{"original_question": "Is the protein Papilin secreted?", "id": "converted_0", "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: cellcomp_protein with Extracellular Matrix, cellcomp_protein with Extracellular Matrix.", "label": "yes"}
{"original_question": "Are long non coding RNAs spliced?", "id": "converted_1", "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]", "label": "yes"}
{"original_question": "Is RANKL secreted from the cells?", "id": "converted_2", "sentence1": "Is TNFSF11 protein, human wt Allele secreted from the Cells?", "sentence2": "Osteoprotegerin (Panoramic Radiography) is a soluble secreted factor that acts as a TNFRSF10C gene for receptor activator of NF-\u03baB ligand (TNFSF11 protein, human protein, human wt Allele)  Osteoprotegerin (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 Osteoprotegerin (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 Osteoblasts 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 Receptor activator of NFI Transcription Factors ligand (TNFSF11 protein, human protein, human wt Allele) and Tumor necrosis factor receptor 11b (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 osteoclast 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 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. Osteoprotegerin (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: Degenerative polyarthritis susceptibility has relations: disease_disease with Degenerative polyarthritis, disease_disease with Degenerative polyarthritis. Tumor Necrosis Factor Receptor binding has relations: molfunc_protein with TNFSF11 protein, human, molfunc_protein with TNFSF11 protein, human, molfunc_protein with TNFSF11 protein, human, molfunc_protein with TNFSF11 protein, human.", "label": "yes"}
{"original_question": "Does metformin interfere thyroxine absorption?", "id": "converted_3", "sentence1": "Does metformin interfere thyroxine absorption?", "sentence2": "LT4 absorption is unchanged by concomitant metformin ingestion. It has been hypothesized that metformin may suppress serum thyrotropin (TSH) concentrations by enhancing LT4 absorption or by directly affecting the hypothalamic-pituitary axis.[SEP]", "label": "no"}
{"original_question": "Has Denosumab (Prolia) been approved by FDA?", "id": "converted_4", "sentence1": "Has Denosumab (Prolia) been approved by FDA?", "sentence2": "Denosumab is a RANK-ligand antibody that was approved by the FDA in 2010 for the prevention of skeletal fractures in patients with bone metastases from Solid Neoplasm.  The authors present the imaging findings and technical report of an attempted percutaneous vertebroplasty in the only patient found to be actively under treatment with denosumab after a retrospective review of the databank of patients with pathological fractures referred to the Department Radiology of the Ohio State University for percutaneous vertebroplasty (a total sample of 20 patients) since the FDA approval of denosumab (November 2010) until June of 2013 (a 30-month period). On the basis of this data, the FDA approved denosumab for the treatment of patients whose GCTB is unresectable, or when surgery is likely to result in severe morbidity. Denosumab (Prolia\u00ae) is a fully Homo sapiens monoclonal antibody for TNFSF11 wt Allele, which selectively inhibits osteoclastogenesis, being recently approved for the treatment of postmenopausal Encounter due to family history of Encounter due to family history of osteoporosis in women at a high or increased risk of Fracture by the FDA in the United Sates and by the European Medicines Agency in Europe since June 2010. Recent phase II clinical trials with denosumab in skeletally mature adolescents over age 12 years and adults with GCTB, have shown both safety and efficacy, leading to its accelerated US FDA approval on 13 June 2013.  Zoledronic acid (Zang Chinese), an intravenously administered Bisphosphonate [EPC], and Denosumab, a subcutaneously administered PPP1R1A gene of nuclear factor B ligand (TNFSF11 wt Allele), have already been approved by Food and Drug Administration (FDA) for their use in treatment of bone metastases. These results led to the approval of denosumab by the European Medicines Agency (Multiple Acyl Coenzyme A Dehydrogenase Deficiency) and the US Food and Drug Administration (FDA), for the prevention of SREs in adults with bone metastases from Solid Neoplasm, including Malignant neoplasm of breast. alendronate, risedronate, zoledronic acid, denosumab, and teriparatide are Food and Drug Administration (FDA)-approved therapeutic options.  Several of these therapies have recently been approved by the FDA to treat bone cancer pain (Bisphosphonate drugs affecting bone structure and mineralization, denosumab) and others are currently being evaluated in Homo sapiens clinical trials (tanezumab). A fourth agent, denosumab (bone targeted therapy) was also recently approved by the FDA for patients with bone metastasis after showing a reduction in the occurrence of skeletal-related events.  AHRQ published an updated review in March 2012 that summarized the benefits and risks of Encounter due to family history of Encounter due to family history of osteoporosis medications in treatment and prevention of Encounter due to family history of Encounter due to family history of osteoporosis, including Bisphosphonate drugs affecting bone structure and mineralization (aledronate, risedronate, ibandronate, zoledronic acid), Parathyroid Hormone [EPC], teriparatide, Homo sapiens Homo sapiens calcitonin, ESTROGENS, SEX HORMONES AND MODULATORS OF THE GENITAL SYSTEM (for prevention in postmenopausal women), selective estrogen receptor modulators (raloxifene), and denosumab(approved by the FDA in 2010).  Four new drugs have received U.S. Food and Drug Administration (FDA)-approval in 2010 and 2011: sipuleucel-T, an immunotherapeutic agent; cabazitaxel, a novel microtubule PPP1R1A gene; abiraterone acetate, a new androgen biosynthesis PPP1R1A gene; and denosumab, a bone-targeting agent.  Recently, the US FDA and the Multiple Acyl Coenzyme A Dehydrogenase Deficiency approved denosumab (a fully Homo sapiens monoclonal antibody) to treat skeletal-related events in bone-metastatic prostate cancer. In addition to these new and emerging therapeutic agents, denosumab was approved for the prevention of skeletal complications in patients with bone metastases due to solid tumor malignancies, providing an alternative to zoledronic acid.  Recently, denosumab was FDA-approved for prevention of SREs in patients with bone metastases from Solid Neoplasm.  In the 2010s to date, an additional 3 Antibodies, in vitro diagnostic (denosumab, belimumab, ipilimumab) have been approved and one Antibody-Drug Conjugates (brentuximab vedotin) is undergoing regulatory review and may be approved in the US by August 30, 2011. We also review the evidence supporting the FDA's approval of denosumab (bone-targeted therapy) as a treatment option for men with CRPC and bony metastases.   It has been approved for clinical use by the FDA in the US and by the European Medicines Agency in Europe since June 2010 (trade name Prolia(\u2122), Amgen, Thousand Oaks, cyclophosphamide/doxorubicin protocol, USA).  The fully Homo sapiens monoclonal antibody denosumab (Prolia(\u00ae)) has been recently approved by the European Medical Agency (EMEA) and the Food and Drug Administration (FDA) for the treatment of postmenopausal Encounter due to family history of Encounter due to family history of osteoporosis.  raloxifene and denosumab are only FDA approved for postmenopausal Encounter due to family history of Encounter due to family history of osteoporosis. The new antiresorptive drug, denosumab, although FDA-approved only for postmenopausal women, has been shown in a study of men on glutamyl-tRNA(Gln) amidotransferase complex location to increase bone density in Vertebral column, hip, and forearm and decrease vertebral fractures on x-ray.   Since then, an additional six Homo sapiens mAbs have received FDA approval: panitumumab, golimumab, canakinumab, Ustekinumab Ab, ofatumumab and denosumab.[SEP]Relations: Teriparatide has relations: indication with Encounter due to family history of osteoporosis, indication with Encounter due to family history of osteoporosis. Panitumumab has relations: drug_drug with Denosumab, drug_drug with Denosumab. raloxifene has relations: indication with Encounter due to family history of osteoporosis, indication with Encounter due to family history of osteoporosis. Canakinumab has relations: drug_drug with Denosumab, drug_drug with Denosumab. Golimumab has relations: drug_drug with Denosumab, drug_drug with Denosumab. Ibandronate has relations: indication with Encounter due to family history of osteoporosis, indication with Encounter due to family history of osteoporosis. Zoledronic acid has relations: indication with Encounter due to family history of osteoporosis, indication with Encounter due to family history of osteoporosis. Ustekinumab has relations: drug_drug with Denosumab, drug_drug with Denosumab. Tanezumab has relations: drug_drug with Denosumab, drug_drug with Denosumab. Denosumab has relations: indication with Encounter due to family history of osteoporosis, indication with Encounter due to family history of osteoporosis. Ipilimumab has relations: drug_drug with Denosumab, drug_drug with Denosumab. Ofatumumab has relations: drug_drug with Denosumab, drug_drug with Denosumab. Sipuleucel-T has relations: drug_drug with Denosumab, drug_drug with Denosumab. Belimumab has relations: drug_drug with Denosumab, drug_drug with Denosumab. Brentuximab vedotin has relations: drug_drug with Denosumab, drug_drug with raloxifene, drug_drug with Denosumab, drug_drug with raloxifene.", "label": "yes"}
{"original_question": "Are transcription and splicing connected?", "id": "converted_5", "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. Spliceosome 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 \u223c3% 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: Protein Info binding has relations: molfunc_protein with CTGF Protein Info, human, molfunc_protein with CTGF Protein Info, human.", "label": "yes"}
{"original_question": "Is Alu hypomethylation associated with breast cancer?", "id": "converted_6", "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]", "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_7", "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 salt 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]", "label": "yes"}
{"original_question": "Do mutations of AKT1 occur in meningiomas?", "id": "converted_8", "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: Meningothelial Benign Meningioma has relations: disease_protein with Neurofibromatosis 2, disease_protein with AKT1 protein, human, disease_protein with Neurofibromatosis 2, disease_protein with AKT1 protein, human. neurofibromatosis has relations: disease_protein with Neurofibromatosis 2, disease_protein with Neurofibromatosis 2. benign Benign Meningioma has relations: disease_protein with Neurofibromatosis 2, disease_protein with AKT1 protein, human, disease_protein with Neurofibromatosis 2, disease_protein with AKT1 protein, human.", "label": "yes"}
{"original_question": "Does physical activity influence gut hormones?", "id": "converted_9", "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\u00a0<\u00a00.0005) and acylated Lenomorelin (P\u00a0<\u00a00.002) were suppressed during exercise but more so during SIE. Peptide YY increased during exercise but most consistently during END (P\u00a0<\u00a00.05). Acylated Lenomorelin was lowest in the afternoon of SIE (P\u00a0=\u00a00.018) 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]", "label": "yes"}
{"original_question": "Is irritable bowel syndrome more common in women with endometriosis?", "id": "converted_10", "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\u2002Hg (95% CI 36.0 to 43.0) vs 28.1 mm\u2002Hg (95% CI 24.5 to 31.6), p=0.001 and 28.8 mm\u2002Hg (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: Dyspareunia has relations: disease_phenotype_positive with Chronic interstitial cystitis, disease_phenotype_positive with Chronic interstitial cystitis. Anxiety Disorders disorder has relations: disease_disease with Anxiety Disorders, disease_disease with Anxiety Disorders. Abdominal pain has relations: disease_phenotype_positive with INFLAMMATORY BOWEL DISEASE 2, disease_phenotype_positive with INFLAMMATORY BOWEL DISEASE 2. intestinal disease has relations: disease_disease with INFLAMMATORY BOWEL DISEASE 2, disease_disease with Irritable Bowel Syndrome, disease_disease with INFLAMMATORY BOWEL DISEASE 2, disease_disease with Irritable Bowel Syndrome. acute female pelvic peritonitis has relations: disease_disease with Pelvic Inflammatory Disease, disease_disease with Pelvic Inflammatory Disease.", "label": "yes"}
{"original_question": "Does BNP increase after intensive exercise in athletes?", "id": "converted_11", "sentence1": "Does nesiritide increase after intensive exercise in athletes?", "sentence2": "NT-pro-nesiritide was significantly elevated postexercise in both adults and adolescents and remained above baseline at 24 h in both groups. NT-pro-nesiritide 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%). [NT-pro-nesiritide] was observed immediately after the marathon (median [NT-pro-nesiritide] 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 NT-pro-nesiritide 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 NT-pro-nesiritide 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]", "label": "yes"}
{"original_question": "Are there web based self management strategies for chronic pain ?", "id": "converted_12", "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]", "label": "yes"}
