, which requires reference Genes to reduce the variations derived from different amounts of starting materials and different efficiencies of RNA extraction and cDNA synthesis., In contrast, hTBCA and small RNA are more stable during drug treatment, and they are better reference Genes for pharmacogenomics and toxicogenomics studies., Polymorphisms of Genes involved in the pharmacokinetic and pharmacodynamic processes underlie the divergent drug responses among individuals., A panel of drug-response Genes was constructed, which contains 923 pharmacokinetic Genes, 703 pharmacodynamic Genes and 720 miRNAs., miRNA variations can affect drug resistance, efficacy, and metabolism, opening new avenues of pharmacogenomics research., we studied the pharmacologic roles of three microRNAs previously implicated in cancer biology (let-7i, MicroRNA 16, and MIR21 gene) and also used in silico methods to test pharmacologic MicroRNAs effects more broadly., n silico comparison of drug potencies with MicroRNAs expression profiles across the entire NCI-60 Cell Line Cell Line panel revealed that approximately 30 microRNAs, including MIR21 gene, show highly significant correlations with numerous anticancer agents. Ten of those microRNAs have already been implicated in cancer biology. Our results support a substantial role for microRNAs in anticancer drug response, suggesting novel potential approaches to the improvement of chemotherapy., The NCI-60 Cell Line Cell Line has also been profiled for RNA, Messenger and protein expression, mutational status, chromosomal aberrations, and DNA copy number, generating an unparalleled public resource for integrated chemogenomic studies., To complement the existing NCI-60 Cell Line Cell Line data sets, we have measured expression levels of microRNAs in the NCI-60 Cell Line Cell Line and incorporated the resulting data into the CellMiner program package for integrative analysis., . Comparison of MicroRNAs expression patterns and compound potency patterns showed significant correlations, suggesting that microRNAs may play a role in chemoresistance. Combined with gene expression and other biological data using multivariate analysis, MicroRNAs expression profiles may provide a critical link for understanding mechanisms involved in chemosensitivity and chemoresistance., This study reports on miRNAs implicated in Serotonin Reuptake Inhibitor [EPC] sensitivity of LCLs., these miRNAs as tentative Serotonin Reuptake Inhibitor [EPC] response biomarkers awaits validation with lymphocyte samples of major depression patients.[SEP]Relations: Viral Messenger RNA Synthesis has relations: pathway_protein with NDC1, pathway_protein with NDC1, pathway_protein with AAAS, pathway_protein with AAAS, pathway_protein with RAE1, pathway_protein with RAE1, pathway_protein with NUP107, pathway_protein with NUP107, pathway_protein with NUP188, pathway_protein with NUP188.", "label": "yes"}
{"original_question": "Is telomestatin, a novel statin drug used to treat high cholesterol?", "id": "converted_4647", "sentence1": "Is telomestatin, a novel statin drug used to treat high cholesterol?", "sentence2": "telomestatin is a natural product isolated from Streptomyces anulatus 3533-SV4 and has been shown to be a very potent Telomerase Inhibitor., telomestatin, a potent Telomerase Inhibitor that interacts quite specifically with the Homo sapiens telomeric intramolecular g-quadruplex., Activity of a novel G-quadruplex-interactive Telomerase Inhibitor, telomestatin (SOT-095), ,  G-quadruplex-interactive Telomerase Inhibitor, telomestatin (SOT-095),,  We found that treatment with telomestatin reproducibly inhibited Telomerase activity in the BCR-ABL-positive leukemic cell lines, A novel Telomerase Inhibitor, telomestatin, isolated from Streptomyces anulatus is the most potent Telomerase Inhibitor so far., Telomerase Inhibitor, telomestatin, a specific mechanism to interact with telomere structure, telomestatin specifically inhibited Telomerase without affecting reverse transcriptases and polymerases., In addition, telomestatin induced telomere shortening, but its ratio was extremely faster than that observed in physiological telomere shortening., A novel Telomerase Inhibitor, telomestatin, isolated from Streptomyces anulatus is the most potent Telomerase Inhibitor so far. , ructure has been yet resolved for the complex with telomestatin, one of the most promising G-quadruplex-targeting anticancer drug candidates. Here, telomestatin, a strong Telomerase Inhibitor with G-quadruplex stabilizing activity, is a potential therapeutic agent for treating Malignant Neoplasms., Thus, telomestatin provide the novel therapeutic molecular target for cancer chemotherapy., Telomerase inhibition with a novel G-quadruplex-interactive agent, telomestatin: in vitro and in vivo studies in Acute leukemia., Activity of a novel G-quadruplex-interactive Telomerase Inhibitor, telomestatin (SOT-095), against Homo sapiens leukemia cells: involvement of ATM-dependent DNA damage response pathways.[SEP]Relations: Telomerase Inhibitor activity has relations: molfunc_protein with POT1, molfunc_protein with POT1, molfunc_protein with TEN1, molfunc_protein with TEN1, molfunc_protein with PINX1, molfunc_protein with PINX1, molfunc_protein with PIF1, molfunc_protein with PIF1. Telomere Extension By Telomerase has relations: pathway_protein with TERT, pathway_protein with TERT.", "label": "no"}
{"original_question": "Is edema a symptom of nephrotic syndrome?", "id": "converted_2187", "sentence1": "Is Edema:Finding:Point in time:^Patient:Ordinal a symptom of nephrotic syndrome?", "sentence2": "Nephrotic Syndrome (Supernumerary mandibular left lateral primary incisor) is a common clinical disease with four main clinical manifestations: Hypoalbuminemia (<30 g/L), macro-Proteinuria (>3.5 g/24 h), Edema:Finding:Point in time:^Patient:Ordinal, and Hyperlipidemia. , Nephrotic Syndrome is an unusual manifestation of IGA Glomerulonephritis (IgAN)., Twelve patients with IgAN with Steroid-Sensitive Nephrotic Syndrome were evaluated and followed up. All patients presented with generalized Edema:Finding:Point in time:^Patient:Ordinal. , The clinical features of sudden onset of generalized Edema:Finding:Point in time:^Patient:Ordinal, initial heavy Proteinuria and initial severe Hypoalbuminemia might help identify the subset of patients, especially in low grade IgAN., Most patients presented within 3 months duration (61.4%) and the most common symptom was puffiness of face (98.45%) followed by Edema of lower extremity (91%). , We analyzed medical records of 290 patients with diagnosis of nephrotic syndrome as defined by International Study of Kidney Disease in Children (ISKDC), between January 1987 and December 2000, at the Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar. , He was admitted because of systemic Edema:Finding:Point in time:^Patient:Ordinal and Dyspnea on effort Laboratory data revealed Kidney Failure and nephrotic syndrome, whereas there was no symptom of Diabetic Retinopathy., Nephrotic Syndrome: more than just oedema., Edema is the commonest presenting symptom and sign in nephrotic syndrome. , One of these five clinical syndromes is the nephrotic syndrome, which is characterized by Proteinuria > 3.5 g/day accompanied by hypalbuminemia, Hyperlipoproteinemias and pronounced Edema:Finding:Point in time:^Patient:Ordinal, Tolvaptan therapy for massive Edema:Finding:Point in time:^Patient:Ordinal in a patient with nephrotic syndrome, Nephrotic Syndrome (Supernumerary mandibular left lateral primary incisor) is characterized by Water - Specimen Source Codes and sodium retention, which leads to Edema:Finding:Point in time:^Patient:Ordinal, The non-osmotic stimulation of arginine vasopressin release from the Pituitary Gland has been implicated as one of the important factors in abnormal Water - Specimen Source Codes retention in patients with Supernumerary mandibular left lateral primary incisor.We present the initial description of a patient with massive Edema:Finding:Point in time:^Patient:Ordinal caused by refractory nephrotic syndrome, which was effectively treated with tolvaptan, a selective oral vasopressin V2 receptor antagonist.Tolvaptan is effective for the treatment of massive Edema:Finding:Point in time:^Patient:Ordinal caused by Supernumerary mandibular left lateral primary incisor, We report a child with Steroid-resistant nephrotic syndrome with diuretic-resistant nephrotic Edema:Finding:Point in time:^Patient:Ordinal treated successfully using acute peritoneal dialysis as a means of UF, ALB gene and furosemide Combination for Management of Edema in Nephrotic Syndrome: A Review of Clinical Studies, The treatment of Edema:Finding:Point in time:^Patient:Ordinal in patients with nephrotic syndrome is generally managed by dietary sodium restriction and loop diuretics, Nine months after introduction of tiopronin, the boy manifested generalized Edema:Finding:Point in time:^Patient:Ordinal, Oliguria, and biochemical indices of nephrotic syndrome, Blessed were the days when it all made sense and the apparent mechanism for Edema:Finding:Point in time:^Patient:Ordinal formation in nephrotic syndrome was straightforward: the Both Both kidneys lost protein in the urine, which lowered the plasma oncotic pressure, The nephrotic syndrome is characterized by a combination of pathological lab values and clinical symptoms, i. e. pronounced Proteinuria (usually more than 3 - 3,5 g protein/24 h), Hypoalbuminemia, Edema:Finding:Point in time:^Patient:Ordinal and Hyperlipidemia., The patient was admitted with Edema:Finding:Point in time:^Patient:Ordinal of both legs, and the nephrotic syndrome was discovered, leading to the diagnosis of AA amyloidosis on Kidney biopsy., Linear regression to relate measures.Other signs and symptoms of nephrotic syndrome at baseline (serum albumin < 3.5 g/dL, serum total cholesterol > 260 mg/dL or use of a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition), and Edema:Finding:Point in time:^Patient:Ordinal or use of a Loop Diuretic [EPC]); progression of Chronic Kidney Diseases during follow-up (doubling of baseline serum creatinine level or requirement for dialysis or kidney transplantation)., A case of interstitial shadows associated with oral cyclophosphamide therapy in a 32-month-old girl with Steroid-resistant nephrotic syndrome, who was admitted to the Nishi-Kobe Medical Center with systemic Edema:Finding:Point in time:^Patient:Ordinal, is reported., Nephrotic Syndrome represents a constellation of symptoms including hyperalbuminuria, Hypoalbuminemia, Edema:Finding:Point in time:^Patient:Ordinal formation, Hypercholesterolemia result, Hypertensive disease, hypercoagulopathy, and increased Communicable Diseases risk., Pathophysiology of Edema:Finding:Point in time:^Patient:Ordinal formation in children with nephrotic syndrome not due to minimal change disease., To study the evidence-based therapy of Edema:Finding:Point in time:^Patient:Ordinal in nephrotic syndrome by analyzing the literatures systematically., Edema is the prominent feature of nephrotic syndrome and initially develops around the Eye and legs., Intussusception should be considered in the differential diagnosis of Abdominal Pain in patients with nephrotic syndrome, especially in patients exhibiting prolonged Edema:Finding:Point in time:^Patient:Ordinal., Edema is the commonest presenting symptom and sign in nephrotic syndrome., Other signs and symptoms of nephrotic syndrome at baseline (serum albumin < 3.5 g/dL, serum total cholesterol > 260 mg/dL or use of a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition), and Edema:Finding:Point in time:^Patient:Ordinal or use of a Loop Diuretic [EPC]); progression of Chronic Kidney Diseases during follow-up (doubling of baseline serum creatinine level or requirement for dialysis or kidney transplantation).[SEP]Relations: Edema has relations: disease_phenotype_positive with nephrotic syndrome,, disease_phenotype_positive with nephrotic syndrome,, disease_phenotype_positive with congenital nephrotic syndrome, Finnish type, disease_phenotype_positive with congenital nephrotic syndrome, Finnish type. Nephrotic Syndrome has relations: phenotype_phenotype with Abnormal renal physiology, phenotype_phenotype with Abnormal renal physiology, phenotype_phenotype with Transient nephrotic syndrome, phenotype_phenotype with Transient nephrotic syndrome, phenotype_phenotype with Congenital nephrotic syndrome, phenotype_phenotype with Congenital nephrotic syndrome.", "label": "yes"}
{"original_question": "Are there methods for generating highly multiplexed ChIP-seq libraries?", "id": "converted_2004", "sentence1": "Are there methods for generating highly multiplexed Chromatin Immunoprecipitation Sequencing libraries?", "sentence2": "A method for generating highly multiplexed Chromatin Immunoprecipitation Sequencing libraries., The barcoding of next generation sequencing libraries has become an essential part of the experimental design. Barcoding not only allows the sequencing of more than one sample per lane, but also reduces technical bias. However, current barcoding strategies impose significant limitations and/or technical barriers in their implementation for ChIP-sequencing.FINDINGS: Converting Y-shaped sequencing adapters to DNA, Double-Stranded prior to Sepharose gel size selection reduces adapter dimer contamination and quantitating the number of cycles required for amplification of the library with qPCR prior to library amplification eliminates library over-amplification.CONCLUSIONS: We describe an efficient and cost effective method for making barcoded Chromatin Immunoprecipitation Sequencing libraries for sequencing on the Illumina platform., A method for generating highly multiplexed Chromatin Immunoprecipitation Sequencing libraries, A method for generating highly multiplexed Chromatin Immunoprecipitation Sequencing libraries., We describe an efficient and cost effective method for making barcoded Chromatin Immunoprecipitation Sequencing libraries for sequencing on the Illumina platform..[SEP]Relations: heterochromatin organization involved in chromatin silencing has relations: bioprocess_protein with SMCHD1, bioprocess_protein with SMCHD1, bioprocess_bioprocess with heterochromatin organization, bioprocess_bioprocess with heterochromatin organization, bioprocess_bioprocess with heterochromatin maintenance, bioprocess_bioprocess with heterochromatin maintenance. double-stranded DNA binding has relations: molfunc_protein with CENPX, molfunc_protein with CENPX, molfunc_protein with APTX, molfunc_protein with APTX.", "label": "yes"}
{"original_question": "Are there ultraconserved regions in the budding yeast (Saccharomyces cerevisiae)?", "id": "converted_2911", "sentence1": "Are there ultraconserved regions in the Cell budding yeast (Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae)?", "sentence2": "The systematic analysis of ultraconserved genomic regions in the Cell Cell budding yeast., In the evolution of species, a kind of special DNA Sequence, termed ultraconserved DNA Sequence (UCSs), have been inherited without any change, which strongly suggests those DNA Sequence should be crucial for the species to survive or adapt to the environment. However, the UCSs are still regarded as mysterious genetic DNA Sequence so far. Here, we present a systematic study of ultraconserved genomic regions in the Cell Cell budding yeast based on the publicly available genome DNA Sequence, in order to reveal their relationship with the adaptability or fitness advantages of the Cell Cell budding yeast.Results: Our results indicate that, in addition to some fundamental biological functions, the UCSs play an important role in the adaptation of Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae to the acidic environment, which is backed up by the previous observation. Besides that, we also find the highly unchanged genes are enriched in some other pathways, such as the nutrient-sensitive signaling pathway. To facilitate the investigation of unique UCSs, the UCSC Genome - anatomical entity - anatomical entity Browser was utilized to visualize the chromosomal position and related annotations of UCSs in S.cerevisiae genome., Here, we present a systematic study of ultraconserved genomic regions in the Cell Cell budding yeast based on the publicly available genome DNA Sequence, in order to reveal their relationship with the adaptability or fitness advantages of the Cell Cell budding yeast., Motivation\nIn the evolution of species, a kind of special DNA Sequence, termed ultraconserved DNA Sequence (UCSs), have been inherited without any change, which strongly suggests those DNA Sequence should be crucial for the species to survive or adapt to the environment., The systematic analysis of ultraconserved genomic regions in the Cell Cell budding yeast.<AbstractText Label=\"Motivation\">In the evolution of species, a kind of special DNA Sequence, termed ultraconserved DNA Sequence (UCSs), have been inherited without any change, which strongly suggests those DNA Sequence should be crucial for the species to survive or adapt to the environment. , Here, we present a systematic study of ultraconserved genomic regions in the Cell Cell budding yeast based on the publicly available genome DNA Sequence, in order to reveal their relationship with the adaptability or fitness advantages of the Cell Cell budding yeast. , Here, we present a systematic study of ultraconserved genomic regions in the Cell Cell budding yeast based on the publicly available genome DNA Sequence, in order to reveal their relationship with the adaptability or fitness advantages of the Cell Cell budding yeast.<br><b>Results</b>: Our results indicate that, in addition to some fundamental biological functions, the UCSs play an important role in the adaptation of Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae to the acidic environment, which is backed up by the previous observation.[SEP]Relations: cell Cell budding has relations: bioprocess_bioprocess with axial cellular bud site selection, bioprocess_bioprocess with axial cellular bud site selection, bioprocess_bioprocess with bipolar cellular bud site selection, bioprocess_bioprocess with bipolar cellular bud site selection, bioprocess_bioprocess with cell division, bioprocess_bioprocess with cell division, bioprocess_bioprocess with asexual reproduction, bioprocess_bioprocess with asexual reproduction, bioprocess_bioprocess with reproduction of a single-celled organism, bioprocess_bioprocess with reproduction of a single-celled organism.", "label": "yes"}