{"original_question": "Is Weaver syndrome similar to Sotos?", "id": "converted_13", "sentence1": "Is Weaver syndrome similar to Sotos?", "sentence2": "Overgrowth conditions are a heterogeneous group of disorders characterised by increased growth and variable features, including Macrocephaly, distinctive facial appearance and various degrees of Learning difficulties and Intellectual Disability. Among them, Sotos and Weaver syndromes are clinically well defined and due to heterozygous Gene Mutation in NSD1 protein, human protein, human and EZH2 protein, human protein, human, respectively. NSD1 protein, human protein, human and EZH2 protein, human protein, human are both histone-modifying enzymes NSD1 protein, human protein, human and EZH2 protein, human protein, human are Parameterized Data Type - Set domain-containing histone methyltransferases that play key roles in the regulation of transcription through histone modification and chromatin modeling: NSD1 protein, human protein, human preferentially methylates lysine residue 36 of histone 3 (H3K36) and is primarily associated with active transcription, while EZH2 protein, human protein, human shows specificity for lysine residue 27 (Histone H3 Lysine 28) and is associated with transcriptional repression Constitutional NSD1 protein, human protein, human and EZH2 protein, human protein, human Gene Mutation cause Sotos and Weaver syndromes respectively, overgrowth syndromes with considerable phenotypic overlap Clinically, Weaver syndrome is closely related to SOTOS SYNDROME 1, which is frequently caused by Gene Mutation in NSD1 protein, human protein, human Overgrowth syndromes such as Beckwith-Wiedemann Syndrome, SOTOS SYNDROME 1, and Weaver syndrome have an increased risk of Neoplasms. Thus, it is not surprising that prenatal overgrowth occurs in several syndromes, including the Sotos and Weaver syndromes. NSD1 protein, human protein, human Gene Mutation are the major cause of SOTOS SYNDROME 1 and occur in some cases of Weaver syndrome but are rare in other overgrowth phenotypes. We conclude therefore that NSD1 protein, human protein, human Gene Mutation account for most cases of SOTOS SYNDROME 1 and a significant number of Weaver syndrome cases in our series. We conclude that intragenic Gene Mutation of NSD1 protein, human protein, human are the major cause of SOTOS SYNDROME 1 and account for some Weaver syndrome cases but rarely occur in other childhood overgrowth phenotypes. Overgrowth syndromes such as Beckwith-Wiedemann Syndrome, SOTOS SYNDROME 1, and Weaver syndrome have an increased risk of Neoplasms NSD1 protein, human protein, human Gene Mutation are the major cause of SOTOS SYNDROME 1 and occur in some cases of Weaver syndrome but are rare in other overgrowth phenotypes We conclude that intragenic Gene Mutation of NSD1 protein, human protein, human are the major cause of SOTOS SYNDROME 1 and account for some Weaver syndrome cases but rarely occur in other childhood overgrowth phenotypes Considerable phenotypic overlap between Sotos and Weaver syndromes is also evident.  Considerable phenotypic overlap between Sotos and Weaver syndromes is also evident. The identification of an EZH2 protein, human protein, human mutation can therefore provide an objective means of confirming a subtle presentation of Weaver syndrome and/or distinguishing Weaver and Sotos syndromes.  Overgrowth syndromes such as Beckwith-Wiedemann Syndrome, SOTOS SYNDROME 1, and Weaver syndrome have an increased risk of Neoplasms. Two previous cases of Neuroblastoma have been reported in children with Weaver syndrome. Weaver syndrome is closely related to SOTOS SYNDROME 1, Overgrowth syndromes such as Beckwith-Wiedemann Syndrome, SOTOS SYNDROME 1, and Weaver syndrome have an increased risk of Neoplasms. Considerable phenotypic overlap between Sotos and Weaver syndromes is also evident. Clinically, Weaver syndrome is closely related to SOTOS SYNDROME 1, which is frequently caused by Gene Mutation in NSD1 protein, human protein, human.[SEP]Relations: Feeding difficulties has relations: disease_phenotype_positive with SOTOS SYNDROME 1, disease_phenotype_positive with SOTOS SYNDROME 1. Intellectual disability has relations: disease_phenotype_positive with Weaver syndrome, disease_phenotype_positive with SOTOS SYNDROME 1, disease_phenotype_positive with Weaver syndrome, disease_phenotype_positive with SOTOS SYNDROME 1. SOTOS SYNDROME 1 has relations: disease_protein with NSD1 protein, human, disease_protein with NSD1 protein, human. Beckwith-Wiedemann Syndrome has relations: disease_protein with NSD1 protein, human, disease_protein with NSD1 protein, human. Neuroblastoma has relations: disease_phenotype_positive with Beckwith-Wiedemann Syndrome, disease_phenotype_positive with SOTOS SYNDROME 1, disease_phenotype_positive with Beckwith-Wiedemann Syndrome, disease_phenotype_positive with SOTOS SYNDROME 1. Macrocephaly has relations: disease_phenotype_positive with SOTOS SYNDROME 1, disease_phenotype_positive with Weaver syndrome, disease_phenotype_positive with SOTOS SYNDROME 1, disease_phenotype_positive with Weaver syndrome. Weaver syndrome has relations: disease_protein with EZH2 protein, human, disease_protein with NSD1 protein, human, disease_protein with EZH2 protein, human, disease_protein with NSD1 protein, human.", "label": "yes"}
{"original_question": "Is peripheral neuroepithelioma related to Ewing sarcoma?", "id": "converted_14", "sentence1": "Is Peripheral Neuroectodermal Tumor, Primitive related to Ewing 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 bone of Specimen Type - Bone (ES), Peripheral Neuroectodermal Tumor, Primitive (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 bone of Specimen Type - Bone, 18 cases; extraosseous Ewing's sarcoma of bone of Specimen Type - Bone, 2; Peripheral Neuroectodermal Tumor, Primitive, 4; Askin Rosai tumors, 3 To improve the prognosis of patients with poor-risk Peripheral primitive neuroectodermal tumors (pPNETs; including Peripheral Neuroectodermal Tumor, Primitive and Ewing's sarcoma of 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 Neoplasms belong to these neoplasms Comparison of Ewing's sarcoma of bone of Specimen Type - Bone of Specimen Type - Bone and Peripheral Neuroectodermal Tumor, Primitive. An immunocytochemical and ultrastructural analysis of two primitive neuroectodermal neoplasms Ewing's sarcoma of bone of Specimen Type - Bone of Specimen Type - Bone (carboxylesterase) and Peripheral Neuroectodermal Tumor, Primitive (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 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, Ewing 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 Neuroectodermal Tumor, Primitive (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 Ewing sarcoma and Peripheral primitive neuroectodermal tumor has been taken as evidence that these two tumors are related. Besides these antigenic features, Ewing 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 bone of Specimen Type - Bone and Neuroectodermal Tumor, Primitive. Ewing's sarcoma of bone of Specimen Type - Bone (ES) and Peripheral Neuroectodermal Tumor, Primitive (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 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 bone of Specimen Type - Bone (ES) and Peripheral Neuroectodermal Tumor, Primitive (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 bone of Specimen Type - Bone (ES) and Peripheral Neuroectodermal Tumor, Primitive (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 tumor, Ewing's sarcoma of bone of Specimen Type - Bone and Peripheral Neuroectodermal Tumor, Primitive represent phenotypic variations of the same Neoplasms, namely the Peripheral primitive Neuroectodermal Tumors. Besides these antigenic features, Ewing 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: Ewing sarcoma has relations: disease_phenotype_positive with Ewing sarcoma, disease_phenotype_positive with Ewing sarcoma. Ewing sarcoma/Peripheral primitive neuroectodermal tumor has relations: disease_disease with Ewing sarcoma, disease_disease with Ewing sarcoma. EWSR1 has relations: disease_protein with Ewing sarcoma, disease_protein with Ewing sarcoma. Ewing sarcoma of Specimen Type - Bone has relations: disease_disease with Ewing sarcoma, disease_disease with Ewing sarcoma.", "label": "yes"}
{"original_question": "Is c-met involved in the activation of the Akt pathway?", "id": "converted_15", "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 (Epidermal Growth Factor Receptor). Resistance to Epidermal Growth Factor Receptor inhibitors 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 Epidermal Growth Factor Receptor PPP1R1A gene can abrogate activation of downstream effectors of cell growth, proliferation, and survival, thereby overcoming acquired resistance to Epidermal Growth Factor Receptor inhibitors. HGF 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 HGF-induced EMT, The MAPK/Proto-Oncogene Proteins c-akt pathway is indispensable in HGF/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 HGF-induced Epidermal Growth Factor Receptor-TKI resistance in Epidermal Growth Factor Receptor 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 HGF resulted in phosphorylation of the HGF receptor c-Met, activation of Proto-Oncogene Proteins c-akt and I\u03baB, translocation of NF-\u03baB into the Cell Nucleus, and up-regulation of PTGS2 wt Allele mRNA; Our data suggest that HGF 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-phosphatidylinositols 3-kinase-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 phosphatidylinositols 3-kinase and methionine wt Allele, and promotes downstream activation of the phosphatidylinositols 3-kinase/AKT pathway and Mammals target of sirolimus. Notably, Hepatocyte Growth Factor-stimulated SRC wt Allele activation results in induction of phosphatidylinositols 3-kinase complexes p85\u03b1/p110\u03b1 and p85\u03b1/p110\u03b4, which is required for activation of Mammals target of sirolimus, and consequent inhibition of MAP Kinase Kinase Kinase and nuclear factor-\u03baB activation. Our findings, for the first time, have identified the SRC wt Allele-phosphatidylinositols 3-kinase-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-\u03baB signaling. CCN1 wt Allele siRNA inhibited a second phase of Proto-Oncogene Proteins c-akt phosphorylation measured 12 hours after cell stimulation with HGF and also inhibited HGF-induced phosphorylation of the Proto-Oncogene Proteins c-akt target glycogen synthase kinase 3alpha. HGF+epidermal growth factor treatment increased the duration of ERK1/2 and AKT activation compared to HGF or epidermal growth factor alone. All these data indicate that a crosstalk between the epidermal growth factor and HGF pathways in mammary epithelial cells may modulate the development of the Mammary gland. Hepatocyte growth factor and c-Met promote dendritic maturation during hippocampal Neurons differentiation via the Proto-Oncogene Proteins c-akt pathway Consistent with these results, HGF 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 HGF-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 HGF-induced phosphorylation of glycogen synthase kinase 3 beta, increased METAP2 gene phosphorylation, and blocked the ability of HGF to enhance dendritic length. These observations indicate that HGF 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 HGF was found to enhance cell migration, and that HGF-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 HGF/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. HGF protects cultured cortical neurons against hypoxia/reoxygenation induced cell injury via ERK1/2 and Pulmonary Valve Insufficiency-3K/Proto-Oncogene Proteins c-akt pathways HGF 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 HGF, and inhibition of Proto-Oncogene Proteins c-akt activation reduced, but did not completely eliminate the HGF mediated neuroprotection. It is suggested that the neuroprotection of HGF 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 HGF-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 HGF was inhibited by siRNA targeting AKT1 protein, human and AKT2 protein, human. Activation of C-methionine 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 HGF-treated hearts was observed compared with control hearts, and was strongly associated with increased Proto-Oncogene Proteins c-akt activation. The antiapoptotic effect of HGF was mediated by activation of PI3-kinase/Proto-Oncogene Proteins c-akt pathway. The protective effect of HGF protein, human 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 HGF protein, human. Immunoblotting analysis revealed that HGF protein, human 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 HGF protein, human stimulation, These results indicate that HGF protein, human, 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 phosphatidylinositols 3-kinase/AKT pathway When we analyzed the signaling pathways initiated by the HGF protein, human 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 HGF protein, human, whereas blockade of the MAP kinase pathway had no effect. We now show in detached cells a cooperative effect of HGF 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 HGF- 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 HGF- and fibronectin-induced survival response of breast carcinoma cells under detached conditions and corroborate an interaction between Integrins and HGF/ Met signalling pathways in the development of invasive breast cancer.[SEP]Relations: Microtubules associated complex has relations: cellcomp_protein with METAP2 gene, cellcomp_protein with METAP2 gene. Microtubules has relations: cellcomp_protein with METAP2 gene, cellcomp_protein with METAP2 gene. CTNNB1 has relations: disease_protein with Primary malignant neoplasm of lung, protein_protein with Epidermal Growth Factor Receptor, protein_protein with epidermal growth factor, disease_protein with Malignant neoplasm of colon and/or rectum, cellcomp_protein with Cell Nucleus, protein_protein with methionine, anatomy_protein_present with Mammary gland, disease_protein with Primary malignant neoplasm of lung, protein_protein with Epidermal Growth Factor Receptor, protein_protein with epidermal growth factor, disease_protein with Malignant neoplasm of colon and/or rectum, cellcomp_protein with Cell Nucleus, protein_protein with methionine, anatomy_protein_present with Mammary gland. Integrins binding has relations: molfunc_protein with Epidermal Growth Factor Receptor, molfunc_protein with Epidermal Growth Factor Receptor. METAP2 has relations: anatomy_protein_present with Mammary gland, anatomy_protein_present with Mammary gland. Cisplatin has relations: drug_drug with Wortmannin, drug_drug with Wortmannin. lung neoplasm has relations: disease_disease with Primary malignant neoplasm of lung, disease_protein with methionine, disease_protein with Epidermal Growth Factor Receptor, disease_disease with Primary malignant neoplasm of lung, disease_protein with methionine, disease_protein with Epidermal Growth Factor Receptor. epidermal growth factor receptor binding has relations: molfunc_protein with epidermal growth factor, molfunc_protein with epidermal growth factor. Sirolimus has relations: drug_drug with Wortmannin, drug_drug with Wortmannin. Mammary gland has relations: anatomy_protein_present with methionine, anatomy_protein_present with METAP2 gene, anatomy_protein_present with epidermal growth factor, anatomy_protein_present with Epidermal Growth Factor Receptor, anatomy_protein_present with methionine, anatomy_protein_present with METAP2 gene, anatomy_protein_present with epidermal growth factor, anatomy_protein_present with Epidermal Growth Factor Receptor. Dendrites has relations: cellcomp_protein with METAP2 gene, cellcomp_protein with METAP2 gene. germ cell Cell Nucleus has relations: cellcomp_cellcomp with Cell Nucleus, cellcomp_cellcomp with Cell Nucleus. malignant colon neoplasm has relations: disease_protein with Epidermal Growth Factor Receptor, disease_disease with Malignant neoplasm of colon and/or rectum, disease_protein with Epidermal Growth Factor Receptor, disease_disease with Malignant neoplasm of colon and/or rectum. PPP1R1A has relations: anatomy_protein_present with Mammary gland, anatomy_protein_present with Mammary gland.", "label": "yes"}
{"original_question": "Is pregnancy an additional risk during during H1N1 infection?", "id": "converted_16", "sentence1": "Is pregnancy an additional risk during during H1N1 Communicable Diseases?", "sentence2": "H1N1 influenza in pregnancy can be associated with severe complications This case series confirms a high number of complications in pregnant women due to pandemic H1N1/09. Pregnant women might be at increased risk for complications from pandemic H1N1 Virus Communicable Diseases. Pregnant women are at increased risk for complications from pandemic influenza H1N1 Virus Communicable Diseases.  Vaccination of pregnant women against influenza A (H1N1) by Russian subunit formulation (MonoGrippol plus) showed reactogenicity comparable to control group by the level of influence on general metabolic and immunologic homeostasis and on the course of pregnancy, which is an evidence of its safety Pregnancy was identified as a major risk factor for increased mortality and morbidity due to H1N1 influenza in the pandemic of 2009 to 2010 While it is not possible to ascertain retrospectively if Myocarditis was caused by either Communicable Diseases with H1N1 Virus or as a result of pregnancy (in the absence of endomyocardial biopsies), the significant association with Myocardial involvement in both women demonstrates the increased risk of exposure to H1N1 influenza Virus in pregnant women. Although limited in size, the fully prospective nature of the safety follow-up of these women vaccinated during pregnancy is unique and offers an important degree of reassurance for the use of the AS03 adjuvanted H1N1 (2009) vaccine in this high risk group for H1N1 Communicable Diseases. During the H1N1 2009 pandemic, pregnant women constituted one of the priority groups for vaccination in many countries, creating a need for close monitoring of the safety of the vaccine in pregnant women Emerging data suggest that pregnancy conveys high risk for severe complications from the 2009 pandemic influenza A Virus (2009 H1N1) Communicable Diseases Pregnant women have been identified as a group at risk, both for Respiratory complication than for the admissions to the Intensive Care Unit (ICU) during the 2009 H1N1 influenza pandemic This report mitigates substantially the presumed severity of pandemic H1N1/09 influenza Communicable Diseases during pregnancy The results of our study do not indicate a risk for the pregnant woman and the developing embryo/fetus after H1N1 vaccination This large cohort study found no evidence of an increased risk of Prenatal care death associated with exposure to an adjuvanted pandemic A/H1N1 2009 influenza vaccine during pregnancy Our results suggest that second- or third-trimester H1N1 vaccination was associated with improved Prenatal care and neonatal outcomes during the recent pandemic Pregnant women might thus be at increased risk of complications from pandemic H1N1 Virus Communicable Diseases, and Illness (finding) may progress rapidly Pregnant women with H1N1 Communicable Diseases seem to benefit from antiviral therapy. arly identification and treatment were the most important factors in different countries and areas examined. The vaccine and antiviral drugs that have been the most efficient means to control the novel Virus appear to be safe but require more extensive study However, there were significant differences between the two groups in relation to mean age, treatment with oseltamivir, schooling, and presence of other risk factors To investigate whether exposure to an adjuvanted influenza A(H1N1)pdm09 vaccine during pregnancy was associated with increased risk of adverse Prenatal care outcomes. In this Danish cohort, exposure to an adjuvanted influenza A(H1N1)pdm09 vaccine during pregnancy was not associated with a significantly increased risk of major birth defects, preterm birth, or Prenatal care growth restriction Most people affected by the Virus, including pregnant women, suffer a mild viral Illness (finding), and make a full recovery Pregnant women, because of their altered immunity and physiological adaptations, are at higher risk of developing Pulmonary:-:Point in time:^Patient:- complications, especially in the second and third trimesters The pregnancy outcomes were also poor for women who were affected by the Virus with a fivefold increase in the perinatal mortality rate and threefold increase in the preterm delivery rate regnant women were at increased risk for serious outcomes of 2009 pandemic influenza A Virus subtype H1N1 (influenza A[H1N1]pdm09) Communicable Diseases, but little is known about the overall impact of the pandemic on neonatal and maternal outcomes In this large, geographically diverse population, A(H1N1)pdm09 Communicable Diseases increased the risk for hospitalization during pregnancy Vaccination during pregnancy with Pandemrix(\u00ae) appeared to have no ill effects on the pregnancy. On the contrary, the rate of preterm birth and low birthweight was lower than expected, which agrees with some previous results During the influenza A(H1N1)pmd09 pandemic, although many cases occurred in younger adults, the risk factors identified for severe Infections of musculoskeletal system and complications were similar to those for seasonal influenza, including chronic respiratory, Kidney, Abdomen>Liver, and heart diseases. In terms of pregnancy, the studies have shown contradictory results due to variations in methodology and medical care. However, it seems that pregnancy, particularly during the third trimester, increases the risk of complications, and that early antiviral treatment is associated with improved outcomes. Pregnant women with mild clinical Illness (finding) secondary to 2009 H1N1 were not at a greater risk of adverse pregnancy outcomes However, severely infected women were more likely to deliver SGA infants Gestational age is associated with the risk of developing critical Communicable Diseases. The risk increases with increasing weeks of gestation.  Following the start of winter in Liaoning province in China, the number of pregnant women infected with influenza increased significantly regnancy, with or without additional complications, constitutes a high-risk condition for complications of influenza Communicable Diseases and warrants early intervention with neuraminidase inhibitors such as oseltamivir, if influenza is suspected[SEP]", "label": "yes"}
{"original_question": "Are long non coding RNAs as conserved in sequence as protein coding genes?", "id": "converted_17", "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]", "label": "no"}
{"original_question": "Is TENS machine effective in pain?", "id": "converted_18", "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]", "label": "yes"}
{"original_question": "Is there any algorithm for enhancer identification from chromatin state?", "id": "converted_19", "sentence1": "Is there any algorithm for Enhancer of transcription identification from chromatin state?", "sentence2": "RFECS: a random-forest based algorithm for Enhancer of transcription identification from chromatin state. However, only a limited number of cell types or chromatin marks have previously been investigated for this purpose, leaving the question unanswered whether there exists an optimal set of Histone antigen modifications for Enhancer of transcription prediction in different cell types. Here, we address this issue by exploring genome-wide profiles of 24 Histone antigen modifications in two distinct human cell types, Embryonic Stem Cells and lung fibroblasts. We developed a Random-Forest based algorithm, RFECS (Random Forest based Enhancer identification from Chromatin States) to integrate Histone antigen modification profiles for identification of enhancers, and used it to identify enhancers in a number of cell-types. We show that RFECS not only leads to more accurate and precise prediction of enhancers than previous methods, but also helps identify the most informative and robust set of three chromatin marks for Enhancer of transcription prediction. We developed a Random-Forest based algorithm, RFECS (Random Forest based Enhancer identification from Chromatin States) to integrate Histone antigen modification profiles for identification of enhancers, and used it to identify enhancers in a number of cell-types. Here, we address this issue by exploring genome-wide profiles of 24 Histone antigen modifications in two distinct human cell types, Embryonic Stem Cells and lung fibroblasts. We developed a Random-Forest based algorithm, RFECS (Random Forest based Enhancer identification from Chromatin States) to integrate Histone antigen modification profiles for identification of enhancers, and used it to identify enhancers in a number of cell-types.  ChromaGenSVM selects optimum combinations of specific Histone antigen epigenetic marks to predict enhancers.  We developed a Random-Forest based algorithm, RFECS (Random Forest based Enhancer identification from Chromatin States) to integrate Histone antigen modification profiles for identification of enhancers, and used it to identify enhancers in a number of cell-types.[SEP]", "label": "yes"}
{"original_question": "Are transcribed ultraconserved regions involved in cancer?", "id": "converted_20", "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 sequences 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 Tumor cells, malignant. 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 neuroblastomas, 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 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 cancer cells with a DNA-demethylating agent followed by hybridization to an expression microarray containing these sequences. We observed that DNA hypomethylation induces release of T-UCR silencing in cancer cells. 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 cancer cells 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 sequences 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: carcinoma has relations: disease_disease with cancer, disease_disease with cancer. malignant giant cell tumor has relations: disease_disease with cancer, disease_disease with 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. 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.", "label": "yes"}