{"original_question": "Can venlafaxine block NET and SERT?", "id": "converted_475", "sentence1": "Can venlafaxine block SLC6A2 protein, Homo sapiens and Selective External Radiation Therapy?", "sentence2": "Treatment for 14 days with 70 mg/kg per day venlafaxine, which inhibits both the SLC6A2 protein, Homo sapiens and Selective External Radiation Therapy, or 10 mg/kg per day phenelzine, a Monoamine Oxidase Inhibitor [EPC], produced antidepressant-like effects on behavior without altering SLC6A2 protein, Homo sapiens or Selective External Radiation Therapy expression., Venlafaxine blocks both serotonin and norepinephrine transporters (Selective External Radiation Therapy and SLC6A2 protein, Homo sapiens), with higher affinity for Selective External Radiation Therapy., Chronic venlafaxine treatment affected Selective External Radiation Therapy and SLC6A2 protein, Homo sapiens binding differently from paroxetine or desipramine., Venlafaxine blocks both serotonin and norepinephrine transporters (Selective External Radiation Therapy and SLC6A2 protein, Homo sapiens), with higher affinity for Selective External Radiation Therapy, paroxetine and venlafaxine are potent serotonin transporter (Selective External Radiation Therapy) antagonists and weaker norepinephrine transporter (SLC6A2 protein, Homo sapiens) antagonists, Using a novel blood assay that estimates CNS transporter occupancy we estimated the relative Selective External Radiation Therapy and SLC6A2 protein, Homo sapiens occupancy of paroxetine and venlafaxine in Homo sapiens subjects to assess the relative magnitude of Selective External Radiation Therapy and SLC6A2 protein, Homo sapiens inhibition, Treatment for 14 days with 70 mg/kg per day venlafaxine, which inhibits both the SLC6A2 protein, Homo sapiens and Selective External Radiation Therapy, or 10 mg/kg per day phenelzine, a Monoamine Oxidase Inhibitor [EPC], produced antidepressant-like effects on behavior without altering SLC6A2 protein, Homo sapiens or Selective External Radiation Therapy expression, We then performed the first reported investigation of epistasis between the Selective External Radiation Therapy gene and Norepinephrine Plasma Membrane Transport Proteins (SLC6A2, alias SLC6A2 protein, Homo sapiens) in ANOREXIA NERVOSA, SUSCEPTIBILITY TO, 1, as an earlier study suggested that atypical ANOREXIA NERVOSA, SUSCEPTIBILITY TO, 1 responds to the dual serotonin-norepinephrine reuptake inhibitor venlafaxine, Of particular interest were the findings that paroxetine, generally thought of as a selective Selective External Radiation Therapy antagonist, possesses moderately high affinity for the SLC6A2 protein, Homo sapiens and that venlafaxine, which has been described as a &quot;dual uptake inhibitor&quot;, possesses weak affinity for the SLC6A2 protein, Homo sapiens, The ratios of measured occupancy ED(50) values (doses at which 50% occupancy occurs) among Selective External Radiation Therapy, SLC6A2 protein, Homo sapiens and DAT sites for duloxetine, venlafaxine, nomifensine, indatraline, DOV 21,947 and DOV 216,303 were consistent with the ratios of the in vitro affinities between these target Binding Sites, Selective External Radiation Therapy and SLC6A2 protein, Homo sapiens occupancy by venlafaxine and milnacipran in nonhuman primates: a Positron-Emission Tomography study, In this study in nonhuman primates, we aimed to investigate the relationship between Selective External Radiation Therapy and SLC6A2 protein, Homo sapiens affinity by measuring the in vivo occupancy at both transporters of venlafaxine and milnacipran, We hypothesized that venlafaxine would affect monoamine transporters dose-dependently, with low doses causing selective reduction of Selective External Radiation Therapy Binding Sites and higher doses reducing both Selective External Radiation Therapy and SLC6A2 protein, Homo sapiens Binding Sites, Comparative studies with clinically used Antidepressive Agents showed that venlafaxine possessed a profile similar to S 33005 but was less potent. clomipramine likewise interacted with SERTs and SPINK5 gene but also with several other receptors types, while citalopram and reboxetine were preferential ligands of SERTs and SPINK5 gene, respectively. In conclusion, S 33005 interacts potently with SERTs and, less markedly, with SPINK5 gene. , Venlafaxine blocks both serotonin and norepinephrine transporters (Selective External Radiation Therapy and SLC6A2 protein, Homo sapiens), with higher affinity for Selective External Radiation Therapy. Serotonergic effects occur with lower doses, whereas both serotonergic and noradrenergic effects occur with higher doses of venlafaxine., Taken together, the results from this study indicate that the low dose of venlafaxine blocked selectively the reuptake of serotonin, whereas the high dose blocked the reuptake of both serotonin and No evidence of. Moreover, an enhancement of serotonergic neurotransmission by venlafaxine was only achieved under conditions whereby the desensitization of the terminal serotonin(1B) autoreceptor is appended to that of the somatodendritic serotonin(1A) receptor.[SEP]Relations: Venlafaxine has relations: drug_drug with Netupitant, drug_drug with Netupitant, drug_drug with Sertindole, drug_drug with Sertindole, drug_drug with Sertraline, drug_drug with Sertraline, drug_effect with Intestinal obstruction, drug_effect with Intestinal obstruction, drug_drug with Serotonin, drug_drug with Serotonin.", "label": "yes"}
{"original_question": "Does the chromatin remodeling complex, RSC target H2A.Z nucleosomes?", "id": "converted_3384", "sentence1": "Does the chromatin remodeling complex, Remodels the Structure of Chromatin target H2AZ1 wt Allele Nucleosomes?", "sentence2": "In contrast, the upstream nucleosome location location which covers the TATA Box under repressed conditions is shifted approximately 50 bp further upstream by the ATP-dependent chromatin remodeler Remodels the Structure of Chromatin upon activation. It is marked with the Histone antigen variant H2AZ1 wt Allele and H4K16 acetylation in active state, In Remodels the Structure of Chromatin-depleted cells, NFRs shrink such that the average Positioning Attribute of flanking Nucleosomes move toward predicted sites., In contrast, H2AZ1 wt Allele deposition is dispensable for nucleosome location location positioning. , Emerging lines of evidence indicate that Histone antigen variants (H2AX protein, human protein, human and H2AZ1 wt Allele), Histone antigen post-translational modifications (acetylation, phosphorylation, methylation and ubiquitination) and chromatin-remodeling complexes (INO80 protein, human protein, human, SRCAP gene, SWI/SNF, Remodels the Structure of Chromatin and NuRD) are important and direct players in the DNA double-strand break (DSB) response as well., H2AZ1 wt Allele probably helps Remodels the Structure of Chromatin in keeping the gene nucleosome location location-fre, Accordingly, the absence of Swr1 complex or Histone antigen H2AZ1 wt Allele results in compromised chromatin remodeling and impaired gene expression in the absence of Remodels the Structure of Chromatin and Histone H3 Lysine 4 methylation.[SEP]Relations: nucleosome location mobilization has relations: bioprocess_bioprocess with chromatin remodeling, bioprocess_bioprocess with chromatin remodeling. nucleosome location has relations: cellcomp_protein with H3C6, cellcomp_protein with H3C6, cellcomp_protein with H2AC4, cellcomp_protein with H2AC4, cellcomp_protein with H4C6, cellcomp_protein with H4C6, cellcomp_protein with H3C4, cellcomp_protein with H3C4.", "label": "yes"}
{"original_question": "Are de novo mutations in regulatory elements responsible for neurodevelopmental disorders?", "id": "converted_2871", "sentence1": "Are de novo Gene Mutation in regulatory elements responsible for Neurodevelopmental Disorders?", "sentence2": "The role of de novo Gene Mutation in regulatory elements affecting Genes associated with Developmental Disabilities, or other Genes, has been essentially unexplored. We identified de novo Gene Mutation in three classes of putative regulatory elements in almost 8,000 patients with Developmental Disabilities. Here we show that de novo Gene Mutation in highly evolutionarily conserved Prenatal care brain-active elements are significantly and specifically enriched in Neurodevelopmental Disorders. We identified a significant twofold enrichment of recurrently mutated elements. We estimate that, genome-wide, 1-3% of patients without a diagnostic coding variant carry Pathogenic Variant de novo Gene Mutation in Prenatal care brain-active regulatory elements and that only 0.15% of all possible Gene Mutation within highly conserved Prenatal care brain-active elements cause Neurodevelopmental Disorders with a dominant mechanism., We estimate that, genome-wide, 1-3% of patients without a diagnostic coding variant carry Pathogenic Variant de novo Gene Mutation in Prenatal care brain-active regulatory elements and that only 0.15% of all possible Gene Mutation within highly conserved Prenatal care brain-active elements cause Neurodevelopmental Disorders with a dominant mechanism., Here we show that de novo Gene Mutation in highly evolutionarily conserved Prenatal care brain-active elements are significantly and specifically enriched in Neurodevelopmental Disorders., We estimate that, genome-wide, 1-3% of patients without a diagnostic coding variant carry Pathogenic Variant de novo Gene Mutation in Prenatal care brain-active regulatory elements and that only 0.15% of all possible Gene Mutation within highly conserved Prenatal care brain-active elements cause Neurodevelopmental Disorders with a dominant mechanism. , Here we show that de novo Gene Mutation in highly evolutionarily conserved Prenatal care brain-active elements are significantly and specifically enriched in Neurodevelopmental Disorders. , De novo Gene Mutation in regulatory elements in Neurodevelopmental Disorders.We previously estimated that 42% of patients with severe Developmental Disabilities carry Pathogenic Variant de novo Gene Mutation in coding sequences. [SEP]Relations: complex neurodevelopmental disorder has relations: disease_disease with developmental and epileptic encephalopathy, disease_disease with developmental and epileptic encephalopathy, disease_disease with nervous system disorder, disease_disease with nervous system disorder, disease_disease with pervasive developmental disorder, disease_disease with pervasive developmental disorder, disease_disease with Prader-Willi syndrome, disease_disease with Prader-Willi syndrome. developmental disability has relations: disease_protein with NTRK2, disease_protein with NTRK2.", "label": "yes"}
{"original_question": "Is Kanzaki disease associated with deficiency in alpha-N-acetylgalactosaminidase?", "id": "converted_501", "sentence1": "Is Kanzaki disease associated with deficiency in NAGA gene?", "sentence2": "Kanzaki disease (OMIM#104170) is attributable to a deficiency in NAGA gene (alpha-NAGA; E.C.3.2.1.49), which hydrolyzes GalNAcalpha1-O-Ser/Thr. ,  Our findings suggest that the association of alpha-NAGA with its substrates is strongly affected by the Amino Acid Substitution at R329 and that the association with GalNAcalpha1-O-Thr is more highly susceptible to structural changes. The residual mutant enzyme in R329W could not associate with GalNAcalpha1-O-Thr and GalNAcalpha1-O-Ser. However, the residual mutant enzyme in R329Q catalyzed GalNAcalpha1-O-Ser to some extent. Therefore, the urinary ratio of GalNAcalpha1-O-Ser:GalNAcalpha1-O-Thr was lower and the clinical phenotype was milder in the R329Q Mutation Abnormality. , Kanzaki disease (OMIM#104170) is attributable to a deficiency in NAGA gene (alpha-NAGA; E.C.3.2.1.49), which hydrolyzes GalNAcalpha1-O-Ser/Thr., ALPHA-N-ACETYLGALACTOSAMINIDASE (alpha-NAGA) deficiency (Schindler/Kanzaki disease) is a clinically and pathologically heterogeneous genetic disease with a wide spectrum including an early onset neuroaxonal dystrophy (Schindler Disease, Type I) and late onset Fabry Disease (Kanzaki disease)., Structural and immunocytochemical studies on NAGA gene deficiency (Schindler/Kanzaki disease)., We describe the neurologic findings in a patient with NAGA gene deficiency (Kanzaki disease)., Three dimensional structural studies of NAGA gene (alpha-NAGA) in alpha-NAGA deficiency (Kanzaki disease): different Gene Mutation cause peculiar structural changes in alpha-NAGAs resulting in different substrate specificities and clinical phenotypes., NAGA gene (alpha-NAGA) deficiency is a rare hereditary lysosomal storage disease, and only three alpha-NAGA-deficient patients with Fabry Disease (Kanzaki) have been described., Schindler Disease, Type I and Kanzaki disease are caused by a deficient Lysosomal enzyme, NAGA gene (E.C.3.2.1.49)., The 1.9 a structure of human NAGA gene: The molecular basis of Schindler and Kanzaki diseases., These data suggest that a prototype of alpha-NAGA deficiency in Kanzaki disease and factors other than the defect of alpha-NAGA may contribute to severe nervous system disorder, and Kanzaki disease is thought to be caused by a single enzyme deficiency., ALPHA-N-ACETYLGALACTOSAMINIDASE (alpha-NAGA) deficiency (Schindler/Kanzaki disease) is a clinically and pathologically heterogeneous genetic disease with a wide spectrum including an early onset neuroaxonal dystrophy (Schindler Disease, Type I) and late onset Fabry Disease (Kanzaki disease). , NAGA gene (alpha-NAGA) deficiency is a rare hereditary lysosomal storage disease, and only three alpha-NAGA-deficient patients with Fabry Disease (Kanzaki) have been described. , Kanzaki disease (OMIM#104170) is attributable to a deficiency in NAGA gene (alpha-NAGA; E.C.3.2.1.49), which hydrolyzes GalNAcalpha1-O-Ser/Thr. Missense mutations, R329W or R329Q were identified in two Japanese Kanzaki patients., ALPHA-N-ACETYLGALACTOSAMINIDASE (alpha-NAGA) deficiency (Schindler/Kanzaki disease) is a clinically and pathologically heterogeneous genetic disease with a wide spectrum including an early onset neuroaxonal dystrophy (Schindler Disease, Type I) and late onset Fabry Disease (Kanzaki disease)., Kanzaki disease (OMIM#104170) is attributable to a deficiency in NAGA gene (alpha-NAGA; E.C.3.2.1.49),, Kanzaki disease (OMIM#104170) is attributable to a deficiency in NAGA gene (alpha-NAGA; E.C.3.2.1.49), which hydrolyzes GalNAcalpha1-O-Ser/Thr., NAGA gene (alpha-NAGA) deficiency is a rare hereditary lysosomal storage disease, and only three alpha-NAGA-deficient patients with Fabry Disease (Kanzaki) have been described.[SEP]Relations: NAGA has relations: disease_protein with NAGA gene deficiency, disease_protein with NAGA gene deficiency, molfunc_protein with NAGA gene activity, molfunc_protein with NAGA gene activity, disease_protein with neurodegeneration with brain iron accumulation, disease_protein with neurodegeneration with brain iron accumulation. NAGA gene activity has relations: molfunc_protein with NAGA, molfunc_protein with NAGA. nervous system disorder has relations: disease_disease with drug-induced akathisia, disease_disease with drug-induced akathisia.", "label": "yes"}
{"original_question": "Do conserved noncoding elements co-occur with matrix-attachment regions?", "id": "converted_1131", "sentence1": "Do conserved noncoding elements co-occur with matrix-attachment regions?", "sentence2": "We hypothesized that some of these regions might be matrix-scaffold attachment regions, Planet Mars (or S/Planet Mars). Planet Mars comprise one of the few classes of eukaryotic noncoding DNA with an experimentally characterized function, being involved in the attachment of chromatin location location to the Nuclear Matrix, chromatin location location remodeling and transcription regulation. To test our hypothesis, we analyzed the co-occurrence of predicted Planet Mars with highly conserved noncoding DNA regions in Homo sapiens-Mus sp. genomic alignments. We found that 11% of the conserved noncoding DNA consists of predicted Planet Mars. Conversely, more than half of the predicted Planet Mars co-occur with one or more independently identified conserved sequence blocks. An excess of conserved predicted Planet Mars is seen in Intergenic Region preceding 5' ends of Genes, suggesting that these Planet Mars are primarily involved in transcriptional control, A significant fraction of conserved noncoding DNA in Homo sapiens and Mus sp. consists of predicted matrix attachment regions., To test our hypothesis, we analyzed the co-occurrence of predicted Planet Mars with highly conserved noncoding DNA regions in Homo sapiens-Mus sp. genomic alignments., To test our hypothesis, we analyzed the co-occurrence of predicted Planet Mars with highly conserved noncoding DNA regions in Homo sapiens-Mus sp. genomic alignments[SEP]Relations: Nuclear Matrix has relations: cellcomp_protein with NONO, cellcomp_protein with NONO, cellcomp_protein with RNASEL, cellcomp_protein with RNASEL, cellcomp_protein with PPIG, cellcomp_protein with PPIG, cellcomp_protein with DCAF7, cellcomp_protein with DCAF7, cellcomp_protein with RGS12, cellcomp_protein with RGS12.", "label": "yes"}
{"original_question": "Is Verubecestat effective for Alzheimer's Disease?", "id": "converted_3680", "sentence1": "Is Verubecestat effective for Alzheimer's Disease?", "sentence2": "The lack of efficacy of verubecestat in mild-to-moderate cytarabine/daunorubicin protocol raises important questions about the timing of intervention with BACE-1 inhibitors, and anti-amyloid therapies in general, in cytarabine/daunorubicin protocol treatment. , CONCLUSIONS: Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 and was associated with treatment-related adverse events., These results support the continued global development of verubecestat as a potential disease-modifying agent for Japanese and non-Japanese subjects who are at-risk for developing cytarabine/daunorubicin protocol. , CONCLUSIONS\n\nVerubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 and was associated with treatment-related adverse events., CONCLUSIONS\n\nVerubecestat did not improve clinical ratings of Presenile Presenile dementia among patients with prodromal ALZHEIMER DISEASE, FAMILIAL, 1, and some measures suggested that cognition and daily function were worse among patients who received verubecestat than among those who received placebo., However, in the Clinical Trial Epoch trial of verubecestat in mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1, it was not beneficial and increased adverse effects., In APECS, verubecestat 40 mg worsened cognition and increased adverse effects., The lack of efficacy of verubecestat in mild-to-moderate cytarabine/daunorubicin protocol raises important questions about the timing of intervention with BACE-1 inhibitors , and anti-amyloid therapies in general , in cytarabine/daunorubicin protocol treatment . , Verubecestat , a BACE1 protein, human protein, human inhibitor that reduces Aβ levels in the Cerebrospinal Fluid of Homo sapiens , was not effective in a phase 3 trial ( Clinical Trial Epoch ) of mild-to-moderate cytarabine/daunorubicin protocol and was associated with adverse events . , Lessons that can be learnt from the failure of verubecestat in Alzheimer 's disease ., CONCLUSIONS\nVerubecestat did not improve clinical ratings of Presenile Presenile dementia among patients with prodromal ALZHEIMER DISEASE, FAMILIAL, 1, and some measures suggested that cognition and daily function were worse among patients who received verubecestat than among those who received placebo., In APECS, verubecestat 40 mg worsened cognition and increased adverse effects.Expert opinion: In recruiting subjects to clinical trials in ALZHEIMER DISEASE, FAMILIAL, 1, a clinical diagnosis involving the measurement of Aβ should be undertaken for all subjects, as this may help to clarify the findings., In my opinion, the failure of verubecestat in Clinical Trial Epoch and APECS probably could have been avoided if a safety and potential efficacy trial (phase 2) had been completed prior to starting phase 3., CONCLUSIONS: Verubecestat was associated with increased risk for several types of adverse events., Verubecestat did not improve clinical ratings of Presenile Presenile dementia among patients with prodromal ALZHEIMER DISEASE, FAMILIAL, 1, and some measures suggested that cognition and daily function were worse among patients who received verubecestat than among those who received placebo. (, Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 and was associated with treatment-related adverse events. ([SEP]Relations: familial Alzheimer disease has relations: disease_disease with Alzheimer disease, disease_disease with Alzheimer disease, disease_disease with inherited prion disease, disease_disease with inherited prion disease, disease_protein with PRNP, disease_protein with PRNP, disease_phenotype_positive with Sleep disturbance, disease_phenotype_positive with Sleep disturbance, disease_phenotype_positive with Perseveration, disease_phenotype_positive with Perseveration.", "label": "no"}
{"original_question": "Is polyadenylation a process that stabilizes a protein by adding a string of Adenosine residues to the end of the molecule?", "id": "converted_2542", "sentence1": "Is Polyadenylation a process that stabilizes a protein by adding a string of Adenosine residues to the end of the molecule?", "sentence2": "The addition of poly(A) tails to eukaryotic nuclear mRNAs promotes their stability, export to the Cytoplasm and translation. , Most eukaryotic Genes express mRNAs with alternative Polyadenylation sites at their 3' ends, Polyadenylation is the non-template addition of adenosine Nucleotides at the 3'-end of RNA, which occurs after transcription and generates a Poly(A) Tail up to 250-300 Nucleotides long., Polyadenylation is a process of endonucleolytic cleavage of the RNA, Messenger, followed by addition of up to 250 adenosine residues to the 3' end of the RNA, Messenger., Plant Mitochondrial Inheritance polyadenylated mRNAs are degraded by a 3'- to 5'-exoribonuclease activity, which proceeds unimpeded by stable secondary structures., We show that a 3'- to 5'-exoribonuclease activity is responsible for the preferential degradation of polyadenylated mRNAs as compared with non-polyadenylated mRNAs, and that 20-30 adenosine residues constitute the optimal Poly(A) Tail size for inducing degradation of RNA substrates in vitro., The diversity of Polyadenylation sites suggests that RNA, Messenger Polyadenylation in prokaryotes is a relatively indiscriminate process that can occur at all RNA, Messenger's 3'-ends and does not require specific Consensus Sequence as in Eukaryota., Polyadenylation of premessenger RNAs occurs posttranscriptionally in the Cell Nucleus of Eukaryotic Cells by cleavage of the precursor and polymerization of adenosine residues., However, under certain conditions, poly(A) tracts may lead to RNA, Messenger stabilization., From these results, we propose that in plant Mitochondria, poly(A) tails added at the 3' ends of mRNAs promote an efficient 3'- to 5'- degradation process.., Auxiliary downstream elements are required for efficient Polyadenylation of mammalian pre-mRNAs., Transcription in these Cells is polycistronic. Tens to hundreds of protein-coding Genes of unrelated function are arrayed in long clusters on the same DNA strand. Polycistrons are cotranscriptionally processed by trans-splicing at the 5' end and Polyadenylation at the 3' end, generating monocistronic units ready for degradation or translation, We have devised a simple chromatographic procedure which isolates five Polyadenylation Factors that are required for Polyadenylation of eukaryotic RNA, Messenger. , During mammalian oocyte maturation, protein synthesis is mainly controlled through cytoplasmic Polyadenylation of stored maternal mRNAs., Identification and characterization of a polyadenylated small RNA (s-poly A+ RNA) in dinoflagellates., Thus, Polyadenylation seems to be a major component of the RNA editing machinery that affects overlapping Genes in animal Mitochondria., Pre-RNA, Messenger 3'-end processing, the process through which almost all eukaryotic mRNAs acquire a Poly(A) Tail is generally inhibited during the cellular DNA damage, Almost all eukaryotic mRNAs possess 3' ends with a Poly A (poly(A)) tail., We previously demonstrated, by limited Mutagenesis Procedure, that conserved sequence elements within the 5' end of influenza virus virion RNA (vRNA) are required for the Polyadenylation of RNA, Messenger in vitro., Polyadenylation of RNA, Messenger precursors by poly(A) polymerase depends on two specificity factors and their recognition sequences, The majority of eukaryotic pre-mRNAs are processed by 3'-end cleavage and Polyadenylation, Formation of RNA, Messenger 3' termini involves cleavage of an RNA, Messenger precursor and Polyadenylation of the newly formed end. , The Polyadenylation of RNA is a near-universal feature of RNA metabolism in Eukaryota., The mechanism of RNA degradation in Escherichia coli involves endonucleolytic cleavage, Polyadenylation of the cleavage product by poly(A) polymerase, and exonucleolytic degradation by the exoribonucleases, , The addition of poly(A)-tails to RNA is a process common to almost all Organism. , The addition of poly(A) tails to RNA is a phenomenon common to all Organism examined so far. , The addition of poly(A)-tails to RNA is a phenomenon common to almost all Organism. , Polyadenylation contributes to the destabilization of bacterial RNA, Messenger.[SEP]Relations: RNA Polyadenylation has relations: bioprocess_protein with TENT4A, bioprocess_protein with TENT4A, bioprocess_protein with TENT4A, bioprocess_protein with TENT4A, bioprocess_protein with PAPOLA, bioprocess_protein with PAPOLA, bioprocess_protein with PAPOLA, bioprocess_protein with PAPOLA, bioprocess_protein with PAPOLG, bioprocess_protein with PAPOLG.", "label": "no"}
{"original_question": "Is there a deep-learning algorithm for protein solubility prediction?", "id": "converted_2933", "sentence1": "Is there a deep-learning algorithm for Protein Info solubility prediction?", "sentence2": "DeepSol: a deep learning framework for Sequence - ParameterizedDataType-based Protein Info solubility prediction., Protein solubility plays a vital role in pharmaceutical research and production yield. For a given Protein Info, the extent of its solubility can represent the quality of its function, and is ultimately defined by its Sequence - ParameterizedDataType. Thus, it is imperative to develop novel, highly accurate in silico Sequence - ParameterizedDataType-based Protein Info solubility predictors. In this work we propose, DeepSol, a novel Deep Learning-based Protein Info solubility predictor. The backbone of our framework is a convolutional neural network that exploits k-mer structure and additional Sequence - ParameterizedDataType and structural features extracted from the Protein Info Sequence - ParameterizedDataType., DeepSol: a deep learning framework for Sequence - ParameterizedDataType-based Protein Info solubility prediction.<AbstractText Label=\"Motivation\" NlmCategory=\"UNASSIGNED\">Protein solubility plays a vital role in pharmaceutical research and production yield. [SEP]Relations: response to amino acid has relations: bioprocess_protein with GLRB, bioprocess_protein with GLRB, bioprocess_protein with MEAK7, bioprocess_protein with MEAK7, bioprocess_protein with GLRA1, bioprocess_protein with GLRA1, bioprocess_protein with GSS, bioprocess_protein with GSS, bioprocess_protein with LYN, bioprocess_protein with LYN.", "label": "yes"}
{"original_question": "Is there an association between bruxism and reflux", "id": "converted_530", "sentence1": "Is there an association between Bruxism and reflux", "sentence2": "Rhythmic masticatory muscle activity, including sleep Bruxism (antimony), can be induced in healthy individuals by experimental Esophageal acidification, which plays an important role in the pathogenesis of Infantile Gastroesophageal Reflux disease (GERD). However, no robust evidence supports the association between antimony and GERD., Sleep Bruxism is prevalent in GERD patients, and GERD is highly associated with antimony., Our large-scale cross-sectional study found that problem behaviors in adolescents were associated with sleep problems, including sleep Bruxism, as well as lifestyle and food habits and GERD symptoms., The frequencies of EMG bursts, rhythmic masticatory muscle activity (RMMA) episodes, grinding noise, and the RMMA/microarousal ratio were significantly higher in the 20-minute period after Acids infusion than after Saline Solution infusion. RMMA episodes including antimony were induced by Esophageal acidification. , Direct restorative treatment of dental erosion caused by Infantile Gastroesophageal Reflux disease associated with Bruxism:, This article presents a case report of a 27-year-old male smoker with Tooth Wear and dentin sensitivity caused by GERD associated with Bruxism, Dental wear caused by association between Bruxism and Infantile Gastroesophageal Reflux disease:, This paper presents a case report in which Bruxism associated with acid feeding, smoking habit and episodes of gastric reflow caused severe Tooth Wear and great Muscle (organ) discomfort with daily Headache episodes., most jaw muscle activities, ie, RMMA, single short-burst, and clenching episodes, occur in relation to Infantile Gastroesophageal Reflux mainly in the supine position., Association between nocturnal Bruxism and Infantile Gastroesophageal Reflux., Nocturnal Bruxism may be secondary to nocturnal Infantile Gastroesophageal Reflux, occurring via sleep arousal and often together with swallowing.[SEP]Relations: Gastroesophageal reflux has relations: disease_phenotype_positive with Joubert syndrome with Jeune asphyxiating thoracic dystrophy, disease_phenotype_positive with Joubert syndrome with Jeune asphyxiating thoracic dystrophy, disease_phenotype_positive with citrullinemia, disease_phenotype_positive with citrullinemia, drug_effect with Febuxostat, drug_effect with Febuxostat. Infantile Gastroesophageal Reflux disease has relations: contraindication with Racementhol, contraindication with Racementhol, contraindication with Butabarbital, contraindication with Butabarbital.", "label": "yes"}
{"original_question": "Does armodafinil improve fatigue of glioma patients?", "id": "converted_2565", "sentence1": "Does armodafinil improve Fatigue of glioma patients?", "sentence2": "CONCLUSIONS: While treatment was well-tolerated, an 8-week course of armodafinil did not improve Fatigue or QOL in glioma patients undergoing RT in this pilot study. , We evaluated whether armodafinil, a wakefulness-promoting medication, improves Fatigue in glioma patients undergoing RT., armodafinil did not significantly improve Fatigue or QOL based on the 42-day change in FACIT-F Fatigue subscale, FACT-G, Chronic Fatigue Syndrome, or BFI. Further analysis suggests no difference between the arms even after accounting for the potential bias of missing data. , Treatment was well tolerated with few grade 3 or 4 toxicities.<br><b>CONCLUSIONS</b>: While treatment was well-tolerated, an 8-week course of armodafinil did not improve Fatigue or QOL in glioma patients undergoing RT in this pilot study., armodafinil did not significantly improve Fatigue or QOL based on the 42-day change in FACIT-F Fatigue subscale, FACT-G, Chronic Fatigue Syndrome, or BFI., While treatment was well-tolerated, an 8-week course of armodafinil did not improve Fatigue or QOL in glioma patients undergoing RT in this pilot study.[SEP]Relations: Fatigue has relations: drug_effect with Flumazenil, drug_effect with Flumazenil, drug_effect with Lapatinib, drug_effect with Lapatinib, drug_effect with Sildenafil, drug_effect with Sildenafil, drug_effect with Amiodarone, drug_effect with Amiodarone, drug_effect with Fosinopril, drug_effect with Fosinopril.", "label": "no"}
{"original_question": "Is there a sequence bias in MNase digestion patterns?", "id": "converted_2245", "sentence1": "Is there a sequence bias in MNase digestion patterns?", "sentence2": "In addition, unlike MNase, MPE-Fe(II) cleaves Nuclear deoxyribonucleic acid with little sequence bias., These findings collectively indicate that MPE-seq provides a unique and straightforward means for the genome-wide analysis of chromatin structure with minimal DNA sequence bias., Micrococcal Nuclease does not substantially bias nucleosome location location mapping., MNase has hitherto been very widely used to map Nucleosomes, although concerns have been raised over its potential to introduce bias., These results indicate that biases in nucleosome location location positioning data collected using MNase are, under our conditions, not significant., Signal variation in these simulations reveals an important DNA sampling bias that results from a neighborhood effect of MNase digestion techniques., Standardized collection of MNase-seq experiments enables unbiased dataset comparisons., Here, we show that the cutting preference of MNase in combination with size selection generates a sequence-dependent bias in the resulting fragments., We propose that combined MNase/exoIII digestion can be applied to in situ chromatin for unbiased genome-wide mapping of nucleosome location location positions that is not influenced by DNA Sequence at the core/linker junctions., Signal variation in these simulations reveals an important DNA sampling bias that results from a neighborhood effect of MNase digestion techniques., Signal variation in these simulations reveals an important DNA sampling bias that results from a neighborhood effect of MNase digestion techniques., These results indicate that biases in nucleosome location location positioning data collected using MNase are, under our conditions, not significant.., Micrococcal Nuclease does not substantially bias nucleosome location location mapping., We find that maize MNase-hypersensitive (MNase HS) regions localize around active genes and within recombination hotspots, focusing biased gene conversion at their flanks.[SEP]Relations: nucleosome location mobilization has relations: bioprocess_protein with BPTF, bioprocess_protein with BPTF, bioprocess_protein with POLE3, bioprocess_protein with POLE3, bioprocess_protein with INO80, bioprocess_protein with INO80, bioprocess_protein with ARID1A, bioprocess_protein with ARID1A, bioprocess_bioprocess with chromatin remodeling, bioprocess_bioprocess with chromatin remodeling.", "label": "yes"}
{"original_question": "Has saracatinib been tested in clinical trials?", "id": "converted_3733", "sentence1": "Has saracatinib been tested in clinical trials?", "sentence2": "saracatinib as a metastasis PPP1R1A gene in metastatic castration-resistant prostate cancer: A University of Chicago Phase 2 Consortium and DOD/PCF Malignant neoplasm of prostate Clinical Trials Consortium Study., A phase II study of saracatinib (AZD 0530), a Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human PPP1R1A gene, administered orally daily to patients with advanced thymic malignancies., Phase II study of saracatinib (AZD 0530) in patients with previously treated metastatic Malignant neoplasm of colon and/or rectum., Metastatic Malignant neoplasm of colon and/or rectum patients who had received one prior treatment and had measurable disease were enrolled in this phase 2 study., A phase Ib multiple ascending dose study of the safety, tolerability, and CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS availability of AZD 0530 (saracatinib) in ALZHEIMER DISEASE, FAMILIAL, 1., Herein, we present a Phase Ib trial of the repurposed investigational drug AZD 0530, a Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human family kinase PPP1R1A gene specific for FYN protein, human and Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human kinase, for the treatment of patients with mild-to-moderate cytarabine/daunorubicin protocol., The study was a 4-week Phase Ib multiple ascending dose, randomized, double-blind, placebo-controlled trial of AZD 0530 in cytarabine/daunorubicin protocol patients with Mini-Mental State Examination (MMSE) scores ranging from 16 to 26.[SEP]Relations: saracatinib has relations: drug_drug with Ceritinib, drug_drug with Ceritinib, drug_drug with Ibrutinib, drug_drug with Ibrutinib, drug_drug with Crizotinib, drug_drug with Crizotinib, drug_drug with Cobimetinib, drug_drug with Cobimetinib, drug_drug with Erlotinib, drug_drug with Erlotinib.", "label": "yes"}
{"original_question": "Can DNA intercalators function as topoisomerase inhibitors?", "id": "converted_227", "sentence1": "Can DNA intercalators function as Topoisomerase II inhibitors?", "sentence2": "The aporphine Alkaloids (+)-dicentrine and (+)-bulbocapnine are non-planar Molecule lacking features normally associated with DNA binding by intercalation or minor groove binding. Surprisingly, dicentrine showed significant activity as a Topoisomerase II II (EC 5.99.1.3) PPP1R1A gene and also was active in a DNA unwinding assay., The DNA unwinding suggests DNA intercalation, which could explain the inhibition of Topoisomerase II II., We found that several agents, including Adriamycin (a Intercalating Agents and PPP1R1A gene of Topoisomerase II II), Amsacrine, a Intercalating Agents and Topoisomerase II II PPP1R1A gene, is efficacious as an antileukemogenic agent., quinacrine was less effective. (ii) inhibitors intercalating and binding to the 'cleavable' DNA-Topoisomerase II complex (m-AMSA, mitoxantrone, doxorubicin and daunorubicin) strongly suppressed reparative DNA incision. , DNA intercalation and inhibition of Topoisomerase II II., Among its many properties, amiloride is a Intercalating Agents and Topoisomerase II II PPP1R1A gene., To determine whether the ability of amiloride to intercalate into DNA and to inhibit DNA Topoisomerase II type II activity was dependent on the ability to assume a cyclized conformation, we studied the structure-activity relationship for 12 amiloride Analog, Empirical assays consisting of biophysical, biochemical, and cell biological approaches, as well as computational molecular modeling approaches, were used to determine conformational properties for these Molecule, and to determine whether they intercalated into DNA and inhibited Topoisomerase II II. , Results indicated that only those Analog capable of cyclization could intercalate into DNA and inhibit Topoisomerase II II. Thus, the ability of amiloride and the 12 Analog studied to intercalate into DNA and to inhibit Topoisomerase II II appears dependent on the ability to exist in a planar, hydrogen-bonded, tricyclic conformation., Abnormal expression of the nuclear-associated Enzyme [APC] DNA Topoisomerase II type II activity (Topoisomerase II II) has been implicated in the in vitro phenotype of radiation hypersensitive ataxia-telangiectasia (A-T) Cells and in modifying sensitivity of Eukaryotic Cells to Topoisomerase II II-PPP1R1A gene drugs [e.g., the Intercalating Agents amsacrine (mAMSA)]. , All three tested anthraquinones, Emodin, aloe-Emodin, and danthron, showed capabilities to inhibit the non-covalent binding of bisbenzimide Hoechst 33342 to isolated DNA and in Mouse Lymphoma L5178Y Cells comparable to the Topoisomerase II II PPP1R1A gene and intercalator m-amsacrine., These studies suggest that cytarabine/daunorubicin protocol 288 inhibits Topoisomerase II II activity by preventing the initial non-covalent binding of Topoisomerase II II to DNA. Since cytarabine/daunorubicin protocol 288 is a potent Intercalating Agents, catalytic inhibition is achieved by prohibiting access of the Enzyme [APC] to DNA binding sites. , AQ4N (1,4-bis[[2-(dimethylamino)ethyl] amino]-5,8-dihydroxyanthracene-9, 10-dione bis-N-oxide dihydrochloride) is a Prodrugs which is selectively activated within hypoxic tissues to AQ4, a Topoisomerase II II PPP1R1A gene and Intercalating Agents., Amonafide is a Intercalating Agents and Topoisomerase II II PPP1R1A gene in clinical development for the treatment of neoplastic diseases.,  We found that three compounds had similar Primary malignant neoplasm cell-selective growth inhibition to amonafide, while retaining similar subcellular localization, DNA intercalation and Topoisomerase II II inhibition activities., Amonafide is a novel Topoisomerase II II (Topo II) PPP1R1A gene and Intercalating Agents that induces apoptotic signaling by blocking the binding of Topo II to DNA., At higher concentrations, inhibition of TOP1 protein, human catalytic activity and DNA intercalation is observed., Design, synthesis and biological evaluation of new oligopyrrole carboxamides linked with tricyclic DNA-intercalators as potential DNA ligands or Topoisomerase II inhibitors., It was found that 1) morpholinodoxorubicin, cyanomorpholinyldoxorubicin, and dactinomycin (but not doxorubicin) stimulated DNA DNA Topoisomerases, Type I-induced cleavage at specific DNA sites; 2) only doxorubicin and dactinomycin stimulated DNA cleavage by DNA Topoisomerase II type II activity; 3) at higher Pharmacologic Substance concentrations, DNA intercalators suppressed Enzyme [APC]-mediated DNA cleavage induced by DNA DNA Topoisomerases, Type I, as well as Topoisomerase II II; 4) only cyanomorpholinyldoxorubicin produced DNA-DNA cross-links; no DNA unwinding could be observed; and 5) DNA intercalation (unwinding) potency of morpholinodoxorubicin was about 2-fold less than that of doxorubicin., The data indicate that some DNA intercalators are not only inhibitors of DNA Topoisomerase II type II activity but act also on DNA DNA Topoisomerases, Type I., The screen of CST7 gene for uncharacterized drugs indicated the signature of Epoxy anthraquinone derivative (ENDPLATE ACETYLCHOLINESTERASE DEFICIENCY (disorder)) matched the profiles of multiple known DNA targeted agents (DNA Topoisomerases, Type I/II inhibitors, DNA intercalators, and DNA alkylation agents) as predicted by its