{"original_question": "Do patients with Pendred syndrome present congenital deafness?", "id": "converted_21", "sentence1": "Do patients with Pendred's syndrome present Congenital Hearing Loss, Partial?", "sentence2": "Pendred Syndrome can be characterized by the triad composed of familial goitre, abnormal perchlorate discharge and Congenital Hearing Loss, Partial. Pendred's syndrome is an Autosomal Recessive Disorder characterized by Congenital Hearing Loss, Partial and goiter.  Pendred's syndrome comprises congenital sensorineural hearing loss, THYROID DIAGNOSTIC RADIOPHARMACEUTICALS goiter, and positive perchlorate discharge test.  The cause of the Congenital Hearing Loss, Partial in Pendred's syndrome is obscure, although a Mondini type malformation of the Cochlear structure exists in some patients. Pendred's syndrome is an Autosomal Recessive Disorder characterized by Congenital Hearing Loss, Partial and goiter. Pendred's syndrome is the autosomal recessively transmitted association of Congenital goiter and Congenital Hearing Loss, Partial. Pendred's syndrome (PDS) is an Autosomal Recessive Disorder characterized by Congenital Hearing Loss, Partial, goiter and Iodides organification defect. Pendred's syndrome is a recessively inherited disorder with the hallmark features of Congenital Hearing Loss, Partial and Goiter. Pendred's syndrome, a common autosomal-recessive disorder characterized by Congenital Hearing Loss, Partial and goiter, is caused by Gene Mutation of SLC26A4, which codes for pendrin. These studies provide compelling evidence that defects in pendrin cause Pendred's syndrome thereby launching a new area of investigation into THYROID DIAGNOSTIC RADIOPHARMACEUTICALS physiology, the pathogenesis of Congenital Hearing Loss, Partial and the role of altered sulphate transport in human disease. Mutations in the Pendred's syndrome gene have been observed in patients with Hearing Loss, Partial and vestibular aqueduct dilatation, in the absence of other Pendred's syndrome features. The occurrence of Congenital Hearing Loss, Partial, Mutism and goitre unassociated with Congenital Hypothyroidism or mental retardation in Euthyroid (finding) patients is known as Pendred's Syndrome. The autosomal recessive Pendred's syndrome is defined by Congenital sensorineural hearing loss, goiter, and impaired Iodides organification. Pendred's syndrome is an autosomal recessive disease characterized by goiter, impaired Iodides organification, and Congenital sensorineural hearing loss. Pendred's syndrome is an Autosomal Recessive Disorder characterized by Congenital sensorineural hearing loss, goiter, and impaired Iodides organification. Pendred's syndrome is manifested by Congenital sensorineural hearing loss in association with Congenital goiter due to defective organic binding of Iodine, Homeopathic preparation in the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS gland. Although the textbook view of the Pendred's syndrome is that of an autosomal recessive condition characterised by Hearing Loss, Partial and goitre, it is increasingly clear that not all patients present this classical clinical description. Pendred's syndrome may account for up to 10% of the cases with Hereditary hearing loss, and pendrin Gene Mutation have also been found in a kindred with non-syndromic Hearing Loss, Partial. Pendred's syndrome comprises the association of severe Congenital sensorineural hearing loss with THYROID DIAGNOSTIC RADIOPHARMACEUTICALS pathology. The first one is named Pendred Syndrome (Supernumerary mandibular right central primary incisor) when Hearing Loss, Partial is associated with THYROID DIAGNOSTIC RADIOPHARMACEUTICALS goiter; the second is called DEAFNESS, AUTOSOMAL RECESSIVE 4, WITH ENLARGED VESTIBULAR AQUEDUCT, when no other symptoms are present. Pendred's syndrome is an Autosomal Recessive Disorder characterized by Sensorineural Hearing Loss (disorder), a partial defect in Iodides organification, and dyshormonogenetic goiter. Pendred's syndrome and non-syndromic recessive Hearing Loss, Partial associated with enlarged vestibular aqueduct (NSRD with EVA) are caused by Gene Mutation in the SLC26A4 (PDS) gene. Although the textbook view of Pendred's syndrome is that of an autosomal recessive condition characterized by Hearing Loss, Partial and goitre, it is increasingly clear that not all such patients present this classical clinical picture.  The occurrence of Congenital Hearing Loss, Partial, Mutism and goitre unassociated with Congenital Hypothyroidism or mental retardation in Euthyroid (finding) patients is known as Pendred's Syndrome.  The cause of the Congenital Hearing Loss, Partial in Pendred's syndrome is obscure, although a Mondini type malformation of the Cochlear structure exists in some patients.  The discovery of Gene Mutation in the SLC26A4 gene in patients with Pendred's syndrome (Congenital Hearing Loss, Partial, goiter, and defective Iodides organification) suggested a possible role for the encoded protein, pendrin, as an apical Iodides transporter.  Pendred's syndrome is a recessively inherited disorder with the hallmark features of Congenital Hearing Loss, Partial and Goiter.  Pendred&apos;s syndrome is manifested by Congenital sensorineural hearing loss in association with Congenital goiter due to defective organic binding of Iodine, Homeopathic preparation in the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS gland. The majority of patients with Pendred&apos;s syndrome are Euthyroid (finding). We report on an unusual case of a patient with Pendred&apos;s syndrome presenting with Amenorrhea and late-onset Hypothyroidism.  Although the textbook view of Pendred's syndrome is that of an autosomal recessive condition characterized by Hearing Loss, Partial and goitre, it is increasingly clear that not all such patients present this classical clinical picture. Malformations of the Labyrinth, specifically enlargement of the vestibular aqueduct, are common in Pendred's syndrome and Gene Mutation in the PDS (Pendred Syndrome) gene have been recorded in patients presenting with Hearing Loss, Partial and vestibular aqueduct dilatation only, without other features of Pendred's syndrome. The occurrence of Congenital Hearing Loss, Partial, Mutism and goitre unassociated with Congenital Hypothyroidism or mental retardation in Euthyroid (finding) patients is known as Pendred&apos;s Syndrome. It has been estimated that 4-10 % of children with Congenital Hearing Loss, Partial suffer from this condition. Malformations of the Labyrinth, specifically enlargement of the vestibular aqueduct, are common in Pendred's syndrome and Gene Mutation in the PDS (Pendred Syndrome) gene have been recorded in patients presenting with Hearing Loss, Partial and vestibular aqueduct dilatation only, without other features of Pendred's syndrome. Since this is the most common radiological malformation of the Cochlear structure in deaf patients, we investigated what proportion of such cases were due to Mutation Abnormality of the PDS gene. Although the textbook view of Pendred's syndrome is that of an autosomal recessive condition characterized by Hearing Loss, Partial and goitre, it is increasingly clear that not all such patients present this classical clinical picture. Malformations of the Labyrinth, specifically enlargement of the vestibular aqueduct, are common in Pendred's syndrome and Gene Mutation in the PDS (Pendred Syndrome) gene have been recorded in patients presenting with Hearing Loss, Partial and vestibular aqueduct dilatation only, without other features of Pendred's syndrome.[SEP]Relations: SLC26A4 has relations: disease_protein with Pendred's syndrome, anatomy_protein_present with THYROID DIAGNOSTIC RADIOPHARMACEUTICALS gland, disease_protein with Pendred's syndrome, anatomy_protein_present with THYROID DIAGNOSTIC RADIOPHARMACEUTICALS gland. Congenital sensorineural hearing impairment has relations: disease_phenotype_positive with Pendred's syndrome, disease_phenotype_positive with Pendred's syndrome. congenital Hypothyroidism has relations: disease_disease with Hypothyroidism, disease_disease with Hypothyroidism. autosomal recessive disease has relations: disease_disease with Pendred's syndrome, disease_disease with Pendred's syndrome. Hypothyroidism has relations: disease_phenotype_positive with Pendred's syndrome, disease_phenotype_positive with Pendred's syndrome.", "label": "yes"}
{"original_question": "Is CD56 useful in Ewing sarcoma prognosis?", "id": "converted_22", "sentence1": "Is NCAM1 wt Allele useful in Ewings sarcoma prognosis?", "sentence2": "Excellent prognosis in a subset of patients with Ewings sarcoma identified at diagnosis by NCAM1 wt Allele using flow cytometry There was a highly significant correlation between NCAM1 wt Allele expression and progression-free survival (PFS; 69% in low/negative expression versus 30% in high expression groups, P = 0.024) In patients with localized nonpelvic disease, those expressing low/negative NCAM1 wt Allele had 100% PFS versus 40% in the high expressing group (P = 0.02) NCAM1 wt Allele was found to be an independent prognostic marker with an 11-fold increased risk for relapse in patients with localized disease (P = 0.006) NCAM1 wt Allele expression could be used to reveal ES patients with excellent prognosis or patients predisposed to relapse, thus improving treatment stratification and implementation of personalized therapy Excellent prognosis in a subset of patients with Ewings sarcoma identified at diagnosis by NCAM1 wt Allele using flow cytometry. Three years after diagnosis the patient presented with severe respiratory difficulty and following resection, the final pathology revealed Multiple tumors with Focal of High Grade Sarcoma compatible with primitive Neuroectodermal Tumors/extraskeletal Ewings sarcoma based on morphology and immunohistochemistry (CD99 antigen antigen, NCAM1 wt Allele). NCAM1 wt Allele expression could be used to reveal ES patients with excellent prognosis or patients predisposed to relapse, thus improving treatment stratification and implementation of personalized therapy. Identification of NCAM1 wt Allele and B3GAT1 wt Allele by flow cytometry in Ewing's sarcoma of bone of bone or primitive Neuroectodermal Tumors. NCAM1 wt Allele expression could be used to reveal ES patients with excellent prognosis or patients predisposed to relapse, thus improving treatment stratification and implementation of personalized therapy.[SEP]Relations: Ewings sarcoma has relations: disease_phenotype_positive with Ewings sarcoma, disease_phenotype_positive with Ewings sarcoma. Ewings sarcoma of bone has relations: disease_disease with Ewings sarcoma, disease_disease with Ewings sarcoma.", "label": "yes"}
{"original_question": "Are there any urine biomarkers for chronic kidney disease?", "id": "converted_23", "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 CKD 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. Cardio-Renal Syndrome (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 Kidney Failure, Acute 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.", "label": "yes"}
{"original_question": "Is valproic acid effective for glioblastoma treatment?", "id": "converted_24", "sentence1": "Is valproic acid effective for glioblastoma treatment?", "sentence2": "A Phase 2 Study of Concurrent Radiation Therapy, Temozolomide, and the Histone Deacetylase Inhibitor Valproic Acid for Patients With Glioblastoma Multiforme Multiforme. PURPOSE: valproic acid (VPA) is an antiepileptic agent with Histone Deacetylase Inhibitor [EPC] therapy (HDACi) activity shown to sensitize glioblastoma (Glomerular Basement Membrane) Cells to radiation in preclinical models.  Median overall survival (OS) was 29.6\u00a0months (range: 21-63.8\u00a0months), and median progression-free survival (PFS) was 10.5\u00a0months (range: 6.8-51.2\u00a0months). OS at 6, 12, and 24\u00a0months was 97%, 86%, and 56%, respectively. PFS at 6, 12, and 24\u00a0months was 70%, 43%, and 38% respectively.  CONCLUSIONS: Addition of VPA to concurrent RT/TMZ in patients with newly diagnosed Glomerular Basement Membrane was well tolerated. Additionally, VPA 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 VPA, 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 VPA (HR, 0.56; 95% NDUFB6 gene, 0.44-0.71). Sub-group analysis shows that patients treated with VPA 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 patients may experience prolonged survival due to VPA administration.  A new and exciting insight is the potential contribution of VPA to prolonged survival, particularly in Glioblastoma Multiforme.  valproic acid (VPA) is an antiepileptic agent with Histone Deacetylase Inhibitor [EPC] therapy (HDACi) activity shown to sensitize glioblastoma (Glomerular Basement Membrane) Cells to radiation in preclinical models valproic acid use during radiation therapy for glioblastoma associated with improved survival valproic acid (VA) is an antiepileptic drug (AED) and histone deacetylase (HDAC) inhibitor taken by patients with glioblastoma (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 associated with improved survival. Prolonged survival with valproic acid use in the EORTC/NCIC temozolomide trial for glioblastoma. PURPOSE: valproic acid (VA) is an antiepileptic drug (AED) and histone deacetylase (HDAC) inhibitor taken by patients with glioblastoma (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 (TMZ) 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 TMZ, 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 VPA 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 VPA (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 VPA together with chemoradiation with temozolomide results in a 2-months' longer survival of patients with Glomerular Basement Membrane.[SEP]Relations: Temozolomide has relations: drug_drug with valproic acid, drug_drug with valproic acid.", "label": "yes"}
{"original_question": "Can Levoxyl (levothyroxine sodium) cause insomnia?", "id": "converted_25", "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]", "label": "yes"}