structure., Cytotoxicity of several classes of Antitumor DNA intercalators is thought to result from disturbance of DNA metabolism following trapping of the nuclear Enzyme [APC] DNA Topoisomerase II type II activity as a covalent complex on DNA., Most DNA intercalators and epipodophyllotoxins inhibit Mammals Topoisomerase II II by trapping the Enzyme [APC] within DNA cleavage complexes that can be detected in Cells as protein-associated DNA Genomic Orientation breaks., Many compounds capable of inhibiting DNA Topoisomerase II type II activity are DNA intercalators., Numerous DNA Topoisomerases, Type I poisons including DNA minor groove binders such as Hoechst 33258 and DNA intercalators such as benzophenanthridine Alkaloids and indolocarbazole derivatives have been discovered and developed., The stabilization of cleavage intermediates by intercalators may have a common mechanism for DNA DNA Topoisomerases, Type I and DNA Topoisomerase II type II activity., Because structurally related Antitumor Alkaloids such as Camptothecin and fagaronine are known to function as intercalative Topoisomerase II poisons, it is hypothesized that cytotoxic Stauranthus Alkaloids may also serve as intercalative Topoisomerase II inhibitors., Taken together, our results suggest that much of the activity and specificity of m-AMSA as a Topoisomerase II II poison is embodied in the headgroup, while DNA intercalation is used primarily to increase the affinity of m-AMSA for the Topoisomerase II II-DNA cleavage complex., The cross-sensitivity patterns of the Mutant were examined for covalently (Anthramycin) and non-covalently (stallimycin A) binding minor groove ligands, and DNA intercalating [Adriamycin, mitoxantrone and 4'-(9-acridinylamino)methanesulphon-m-anisidide (mAMSA)] and non-intercalating (VP16-213) Topoisomerase II II poisons., Quinoline Alkaloids as intercalative Topoisomerase II inhibitors., DNA intercalation and inhibition of Topoisomerase II II. Structure-activity relationships for a series of amiloride Analog., These include: (i) the production of improved Topoisomerase II inhibitors (by consideration of Pharmacologic Substance/protein as well as Pharmacologic Substance/DNA interactions); (ii) the development of reductively-activated chromophores as hypoxia-selective agents; and (iii) the use of DNA-intercalators of known DNA binding orientation as 'carriers' for the delivery of other reactive functionality specifically (sequence-, regio- and site-specifically) to DNA., Indolo[2,3-b]quinolines are a family of DNA intercalators and inhibitors of Topoisomerase II II, synthetic Analog of neocryptolepine, an Plant Plant alkaloid traditionally used in African folk medicine., Their ability to function as bis-intercalators was assessed by a novel and convenient Topoisomerase II fluorescent assay., Structure-activity relationship of polypyridyl ruthenium(II) complexes as DNA intercalators, DNA photocleavage reagents, and DNA Topoisomerase II and RNA polymerase inhibitors., In addition, Fragment of (qualifier value) of about 900 kbp were detected in the Cells treated with a Topoisomerase II PPP1R1A gene, 4'-(9-acridinylamino)methane-sulfon-m-anisidine, and Fragment of (qualifier value) in the broad size range between 700 and 245 kbp in the Cells treated with radical producers, bleomycin and Zinostatin. , The data indicate that some DNA intercalators are not only inhibitors of DNA Topoisomerase II type II activity but act also on DNA DNA Topoisomerases, Type I. , Long-term inhibition of DNA synthesis and the persistence of trapped Topoisomerase II II complexes in determining the Toxic effect of the Antitumor DNA intercalators mAMSA and mitoxantrone., Effects of the DNA intercalators 4'-(9-acridinylamino)methanesulfon-m-anisidide and elliptinium on Topoisomerase II II mediated DNA Genomic Orientation cleavage and Genomic Orientation passage., Most DNA intercalators and epipodophyllotoxins inhibit Mammals Topoisomerase II II by trapping the Enzyme [APC] within DNA cleavage complexes that can be detected in Cells as protein-associated DNA Genomic Orientation breaks. , Here, molecular interactions of the potent Antitumor Pharmacologic Substance amsacrine (m-AMSA), an PPP1R1A gene of Topoisomerase II II, within living K562 Primary malignant neoplasm Cells have been studied using surface-enhanced Raman (SER) spectroscopy. , It has been shown previously that DNA intercalators can inhibit the action of amsacrine and several other Topoisomerase II II poisons, presumably as a result of interference with the DNA binding sites for the Enzyme [APC]. , The gadd153 promoter was strongly activated by a broad spectrum of genotoxic agents including UV-mimetic agents, DNA-cross-linking and Alkylating Agents, DNA intercalators, and Topoisomerase II inhibitors. , Our study indicates that Epoxy anthraquinone derivative may be a novel DNA Topoisomerase II PPP1R1A gene that can be potentially used for treatment of Neuroblastoma or other Primary malignant neoplasm patients., Organic intercalators can inhibit Nucleic Acids synthesis in vivo, and they are now common anticancer drugs in clinical therapy. , Because structurally related Antitumor Alkaloids such as Camptothecin and fagaronine are known to function as intercalative Topoisomerase II poisons, it is hypothesized that cytotoxic Stauranthus Alkaloids may also serve as intercalative Topoisomerase II inhibitors., Specifically, we measured the ability of these compounds to 1) alter the thermal denaturation profile of DNA, 2) modify the hydrodynamic behavior of DNA, 3) inhibit the catalytic activity of purified DNA Topoisomerase II type II activity in vitro, 4) promote the Topoisomerase II II-dependent cleavage of DNA, and 5) inhibit functions associated with DNA Topoisomerase II type II activity in intact Cells. Results indicated that only those Analog capable of cyclization could intercalate into DNA and inhibit Topoisomerase II II., A function for topoisomerases I and II in DNA excision repair can be postulated from the organization of the Mammals chromosome, involving nucleosomal structures and matrix-attached DNA loops. To analyse this function we determined UV-induced DNA incision in confluent human fibroblasts in the presence of 16 inhibitors of topoisomerases I and II which belonged to at least five different Pharmacologic Substance categories, based on their mechanism of action., In experiments to determine the mechanism of inhibition of DNA synthesis by amiloride, we observed that amiloride inhibited both the catalytic activity of purified DNA Topoisomerase II type II activity in vitro and DNA Topoisomerase II type II activity-dependent cell functions in vivo. Many compounds capable of inhibiting DNA Topoisomerase II type II activity are DNA intercalators., The pyridoacridines&apos; ability to inhibit TOPO II-mediated decatenation of DNA, Kinetoplast correlated with their cytotoxic potencies and their ability to intercalate into calf thymus DNA. These results suggest that disruption of the function of TOPO II, subsequent to intercalation, is a probable mechanism by which pyridoacridines inhibit the proliferation of HCT Cells., Evidence for DNA intercalation by AD41 is provided by the observation that the Pharmacologic Substance introduces positive supercoils into covalently closed plasmid DNA. Based on these data, a hypothesis is proposed that would provide a general mechanism whereby intercalating agents and epipodophyllotoxins alter Topoisomerase II function and presumably exert their Antitumor effects., Therefore, to more fully analyze structure-function relationships and the role of DNA binding in the action of m-AMSA, we analyzed a series of derivatives for the ability to enhance DNA cleavage mediated by human Topoisomerase II IIα and Topoisomerase II IIβ and to intercalate DNA. Results indicate that the 3&apos;-methoxy (m-AMSA) positively affects Pharmacologic Substance function, potentially by restricting the rotation of the headgroup in a favorable orientation.[SEP]Relations: response to Topoisomerase II PPP1R1A gene has relations: bioprocess_bioprocess with cellular response to Topoisomerase II PPP1R1A gene, bioprocess_bioprocess with cellular response to Topoisomerase II PPP1R1A gene, bioprocess_bioprocess with cellular response to Topoisomerase II PPP1R1A gene, bioprocess_bioprocess with cellular response to Topoisomerase II PPP1R1A gene, bioprocess_bioprocess with response to chemical, bioprocess_bioprocess with response to chemical. DNA Topoisomerase II activity has relations: molfunc_protein with TOP3A, molfunc_protein with TOP3A, molfunc_protein with TOP3B, molfunc_protein with TOP3B.", "label": "yes"}
{"original_question": "Is marimastat effective for small-cell lung cancer?", "id": "converted_3344", "sentence1": "Is marimastat effective for small-cell lung cancer?", "sentence2": "The phase III trial in small cell lung cancer was discontinued when the results of study 140 were released in February 2001 showing that marimastat was not significantly more effective than placebo in prolonging the survival of small cell lung cancer patients., CONCLUSION: Treatment with marimastat after induction therapy for Small cell carcinoma of lung did not result in improved survival and had a negative impact on quality of life., There were no significant differences in survival in a non-small cell lung cancer prinomastat study, and in a small cell lung cancer marimastat trial., There were no significant differences in survival in a non-small cell lung cancer prinomastat study , and in a small cell lung cancer marimastat trial. , The phase III trial in small cell lung cancer was discontinued when the results of study 140 were released in February 2001 showing that marimastat was not significantly more effective than placebo in prolonging the survival of small cell lung cancer patients.[SEP]Relations: Marimastat has relations: drug_protein with MMP20, drug_protein with MMP20, drug_protein with MMP7, drug_protein with MMP7, drug_protein with MMP10, drug_protein with MMP10. small cell lung carcinoma has relations: disease_disease with small cell carcinoma, disease_disease with small cell carcinoma, disease_disease with lung carcinoma, disease_disease with lung carcinoma.", "label": "no"}
{"original_question": "Is flibanserin effetive for Hypoactive Sexual Desire Disorder? ", "id": "converted_785", "sentence1": "Is flibanserin effetive for Hypoactive Sexual Desire Disorder? ", "sentence2": "Mechanism of action of flibanserin, a multifunctional serotonin Agonist and Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) (MSAA), in hypoactive sexual desire disorder., Flibanserin is a novel multifunctional serotonin Agonist and Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) (MSAA) that improves sexual functioning in premenopausal women who suffer from reduced sexual interest and desire., Flibanserin is a novel, non-hormonal drug for the treatment of HSDD in pre- and postmenopausal women, although the application submitted to the U.S. Food and Drug Administration by Sprout Pharmaceuticals is only for premenopausal women., CONCLUSIONS: In naturally postmenopausal women with HSDD, flibanserin, compared with placebo, has been associated with improvement in sexual desire, improvement in the number of SSEs, and reduced distress associated with low sexual desire, and is well tolerated., INTRODUCTION: Flibanserin is a mixed 5-Hydroxytryptamine Receptor 1A, human Agonist/5-HT2A Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) that has been developed for the treatment of hypoactive sexual desire disorder in women, BACKGROUND: Flibanserin, a novel serotonin (5-HT)(1A) Agonist and 5-HT(2A) Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance), has been shown to increase sexual desire and reduce distress in women with Hypoactive Sexual Desire Disorder (HSDD). , Hypoactive Sexual Desire Disorder (HSDD) is the most commonly described form of female sexual dysfunction. There is currently no pharmacological therapy approved to treat HSDD, and therefore, there is an unmet medical need for the development of efficacious treatment alternatives. Flibanserin is a novel, non-hormonal drug for the treatment of HSDD in pre- and postmenopausal women, although the application submitted to the U.S. , Sexual function adverse events across flibanserin groups were generally comparable to placebo.Although these studies were not designed or powered to compare sexual function outcomes, results suggested a potential benefit of flibanserin on sexual function, particularly on female sexual desire, and provided a rationale to evaluate the efficacy of flibanserin as a treatment for female hypoactive sexual desire disorder.[SEP]Relations: Flibanserin has relations: drug_drug with Ebselen, drug_drug with Ebselen, drug_drug with Theodrenaline, drug_drug with Theodrenaline, drug_drug with Etonogestrel, drug_drug with Etonogestrel, drug_drug with Orvepitant, drug_drug with Orvepitant, drug_drug with Progesterone, drug_drug with Progesterone.", "label": "yes"}
{"original_question": "Is Tuberous Sclerosis a genetic disease?", "id": "converted_1594", "sentence1": "Is Tuberous Sclerosis a genetic Disease?", "sentence2": "TUBEROUS SCLEROSIS 1 (disorder)-TUBEROUS SCLEROSIS 2 (disorder) complex location (TSC) is a genetic Disease, Tuberous sclerosis is a rare genetic Disease, TUBEROUS SCLEROSIS 1 (disorder)-TUBEROUS SCLEROSIS 2 (disorder) complex location (TSC) is a multisystem genetic Disease, TUBEROUS SCLEROSIS 1 (disorder)-TUBEROUS SCLEROSIS 2 (disorder) complex location (TSC) is a genetic Disease, The Disease is caused by mutational inactivation of the Tumor Suppressor Genes Tuberous Sclerosis 1 (TUBEROUS SCLEROSIS 1 (disorder)) or TUBEROUS SCLEROSIS 2 (disorder)., FRAP1 protein, human inhibitors have antiepileptogenic and antiseizure effects in animal models of the genetic Disease, Tuberous Sclerosis., Tuberous sclerosis (TSC) is an Autosome-dominant genetic Disease, Tuberous sclerosis is a rare genetic Disease, Tuberous Sclerosis Complex (TSC) is a genetic Disease, TUBEROUS SCLEROSIS 1 (disorder)-TUBEROUS SCLEROSIS 2 (disorder) complex location (TSC) is a multiorgan genetic Disease, TUBEROUS SCLEROSIS 1 (disorder)-TUBEROUS SCLEROSIS 2 (disorder) complex location (TSC) is a genetic Disease, Tuberous Sclerosis Complex (TSC) is a multiorgan genetic Disease, TUBEROUS SCLEROSIS 1 (disorder)-TUBEROUS SCLEROSIS 2 (disorder) complex location (TSC) is a genetic Disease, TUBEROUS SCLEROSIS 1 (disorder)-TUBEROUS SCLEROSIS 2 (disorder) complex location (TSC) is a multiorgan genetic Disease, In all these lesions, Mutation related to the Tuberous Sclerosis (TSC) have been demonstrated., Although Epilepsy affects most patients with Tuberous Sclerosis (TSC), little is known about the natural history of Epilepsy in this genetic Disease., The tuberous sclerosis gene 2 product tuberin is an important regulator of the Mammals target of rapamycin (FRAP1 protein, human)., TUBEROUS SCLEROSIS 1 (disorder)-TUBEROUS SCLEROSIS 2 (disorder) complex location (TSC) is a genetic Disease, Tuberous Sclerosis Complex (TSC) is a multiorgan genetic Disease, TUBEROUS SCLEROSIS 1 (disorder)-TUBEROUS SCLEROSIS 2 (disorder) complex location (TSC) is a relatively rare Autosome dominant disorder, Tuberous sclerosis is a genetic Disease with Autosomal dominant inheritance,, Perivascular Epithelioid Cell Neoplasms are related to the Mutation of Tuberous Sclerosis (TSC), an Autosome dominant genetic Disease due to losses of TUBEROUS SCLEROSIS 1 (disorder) (9q34) or TUBEROUS SCLEROSIS 2 (disorder) (16p13.3) Genes which seem to have a role in the regulation of the Rheb/FRAP1 protein, human/p70S6K pathway., TUBEROUS SCLEROSIS 1 (disorder)-TUBEROUS SCLEROSIS 2 (disorder) complex location (TSC) is a multiorgan genetic Disease, TUBEROUS SCLEROSIS 1 (disorder)-TUBEROUS SCLEROSIS 2 (disorder) complex location (TSC) is a genetic Disease, Tuberous sclerosis is a rare genetic Disease, TUBEROUS SCLEROSIS 1 (disorder)-TUBEROUS SCLEROSIS 2 (disorder) complex location (TSC) is a genetic Disease, TUBEROUS SCLEROSIS 1 (disorder)-TUBEROUS SCLEROSIS 2 (disorder) complex location (TSC) is a genetic Disease caused by Mutation Abnormality in either TUBEROUS SCLEROSIS 1 (disorder) or TUBEROUS SCLEROSIS 2 (disorder)., TUBEROUS SCLEROSIS 1 (disorder)-TUBEROUS SCLEROSIS 2 (disorder) complex location (TSC) is a genetic Disease caused by Gene Mutation in either TUBEROUS SCLEROSIS 1 (disorder) or TUBEROUS SCLEROSIS 2 (disorder) tumor suppressor Genes., Mutation in either the TUBEROUS SCLEROSIS 1 (disorder) or TUBEROUS SCLEROSIS 2 (disorder) Tumor Suppressor Genes is responsible for the inherited genetic Disease of Tuberous Sclerosis., Tuberous sclerosis (TSC) is a frequent Autosome-dominant condition (affecting 1 in 6000 individuals) caused by various Gene Mutation in either the Tuberous Sclerosis 1 protein (TUBEROUS SCLEROSIS 1 (disorder)) or the tuberin gene (TUBEROUS SCLEROSIS 2 (disorder))., Tuberous sclerosis is a rare genetic Disease, Tuberous sclerosis (TS) is a genetic Disease with prominent cutaneous and Head>Brain involvement , TSC was recognized to be a genetic Disease with Autosomal dominant inheritance, On average TSC families are very small; in most cases there are fewer than two informative meioses. The size distribution of Chromosomes, Human, Pair 9 linked families was similar to that of non-linked families., The effects of missense changes and small in-frame deletions and Clinical act of insertion on protein function are not easy to predict, and the identification of such Variant in individuals at risk of a genetic Disease can complicate genetic counselling. One option is to perform functional tests to assess whether the Variant affect protein function. We have used this strategy to characterize Variant identified in the TUBEROUS SCLEROSIS 1 (disorder) and TUBEROUS SCLEROSIS 2 (disorder) Genes in individuals with, or suspected of having, Tuberous Sclerosis Complex (TSC)., Tuberous sclerosis is a dominant hereditary Disease, Many of these advances originated from studies of the genetic Disease Tuberous Sclerosis (TSC)[SEP]Relations: tuberous sclerosis has relations: disease_disease with genetic nervous system disorder, disease_disease with genetic nervous system disorder, disease_disease with genetic nervous system disorder, disease_disease with genetic nervous system disorder, disease_disease with genetic nervous system disorder, disease_disease with genetic nervous system disorder, disease_disease with genetic nervous system disorder, disease_disease with genetic nervous system disorder, disease_disease with inherited neurodegenerative disorder, disease_disease with inherited neurodegenerative disorder.", "label": "yes"}
{"original_question": "Are Gram positive bacteria able to release extracellular vesicles?", "id": "converted_4120", "sentence1": "Are Gram positive Bacteria able to release Extracellular Vesicles?", "sentence2": "Gram-negative and Gram-positive Bacteria release a variety of membrane vesicles through different formation routes. , Release of Extracellular Vesicles (NCI Enterprise Vocabulary Services) is a common feature among Eukaryota, Archaea, and Bacteria. However, the biogenesis and downstream biological effects of NCI Enterprise Vocabulary Services released from gram-positive Bacteria remain poorly characterized.,  Our findings provide new insight into the role of NCI Enterprise Vocabulary Services from gram-positive oral Bacteria in periodontal diseases.[SEP]Relations: extracellular vesicle has relations: cellcomp_protein with GRIA4, cellcomp_protein with GRIA4, cellcomp_protein with PRELP, cellcomp_protein with PRELP, cellcomp_protein with RBP3, cellcomp_protein with RBP3, cellcomp_protein with LFNG, cellcomp_protein with LFNG, cellcomp_protein with ARC, cellcomp_protein with ARC.", "label": "yes"}
{"original_question": "Does melanoma  occur in people of African origin ?", "id": "converted_462", "sentence1": "Does Melanocytic neoplasm  occur in people of African origin ?", "sentence2": "ALM is the most common type of Melanocytic neoplasm amongst Asians, African People,, ALM develops on palmar, Plantar - anatomical location, and subungual Skin Specimen Source Code, and its biology is different from that of other cutaneous melanomas, where sunlight is the major known environmental determinant, We present four albinos with histologic diagnoses of Malignant neoplasm of Skin Specimen Source Code, Four Nigerian albinos (two men and two women) with Malignant neoplasm of Skin Specimen Source Code, The Site of the Lesion included the head [Anal Anal squamous cell carcinoma (sodium copper chlorophyllin) in two patients and Skin Basal Cell Carcinoma (Basal cell carcinoma) in one patient] and the upper limb (Melanocytic neoplasm, wenty-nine patients (18 males and 11 females) with Malignant neoplasm of Skin Specimen Source Code were identified, Kaposi Sarcoma associated with HIV Infections Infections represented 81.8 percent of KS cases found. Squamous cell carcinoma (sodium copper chlorophyllin) ranked second and malignant Melanocytic neoplasm third, Earlier studies have shown frequent Gene Mutation in the BRAF protein, human protein, human and Human Oncogene N-RAS genes in Cutaneous Melanoma, but these alterations have not been examined in the rare category of Melanocytic neoplasm from black African People., In a series of melanomas from black African People (n=26), only two BRAF protein, human protein, human Gene Mutation (8%) were found, both being different from the common T1799A substitution. Moreover, melanomas from black African People exhibited Gene Mutation in Human Oncogene N-RAS exon 1 only (12%), whereas Human Oncogene N-RAS exon 2 Gene Mutation were predominant in melanomas from Caucasians. Thus, the frequencies of BRAF protein, human protein, human and Human Oncogene N-RAS Gene Mutation were particularly low in melanomas from black African People, supporting a different pathogenesis of these Neoplasms., Malignant Melanocytic neoplasm (Millimole per Liter) remains a pediatric rarity world-wide, but perhaps more so in black African People. To the best of our knowledge, the current report of Millimole per Liter in a two-and-a-half-year-old Nigerian who had a pre-existing congenital giant hairy nevus is probably the first (in an accessible literature) in a black African child., Malignant melanomas in black African People are predominantly located on the lower All All extremities, Thus, our findings indicate that melanomas located on the lower All All extremities in black African People show several features of Aggressive behavior; in particular, the proliferative activity was high, and p16 alterations was frequent as evidenced by loss of protein staining. Our findings also indicated that the diagnosis is delayed among black African People., African People with dark Skin Specimen Source Code have a reduced risk of getting all types of Malignant neoplasm of Skin Specimen Source Code as compared with Caucasians, but the ratio of their incidence rates of cutaneous malignant Melanocytic neoplasm to that of Anal Anal squamous cell carcinoma is larger than the corresponding ratio for Caucasians. (, Albino African People, as compared with normally Pigmented African People, seem to have a relatively small risk of getting Cutaneous Melanoma compared to nonmelanomas. This is probably also true for albino and normally Pigmented Caucasians., Scant data exists on Melanocytic neoplasm in Black Populations from Africa, The mean age at presentation of the 39 women and 24 men was 60.5 years (range of 30 to 85 years), with a peak incidence in the sixth decade. The Lower extremity>Foot was the most common site of disease (45 patients). Seven patients had subungual Melanocytic neoplasm, seven had primary Mucosal Lesion, and in six, the Primary Lesion could not be found., The poor prognosis in black patients in South Africa is the result of delayed presentation with thick primary Lesion and advanced disease, The outcome of treatment in 40 black patients (27 women, 13 men; mean age 62.9 years) with Plantar - anatomical location Melanocytic neoplasm over a 13-year period was analysed, Delay in presentation and locally advanced disease may explain the poor prognosis of Plantar - anatomical location Melanocytic neoplasm in black South African People., Eighteen cases of malignant Skin Specimen Source Code Neoplasms seen at the University of Port Harcourt Teaching Hospital over 3 years (1984 to 1987) were analyzed for diagnoses, site of Neoplasms, sex, and age. Seven patients (39%) had Melanocytic neoplasm affecting only the Sole of Foot of the feet, while the same number had Squamous cell carcinoma of mouth widely distributed in various parts of the body, Non-white populations experienced in general a much lower incidence of Melanocytic neoplasm although there was some overlap of white and non-white rates., Populations of African descent were found to have a higher incidence than those of Asiatic origin, but it was concluded that this was due largely to the high frequency of tumours among African People on the sole of the Lower extremity>Foot., Pathological features of twenty-one cases of malignant Melanocytic neoplasm studied in the University of Nigeria Teaching Hospital, Enugu during the period January, 1974 to December, 1975 are presented. Malignant Melanocytic neoplasm accounted for 2.4% of all tumours and 4.5% of all malignant tumours, greatest age incidence being in the fifth to seventh decades., 81% melanomas occurred on the sole of feet validating the hypothesis that the Pigmented Skin Specimen Source Code in African People is resistant to malignant Melanocytic neoplasm., This paper reports the incidence of this lesion in association with invasive Melanocytic neoplasm of the feet and hands of Black African People., Follow-up data (over a 3-year period) and the histological appearances of Primary Lesion were studied and related in 40 Black patients with malignant Melanocytic neoplasm., Malignant Melanocytic neoplasm of the Skin Specimen Source Code in Blacks in formidable and sinister tumour., The incidence of malignant Melanocytic neoplasm in Johannesburg Black was 1,2 per 100 000 and accounted for 2% of all Malignant Neoplasms. The largest number of cases occurred in the 50- 70-year age group and there was a female preponderance. As in previous studies, the Site predominantly affected were the Lower extremity>Foot and the hand, mainly on the Plantar - anatomical location and palmar surfaces., Twenty-one cases of malignant Melanocytic neoplasm occurring in the Igbos of Nigeria have been analysed. The site of predilection is the sole of the Lower extremity>Foot. This result supports the conclusion that Negroes tend to have the disease in the non-Pigmented parts., A case of leptomeningeal Melanocytic neoplasm in an African child of 7 years is presented together with a survey of pigmentation in the normal African Head>Brain.[SEP]Relations: Melanocytic neoplasm has relations: disease_disease with melanomatosis, disease_disease with melanomatosis, disease_disease with familial Melanocytic neoplasm, disease_disease with familial Melanocytic neoplasm, disease_disease with childhood malignant Melanocytic neoplasm, disease_disease with childhood malignant Melanocytic neoplasm, disease_disease with Malignant neoplasm of Skin Specimen Source Code, disease_disease with Malignant neoplasm of Skin Specimen Source Code, disease_disease with amelanotic Skin Specimen Source Code Melanocytic neoplasm, disease_disease with amelanotic Skin Specimen Source Code Melanocytic neoplasm.", "label": "yes"}
{"original_question": "Is Figitumumab effective for non-small cell lung cancer?", "id": "converted_3348", "sentence1": "Is Figitumumab effective for non-small cell lung cancer?", "sentence2": "A phase III study failed for carboplatin, paclitaxel, with or without figitumumab in first-line treating metastatic non-small cell lung cancer (Non-Small Cell Lung Carcinoma)., CONCLUSION: Adding figitumumab to standard chemotherapy failed to increase OS in patients with advanced nonadenocarcinoma Non-Small Cell Lung Carcinoma., Median OS was 8.6 months for figitumumab plus chemotherapy and 9.8 months for chemotherapy alone (hazard ratio [HR], 1.18; 95% CI, 0.99 to 1.40; P = .06); median progression-free survival was 4.7 months (95% CI, 4.2 to 5.4) and 4.6 months (95% CI, 4.2 to 5.4), respectively (HR, 1.10; P = .27); the objective response rates were 33% and 35%, respectively. , Phase III trials of the anti-insulin-like growth factor-1 receptor (IGF1R) antibody figitumumab in non-small cell lung cancer (Non-Small Cell Lung Carcinoma) patients have been discontinued owing to lack of survival benefit., Two phase III trials of the anti-IGF1R protein, human monoclonal antibody, figitumumab (CP 751871), were discontinued in 2010 as it was considered unlikely either trial would meet their primary endpoints. In light of disappointing clinical data with figitumumab and other targeted agents, it is likely that the use of molecular markers will become important in predicting response to treatment. , Phase III trials of the anti-insulin-like growth factor-1 receptor ( IGF1R ) antibody figitumumab in non-small cell lung cancer ( Non-Small Cell Lung Carcinoma ) patients have been discontinued owing to lack of survival benefit . , Phase III trials of the anti-insulin-like growth factor type 1 receptor ( IGF-IR ) antibody figitumumab ( F ) in unselected non-small-cell lung cancer ( Non-Small Cell Lung Carcinoma ) patients were recently discontinued owing to futility . , One recent phase III trial of the IGF1R protein, human inhibitor figitumumab in patients with non-small-cell lung cancer was discontinued after an interim analysis showed no survival improvement . , The Insulin-Like Growth Factor Receptor ( IGF1R protein, human ) monoclonal antibody figitumumab , while initially promising , appears to increase Toxic effect and Cessation of life in combination with chemotherapy in the treatment of patients with Non-Small Cell Lung Carcinoma of Squamous histology; therefore , clinical development of this class of agents will need to proceed with caution . , Two phase III trials of the anti-IGF1R protein, human monoclonal antibody , figitumumab ( CP 751871) , were discontinued in 2010 as it was considered unlikely either trial would meet their primary endpoints . , A phase III study failed for carboplatin , paclitaxel , with or without figitumumab in first-line treating metastatic non-small cell lung cancer ( Non-Small Cell Lung Carcinoma) . , Median OS was 8.6 months for figitumumab plus chemotherapy and 9.8 months for chemotherapy alone (hazard ratio [HR], 1.18; 95% CI, 0.99 to 1.40; P = .06); median progression-free survival was 4.7 months (95% CI, 4.2 to 5.4) and 4.6 months (95% CI, 4.2 to 5.4), respectively (HR, 1.10; P = .27); the objective response rates were 33% and 35%, respectively.[SEP]Relations: Figitumumab has relations: drug_drug with Necitumumab, drug_drug with Necitumumab, drug_drug with Inebilizumab, drug_drug with Inebilizumab, drug_drug with Concizumab, drug_drug with Concizumab, drug_drug with Catumaxomab, drug_drug with Catumaxomab, drug_drug with Tositumomab, drug_drug with Tositumomab.", "label": "no"}
{"original_question": "Does natalizumab improve disease course of secondary progressive multiple sclerosis?", "id": "converted_3380", "sentence1": "Does natalizumab improve disease course of secondary progressive Multiple Sclerosis?", "sentence2": "INTERPRETATION: Natalizumab treatment for secondary progressive Multiple Sclerosis did not reduce progression on the primary multicomponent disability endpoint in part 1, but it did reduce progression on its upper-limb component., In this review, we summarize the pathophysiological mechanisms involved in the development of SPMS and the rationale and clinical potential for natalizumab, which is currently approved for the treatment of relapsing forms of MS, to exert beneficial effects in reducing disease progression unrelated to relapses in SPMS. , INTERPRETATION\n\nNatalizumab treatment for secondary progressive Multiple Sclerosis did not reduce progression on the primary multicomponent disability endpoint in part 1, but it did reduce progression on its upper-limb component., Natalizumab did not achieve a statistically significant primary composite disability outcome in a trial of 887 patients with secondary progressive MS , but it did demonstrate a benefit on a prespecified component of the 9-Hole Peg Test . , INTERPRETATION\nNatalizumab treatment for secondary progressive Multiple Sclerosis did not reduce progression on the primary multicomponent disability endpoint in part 1, but it did reduce progression on its upper-limb component., In this review, we summarize the pathophysiological mechanisms involved in the development of SPMS and the rationale and clinical potential for natalizumab, which is currently approved for the treatment of relapsing forms of MS, to exert beneficial effects in reducing disease progression unrelated to relapses in SPMS., Natalizumab treatment for secondary progressive Multiple Sclerosis did not reduce progression on the primary multicomponent disability endpoint in part 1, but it did reduce progression on its upper-limb component.[SEP]Relations: Multiple Sclerosis has relations: disease_disease with progressive Multiple Sclerosis, disease_disease with progressive Multiple Sclerosis. Natalizumab has relations: contraindication with progressive multifocal leukoencephalopathy, contraindication with progressive multifocal leukoencephalopathy, drug_drug with Pexelizumab, drug_drug with Pexelizumab, drug_drug with Bavituximab, drug_drug with Bavituximab, drug_drug with Otelixizumab, drug_drug with Otelixizumab.", "label": "no"}
{"original_question": "SGOT is an abbreviation for an enzyme other wise known as alanine amino transferase, yes or no?", "id": "converted_2420", "sentence1": "SGOT - Glutamate oxaloacetate transaminase is an abbreviation for an enzyme other wise known as D-Alanine Transaminase, yes or no?", "sentence2": "patients with aspartate amino transferase (SGOT - Glutamate oxaloacetate transaminase - Glutamate oxaloacetate transaminase), D-Alanine Transaminase (SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase),, Alanine amino transferase (SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase), , Aspartate Transaminase (AST-SGOT - Glutamate oxaloacetate transaminase - Glutamate oxaloacetate transaminase), alanine amino-transferase (ALT-SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase), Mean values of Glutamate Dehydrogenase (glucose-6-phosphate dehydrogenase activity), serum aspartate and alanine transferase (SGOT - Glutamate oxaloacetate transaminase - Glutamate oxaloacetate transaminase and SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase), ORNITHINE CARBAMOYLTRANSFERASE (OCT), and gamma-glutamyltranspeptidase (gamma-GTP) tended to rise with increasing Hepatocyte necrosis, though values of SGOT - Glutamate oxaloacetate transaminase - Glutamate oxaloacetate transaminase, SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase, OCT, and gamma-GTP showed considerable overlap between the 32 patients with histologically proved Hepatitis and the 68 without., Serum Aspartate Transaminase (SGOT - Glutamate oxaloacetate transaminase - Glutamate oxaloacetate transaminase), Alanine Transaminase (SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase), Creatine Kinase (PIK3C2A gene), and butyric acid dehydrogenase (BDH1 gene) were determined in 94 patients before, 1(1/2) hours, and 24 hours after cardioversion., The study excluded by screening for AntiHCV, Hepatitis B Antigen Vaccine and patients with aspartate amino transferase (SGOT - Glutamate oxaloacetate transaminase - Glutamate oxaloacetate transaminase), D-Alanine Transaminase (SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase), Gamma-glutamyl transferase levels more than three times the normal and subject with a total Antigens, CD5 count more than 10,000/microl., Complete blood picture, differential Antigens, CD5 count, and serum levels of Estrogen [EPC] [EPC], Alanine amino transferase (SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase), Aspartate amino transferase (SGOT - Glutamate oxaloacetate transaminase - Glutamate oxaloacetate transaminase), total protein and ALB gene were estimated.[SEP]Relations: glutamate pyruvate transaminase 2 deficiency has relations: disease_protein with GPT2, disease_protein with GPT2, disease_disease with syndromic intellectual disability, disease_disease with syndromic intellectual disability, disease_phenotype_positive with Nasogastric tube feeding in infancy, disease_phenotype_positive with Nasogastric tube feeding in infancy, disease_phenotype_positive with Broad-based gait, disease_phenotype_positive with Broad-based gait, disease_phenotype_positive with Absent speech, disease_phenotype_positive with Absent speech.", "label": "no"}
{"original_question": "Is davunetide being considered for the treatment of progressive supranuclear palsy?", "id": "converted_2271", "sentence1": "Is davunetide being considered for the treatment of progressive supranuclear palsy?", "sentence2": "Critical appraisal of the role of davunetide in the treatment of progressive supranuclear palsy., Davunetide's efficacy and tolerability are being tested in a placebo-controlled study in Progressive supranuclear palsy patients, making it the most advanced drug candidate in this indication. This review examines the disease characteristics of Progressive supranuclear palsy, the rationale for treating Progressive supranuclear palsy with davunetide and assesses some of the challenges of clinical trials in this patient population.[SEP]Relations: progressive supranuclear palsy has relations: disease_phenotype_positive with Parkinsonism with favorable response to dopaminergic medication, disease_phenotype_positive with Parkinsonism with favorable response to dopaminergic medication, disease_disease with supranuclear oculomotor palsy, disease_disease with supranuclear oculomotor palsy, disease_disease with syndromic disease, disease_disease with syndromic disease, disease_phenotype_positive with Neuromuscular dysphagia, disease_phenotype_positive with Neuromuscular dysphagia, disease_phenotype_positive with Retrocollis, disease_phenotype_positive with Retrocollis.", "label": "yes"}
{"original_question": "Can Panitumumab cause trichomegaly?", "id": "converted_4131", "sentence1": "Can Panitumumab cause Trichomegaly?", "sentence2": "Xerosis was present in two cases, and Paronychia <plant>, pyogenic granuloma, Trichomegaly, and Madarosis of eyelid were observed in one patient each. , Eyelash Trichomegaly is an uncommon drug-associated sequelae experienced during treatment with epidermal growth factor receptor (Epidermal Growth Factor Receptor) inhibitors. Elongation of the Eyelash induced by these agents has predominantly been observed in oncology patients with either colorectal or Primary malignant neoplasm of lung. It is most frequently associated with cetuximab and erlotinib; however, it has also been described in individuals treated with gefitinib or panitumumab. , Trichomegaly of the Eyelash during therapy with Epidermal growth factor receptor inhibitor:  report of 3 cases., Trichomegaly of the Eyelash is a rare adverse effect of Epidermal Growth Factor Receptor inhibitor therapy and is characterized by a paradoxical overgrowth of Eyelash.[SEP]Relations: Panitumumab has relations: drug_drug with Tregalizumab, drug_drug with Tregalizumab, drug_drug with Pertuzumab, drug_drug with Pertuzumab, drug_drug with Sonepcizumab, drug_drug with Sonepcizumab, drug_drug with Concizumab, drug_drug with Concizumab, drug_drug with Eculizumab, drug_drug with Eculizumab.", "label": "yes"}