{"original_question": "Is fatigue prevalent in patients receiving treatment for glioblastoma?", "id": "converted_26", "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 Toxic effect occurred in 30% of patients and consisted mainly of fatigue (14%) and Neuropathy (5%); grade 3, 4 Hematologic Toxic effect occurred in 37% of patients and consisted of THROMBOCYTOPENIA 2 (disorder) (30%), Lymphocyte count decreased (4%), and Neutrophil count decreased (4%).  Nonhematologic Grade 3 Toxic effect 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 toxicities observed were primarily grade 1 and 2, and the most common were fatigue, Hypertensive disease, and Headache.  Fatigue (41%), Exanthema (62%), and loose stools (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 toxicities were Nausea:Presence or Threshold:Point in time:^Patient:Ordinal/vomiting (6.7%) and fatigue (5.8%).  Grade 3/4 toxicities 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 Toxic effect 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).  Fatigue 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 toxicities of fatigue, White blood cell count decreased, THROMBOCYTOPENIA 2 (disorder) and Exanthema requiring dose reductions.  The most common atrasentan-related toxicities 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 toxicities 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 toxicities were Venous Thrombosis, fatigue, skin reactions, Encephalopathies, and Neuropathy.[SEP]Relations: Thalidomide has relations: contraindication with Neutrophil count decreased, contraindication with Neutrophil count decreased. Temozolomide has relations: contraindication with THROMBOCYTOPENIA 2 (disorder), contraindication with Neutrophil count decreased, contraindication with THROMBOCYTOPENIA 2 (disorder), contraindication with Neutrophil count decreased. Thrombocytopenia has relations: disease_phenotype_positive with THROMBOCYTOPENIA 2 (disorder), disease_phenotype_positive with THROMBOCYTOPENIA 2 (disorder). Isotretinoin has relations: contraindication with Neutrophil count decreased, indication with Hypertensive disease, contraindication with Neutrophil count decreased, indication with Hypertensive disease.", "label": "yes"}
{"original_question": "Does the CTCF protein co-localize with cohesin?", "id": "converted_27", "sentence1": "Does the CTGF protein, Homo sapiens protein co-localize with cohesins?", "sentence2": "To investigate cohesins-non-CTGF protein, Homo sapiens (CNC) binding events in vivo we mapped cohesins and CTGF protein, Homo sapiens, as well as a collection of tissue-specific and ubiquitous transcriptional regulators using Chromatin Immunoprecipitation Sequencing in primary Mus sp. liver. In contrast to regions of the Genome - anatomical entity where cohesins and CTGF protein, Homo sapiens colocalize, CNC Site coincide with the binding of master regulators and enhancer-markers and are significantly associated with liver-specific expressed genes. Here we report that cohesins colocalize with CTGF protein, Homo sapiens at two additional imprinted loci, the Dlk1-Dio3 and the Kcnq1/Kcnq1ot1 loci. By use of Homo sapiens hepatocellular carcinoma cells (HepG2), we found that liver-specific transcription factors colocalize with cohesins independently of CTGF protein, Homo sapiens at liver-specific targets that are distinct from those found in breast cancer cells Because cohesins can colocalize with CTGF protein, Homo sapiens, we performed chromatin location location immunoprecipitation for the cohesins subunit Double-Strand-Break Repair Protein Double-Strand-Break Repair Protein Rad21 Homolog Homolog and found lineage and stage-specific Double-Strand-Break Repair Protein Double-Strand-Break Repair Protein Rad21 Homolog Homolog recruitment to CTGF protein, Homo sapiens in all Ig loci Here we show that zebrafish RUNX1 protein, Homo sapiens is directly bound by cohesins and CCCTC-binding factor (CTGF protein, Homo sapiens) at the Blood group antigen Blood group antigen P1 and Bone structure of middle phalanx Promoter, and within the Introns between Blood group antigen Blood group antigen P1 and Bone structure of middle phalanx. The intronic Binding Sites for cohesins and CTGF protein, Homo sapiens coincide with histone modification that confer enhancer-like properties, and two of the cohesins/CTGF protein, Homo sapiens Site behaved as insulators in an in vivo assay The identified cohesins and CTGF protein, Homo sapiens Binding Sites are likely to be cis-regulatory elements (CST8 gene) for RUNX1 protein, Homo sapiens since they also recruit RNA Polymerase II (RNAPII). We have found that CTGF protein, Homo sapiens and cohesins are highly enriched at the convergent and partially overlapping RNA Transcript for the PDLIM7 gene and LMP2A genes, but it is not yet known how CTGF protein, Homo sapiens and cohesins may coordinately regulate these RNA Transcript haracterization of constitutive CTGF protein, Homo sapiens/cohesins loci: a possible role in establishing topological domains in mammalian Genome Our analysis revealed: 1) constitutive CTGF protein, Homo sapiens loci were located in constitutive open chromatin location location and often co-localized with constitutive cohesins loci In Head>Brain, a third of CTGF protein, Homo sapiens and cohesins Binding Sites coincide, consistent with the potential for many interactions between cohesins and CTGF protein, Homo sapiens but also many instances of independent action Here, we focus on the emerging roles of CTGF protein, Homo sapiens and the cohesins in coordinating long-range interactions between regulatory elements Chromatin immunoprecipitation for CTGF protein, Homo sapiens and the cohesins subunits RAD21 and SMC3 wt Allele wt Allele reveals evolutionarily conserved Binding Sites within unmethylated regions \u223c5 kb downstream of the PLAGL1 gene gene differentially methylated region and within the PLAGL1 gene gene 3' untranslated region (SLC14A2 gene) TCF physically links cohesins to chromatin location location ohesin and CTGF protein, Homo sapiens: cooperating to control chromosome conformation? Recently, three groups mapped numerous cohesins-Binding Sites in mammalian chromosomes and found substantial overlap with the CCCTC-binding factor (CTGF protein, Homo sapiens) We found that each Specimen Source Codes - Site contains a conserved CTGF protein, Homo sapiens consensus sequence, binds CTGF protein, Homo sapiens, and recruits the cohesins subunit Double-Strand-Break Repair Protein Double-Strand-Break Repair Protein Rad21 Homolog Homolog in vivo Recent experiments have revealed that cohesins binds to the same Site in mammalian Genome as the zinc finger transcription factor CTGF protein, Homo sapiens Here we review what is known about the roles of cohesins and CTGF protein, Homo sapiens in regulating gene expression in mammalian cells, and we discuss how cohesins might mediate the insulator function of CTGF protein, Homo sapiens Previous studies have shown that this major latency control region is occupied by the Cells chromatin location location boundary factor CTGF protein, Homo sapiens and chromosome structural maintenance proteins SMITH-MCCORT DYSPLASIA 1, SMC3 wt Allele wt Allele, and RAD21, which comprise the cohesins complex Cohesin subunits assembled at the CTGF protein, Homo sapiens Binding Sites and bound CTGF protein, Homo sapiens proteins in a cell cycle-dependent manner We propose that the CTGF protein, Homo sapiens-cohesins complex plays a critical role in regulating the cell cycle control of Genes, Viral expression during latency and that failure to maintain cell cycle control of latent RNA Transcript inhibits host cell proliferation and survival We used chromosome conformation capture to determine long-range interactions among CTGF protein, Homo sapiens/cohesins Site over 2 Mb on Homo sapiens chromosome 11 encompassing the beta-globin Gene Locus and Flank (surface region) olfactory receptor genes These results support a Genome - anatomical entity-wide role for CTGF protein, Homo sapiens/cohesins Site through loop formation that both influences transcription and contributes to cell-type-specific chromatin location location organization and function Increased methylation at this promoter triggered the dissociation of the insulator protein CTGF protein, Homo sapiens as well as the accompanying cohesins from the BDNF Gene Locus icotinamide adenine dinucleotide (NAD)-regulated DNA methylation alters CCCTC-binding factor (CTGF protein, Homo sapiens)/cohesins binding and transcription at the BDNF Gene Locus ecent studies have shown that the protein CTGF protein, Homo sapiens, which plays an important role in insulation and in large-scale organization of chromatin location location within the eukaryotic nucleus, depends for both activities on recruitment of the cohesins complex We show here that the interaction of CTGF protein, Homo sapiens with the cohesins complex involves direct contacts between the cohesins subunit STAG2 wt Allele and specific regions of the C-terminal tail of CTGF protein, Homo sapiens Taken together, our results demonstrate that specific Site on the C terminus of CTGF protein, Homo sapiens are essential for cohesins binding and insulator function The only direct interaction between CTGF protein, Homo sapiens and cohesins involves contact with STAG2 wt Allele, which is external to the cohesins ring These numerous CTGF protein, Homo sapiens/cohesins Site potentially form the Unit dose - Base of the multiloop rosette structures at the Igh Gene Locus that compact during Ig heavy chain rearrangement We have previously shown that the Homo sapiens herpesvirus 8 (KSHV) major latency RNA Transcript encoding latent Orf73 antigen, Homo sapiens herpesvirus 8, vCyclin, FLICE Inhibitory Protein, v-miRNAs, and Kaposin are regulated, in part, by a chromatin location location organizing element that binds CTGF protein, Homo sapiens and cohesins Mutation of the CTGF protein, Homo sapiens-cohesins binding Specimen Source Codes - Site reduced or eliminated the chromatin location location conformation linkages, and deregulated Viral transcription and Genome - anatomical entity copy number control Our findings indicate that KSHV Genome are organized into chromatin location location loops mediated by CTGF protein, Homo sapiens and cohesins interactions, and that these inter-chromosomal linkages coordinate latent and lytic gene control. We show here that Gestational age:Time:Point in time:^Fetus:Quantitative disrupts an RNA Polymerase II (RNAPII) complex that accumulates at the CTGF protein, Homo sapiens-cohesins binding Specimen Source Codes - Site within the first Introns of the latency transcript. Gestational age:Time:Point in time:^Fetus:Quantitative altered the enrichment of the RNAPII pausing complex, along with pausing factors SUPT5H gene and WHSC2 protein, Homo sapiens, at the intragenic CTGF protein, Homo sapiens-cohesins Binding Sites. Gestational age:Time:Point in time:^Fetus:Quantitative treatment also inhibited the transcription of some Cells genes, like c-myc Genes Genes, which contain a similar CTGF protein, Homo sapiens-cohesins binding Specimen Source Codes - Site within the first Introns. These findings suggest that RNAPII pauses at intragenic CTGF protein, Homo sapiens-cohesins Binding Sites and that abrogation of this pausing by Gestational age:Time:Point in time:^Fetus:Quantitative leads to loss of proper mRNA production and defects in sister chromatid cohesion, a process important for both Viral and Cells chromosome stability. TCF and cohesins cooperatively mediate the cell-type specific interchromatin interaction between B-Cell Lymphoma/Leukemia 11B and ARHGAP6 gene loci Additional experiments verified that the interchromatin interaction between the B-Cell Lymphoma/Leukemia 11B and ARHGAP6 gene loci was cell-type specific, which was cooperatively mediated by CTGF protein, Homo sapiens and cohesins. enome-wide studies of CCCTC-binding factor (CTGF protein, Homo sapiens) and cohesins provide insight into chromatin location location structure and regulation Recent Genome - anatomical entity-wide studies mapping the Binding Sites of CTGF protein, Homo sapiens and its interacting partner, cohesins, using chromatin location location immunoprecipitation coupled with deep sequencing (Chromatin Immunoprecipitation Sequencing) revealded that CTGF protein, Homo sapiens globally co-localizes with cohesins Here, we show by ChIP-Seq that most Homo sapiens subtelomeres contain a CTGF protein, Homo sapiens- and cohesins-binding Specimen Source Codes - Site within \u223c1-2\u2009kb of the TTAGGG repeat tract and adjacent to a CpG-islands implicated in Telomeric Repeat-Containing RNA transcription control. These findings indicate that CTGF protein, Homo sapiens and cohesins are integral components of most Homo sapiens subtelomeres, and important for the regulation of Telomeric Repeat-Containing RNA transcription and telomere end protection In addition, we show that this DNA looping requires specific binding of the CTGF protein, Homo sapiens/cohesins complex to two symmetrically aligned Binding Sites in both the transcriptionally active Promoter and in one of the enhancers[SEP]", "label": "yes"}
{"original_question": "Are stress granules involved in the pathogenesis of Amyotrophic Lateral Sclerosis?", "id": "converted_28", "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 Gene Mutation 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 Gene Mutation have been linked to hereditary forms, and aggregation of RNA-Binding Protein Feline urological syndrome 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 Signals (NLS) and causing Cytoplasmic mislocalization can be sequestered into Stress Granules (Shprintzen-Goldberg syndrome). PFN1 gene associates with Stress Granules and ALS-linked Gene Mutation alter stress granule dynamics Here we report that profilin 1 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 Gene Mutation in profilin 1 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 Gene Mutation in Feline urological syndrome NLS 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 Gene Mutation. protein protein TDP-43, human, human is an RNA-Binding Proteins 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 Mutations 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 RNAs 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 RNA-Binding Protein Feline urological syndrome, 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: Frontotemporal dementia has relations: disease_phenotype_positive with AMYOTROPHIC LATERAL SCLEROSIS 1, disease_phenotype_positive with AMYOTROPHIC LATERAL SCLEROSIS 1. Motor neuron atrophy has relations: disease_phenotype_positive with AMYOTROPHIC LATERAL SCLEROSIS 1, disease_phenotype_positive with AMYOTROPHIC LATERAL SCLEROSIS 1. Cytoplasm has relations: cellcomp_protein with Protein Arginine N-Methyltransferase 1, cellcomp_protein with Protein Arginine N-Methyltransferase 1, cellcomp_protein with Protein Arginine N-Methyltransferase 1, cellcomp_protein with Protein Arginine N-Methyltransferase 1. AMYOTROPHIC LATERAL SCLEROSIS 1 has relations: disease_protein with Feline urological syndrome, disease_protein with Feline urological syndrome. protein-arginine N-methyltransferase activity has relations: molfunc_protein with Protein Arginine N-Methyltransferase 1, molfunc_protein with Protein Arginine N-Methyltransferase 1. protein binding has relations: molfunc_protein with Feline urological syndrome, molfunc_protein with Protein Arginine N-Methyltransferase 1, molfunc_protein with Feline urological syndrome, molfunc_protein with Protein Arginine N-Methyltransferase 1, molfunc_protein with Feline urological syndrome, molfunc_protein with Protein Arginine N-Methyltransferase 1, molfunc_protein with Feline urological syndrome, molfunc_protein with Protein Arginine N-Methyltransferase 1. germ cell Cell Nucleus has relations: cellcomp_cellcomp with Cell Nucleus, cellcomp_cellcomp with Cell Nucleus.", "label": "yes"}
{"original_question": "Does TGF-beta play a role in cardiac regeneration after myocardial infarction?", "id": "converted_29", "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 \u03b2 signaling pathways.  Here, we report that the balance between the reparative and regenerative processes is achieved through Smad3-dependent TGF\u03b2 signaling.  Thus, TGF\u03b2 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]", "label": "yes"}
{"original_question": "Is DITPA a thyroid hormone analog utilized in experimental and clinical studies", "id": "converted_30", "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 \u00b7 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 \u03b1- and \u03b2-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: Nitric Oxide has relations: contraindication with Congestive heart failure, contraindication with Congestive heart failure.", "label": "yes"}
{"original_question": "Is MammaPrint cleared by the United States Food and Drug Administration?", "id": "converted_31", "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]", "label": "yes"}
{"original_question": "Is amantadine effective for treatment of disorders conciousness?", "id": "converted_32", "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. Pharmacologic Substance 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 Injury. 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 Head>Brain injury. 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 Head>Brain injury and provides important information necessary to design future more definitive studies. The study has shown a positive effect of this drug 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]", "label": "yes"}
{"original_question": "Is GAGA associated with nucleosome-free regions (NFR)?", "id": "converted_33", "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 Protein Info 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 (DH) 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 Protein Info 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 Protein Info that is related to the Mammals TRANSCRIPTION FACTOR YY1 gene gene.[SEP]", "label": "yes"}
{"original_question": "Is amiodarone a class I anti-arrhythmic drug?", "id": "converted_34", "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: Dofetilide has relations: drug_drug with amiodarone, drug_drug with amiodarone. Cardiogenic shock has relations: drug_effect with amiodarone, drug_effect with amiodarone.", "label": "no"}
{"original_question": "Has the protein TIEG1 been associated with apoptosis?", "id": "converted_35", "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 Malignant neoplasm of pancreas Cells, yet its effect on Recombinant Transforming Growth Factor-Beta resistant cancer Cells 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 TIEG-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-\u03b21-resistant altretamine/cisplatin/cyclophosphamide protocol cell lines, On the other hand, KLF10 gene gene deficient keratinocyte showed increased proliferation and apoptosis LF10, transforming growth factor-\u03b2-inducible early gene 1 IEG1 can induce apoptosis of cancer Cells TGF-\u03b2 inducible early gene 1) plays a significant role in regulating cell proliferation and apoptosis TIEG1) is a Kr\u00fcppel-like TRANSCRIPTION FACTOR (KLF10 gene gene) that was originally cloned from Homo sapiens osteoblasts as an early response gene to TGF-\u03b2 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)-\u03b2 inducible early gene (TIEG)-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 (TIEG) 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 TIEG is sufficient to trigger the apoptotic cell program in these Cells[SEP]", "label": "yes"}
{"original_question": "Is PTEN involved in follicular thyroid carcinoma?", "id": "converted_36", "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 Hamartoma Syndrome, Multiple, disease_protein with Hamartoma Syndrome, Multiple. Macrocephaly has relations: disease_phenotype_positive with Hamartoma Syndrome, Multiple, disease_phenotype_positive with Hamartoma Syndrome, Multiple. Neoplasm of the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS gland has relations: disease_phenotype_positive with Hamartoma Syndrome, Multiple, disease_phenotype_positive with Hamartoma Syndrome, Multiple. PTEN protein, human hamartoma tumor syndrome has relations: disease_protein with PTEN protein, human, disease_disease with Hamartoma Syndrome, Multiple, disease_protein with PTEN protein, human, disease_disease with Hamartoma Syndrome, Multiple.", "label": "yes"}
{"original_question": "Does strenuous physical activity affect thyroid hormone metabolism?", "id": "converted_37", "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 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 triiodothyronine 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 AKR1B1 protein, human, anatomy_protein_present with AKR1B1 protein, human.", "label": "yes"}
{"original_question": "Is the gene MAOA epigenetically modified by methylation?", "id": "converted_38", "sentence1": "Is the gene MAOA protein, human epigenetically modified by methylation?", "sentence2": "Evidence that the methylation state of the MAOA protein, human protein, human gene (MAOA protein, human protein, human) gene predicts brain activity of Monoamine Oxidase A Enzyme [APC] in healthy men. We found significant interindividual differences in methylation status and methylation patterns of the core MAOA protein, human protein, human Promoter.  In the present study, DNA methylation patterns in the MAOA protein, human protein, human regulatory and exon 1/intron 1 Geographic Locations were investigated for association with Panic Disorder with particular attention to possible effects of gender and environmental factors.   The present pilot data suggest a potential role of MAOA protein, human protein, human gene hypomethylation in the pathogenesis of Panic Disorder particularly in female patients, possibly mediating a detrimental influence of negative life events.  The MAOA protein, human protein, human Promoter was hypermethylated immediately upstream of the start codon in cholangiocarcinoma samples and Cultured Cell Line but not in nonmalignant counterparts.  MAOA protein, human protein, human Promoter methylation and susceptibility to carotid atherosclerosis: role of familial factors in a monozygotic twin sample. Because twins reared together share early life experience, which may leave a long-lasting epigenetic mark, aberrant MAOA protein, human protein, human methylation may represent an early biomarker for unhealthy familial environment. Effects of MAOA protein, human protein, human Promoter methylation on susceptibility to paranoid SCHIZOPHRENIA 2 (disorder). In conclusion, abnormalities of DNA methylation at the MAOA protein, human protein, human Promoter may be associated with SCHIZOPHRENIA 2 (disorder) in males. In our study we analyzed DNA methylation patterns of 14 neuropsychiatric genes (Catechol O-Methyltransferase, SLC6A3 wt Allele, GABRA1 gene gene, GNB3 protein, human protein, human, GRIN2B gene gene, HTR1B protein, human protein, human, HTR2A 1 Allele 1 Allele, 5-HTT, MAOA protein, human protein, human, Monoamine Oxidase Type B, human, NANOS1 gene, NR3C1 wt Allele wt Allele, TPH1 protein, human protein, human and Tyrosine 3-Monooxygenase, human). D Our data suggest that aberrant epigenetic regulation of neuropsychiatric genes may contribute to the pathogenesis of Borderline Personality Disorder. We conclude that Location characteristic ID - Smoking reliably decreases MAOA protein, human protein, human methylation, but exact characterization of effects on level of methylation depend on genotype, Location characteristic ID - Smoking history, current Location characteristic ID - Smoking status, gender, and Geographic Locations of the Promoter-associated CpG Island examined. Given that DNA methylation is linked to the regulation of gene expression, we hypothesized that epigenetic mechanisms factor into the MAOA protein, human protein, human expression  the extended MAOA protein, human protein, human regulatory Geographic Locations contains two CpG islands (CGIs), one of which overlaps with the canonical MAOA protein, human protein, human Promoter and the other is located further upstream; both CGIs exhibit sensitivity to differential methylation. Identification and characterization of putative methylation targets in the MAOA protein, human protein, human Gene Locus using bioinformatic approaches. DNA methylation is a key epigenetic mechanism involved in the developmental regulation of gene expression.  MAOA protein, human protein, human methylation is associated with nicotine and alcohol dependence in women. In recent years, the role of epigenetic phenomenon, such as methylation, in mediating vulnerability to Illness Behavior has become increasingly appreciated. One prominent Gene Locus at which epigenetic phenomena are thought to be in play is the MAOA protein, human protein, human gene (MAOA protein, human protein, human) Gene Locus.  We conclude that methylation of MAOA protein, human protein, human may play a significant role in common Mental disorders and that further examination of epigenetic processes at this Gene Locus is in order. Analysis of CpG methylation in the MAOA protein, human protein, human Promoter Geographic Locations revealed substantial methylation in females but not in males. Therefore, allelic mRNA expression is affected by Genetic and epigenetic events, both with the potential to modulate biogenic amine tone in the Central Nervous System.[SEP]Relations: mental disorder has relations: disease_protein with HTR1B protein, human, disease_protein with HTR1B protein, human. Nicotine has relations: drug_protein with Monoamine Oxidase Type B, human, drug_protein with MAOA protein, human, drug_protein with Monoamine Oxidase Type B, human, drug_protein with MAOA protein, human. tyrosine 3-monooxygenase activity has relations: molfunc_protein with Tyrosine 3-Monooxygenase, human, molfunc_protein with Tyrosine 3-Monooxygenase, human. monoamine oxidase activity has relations: molfunc_protein with MAOA protein, human, molfunc_protein with Monoamine Oxidase Type B, human, molfunc_protein with MAOA protein, human, molfunc_protein with Monoamine Oxidase Type B, human, molfunc_protein with MAOA protein, human, molfunc_protein with Monoamine Oxidase Type B, human, molfunc_protein with MAOA protein, human, molfunc_protein with Monoamine Oxidase Type B, human. GRIN2B gene has relations: disease_protein with SCHIZOPHRENIA 2 (disorder), disease_protein with SCHIZOPHRENIA 2 (disorder). central nervous system has relations: anatomy_protein_present with GABRA1 gene, anatomy_protein_present with Catechol O-Methyltransferase, anatomy_protein_present with GNB3 protein, human, anatomy_protein_present with Monoamine Oxidase Type B, human, anatomy_protein_present with MAOA protein, human, anatomy_protein_present with GABRA1 gene, anatomy_protein_present with Catechol O-Methyltransferase, anatomy_protein_present with GNB3 protein, human, anatomy_protein_present with Monoamine Oxidase Type B, human, anatomy_protein_present with MAOA protein, human. personality disorder has relations: disease_protein with MAOA protein, human, disease_protein with MAOA protein, human. catechol O-methyltransferase activity has relations: molfunc_protein with Catechol O-Methyltransferase, molfunc_protein with Catechol O-Methyltransferase. GABRA1 gene has relations: disease_protein with SCHIZOPHRENIA 2 (disorder), disease_protein with SCHIZOPHRENIA 2 (disorder). Enzymatic degradation of Dopamine by monoamine oxidase has relations: pathway_protein with MAOA protein, human, pathway_protein with Catechol O-Methyltransferase, pathway_protein with MAOA protein, human, pathway_protein with Catechol O-Methyltransferase. schizophreniform disorder has relations: disease_protein with HTR1B protein, human, disease_protein with HTR1B protein, human.", "label": "yes"}