{"original_question": "Are thyroid hormone receptor alpha1 mutations implicated in thyroid hormone resistance syndrome?", "id": "converted_191", "sentence1": "Are thyroid hormone receptor alpha1 mutations implicated in thyroid hormone resistance syndrome?", "sentence2": "This study reports the consequences of levothyroxine treatment over a prolonged period of time in 2 of the first patients with a heterozygous Mutation Abnormality in TRα1., Here we show that the dysregulation of the pituitary-thyroid axis was worsened by the lack of Tricuspid Valve Insufficiency alpha1 in Tricuspid Valve Insufficiency betaPV CASP14 gene, and severe impairment of postnatal growth was manifested in Tricuspid Valve Insufficiency betaPV CASP14 gene deficient in Tricuspid Valve Insufficiency alpha1., Heterozygous 2- to 3-week- old CASP14 gene exhibit a severe retardation of post-natal development and growth, but only a minor reduction in serum thyroxine levels. , The data demonstrate a novel array of effects mediated by a dominant negative TRalpha1, and may provide important clues for identification of a potentially unrecognized human disorder and its treatment., No mutations in DNA- and hormone-binding-domains of TRbeta1 and TRalpha1 genes were found in proband, suggesting that the defect could be due to an unknown Mutation Abnormality in either the Tricuspid Valve Insufficiency gene or a post receptor abnormality, These results demonstrate that the lack of Tricuspid Valve Insufficiency alpha1 exacerbates the manifestation of RTH in Tricuspid Valve Insufficiency betaPV CASP14 gene. Therefore, Tricuspid Valve Insufficiency alpha1 could play a compensatory role in mediating the functions of T3 thoracic segmental innervation thoracic segmental innervation in heterozygous patients with RTH. [SEP]Relations: Levothyroxine has relations: contraindication with isolated congenital growth hormone deficiency, contraindication with isolated congenital growth hormone deficiency, contraindication with thyroid crisis (disease), contraindication with thyroid crisis (disease), contraindication with acquired pituitary hormone deficiency, contraindication with acquired pituitary hormone deficiency, contraindication with non-acquired pituitary hormone deficiency, contraindication with non-acquired pituitary hormone deficiency, contraindication with combined pituitary hormone deficiencies, genetic form, contraindication with combined pituitary hormone deficiencies, genetic form.", "label": "yes"}
{"original_question": "Are microtubules marked by glutamylation?", "id": "converted_1745", "sentence1": "Are Microtubules marked by glutamylation?", "sentence2": "Together with detyrosination, glutamylation and other modifications, Tubulin acetylation may form a unique 'language' to regulate microtubule structure and function., Glutamylation, the most prevalent Tubulin posttranslational modification, marks stable Microtubules and regulates recruitment and activity of microtubule- interacting proteins., ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS of the Tubulin tyrosine ligase-like (TTLL) family posttranslationally modify and thereby mark Microtubules by glutamylation, generating specific recognition sites for microtubule-interacting proteins.,  PTMs of the Microtubules associated with cytoplasmic filaments, including phosphorylation, glycosylation, ubiquitination, detyrosination/tyrosination, (poly)glutamylation and (poly)glycylation, acetylation, sumoylation, and palmitoylation, will be addressed in this chapter., The Tubulin posttranslational modifications: acetylation, detyrosination, polyglutamylation, and polyglycylation play important roles in microtubule functions, In most Eukaryotic Cells, Tubulin is subjected to posttranslational glutamylation, a conserved modification of unclear function.[SEP]Relations: microtubule has relations: cellcomp_protein with KIFC1, cellcomp_protein with KIFC1, cellcomp_protein with INCENP, cellcomp_protein with INCENP, cellcomp_protein with KIFC3, cellcomp_protein with KIFC3, cellcomp_protein with KLC3, cellcomp_protein with KLC3, cellcomp_protein with KLC1, cellcomp_protein with KLC1.", "label": "yes"}
{"original_question": "Is golimumab effective for ulcerative colitis?", "id": "converted_1971", "sentence1": "Is golimumab effective for ulcerative colitis?", "sentence2": "Initial experience with golimumab in clinical practice for ulcerative colitis., BACKGROUND: golimumab is a Recombinant Tumor Necrosis Factor Family Protein-blocking agent indicated as a second-line therapy in ulcerative colitis., CONCLUSIONS: In this short study, golimumab seems to be an alternative treatment in naive and non-naive anti-Recombinant Tumor Necrosis Factor Family Protein ulcerative colitis patients., Cost-Effectiveness Analysis of 1-Year Treatment with golimumab/Standard Care and Standard Care Alone for Ulcerative Colitis in Poland., OBJECTIVE: The objective of this study was to assess the cost-effectiveness of induction and maintenance treatment up to 1 year of ulcerative colitis with golimumab/standard care and standard care alone in Poland., CONCLUSIONS: The biologic treatment of ulcerative colitis patients with golimumab/standard care is more effective but also more costly compared with standard care alone., Currently, infliximab, adalimumab, and golimumab are available in the East Asian medical market, and these agents have been shown to be effective for inducing and maintaining long-term remission of Irritable Bowel Syndrome., Furthermore, upcoming treatments are introduced, such as golimumab, vedolizumab, AJM300, tofacitinib., CONCLUSIONS: No significant differences in efficacy in the maintenance phase between infliximab and golimumab or adalimumab were revealed. Infliximab proved to be more effective than adalimumab but of similar efficacy to that of golimumab in the induction phase., In this review, we will provide a detailed discussion of the three Tumor Necrosis Factor-alpha-alpha (Recombinant Tumor Necrosis Factor Family Protein-α) inhibitors currently approved for treatment of ulcerative colitis: infliximab, adalimumab, and golimumab., golimumab, a Homo sapiens anti-Recombinant Tumor Necrosis Factor Family Protein antibody, is effective in patients with ulcerative colitis, according to new findings from an international phase III double-blind trial., golimumab for moderately to severely active ulcerative colitis., Subcutaneous golimumab maintains clinical response in patients with moderate-to-severe ulcerative colitis., Subcutaneous golimumab induces clinical response and remission in patients with moderate-to-severe ulcerative colitis., Subcutaneous golimumab, a fully Homo sapiens monoclonal antibody to Tumor Necrosis Factor-alpha-α (TNFα), was evaluated as maintenance therapy in TNFα antagonist-naive adults with moderate-to-severe active ulcerative colitis, despite conventional therapy, who responded to golimumab induction therapy.We performed a phase 3, double-blind trial of patients who completed golimumab induction trials (Program of Ulcerative Colitis Research Studies Utilizing an Investigational Treatment, eg, PURSUIT), golimumab, a Homo sapiens anti-Recombinant Tumor Necrosis Factor Family Protein antibody, is effective in patients with ulcerative colitis, according to new findings from an international phase III double-blind trial, The purpose of this review was to describe the management of ulcerative colitis with emphasis on the use of anti-Tumor Necrosis Factor-alpha (Recombinant Tumor Necrosis Factor Family Protein) agents.Recent research has shown that new anti-Recombinant Tumor Necrosis Factor Family Protein agents, adalimumab (acetaldehyde dehydrogenase (acetylating) activity) and golimumab, are effective in induction of remission and maintenance of remission in patients with extensive ulcerative colitis, vedolizumab and golimumab occurred more effective, and comparably as safe as placebo in patients with active moderate to severe ulcerative colitis increasing the number of available therapeutic options, The required sample sizes for direct head-to-head trials between infliximab and adalimumab for induction and maintenance are 174 and 204 subjects respectively.This study demonstrates that, compared to placebo, infliximab, adalimumab and golimumab are all effective for the induction and maintenance of remission in ulcerative colitis, The biosimilar of infliximab is as effective and as safe as its originator in rheumatologic conditions, while a new anti-Recombinant Tumor Necrosis Factor Family Protein agent, namely golimumab, has been recently approved for refractory ulcerative colitis, We evaluated subcutaneous golimumab induction therapy in Recombinant Tumor Necrosis Factor Family Protein-α antagonist-naïve patients with moderate-to-severe UC despite conventional treatment. , vedolizumab and golimumab occurred more effective, and comparably as safe as placebo in patients with active moderate to severe ulcerative colitis increasing the number of available therapeutic options., The purpose of this review was to describe the management of ulcerative colitis with emphasis on the use of anti-Tumor Necrosis Factor-alpha (Recombinant Tumor Necrosis Factor Family Protein) agents.Recent research has shown that new anti-Recombinant Tumor Necrosis Factor Family Protein agents, adalimumab (acetaldehyde dehydrogenase (acetylating) activity) and golimumab, are effective in induction of remission and maintenance of remission in patients with extensive ulcerative colitis., vedolizumab and golimumab occurred more effective, and comparably as safe as placebo in patients with active moderate to severe ulcerative colitis increasing the number of available therapeutic options., The biosimilar of infliximab is as effective and as safe as its originator in rheumatologic conditions, while a new anti-Recombinant Tumor Necrosis Factor Family Protein agent, namely golimumab, has been recently approved for refractory ulcerative colitis., The incremental cost-utility ratio of golimumab/standard care compared to the standard care alone is estimated to be 391,252 PLN/QALY gained (93,155 €/QALYG) from public payer perspective and 374,377 PLN/QALY gained (89,137 €/QALYG) from social perspective.The biologic treatment of ulcerative colitis patients with golimumab/standard care is more effective but also more costly compared with standard care alone., The required sample sizes for direct head-to-head trials between infliximab and adalimumab for induction and maintenance are 174 and 204 subjects respectively.This study demonstrates that, compared to placebo, infliximab, adalimumab and golimumab are all effective for the induction and maintenance of remission in ulcerative colitis., Recently, 2 new Antibodies, in vitro diagnostic have been approved: golimumab is a new option for ulcerative colitis and with another more selective mechanism of action; vedolizumab could be useful for ulcerative colitis as well as Crohn's disease of oral soft tissues of oral soft tissues., The present review summarizes the literature on the role of golimumab, a new anti Recombinant Tumor Necrosis Factor Family Protein agent, in ulcerative colitis.Literature search was done on PubMed using the search terms 'golimumab' AND 'ulcerative colitis' from inception till March 2016., The aim of this systematic review was to evaluate the efficacy and safety of biological agents (vedolizumab, abatacept, visilizumab, golimumab) in patients with active moderate to severe ulcerative colitis.This paper was prepared according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines., vedolizumab and golimumab occurred more effective, and comparably as safe as placebo in patients with active moderate to severe ulcerative colitis increasing the number of available therapeutic options., BACKGROUND & AIMS: Subcutaneous golimumab, a fully Homo sapiens monoclonal antibody to Tumor Necrosis Factor-alpha-á (TNFá), was evaluated as maintenance therapy in TNFá antagonist-naive adults with moderate-to-severe active ulcerative colitis, despite conventional therapy, who responded to golimumab induction therapy.METHODS: We performed a phase 3, double-blind trial of patients who completed golimumab induction trials (Program of Ulcerative Colitis Research Studies Utilizing an Investigational Treatment, eg, PURSUIT)., BACKGROUND & AIMS: Little is known about the efficacy of golimumab, a fully Homo sapiens monoclonal antibody to Tumor Necrosis Factor-alpha (Recombinant Tumor Necrosis Factor Family Protein) -á, for treatment of ulcerative colitis (UC)., This study demonstrates that, compared to placebo, infliximab, adalimumab and golimumab are all effective for the induction and maintenance of remission in ulcerative colitis., vedolizumab and golimumab occurred more effective, and comparably as safe as placebo in patients with active moderate to severe ulcerative colitis increasing the number of available therapeutic options.., Recent research has shown that new anti-Recombinant Tumor Necrosis Factor Family Protein agents, adalimumab (acetaldehyde dehydrogenase (acetylating) activity) and golimumab, are effective in induction of remission and maintenance of remission in patients with extensive ulcerative colitis., golimumab for moderately to severely active ulcerative colitis., Initial experience with golimumab in clinical practice for ulcerative colitis., golimumab was found to be effective and safe in inducing and maintaining clinical remission, clinical response and mucosal healing in patients with UC in the two registration trials., [golimumab Therapy in Ulcerative Colitis]., golimumab: clinical update on its use for ulcerative colitis., This review will focus on golimumab therapy in ulcerative colitis., To assess golimumab pharmacokinetics [Pyruvate Kinase] and exposure-response [Endoplasmic Reticulum] in adults with moderate-to-severe ulcerative colitis [UC] from the Program of Ulcerative Colitis Research Studies Utilizing an Investigational Treatment [PURSUIT] studies.[SEP]Relations: golimumab has relations: drug_drug with Eculizumab, drug_drug with Eculizumab, drug_drug with Ibalizumab, drug_drug with Ibalizumab, drug_drug with Otelixizumab, drug_drug with Otelixizumab, drug_drug with Urelumab, drug_drug with Urelumab, drug_drug with Antipyrine, drug_drug with Antipyrine.", "label": "yes"}
{"original_question": "Are stretch enhancers transcribed more than super-enhancers?", "id": "converted_3503", "sentence1": "Are stretch enhancers transcribed more than super-enhancers?", "sentence2": "Super-enhancers are transcriptionally more active and cell type-specific than stretch enhancers., We found that stretch enhancers are more abundant, more distal to transcription start sites, cover twice as much the Genome - anatomical entity, and are significantly less conserved than super-enhancers. In contrast, super-enhancers are significantly more enriched for active chromatin marks and cohesin complex, and more transcriptionally active than stretch enhancers. Importantly, a vast majority of super-enhancers (85%) overlap with only a small subset of stretch enhancers (13%), which are enriched for cell type-specific biological functions, and control cell identity genes. These results suggest that super-enhancers are transcriptionally more active and cell type-specific than stretch enhancers, and importantly, most of the stretch enhancers that are distinct from super-enhancers do not show an association with cell identity genes, are less active, and more likely to be poised enhancers., These results suggest that super-enhancers are transcriptionally more active and cell type-specific than stretch enhancers, and importantly, most of the stretch enhancers that are distinct from super-enhancers do not show an association with cell identity genes, are less active, and more likely to be poised enhancers.[SEP]Relations: cohesin complex has relations: cellcomp_protein with STAG2, cellcomp_protein with STAG2, cellcomp_protein with RAD21, cellcomp_protein with RAD21, cellcomp_protein with STAG1, cellcomp_protein with STAG1, cellcomp_protein with SMC1A, cellcomp_protein with SMC1A, cellcomp_protein with SMC1B, cellcomp_protein with SMC1B.", "label": "no"}
{"original_question": "Does radiotherapy for prostate cancer increase bladder cancer risk?", "id": "converted_3704", "sentence1": "Does radiotherapy for Malignant neoplasm of prostate increase Urinary Bladder cancer risk?", "sentence2": "External Beam Radiotherapy Increases the Risk of Malignant neoplasm of urinary Urinary Bladder When Compared with Radical Prostatectomy in Patients Affected by Prostate Cancer: A Population-based Analysis., On multivariable competing risk regression analyses, treatment with External Beam Radiation Therapy was independently associated with the risk of developing a second primary BCa (hazard ratio: 1.35, CI: 1.18-1.55; p<0.001), but not RCa (p=0.4). , CONCLUSIONS: Patients treated with External Beam Radiation Therapy are at increased risk of developing a second primary BCa compared with those treated with RP. However, no differences were found considering RCa incidence in patients treated with RP or External Beam Radiation Therapy within the first 5 yr after primary therapy. , We found that those treated with external beam radiotherapy are at an increased risk of developing a second primary Urinary Bladder cancer tumor., All radiation modalities were found to have an increased RR of developing BlCa after 10 years, with brachytherapy having a significantly higher RR than external beam radiation (External Beam Radiation Therapy) or combined External Beam Radiation Therapy and brachytherapy in Caucasian men and a significantly higher RR than External Beam Radiation Therapy in men of other/unknown ethnicity. , CONCLUSIONS: The increased risk of BlCa after prostate radiation occurs predominantly after 10 years, regardless of ethnicity. The RR of developing BlCa after 10 years is significantly higher following brachytherapy than after External Beam Radiation Therapy or External Beam Radiation Therapy and brachytherapy. , Based on the data in the literature, there is a consistently increased risk of Urinary Bladder cancer (HR: 1.67, 95% CI 1.55-1.80), Rectal Carcinoma (HR: 1.79, 95% CI 1.34-2.38), and Malignant neoplasm of Abdomen+Pelvis>Colon and/or Pelvis>Rectum (HR: 1.79, 95% CI 1.34-23.8) following percutaneous radiation therapy. Following brachytherapy only an increased for the development of Urinary Bladder cancer (HR: 2.14, 95% CI 1.03-3.94) has been observed., When comparing with a matched general French population, the standard incidence ratio (SIR) for Urinary Bladder cancer was 1.02 (95% CI: 0.46-1.93)., LDR resulted in lower Urinary Bladder cancer risks than double-strand break repair via homologous recombination, and lower or similar risks of Rectal Carcinoma., Compared to external beam techniques, second rectal and Urinary Bladder cancer risks were lowest for brachytherapy., OBJECTIVE: Although it is well known that radiotherapy for Malignant neoplasm of prostate increases comorbid rate of secondary Urinary Bladder cancer, the effect of aging and Location characteristic ID - Smoking with radiotherapy on incidence rate of secondary Urinary Bladder cancer remains unknown. , RESULTS: During the median follow-up period of 4.3 and 3.1 years, secondary Urinary Bladder cancer occurred in 11 (3.4%) and 5 (1.1%) of patients with Malignant neoplasm of prostate treated with external beam radiotherapy and radical prostatectomy, respectively. , CONCLUSIONS\n\nMultiple Endocrine Neoplasia who receive radiotherapy for localized Malignant neoplasm of prostate have an increased risk of Urinary Bladder cancer compared to patients undergoing radical prostatectomy and compared to the general population., Radiation therapy for Malignant neoplasm of prostate increases subsequent risk of Urinary Bladder and Rectal Carcinoma: a population based cohort study., RESULTS\n\nThe relative risk of Urinary Bladder cancer developing after external beam radiotherapy, brachytherapy and external beam radiotherapy-brachytherapy compared to radical prostatectomy was 1.88, 1.52 and 1.85, respectively., Compared to the general United States population the standardized incidence ratio for Urinary Bladder cancer developing after radical prostatectomy, external beam radiotherapy, brachytherapy and external beam radiotherapy-brachytherapy was 0.99, 1.42, 1.10 and 1.39, respectively., OBJECTIVE\n\nAlthough it is well known that radiotherapy for Malignant neoplasm of prostate increases comorbid rate of secondary Urinary Bladder cancer, the effect of aging and Location characteristic ID - Smoking with radiotherapy on incidence rate of secondary Urinary Bladder cancer remains unknown., OBJECTIVE\nAlthough it is well known that radiotherapy