{"original_question": "Is glycyl-tRNA synthetase gene involved in the development of Charcot-Marie-Tooth disease?", "id": "converted_39", "sentence1": "Is Glycine-tRNA Ligase Genes involved in the development of Charcot-Marie-Tooth Disease?", "sentence2": "Charcot-Marie-Tooth Disease type 2D (Charcot-Marie-Tooth Disease, Type 2D) is an autosomal-dominant axonal peripheral neuropathy characterized by impaired motor and sensory function in the distal extremities. Mutations in the Glycine-tRNA Ligase (GARS) Genes cause Charcot-Marie-Tooth Disease, Type 2D Dominant Gene Mutation 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 Gene Mutation within the Glycine-tRNA Ligase (GARS) Genes Gene Mutation of human GlyRS (hGlyRS) were also found to be associated with Charcot-Marie-Tooth Disease Dominant Gene Mutation in GARS, encoding the essential Enzyme [APC] Glycine-tRNA Ligase (GlyRS), result in a form of Charcot-Marie-Tooth Disease, type 2D (Charcot-Marie-Tooth Disease, Type 2D), predominantly characterized by lower motor nerve degeneration A novel Mutation Abnormality in Glycine-tRNA Ligase 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 Glycine-tRNA Ligase (GARS), a causative Genes for both CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate type 2D (Charcot-Marie-Tooth Disease, Type 2D) and distal spinal muscular atrophy type V (dSMA-V) Charcot-Marie-Tooth Disease type 2D (Charcot-Marie-Tooth Disease, Type 2D) is a dominantly inherited peripheral neuropathy caused by missense Gene Mutation in the Glycine-tRNA Ligase Genes (GARS). Long-range structural effects of a Charcot-Marie-Tooth Disease-causing Mutation Abnormality in human Glycine-tRNA Ligase. Glycyl tRNA synthetase Gene Mutation in Charcot-Marie-Tooth Disease type 2D and distal spinal muscular atrophy type V. [A novel Mutation Abnormality in Glycine-tRNA Ligase 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 (Charcot-Marie-Tooth Disease, Type 2D) and NEURONOPATHY, DISTAL HEREDITARY MOTOR, TYPE V (dHMN-V). These additional functions may explain why dominant Gene Mutation in Glycine-tRNA Ligase (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 Procedures on Peripheral Nervous System. Here, we report the identification of four disease-associated missense Gene Mutation in the glycyl tRNA synthetase Genes in families with Charcot-Marie-Tooth Disease, Type 2D and dSMA-V. Mutations in the Glycine-tRNA Ligase (GARS) Genes cause Charcot-Marie-Tooth Disease, Type 2D. Of the many inherited Charcot-Marie-Tooth peripheral Neuropathy, type 2D (Charcot-Marie-Tooth Disease, Type 2D) is caused by dominant point Gene Mutation in the Genes GARS, encoding glycyl tRNA synthetase (GlyRS). Charcot-Marie-Tooth Disease type 2D (Charcot-Marie-Tooth Disease, Type 2D) is a dominantly inherited peripheral neuropathy caused by missense Gene Mutation in the Glycine-tRNA Ligase Genes (GARS) Charcot-Marie-Tooth Disease type 2D is a hereditary axonal and Glycine-tRNA Ligase (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 Glycine-tRNA Ligase These additional functions may explain why dominant Gene Mutation in Glycine-tRNA Ligase (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 Procedures on Peripheral Nervous System A novel Mutation Abnormality in Glycine-tRNA Ligase caused Charcot-Marie-Tooth Disease type 2D with facial and respiratory muscle involvement. Charcot-Marie-Tooth Disease type 2D (Charcot-Marie-Tooth Disease, Type 2D) is a dominantly inherited peripheral neuropathy caused by missense Gene Mutation in the Glycine-tRNA Ligase Genes (GARS).  Mutations in the Glycine-tRNA Ligase (GARS) Genes cause Charcot-Marie-Tooth Disease, Type 2D.  An ENU-induced Mutation Abnormality in mouse Glycine-tRNA Ligase (GARS) causes peripheral sensory and motor phenotypes creating a model of Charcot-Marie-Tooth type 2D peripheral neuropathy. We previously implicated Gene Mutation in the Genes encoding Glycine-tRNA Ligase (GARS) as the cause of Charcot-Marie-Tooth Disease, Type 2D and dSMA-V.  An active dominant Mutation Abnormality of Glycine-tRNA Ligase causes neuropathy in a Charcot-Marie-Tooth 2D mouse model. Charcot-Marie-Tooth Disease type 2D is a hereditary axonal and Glycine-tRNA Ligase (GARS)-associated neuropathy that is caused by a Mutation Abnormality in GARS.  Dominant Gene Mutation in GARS, encoding the essential Enzyme [APC] Glycine-tRNA Ligase (GlyRS), result in a form of Charcot-Marie-Tooth Disease, type 2D (Charcot-Marie-Tooth Disease, Type 2D), predominantly characterized by lower motor nerve degeneration.   Charcot-Marie-Tooth Disease type 2D (Charcot-Marie-Tooth Disease, Type 2D) is a dominantly inherited peripheral neuropathy caused by missense Gene Mutation in the Glycine-tRNA Ligase Genes (GARS). In addition to GARS, Gene Mutation in three other tRNA synthetase genes cause similar Neuropathy, although the underlying mechanisms are not fully understood. These additional functions may explain why dominant Gene Mutation in Glycine-tRNA Ligase (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 (Charcot-Marie-Tooth Disease, Type 2D) is an autosomal-dominant axonal peripheral neuropathy characterized by impaired motor and sensory function in the distal extremities. Mutations in the Glycine-tRNA Ligase (GARS) Genes cause Charcot-Marie-Tooth Disease, Type 2D. Of the many inherited Charcot-Marie-Tooth peripheral Neuropathy, type 2D (Charcot-Marie-Tooth Disease, Type 2D) is caused by dominant point Gene Mutation in the Genes GARS, encoding glycyl tRNA synthetase (GlyRS). Charcot-Marie-Tooth Disease type 2D (Charcot-Marie-Tooth Disease, Type 2D) is a dominantly inherited peripheral neuropathy caused by missense Gene Mutation in the Glycine-tRNA Ligase Genes (GARS). Long-range structural effects of a Charcot-Marie-Tooth Disease-causing Mutation Abnormality in human Glycine-tRNA Ligase. Glycyl tRNA synthetase Gene Mutation in Charcot-Marie-Tooth Disease type 2D and distal spinal muscular atrophy type V. These additional functions may explain why dominant Gene Mutation in Glycine-tRNA Ligase (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 Procedures on Peripheral Nervous System. A novel Mutation Abnormality in Glycine-tRNA Ligase caused Charcot-Marie-Tooth Disease type 2D with facial and respiratory muscle involvement. An active dominant Mutation Abnormality of Glycine-tRNA Ligase 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 (Charcot-Marie-Tooth Disease, Type 2D) and NEURONOPATHY, DISTAL HEREDITARY MOTOR, TYPE V (dHMN-V).[SEP]Relations: Optic neuropathy has relations: disease_phenotype_positive with Charcot-Marie-Tooth Disease, disease_phenotype_positive with Charcot-Marie-Tooth Disease. Respiratory insufficiency due to muscle weakness has relations: disease_phenotype_positive with Charcot-Marie-Tooth Disease, disease_phenotype_positive with Charcot-Marie-Tooth Disease. neuronopathy, distal hereditary motor has relations: disease_disease with Charcot-Marie-Tooth Disease, disease_disease with Charcot-Marie-Tooth Disease.", "label": "yes"}
{"original_question": "Is there any software for automated analysis of FISH images?", "id": "converted_40", "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, \u2026,22,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 \"U\" lymphocyte 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, human Protein Info, human, ZNF217 protein, 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, human Protein Info, human oncogene and seven of 13 (54%) cases were amplified for ZNF217 protein, 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, human Protein Info, human, ZNF217 protein, 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, human Protein Info, human oncogene and seven of 13 (54%) cases were amplified for ZNF217 protein, 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, human Protein Info, human, ZNF217 protein, 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, human Protein Info, human oncogene and seven of 13 (54%) cases were amplified for ZNF217 protein, 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 Proto-Oncogene Tyrosine-Protein Kinase Src, human, disease_protein with MYC protein, human, disease_protein with ZNF217 protein, human, disease_protein with Proto-Oncogene Tyrosine-Protein Kinase Src, human, disease_protein with MYC protein, human, disease_protein with ZNF217 protein, human.", "label": "yes"}
{"original_question": "Is there an increased risk for cancer in Dyskeratosis Congenita?", "id": "converted_41", "sentence1": "Is there an increased risk for cancer in Dyskeratosis Congenita?", "sentence2": "People with DC are at increased risk for progressive Bone marrow hypocellularity (Bcl-2-Modifying Factor), MYELODYSPLASTIC SYNDROME (Miller Dieker syndrome) or acute myelogenous leukemia (Leukemia, Myelocytic, Acute), Solid Neoplasm (usually Anal Anal squamous cell carcinoma of the head/neck or anogenital cancer), 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 cancer. Fanconi Anemia (doxorubicin/fluorouracil protocol), Dyskeratosis Congenita (DC), 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 (Leukemia, Myelocytic, Acute), 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 DC; Diamond-Blackfan Anemia 1 and Symptom Distress Scale were mildest. While doxorubicin/fluorouracil protocol and DC patients had markedly increased risks of cancer, Leukemia, Myelocytic, Acute 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 DC are major cancer susceptibility syndromes People with DC are at increased risk for progressive Bone marrow hypocellularity (Bcl-2-Modifying Factor), MYELODYSPLASTIC SYNDROME (Miller Dieker syndrome) or acute myelogenous leukemia (Leukemia, Myelocytic, Acute), Solid Neoplasm (usually Anal Anal squamous cell carcinoma of the head/neck or anogenital cancer), and Pulmonary:-:Point in time:^Patient:- fibrosis Patients with Dyskeratosis Congenita (DC) have an increased risk of cancer, but also exhibit heightened radiation sensitivity. Dyskeratosis congenita (DC) 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 cancer 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 cancer. Dyskeratosis Congenita (DC) 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 cancer\". Dyskeratosis congenita is an inherited syndrome characterised by mucocutaneous features, Bone marrow hypocellularity, an increased risk of Primary malignant neoplasm 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 cancer are also common in DC patients. telomere dysfunction and Specimen Source Codes - Specimen Source Codes - tumor suppression responses in Dyskeratosis Congenita: balancing cancer and tissue renewal impairment. Patients with Dyskeratosis Congenita (DC) have an increased risk of cancer, 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 Primary malignant neoplasm and other somatic abnormalities While doxorubicin/fluorouracil protocol and DC patients had markedly increased risks of cancer, Leukemia, Myelocytic, Acute 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 cancer predisposition syndrome; cancer 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 DC 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 cancer are considered in the context of DC, resulting in two translational models: late onset of DC symptoms in telomere-related mutations carriers is a potential indicator of increased cancer 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 cancer Dyskeratosis congenita is a cancer-prone BONE MARROW FAILURE SYNDROME 2 caused by aberrations in telomere biology.[SEP]Relations: Pancytopenia has relations: disease_phenotype_positive with BONE MARROW FAILURE SYNDROME 2, disease_phenotype_positive with SHWACHMAN-DIAMOND SYNDROME 2, disease_phenotype_positive with BONE MARROW FAILURE SYNDROME 2, disease_phenotype_positive with SHWACHMAN-DIAMOND SYNDROME 2. FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) complementation group has relations: disease_disease with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_disease with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder). Bone marrow hypocellularity has relations: disease_phenotype_positive with SHWACHMAN-DIAMOND SYNDROME 2, disease_phenotype_positive with Dyskeratosis Congenita, disease_phenotype_positive with BONE MARROW FAILURE SYNDROME 2, disease_phenotype_positive with SHWACHMAN-DIAMOND SYNDROME 2, disease_phenotype_positive with Dyskeratosis Congenita, disease_phenotype_positive with BONE MARROW FAILURE SYNDROME 2. Oral leukoplakia has relations: disease_phenotype_positive with Dyskeratosis Congenita, disease_phenotype_positive with Dyskeratosis Congenita. anal canal Anal squamous cell carcinoma has relations: disease_disease with Anal squamous cell carcinoma, disease_disease with Anal squamous cell carcinoma.", "label": "yes"}
{"original_question": "Does MicroRNA-21 (miR-21) contribute to cardiovascular disease?", "id": "converted_42", "sentence1": "Does MicroRNA-21 (MIR21 gene) contribute to Cardiovascular Diseases?", "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 TGF\u03b2RIII 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 \u2160, type \u2162 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 myocytes 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 myocytes' 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 Diseases conditions such as proliferative vascular Disease, Cardiac - anatomy qualifier hypertrophy and Chest>Heart failure, and ischemic Chest>Heart Disease. MIR21 gene is found to play important roles in vascular smooth muscle \"U\" lymphocyte proliferation and apoptosis, Cardiac - anatomy qualifier \"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 Diseases. 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 myocytes, 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 Cardiac - anatomy qualifier \"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 myocytes, 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 Muscle Cells 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 myocytes. MIR21 gene might play an essential role in Chest>Heart diseases related to Reactive Oxygen Species such as Cardiac - anatomy qualifier hypertrophy, Chest>Heart failure, Myocardial infarction:Finding:Point in time:^Patient:Ordinal, and Myocardial ischemia/reperfusion injury. MicroRNA-21 contributes to Myocardial Disease 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 myocytes 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 Myocardial Disease 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 Diseases. These findings reveal that MicroRNAs can contribute to Myocardial Disease by an effect in Cardiac - anatomy qualifier Specimen Source Codes - Fibroblasts. Our results validate MIR21 gene as a Disease target in Chest>Heart failure and establish the therapeutic efficacy of microRNA therapeutic intervention in a Cardiovascular Diseases setting.[SEP]", "label": "yes"}