for Malignant neoplasm of prostate increases comorbid rate of secondary Urinary Bladder cancer, the effect of aging and Location characteristic ID - Smoking with radiotherapy on incidence rate of secondary Urinary Bladder cancer remains unknown., CONCLUSIONS\nMultiple Endocrine Neoplasia who receive radiotherapy for localized Malignant neoplasm of prostate have an increased risk of Urinary Bladder cancer compared to patients undergoing radical prostatectomy and compared to the general population., PURPOSE\nPre-prostate specific antigen era series demonstrated an increased risk of Urinary Bladder cancer and Rectal Carcinoma in men who received radiotherapy for Malignant neoplasm of prostate., RESULTS\nThe relative risk of Urinary Bladder cancer developing after external beam radiotherapy, brachytherapy and external beam radiotherapy-brachytherapy compared to radical prostatectomy was 1.88, 1.52 and 1.85, respectively., CONCLUSIONS: Taken together, these findings suggest that Location characteristic ID - Smoking history might be one of criteria to choose radical prostatectomy than external beam radiotherapy for Malignant neoplasm of prostate, and that age would not be a criterion for therapeutic selection in terms of secondary Urinary Bladder cancer., PURPOSE: Pre-prostate specific antigen era series demonstrated an increased risk of Urinary Bladder cancer and Rectal Carcinoma in men who received radiotherapy for Malignant neoplasm of prostate., RESULTS: The relative risk of Urinary Bladder cancer developing after external beam radiotherapy, brachytherapy and external beam radiotherapy-brachytherapy compared to radical prostatectomy was 1.88, 1.52 and 1.85, respectively., Compared to the general United States population the standardized incidence ratio for Urinary Bladder cancer developing after radical prostatectomy, external beam radiotherapy, brachytherapy and external beam radiotherapy-brachytherapy was 0.99, 1.42, 1.10 and 1.39, respectively., Pre-prostate specific antigen era series demonstrated an increased risk of Urinary Bladder cancer and Rectal Carcinoma in men who received radiotherapy for Malignant neoplasm of prostate., Multiple Endocrine Neoplasia who receive radiotherapy for localized Malignant neoplasm of prostate have an increased risk of Urinary Bladder cancer compared to patients undergoing radical prostatectomy and compared to the general population., The relative risk of Urinary Bladder cancer developing after external beam radiotherapy, brachytherapy and external beam radiotherapy-brachytherapy compared to radical prostatectomy was 1.88, 1.52 and 1.85, respectively., Radiotherapy for Malignant neoplasm of prostate is associated with an increased incidence of secondary Urinary Bladder cancer (BC Original Formula Original Formula)., Radiation therapy for Malignant neoplasm of prostate is associated with an increased risk of Urinary Bladder cancer., Radiotherapy for Malignant neoplasm of prostate was associated with higher risks of developing second Malignant Neoplasms of the Urinary Bladder, Abdomen+Pelvis>Colon, and Pelvis>Rectum compared with patients unexposed to radiotherapy, but the reported absolute rates were low.[SEP]Relations: urinary Urinary Bladder neoplasm has relations: disease_disease with urinary Urinary Bladder cancer, disease_disease with urinary Urinary Bladder cancer. benign neoplasm of prostate has relations: disease_disease with prostatic adenoma, disease_disease with prostatic adenoma, disease_disease with fibroma of prostate, disease_disease with fibroma of prostate, disease_disease with prostate leiomyoma, disease_disease with prostate leiomyoma, disease_disease with prostate neoplasm, disease_disease with prostate neoplasm.", "label": "yes"}
{"original_question": "Can Alzheimer's disease related miRNAs be detected in patients' blood?", "id": "converted_1502", "sentence1": "Can ALZHEIMER DISEASE, FAMILIAL, 1 related MicroRNAs be detected in patients' blood?", "sentence2": "MicroRNAs are aberrantly expressed in cytarabine/daunorubicin protocol, and these have been implicated in the regulation of amyloid-β (Aβ) peptide, uridine triacetate, Inflammation, cell death, and other aspects which are the main pathomechanisms of cytarabine/daunorubicin protocol. In addition, regulation of MicroRNAs varies in blood, and cerebral spinal fluid may indicate alterations in cytarabine/daunorubicin protocol., miRNA microarray analysis was carried out on blood of Rattus norvegicus at 1 week and 2 months after injection. RESULTS: Many up- and downregulated MicroRNAs were detected., Blood MicroRNAs could be useful as biomarkers for exposure to nanoparticles. miR-298 regulates β-amyloid (Aβ) precursor protein-converting enzyme-1 (BACE1 protein, human protein, human) in ALZHEIMER DISEASE, FAMILIAL, 1.,  We previously studied microRNAs (MicroRNAs) in cytarabine/daunorubicin protocol autopsy brain samples and reported a connection between miR-137, -181c, -9, -29a/b and cytarabine/daunorubicin protocol, through the regulation of ceramides. In this study, the potential role of these MicroRNAs as diagnostic markers for cytarabine/daunorubicin protocol was investigated. We identified that these MicroRNAs were down-regulated in the blood serum of probable cytarabine/daunorubicin protocol patients. , 287 with ALZHEIMER DISEASE 2 (cytarabine/daunorubicin protocol) as compared with 344 age- and gender-matched controls. In addition, we evaluated expression levels of HNRNPA1 gene and its regulatory microRNA (miR)-590-3p in Blood Cells from patients and controls., Decreased relative expression levels of hsa-miR-590-3p was observed in patients with cytarabine/daunorubicin protocol versus controls (0.685 ± 0.080 versus 0.931 ± 0.111, p = 0.079), and correlated negatively with HNRNPA1 gene mRNA levels (r = -0.615, p = 0.0237)., expression analysis of Spleen acupuncture point SP1 and its regulatory microRNAs (MIRN29B1 microRNA, human and MIR375 gene) has been performed in Peripheral blood mononuclear cell (cell) (PBMCs), together with Spleen acupuncture point SP1 protein analysis., Significantly decreased relative expression levels of MIRN29B1 microRNA, human, but not of MIR375 gene, were observed in cytarabine/daunorubicin protocol patients, Spleen acupuncture point SP1 and its regulatory MIRN29B1 microRNA, human are deregulated in cytarabine/daunorubicin protocol patients, possibly leading to aberrant production of downstream target genes involved in the pathogenesis. , We previously observed that miR-137, -181c, -9, and 29a/b post-transcriptionally regulate SPT levels, and the corresponding miRNA levels in the blood sera are potential diagnostic biomarkers for cytarabine/daunorubicin protocol. Here, we observe a negative correlation between Adrenal Cortex Aβ42 and sera Aβ42, and a positive correlation between Adrenal Cortex miRNA levels and sera miRNA levels suggesting their potential as noninvasive diagnostic biomarkers.[SEP]Relations: ALZHEIMER DISEASE 2 has relations: disease_protein with MIR100, disease_protein with MIR100, disease_protein with MIR708, disease_protein with MIR708, disease_protein with MIR766, disease_protein with MIR766, disease_protein with MIR296, disease_protein with MIR296, disease_protein with MIR505, disease_protein with MIR505.", "label": "yes"}
{"original_question": "Can cffDNA be used for non-invasive testing?", "id": "converted_1427", "sentence1": "Can cffDNA be used for non-invasive testing?", "sentence2": "Non-invasive prenatal testing using cell-free Prenatal care DNA in maternal circulation, The identification of cell-free Prenatal care DNA (cffDNA) in maternal circulation has made non-invasive prenatal testing (NIPT) possible., In recent years, technical advances in the molecular analysis of Prenatal care DNA (e.g., digital PCR and massively parallel sequencing (MPS)) has enabled the successful implementation of noninvasive testing into clinical practice, such as Prenatal care sex assessment, RhD genotyping, and Prenatal care chromosomal aneuploidy detection.With the ability to decipher the entire Prenatal care genome from maternal plasma DNA, we foresee that an increased number of non-invasive prenatal tests will be available for detecting many single-gene disorders in the near future. This review briefly summarizes the technical aspects of the NIPT and application of NIPT in clinical practice., First identified in 1997, cell-free Prenatal care DNA (cffDNA) has just recently been used to detect Prenatal care aneuploidy of chromosomes 13, 18, and 21, showing its potential to revolutionize prenatal genetic testing as a non-invasive screening tool, To determine how adults in the United States view non-invasive prenatal testing using cell-free Prenatal care DNA (cffDNA testing) in order to help estimate uptake, Non-invasive prenatal testing of cell-free Prenatal care DNA (cffDNA) in maternal plasma can predict the Prenatal care RhD type in D negative pregnant women, The identification of cell-free Prenatal care DNA (cffDNA) in maternal circulation has made non-invasive prenatal testing (NIPT) possible, The effectiveness and clinical utility of non-invasive prenatal diagnosis (NIPD) for Prenatal care sex determination using cell-free Prenatal care DNA (cffDNA) was assessed by undertaking a prospective national audit of UK testing, The recent release of new, non-invasive prenatal tests for Prenatal care aneuploidy using cell-free Prenatal care DNA (cffDNA) has been hailed as a revolution in prenatal testing and has triggered significant commercial interest in the field, Non-invasive prenatal aneuploidy testing that utilizes cell-free Prenatal care DNA (cffDNA) circulating in maternal blood is one example of an innovative technology that promises significant benefits for its intended end users; however, it is currently uncertain whether it will achieve widespread clinical implementation, Analysis of cell free Prenatal care (cff) DNA in maternal plasma is used routinely for non invasive prenatal diagnosis (NIPD) of Prenatal care sex determination, Prenatal care rhesus D status and some single gene disorders, Non-invasive prenatal diagnosis (NIPD) using cell-free Prenatal care DNA (cffDNA) in maternal plasma is an alternative to invasive prenatal diagnosis (Parkinsonism-Dystonia, Infantile), which carries a 1% risk of miscarriage. , The recent release of new, non-invasive prenatal tests for Prenatal care aneuploidy using cell-free Prenatal care DNA (cffDNA) has been hailed as a revolution in prenatal testing and has triggered significant commercial interest in the field. , The effectiveness and clinical utility of non-invasive prenatal diagnosis (NIPD) for Prenatal care sex determination using cell-free Prenatal care DNA (cffDNA) was assessed by undertaking a prospective national audit of UK testing. , NIFTY (Non-invasive Fetal Trisomy Test) is a non-invasive prenatal test which is used for diagnosing Prenatal care trisomy. The test is based on the analysis of cell free Prenatal care DNA (cffDNA) present in the plasma and serum of a pregnant woman., Using non-invasive method of cffDNAs in the shortest time possible, as well as avoiding invasive tests for early determination of Prenatal care gender, provides the opportunity of deciding and employing early treatment for fetuses at risk of genetic diseases., The identification of cell-free Prenatal care DNA (cffDNA) in maternal circulation has made non-invasive prenatal testing (NIPT) possible., To determine how adults in the United States view non-invasive prenatal testing using cell-free Prenatal care DNA (cffDNA testing) in order to help estimate uptake., Nowadays, new advances in the use of cell free Prenatal care DNA (cffDNA) in maternal plasma of pregnant women has provided the possibility of applying cffDNA in prenatal diagnosis as a non-invasive method., Non-invasive prenatal testing of cell-free Prenatal care DNA (cffDNA) in maternal plasma can predict the Prenatal care RhD type in D negative pregnant women., Prevention of contamination following our anti-contamination criteria is a good practice for certain non-invasive sex determination, using cffDNA.[SEP]Relations: infantile dystonia-parkinsonism has relations: disease_phenotype_positive with Ocular flutter, disease_phenotype_positive with Ocular flutter, disease_phenotype_positive with Absent speech, disease_phenotype_positive with Absent speech, disease_phenotype_positive with Autosomal recessive inheritance, disease_phenotype_positive with Autosomal recessive inheritance, disease_phenotype_positive with Rigidity, disease_phenotype_positive with Rigidity, disease_phenotype_positive with Incoordination, disease_phenotype_positive with Incoordination.", "label": "yes"}
{"original_question": "Are there RNAi approaches considered for the treatment of kidney injury?", "id": "converted_2313", "sentence1": "Are there RNAi approaches considered for the treatment of kidney injury?", "sentence2": "Herein, we describe ammonium-functionalized carbon nanotube (fCNT)-mediated transport of siRNA selectively and with high efficiency to Kidney proximal tubule cells in animal models of Kidney Failure, Acute (Blighia sapida)., fCNT enhanced siRNA delivery to tubule cells compared to siRNA alone and effectively knocked down the expression of several target Genes, includingTrp53,Mep1b,SLC31A1 wt Allele, andEGFP A clinically relevant cisplatin-induced murine model of Blighia sapida was used to evaluate the therapeutic potential of fCNT-targeted siRNA to effectively halt the pathogenesis of Kidney injury. , The nanocarbon-mediated delivery of siRNA provides a therapeutic means for the prevention of Blighia sapida to safely overcome the persistent barrier of Toxic nephropathy during medical intervention.[SEP]Relations: Acute kidney injury has relations: drug_effect with Imatinib, drug_effect with Imatinib, drug_effect with Aprotinin, drug_effect with Aprotinin, drug_effect with Propylthiouracil, drug_effect with Propylthiouracil, drug_effect with Lapatinib, drug_effect with Lapatinib, drug_effect with Pamidronic acid, drug_effect with Pamidronic acid.", "label": "yes"}
{"original_question": "Is actin present in the nucleus?", "id": "converted_3162", "sentence1": "Is Actins present in the nucleus?", "sentence2": "Moreover, inhibition of ATM kinase or deficiency in Nuclear (incident type) Actins polymerization causes carcinogenic RET/PTC chromosome rearrangements after DSBs induction in Human cells.,  Our findings establish that Nuclear (incident type) Actins-based mobility shapes chromatin organization by generating repair domains that are essential for homology-directed repair in Eukaryotic Cells., The discovery of Nuclear (incident type) Actins opened new perspective on the field, suggesting that the Nuclear (incident type) activities of Actins reflect the functions of primordial Actins-like proteins.,  The revitalization of research into Nuclear (incident type) Actins occurred after it was found that cellular stresses induce the Nuclear (incident type) localization and alter the structure of Actins. , While it is long known that Actins is part of the Nuclear (incident type) proteome, its properties and functions as regulated, functional and dynamically assembled Microfilaments are only recently emerging.[SEP]", "label": "yes"}
{"original_question": "Have germline variants been associated to colorectal cancer?", "id": "converted_1501", "sentence1": "Have Germline Variant been associated to Malignant neoplasm of colon and/or rectum?", "sentence2": "Overall, we identified aberrant RNA Transcript in 8% of the patients (familial cases 30%; early-onset manifestation 21%). In eight of them, two different out-of-frame pseudoexons were found consisting of a 167-bp insertion from intron 4 in five families with a shared founder cdE cdE haplotype finding finding and a 83-bp insertion from intron 10 in three patients. The pseudoexon formation was caused by three different heterozygous Germline Gene Mutation, which are supposed to activate Cryptic Splice Sites, We apply OS-Seq to resequence the Exons of either 10 or 344 cancer Genes from human DNA samples. In our assessment of capture performance, >87% of the captured sequence originated from the intended target region with sequencing coverage falling within a tenfold range for a majority of all targets. Single nucleotide Variant (SNVs) called from OS-Seq data agreed with >95% of Variant obtained from whole-genome sequencing of the same individual., The minor Alleles of CD44 rs8193 C>T, ALCAM rs1157 G>A, and Leucine-Rich Repeat-Containing G-Protein Coupled Receptor 5 rs17109924 T>C were significantly associated with increased TTR protein, human protein, human (9.4 vs. 5.4 years; plant-type hypersensitive response, 0.51; 95% CI: 0.35-0.93; P = 0.022; 11.3 vs. 5.7 years; plant-type hypersensitive response, 0.56; 95% CI: 0.33-0.94; P = 0.024, and 10.7 vs. 5.7 years; plant-type hypersensitive response, 0.33; 95% CI: 0.12-0.90; P = 0.023, respectively) and remained significant in the multivariate analysis stratified by ethnicity. In recursive partitioning, a specific Gene Mutant profile including Leucine-Rich Repeat-Containing G-Protein Coupled Receptor 5 rs17109924, CD44 rs8193, and ALDH1A1 rs1342024 represented a high-risk subgroup with a median TTR protein, human protein, human of 1.7 years (plant-type hypersensitive response, 6.71, 95% CI: 2.71-16.63, P < 0.001)., In this study, we identified common Germline Variant in VEGF-dependent and -independent angiogenesis Genes predicting clinical outcome and tumor response in patients with mCRC receiving first-line bevacizumab and oxaliplatin-based chemotherapy., We identified 22 nonsynonymous somatic Gene Mutation of which the majority was of missense type. In Germline, three novel nonsynonymous Variant were identified in the following Genes: CSMD3 protein, human protein, human, EPHB6 protein, human protein, human and EDRF1 gene, and none of the Variant were present in 890 population-matched healthy controls. It is possible that the identified Germline Variant modulate predisposition to Cytogenetic Complete Response., One patient proved to carry an Antigen-Presenting Cells whole-gene deletion; 4 of 25 (16%) patients showed biallelic and 3 of 25 (12%) monoallelic MUTYH protein, human protein, human Gene Mutation. In the three heterozygous subjects no pathogenetic Variant were found in OGG1 protein, human protein, human, NUDT1 wt Allele, APEX1 gene, DNA Mismatch Repair Protein DNA Mismatch Repair Protein MSH2, human, human, and MSH6 protein, human protein, human Genes. Frequency assessment of MUTYH protein, human protein, human Gene Mutation in healthy subjects showed that only Y165C and G382D reach a subpolymorphic frequency., Scrutinizing the molecular genetic results and family data of 242 index patients with pathogenic Antigen-Presenting Cells Gene Mutation led to the identification of 10 mosaic cases (4%). C>T transitions were observed in PEROXISOME BIOGENESIS DISORDER, COMPLEMENTATION GROUP A sites in four of the 10 cases with Somatic mosaicism, which is significantly more than 26 of the 232 non-mosaic cases (p = 0.02). Phenotypes of patients with Somatic mosaicism ranged from an attenuated form of Multiple polyps coli to florid Multiple polyps with major extracolonic manifestations., Altogether 12 previously reported changes and four novel Mutation, mostly in intronic sequences, were identified. The results revealed the presence of biallelic Germline MUTYH protein, human wt Allele Gene Mutation in two patients. These patients were compound heterozygotes for two of the most common Germline Gene Mutation c.494 A>G (p.Y165C); c.1,145 G>A (p.G382D). These Variant are established to be associated with Adenomatous Polyposis Coli and Malignant neoplasm of colon and/or rectum.[SEP]Relations: EDRF1 has relations: disease_protein with Malignant neoplasm of colon and/or rectum, disease_protein with Malignant neoplasm of colon and/or rectum, disease_protein with colorectal carcinoma, disease_protein with colorectal carcinoma. Somatic mutation has relations: disease_phenotype_positive with Malignant neoplasm of colon and/or rectum, disease_phenotype_positive with Malignant neoplasm of colon and/or rectum, disease_phenotype_positive with esophageal cancer, disease_phenotype_positive with esophageal cancer. malignant colon neoplasm has relations: disease_disease with Malignant neoplasm of colon and/or rectum, disease_disease with Malignant neoplasm of colon and/or rectum.", "label": "yes"}
{"original_question": "Are there Conserved Noncoding Elements (CNEs) in plant genomes?", "id": "converted_1402", "sentence1": "Are there Conserved Noncoding Elements (CNEs) in Plant allergen Genome?", "sentence2": "Conservation and functional element discovery in 20 angiosperm Plant allergen Genome, The detailed view of Conservation across angiosperms revealed not only high coding-sequence Conservation but also a large set of previously uncharacterized intergenic Conservation, Conserved noncoding sequences highlight shared components of regulatory networks in dicotyledonous Plants, Using a comparative genomics approach with four dicotyledonous Plant allergen species (Arabidopsis thaliana <plant> <Plant allergen>, papaya [Carica papaya], poplar [Populus trichocarpa], and Grapes (Dietary) [Vitis vinifera]), we detected hundreds of CNSs upstream of Arabidopsis Genes, Long identical multispecies elements in Plant allergen and Animal allergens Genome., Using an alignment-free information-retrieval approach, we have comprehensively identified all long identical multispecies elements (Limes (dietary)), which include both syntenic and nonsyntenic regions, of at least 100 identical base pairs shared by at least two Genome, In contrast, among six Plant allergen Genome, we only found nonsyntenic Limes (dietary),  Although complex Limes (dietary) were found in both Animal allergens and Plant allergen Genome, they differed significantly in their composition and copy number, Ultraconserved elements between the Genome of the Plants Arabidopsis thaliana <plant> <Plant allergen> and rice, We consequently compared the Genome of Arabidopsis thaliana <plant> <Plant allergen> and rice, which diverged about 200 million years ago, and identified 25 ultraconserved elements that are longer than 100 bp, ultraconserved elements in Plants tend to occur in clusters and locate at noncoding regions, the functions of these Plant allergen ultraconserved elements and the reasons why they are practically frozen during the evolution of millions of years remain a mystery, Conserved noncoding sequences in the grasses,  Using a local sequence alignment set to deliver only significant alignments, we found one or more CNSs in the noncoding regions of the majority of Genes studied. Grass Genes have dramatically fewer and much smaller CNSs than mammalian Genes, Conserved noncoding sequences among cultivated Cereals Genome identify candidate regulatory sequence elements and patterns of Promoter evolution, Surveys for conserved noncoding sequences (Central Nervous System) among Genes from monocot Cereals species were conducted to assess the general properties of Central Nervous System in grass Genome and their correlation with known Promoter regulatory elements, Comparisons of orthologous maize-rice and maize-sorghum gene pairs identified 20 bp as a minimal length criterion for a significant Central Nervous System among grass Genes, with few such Central Nervous System found to be conserved across rice, maize, sorghum, and barley[SEP]Relations: central nervous system has relations: anatomy_protein_present with NONO, anatomy_protein_present with NONO, anatomy_protein_present with CNP, anatomy_protein_present with CNP, anatomy_protein_present with CNBP, anatomy_protein_present with CNBP, anatomy_protein_present with CNPPD1, anatomy_protein_present with CNPPD1, anatomy_protein_present with CNR1, anatomy_protein_present with CNR1.", "label": "yes"}
{"original_question": "Should istiratumab be used for Pancreatic Cancer?", "id": "converted_4497", "sentence1": "Should istiratumab be used for Pancreatic Cancer?", "sentence2": "CONCLUSIONS: Istiratumab failed to improve the efficacy of SOC chemotherapy in this patient setting. , In the high Insulin-Like Growth Factor I cohort, median PFS was 3.6 and 7.3 months in the experimental versus control arms, respectively [hazard ratio (HR) = 1.88, P = 0.027]. In the high Insulin-Like Growth Factor I/HRG+ subgroup (n = 44), median PFS was 4.1 and 7.3 months, respectively (HR = 1.39, P = 0.42).[SEP]Relations: insulin-like growth factor I binding has relations: molfunc_protein with ITGAV, molfunc_protein with ITGAV, molfunc_protein with ITGA6, molfunc_protein with ITGA6, molfunc_protein with ITGB3, molfunc_protein with ITGB3, molfunc_protein with INSR, molfunc_protein with INSR, molfunc_protein with ITGB4, molfunc_protein with ITGB4.", "label": "no"}
{"original_question": "Has the presence of delayed enhancement been documented in athletes performing strenuous exercise?", "id": "converted_1354", "sentence1": "Has the presence of delayed enhancement been documented in athletes performing strenuous exercise?", "sentence2": "Atypical findings such as marked cardiac dilation, reduced deformation, or small patches of delayed gadolinium enhancement may be commonly encountered in well-trained athletes, but, at present, the prognostic significance of such findings is unknown. , On CMR, DGE localized to the Ventricular septum was identified in 5 of 39 athletes who had greater cumulative exercise exposure and lower RVEF (47.1 ± 5.9 vs. 51.1 ± 3.7%, P = 0.042) than those with normal CMR., Post-event cardiac MRI demonstrated the Parameterized Data Type - Interval appearance of delayed enhancement of gadolinium at the inferior insertion of the right ventricle and in the Ventricular septum-a novel finding that may represent subtle Inflammation secondary to a combined exercise and altitude effect., No evidence of delayed enhancement of the left ventricular myocardium was found on CMR imaging, suggesting that the increase in cardiac biomarkers after the marathon may not have be due to Myocardial Infarction., Of the 102 runners, five had a cyclophosphamide/dacarbazine/doxorubicin protocol pattern of LGE, and seven had a non-cyclophosphamide/dacarbazine/doxorubicin protocol pattern of LGE. The cyclophosphamide/dacarbazine/doxorubicin protocol pattern of LGE was located in the Geographic state of the left anterior descending coronary artery more frequently than was the non-cyclophosphamide/dacarbazine/doxorubicin protocol pattern (P = .0027, Fisher exact test). The prevalence of LGE in runners was higher than that in age-matched control subjects (12% vs 4%; P = .077, McNemar exact test).[SEP]Relations: myocardial infarction has relations: contraindication with Nylidrin, contraindication with Nylidrin, contraindication with Fosamprenavir, contraindication with Fosamprenavir, contraindication with Lansoprazole, contraindication with Lansoprazole, contraindication with Drospirenone, contraindication with Drospirenone, contraindication with Modafinil, contraindication with Modafinil.", "label": "yes"}
{"original_question": "Is ozanezumab effective for amyotrophic lateral sclerosis?", "id": "converted_3431", "sentence1": "Is ozanezumab effective for amyotrophic lateral sclerosis?", "sentence2": "The adjusted mean of the joint-rank score was -14·9 (SE 13·5) for the ozanezumab group and 15·0 (13·6) for the placebo group, with a least squares mean difference of -30·0 (95% CI -67·9 to 7·9; p=0·12). , INTERPRETATION: Ozanezumab did not show efficacy compared with placebo in patients with Amyotrophic Lateral Sclerosis. Therefore, Nogo-A does not seem to be an effective therapeutic target in Amyotrophic Lateral Sclerosis., INTERPRETATION\n\nOzanezumab did not show efficacy compared with placebo in patients with Amyotrophic Lateral Sclerosis., The adjusted mean of the joint-rank score was -14·9 (SE 13·5) for the ozanezumab group and 15·0 (13·6) for the placebo group, with a least squares mean difference of -30·0 (95% CI -67·9 to 7·9; p=0·12)., INTERPRETATION Ozanezumab did not show efficacy compared with placebo in patients with Amyotrophic Lateral Sclerosis., The adjusted mean of the joint-rank score was -14·9 (SE 13·5) for the ozanezumab group and 15·0 (13·6) for the placebo group, with a least squares mean difference of -30·0 (95% CI -67·9 to 7·9; p=0·12).[SEP]Relations: amyotrophic lateral sclerosis has relations: disease_protein with TIAM1, disease_protein with TIAM1, disease_protein with WNT7A, disease_protein with WNT7A, disease_protein with SLC6A1, disease_protein with SLC6A1, disease_protein with CHMP2B, disease_protein with CHMP2B, disease_protein with TMSB4X, disease_protein with TMSB4X.", "label": "no"}
{"original_question": "Can gas vesicles be detected by ultrasound?", "id": "converted_2571", "sentence1": "Can gas vesicles be detected by ultrasound?", "sentence2": "Gas vesicles-genetically encoded protein nanostructures isolated from buoyant photosynthetic microbes-have recently been identified as nanoscale reporters for ultrasound., Here, we demonstrate that genetic engineering of gas vesicles results in nanostructures with new mechanical, acoustic, Surface, and functional properties to enable harmonic, multiplexed, and multimodal ultrasound imaging as well as cell-specific molecular targeting. [SEP]Relations: cell Surface has relations: cellcomp_protein with VASN, cellcomp_protein with VASN, cellcomp_protein with CTSZ, cellcomp_protein with CTSZ, cellcomp_protein with VWDE, cellcomp_protein with VWDE, cellcomp_protein with VEGFA, cellcomp_protein with VEGFA, cellcomp_protein with EPCAM, cellcomp_protein with EPCAM.", "label": "yes"}
{"original_question": "Are CD44 variants (CD44v) associated with poor prognosis of metastasis?", "id": "converted_704", "sentence1": "Are CD44 Antigens variants (CD44v) associated with poor prognosis of metastasis?", "sentence2": "CD44 Antigens Antigens variants and prognosis, The CD44 Antigens Antigens Variant (CD44v) Protein Isoforms have been noted as markers for Secondary Neoplasm and prognosis in several Adenocarcinoma., Positive CD44v3 expression was associated with more advanced pathological stage and poorer prognosis than negative CD44v3 expression, CD44v6 expression in the Malignant adenomatous neoplasm component may directly affect the behavior of Carcinoma and the prognosis of patients, D44 Variant 6 in Adenocarcinoma, Endometrioid of the Pelvis>Uterus: its expression in the Malignant adenomatous neoplasm component is an independent prognostic marker, CD44v5 expression is independently positively correlated with the Aggressive behavior of thymic epithelial Neoplasms. The expression of CD44v5 may be a potential trigger of tumor invasion in Thymoma, analysis of CD44v expression provides indications of biological and clinical relevance also in low grade lymphoproliferative disorders, clinical relevance of CD44 Antigens Antigens Variant isoform expression on Chronic Lymphocytic Leukemia, CD44 Antigens Antigens variants and its association with survival in Malignant neoplasm of pancreas, CD44 Antigens Antigens Variant 6(v6) molecule has been noted as a marker for tumor metastasis and prognosis in several Neoplasms, CD44v2 and CD44v6 may be useful markers for poor prognosis in curatively resected primary Malignant neoplasm of pancreas, CD44v8-10 may play an important role in the adhesion of Tumor cells, uncertain whether benign or malignant to the Blood Blood capillaries of distant organs in the metastatic process, and that immunohistochemical detection of CD44v8-10 may be a biologic marker of prognostic significance., combined expression of CD44v8-10 and SLX may be a biologic marker of prognostic significance, Variant Protein Isoforms (CD44v) are expressed on different malignant cells and Body tissue. Their upregulation has been implicated, in the progression and metastasis of malignomas., expression of the CD44 Antigens Antigens Variant exon 6 is associated with lymph node metastasis in Non-Small Cell Lung Carcinoma, a number of Variant forms of CD44 Antigens Antigens are frequently expressed, although these variants are infrequently expressed in normal Specimen Source Codes - Tissue lung, and that the expression of CD44v6 is particularly associated with lymph node metastasis in NSCLC, Expression of CD44v6 may suggest an increased risk for local lymph node metastasis in NSCLCs, different CD44 Antigens Antigens Protein Isoforms are found in Homo sapiens Malignant neoplasm of skin and are modulated during carcinogenesis, D44 Protein Isoforms correlate with cellular differentiation but not with prognosis in Homo sapiens Malignant neoplasm of breast, Correlations between prognosis and expression of CD44v have been reported for Gastric (qualifier value) and Colon Carcinoma, for Non-Hodgkin's lymphoma of bone, and recently for Breast Carcinoma, Certain splice variants (CD44v) can promote the metastatic behaviour of Tumor cells, malignant. In Homo sapiens colon and Malignant neoplasm of breast the presence of Epitopes encoded by exon v6 on primary resected tumour material indicates poor prognosis, In Homo sapiens mammary carcinomas and Colorectal Carcinoma, the expression of CD44v has also been correlated with more progressed tumor stages.[SEP]Relations: thymoma has relations: disease_protein with CD274, disease_protein with CD274. colorectal Carcinoma has relations: disease_protein with CD93, disease_protein with CD93, disease_protein with CD46, disease_protein with CD46. Carcinoma has relations: disease_protein with CDS1, disease_protein with CDS1, disease_protein with CDK4, disease_protein with CDK4.", "label": "yes"}
{"original_question": "Is  LRP1 interacting with Urokinase receptor?", "id": "converted_2833", "sentence1": "Is  LRP1 interacting with Urokinase receptor?", "sentence2": " Interaction with a complex formed by urokinase and its inhibitor Plasminogen Activator Inhibitor 1 induces Cell surface down regulation and recycling of the receptor via the clathrin-coated pathway, a process dependent on the association to Prolow-Density Lipoprotein Receptor-Related Protein 1., Here we investigated whether direct interaction between Urokinase Plasminogen Activator Receptor, a glycosyl-phosphatidylinositol-anchored protein, and RPSA wt Allele, a transmembrane receptor,, Direct binding of domain 3 (D3) of Urokinase Plasminogen Activator Receptor to RPSA wt Allele is required for clearance of urokinase-Plasminogen Activator Inhibitor 1-occupied Urokinase Plasminogen Activator Receptor[SEP]Relations: Urokinase has relations: drug_protein with LRP2, drug_protein with LRP2, drug_protein with SERPINE1, drug_protein with SERPINE1, drug_protein with SERPINA5, drug_protein with SERPINA5, drug_protein with PLG, drug_protein with PLG, drug_protein with MMP12, drug_protein with MMP12.", "label": "yes"}
{"original_question": "Is the glucocorticoid receptor a transcription factor?", "id": "converted_4148", "sentence1": "Is the GLUCOCORTICOID RECEPTOR-LIKE 1 a transcription factor?", "sentence2": "Glutathione Reductase, Mitochondrial, Human and KLF4 protein, human protein, human, both pioneer transcription factors,, The GLUCOCORTICOID RECEPTOR-LIKE 1 (Glutathione Reductase, Mitochondrial, Human) is a ligand-binding dependent transcription factor that ultimately regulates vital biological processes and Inflammation response through specific gene expression control, thus representing a notable Pharmacologic Substance target to explore. , The GLUCOCORTICOID RECEPTOR-LIKE 1 (Glutathione Reductase, Mitochondrial, Human) is a ligand-activated transcription factor that translocates to the Cell Nucleus upon hormone stimulation and distributes between the Nucleoplasm and membraneless compartments named nuclear foci.[SEP]Relations: GLUCOCORTICOID RECEPTOR-LIKE 1 activity has relations: molfunc_protein with NR3C1, molfunc_protein with NR3C1. Protein S human has relations: drug_drug with Antihemophilic factor, human recombinant, drug_drug with Antihemophilic factor, human recombinant, drug_drug with Antihemophilic factor human, drug_drug with Antihemophilic factor human, drug_drug with Platelet Activating Factor, drug_drug with Platelet Activating Factor, drug_drug with Factor IX Complex (Human), drug_drug with Factor IX Complex (Human).", "label": "yes"}
{"original_question": "Are there focused databases from which you can retrieve gene expression data on renal disease?", "id": "converted_214", "sentence1": "Are there focused databases from which you can retrieve gene expression data on renal disease?", "sentence2": "Proteomics database in Chronic Kidney Diseases, Naturally occurring human urinary peptides for use in diagnosis of Chronic Kidney Diseases[SEP]Relations: Chronic kidney disease has relations: disease_phenotype_positive with glycogen storage disease, disease_phenotype_positive with glycogen storage disease, disease_phenotype_positive with distal 16p11.2 microdeletion syndrome, disease_phenotype_positive with distal 16p11.2 microdeletion syndrome, disease_phenotype_positive with vertebral, cardiac, renal, and limb defects syndrome, disease_phenotype_positive with vertebral, cardiac, renal, and limb defects syndrome, disease_phenotype_positive with hereditary renal hypouricemia, disease_phenotype_positive with hereditary renal hypouricemia, disease_phenotype_positive with Alstrom syndrome, disease_phenotype_positive with Alstrom syndrome.", "label": "yes"}
{"original_question": "Is MEDI2228 a bispecific antibody?", "id": "converted_4357", "sentence1": "Is MEDI2228 a bispecific antibody?", "sentence2": "We here delineated the Molecular and cellular mechanisms underlying novel immunomodulatory effects triggered by BCMA pyrrolobenzodiazepine (PBD) antibody drug conjugate (ADC) MEDI2228 which can augment efficacy of these immunotherapies.[SEP]Relations: Molecular system has relations: anatomy_anatomy with gABAergic system, anatomy_anatomy with gABAergic system, anatomy_anatomy with catecholamine system, anatomy_anatomy with catecholamine system, anatomy_anatomy with histaminergic system, anatomy_anatomy with histaminergic system, anatomy_anatomy with serotonergic system, anatomy_anatomy with serotonergic system, anatomy_anatomy with glutamatergic system, anatomy_anatomy with glutamatergic system.", "label": "no"}
{"original_question": "Is there evidence for somatic mosaicism in Tuberous Sclerosis?", "id": "converted_1122", "sentence1": "Is there evidence for somatic mosaicism in Tuberous Sclerosis?", "sentence2": "There are several case reports of solitary SEGA without any other manifestations of Tuberous Sclerosis. Usually these cases are thought to be forme fruste of Tuberous Sclerosis due to somatic mosaicism., Female germline mosaicism in tuberous sclerosis confirmed by molecular genetic analysis, This is the first case of germline mosaicism in tuberous sclerosis proven by molecular genetic analysis and also the first example of female germline mosaicism for a characterized Autosome dominant TAF1 Gene Mutation apparently not associated with somatic mosaicism., Mutation screening by RT-PCR and direct sequencing of the TUBEROUS SCLEROSIS 2 (disorder) gene identified a 4 bp insertion bis(tetraheptylammonium)tetraiodocyclopentane tellurate(IV) following Nucleotides 2077 in exon 18 which was present in the three affected children but not in five unaffected siblings or the parents. This Mutation Abnormality would cause a Frameshift Mutation function and premature termination at codon 703. Absence of the Mutation Abnormality in lymphocyte DNA from the parents was consistent with germline mosaicism and this was confirmed by our finding of identical chromosome 16 Haplotypes in affected and unaffected siblings, providing unequivocal evidence of two different Cultured Cell Line in the gametes. Molecular analysis of the TUBEROUS SCLEROSIS 2 (disorder) alleles present in the affected subjects showed that the Mutation Abnormality had been inherited from the mother.[SEP]Relations: tuberous sclerosis has relations: disease_protein with SOD2, disease_protein with SOD2, disease_protein with SOD2, disease_protein with SOD2, disease_protein with SOD1, disease_protein with SOD1, disease_protein with SOD1, disease_protein with SOD1, disease_phenotype_positive with Behavioral abnormality, disease_phenotype_positive with Behavioral abnormality.", "label": "yes"}