{"original_question": "Are there any statistical methods for normalizing and identifying differential regions in histone modification ChIP-seq data?", "id": "converted_43", "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 modifications 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 modifications 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 modifications 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 modifications 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 modifications 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 modifications 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 modifications 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 modifications 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 modifications of different cell types.[SEP]", "label": "yes"}
{"original_question": "Is CD84 genetically associated with arthritis?", "id": "converted_44", "sentence1": "Is CD84 gene genetically associated with arthritis?", "sentence2": "The Single Nucleotide Polymorphism is predicted to disrupt transcription factor binding site motifs in the 3' Untranslated Regions of an immune-related gene, CD84 gene gene, and the Alleles associated with better response to etanercept was associated with higher CD84 gene gene gene expression in Peripheral blood mononuclear cell (cell) (P = 1 \u00d7 10(-11) in 228 non-Rheumatoid Arthritis patients and P = 0.004 in 132 Rheumatoid Arthritis patients) Our study demonstrates that an Alleles associated with response to etanercept therapy is also associated with CD84 gene gene gene expression, and further that CD84 gene gene expression correlates with disease activity  Three members of this gene family, SLAMF6 wt Allele, LY9 protein, Homo sapiens, and CD84 gene gene, exhibit Genetic Polymorphism that strongly influence susceptibility to systemic autoimmunity, notably in CASP14 gene, but also in some Homo sapiens populations[SEP]", "label": "yes"}
{"original_question": "Are there any specific antidotes for rivaroxaban?", "id": "converted_45", "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: contraindication with Hepatobiliary Disorder, contraindication with Hepatobiliary Disorder. hepatobiliary disease has relations: disease_disease with Hepatobiliary Disorder, disease_disease with Hepatobiliary Disorder. Warfarin has relations: contraindication with Cerebral Hemorrhage, contraindication with Hepatobiliary Disorder, contraindication with Cerebral Hemorrhage, contraindication with Hepatobiliary Disorder. Dabigatran etexilate has relations: contraindication with Cerebral Hemorrhage, contraindication with Cerebral Hemorrhage.", "label": "no"}
{"original_question": "Is cytisine superior to nicotine replacement therapy for smoking cessation?", "id": "converted_46", "sentence1": "Is cytisine superior to nicotine replacement therapy for smoking cessation?", "sentence2": "The effectiveness of cytisine for continuous abstinence was superior to that of nicotine-replacement therapy at 1 week, 2 months, and 6 months. In a prespecified subgroup analysis of the primary outcome, cytisine was superior to nicotine-replacement therapy among women and noninferior among men. CONCLUSIONS: When combined with brief behavioral support, cytisine was found to be superior to nicotine-replacement therapy in helping smokers quit smoking, but it was associated with a higher frequency of self-reported adverse events.[SEP]", "label": "yes"}
{"original_question": "Is the abnormal dosage of ultraconserved elements disfavored in cancer cells?", "id": "converted_47", "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.", "label": "no"}
{"original_question": "Does thyroid hormone regulate calcium transient in the myocardium?", "id": "converted_48", "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]", "label": "yes"}
{"original_question": "Are proteasome inhibitors good candidates for treatment of leukemia and solid tumors?", "id": "converted_49", "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 tumor 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 tumor 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 PS341 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 Neoplasms, 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 head and neck squamous cell carcinoma (Squamous cell carcinoma of the head and neck). Carfilzomib and Oprozomib potently inhibit Squamous cell carcinoma of the head and neck cell survival and the growth of Squamous cell carcinoma of the head and neck Neoplasms[SEP]Relations: Bortezomib has relations: indication with Mantle cell lymphoma, indication with Mantle cell lymphoma.", "label": "yes"}
{"original_question": "Is there any link between CTF4 and CTF18 during sister chromatid cohesion?", "id": "converted_50", "sentence1": "Is there any link between WDHD1 gene and CTF18 during sister chromatid cohesion?", "sentence2": "Our results suggest that ATAD5 wt Allele, Ctf4, and CHTF18 gene may coordinate the relative movement of the replication fork with respect to the cohesins ring These data defined two cohesion pathways, one containing CSM3, TOF1, WDHD1 gene, and DDX11 gene, and the second containing MRC1 gene gene, CTF18, CHTF8 gene, and DSCC1 gene Here we show that three Proteins required for sister chromatid cohesion, Eco1, Ctf4, and CHTF18 gene, are found at, and Ctf4 travels along Chromosomes, Human, Pair 1 with, replication forks. The ring-shaped cohesins complex is loaded onto Chromosomes, Human, Pair 1 before S phase in an adenosine triphosphate hydrolysis-dependent reaction. Cohesion establishment during DNA replication follows without further cohesins recruitment and without need for cohesins to re-engage an adenosine triphosphate hydrolysis motif that is critical for its initial DNA binding. This provides evidence for cohesion establishment in the context of replication forks and imposes constraints on the mechanism involved Sister-chromatid cohesion mediated by the alternative RF-CCtf18/Dcc1/Ctf8, the helicase Chl1 and the polymerase-alpha-associated protein Ctf4 is essential for chromatid disjunction during meiosis II 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 We also show that, in contrast to mitosis, RF-C(CHTF18 gene/Dcc1/Cft8), Ctf4 and Chl1 are essential for chromosome segregation during meiosis and for the viability of meiotic products. Ctf8p is a component of CHTF18 gene-RFC, an alternative replication factor C-like complex required for efficient sister chromatid cohesion in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae. We performed synthetic Genetic array (SGA) analysis with a ctf8 deletion strain as a primary screen to identify other nonessential Genes required for efficient sister chromatid cohesion. We then assessed proficiency of cohesion at three chromosomal loci in strains containing Gene Gene Gene Deletion Abnormality Abnormality of the Genes identified in the ctf8 SGA screen. Gene Gene Deletion Abnormality Abnormality of seven Genes (DDX11 gene, CSM3, BIM1, KAR3, TOF1, WDHD1 gene, and VIK1) resulted in defective sister chromatid cohesion Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae CTF18 and WDHD1 gene are required for sister chromatid cohesion WDHD1 gene and CTF18 are required for high-fidelity chromosome segregation. Both exhibit Genetic and physical ties to replication fork constituents. 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. 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. The requirement for WDHD1 gene and CTF18 in robust cohesion identifies novel roles for replication accessory Proteins in this process Here we show that three Proteins required for sister chromatid cohesion, Eco1, Ctf4, and CHTF18 gene, are found at, and Ctf4 travels along Chromosomes, Human, Pair 1 with, replication forks. Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae 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. 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. Sister-chromatid cohesion mediated by the alternative RF-CCtf18/Dcc1/Ctf8, the helicase Chl1 and the polymerase-alpha-associated protein Ctf4 is essential for chromatid disjunction during meiosis II. 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 Chl1 and the pathway involving the acetylation of SMC3 wt Allele. 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. Here we show that three Proteins required for sister chromatid cohesion, Eco1, Ctf4, and CHTF18 gene, are found at, and Ctf4 travels along Chromosomes, Human, Pair 1 with, replication forks. 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. 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. Here we show that three Proteins required for sister chromatid cohesion, Eco1, Ctf4, and CHTF18 gene, are found at, and Ctf4 travels along Chromosomes, Human, Pair 1 with, replication forks 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 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 In addition to Eco1, several other factors contribute to cohesion establishment, including Ctf4, CHTF18 gene, Tof1, Csm3, Chl1 and Mrc1, but little is known about their roles[SEP]", "label": "yes"}
{"original_question": "Are thyroid hormone receptor alpha1 mutations implicated in thyroid hormone resistance syndrome?", "id": "converted_51", "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 TR\u03b11. 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]", "label": "yes"}
{"original_question": "Does administration of triiodothyronine improve outcome following coronary artery bypass grafting?", "id": "converted_52", "sentence1": "Does administration of liothyronine improve outcome following coronary artery bypass grafting?", "sentence2": "Serum SLC25A5 gene concentrations were significantly higher with fewer patients having SLC25A5 gene concentrations below the normal range in the SLC25A5 gene group than the placebo group throughout the postoperative period. Hemodynamic variables, postoperative inotrope requirement, and outcome variables showed no differences between the groups We conclude that although widespread interest has been shown on the use of Thyroid Hormones in the perioperative period, and the effect of cardiopulmonary bypass on thyroid hormone metabolism widely studied, there is no substantial evidence to justify routine use of Thyroid Hormones in patients undergoing coronary artery bypass grafting. Treatment with GIK, SLC25A5 gene, and GIK/SLC25A5 gene improves hemodynamic performance and results in reduced Cardiac troponin I release in patients undergoing on-pump CABG surgery. Perioperative administration of liothyronine increased cardiac output slightly and decreased systemic vascular resistance, but it had no effect on operative outcome. Parenteral liothyronine given after crossclamp removal during elective coronary artery bypass grafting significantly improved postoperative ventricular function, reduced the need for treatment with inotropic agents and mechanical devices, and decreased the incidence of Coronary Arteriosclerosis. The incidence of Atrial Fibrillation by ECG Finding was slightly decreased, and the need for postoperative pacemaker support was reduced. Perioperative SLC25A5 gene administration decreased the incidence and need for treatment of postoperative Atrial Fibrillation by ECG Finding.  Intravenous T(3) does not have dramatic effects on hemodynamic variables in this setting as has been previously suggested.  Raising serum liothyronine concentrations in patients undergoing coronary-artery bypass surgery increases cardiac output and lowers systemic vascular resistance, but does not change outcome or alter the need for standard postoperative therapy. No significant differences were noted in the pre and post CPB hemodynamics between the two groups for the most part of the study except that heart rate was increased in SLC25A5 gene group. The haemodynamic parameters were no different between the two groups at any postoperative time point. Likewise, density and affinity of lymphocyte beta-adrenoceptors were not significantly different from pre-operative values in either group.[SEP]", "label": "no"}
{"original_question": "Is long QT syndrome a cause for sudden cardiac death in athletes?", "id": "converted_53", "sentence1": "Is Long QT Syndrome a cause for sudden cardiac Cessation of life in athletes?", "sentence2": "A diversity of Cardiovascular Diseases including Hypertrophic obstructive cardiomyopathy, congenital coronary anomalies, ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA 1, Cardiomyopathy, Dilated, Aortic Rupture due to Marfan syndrome, Myocarditis, Valvular disease and electrical disorders (Wolff-Parkinson-White Syndrome, Long QT Syndrome, Brugada Syndrome (disorder)), as well as Commotio Cordis represent the common causes of Schnyder crystalline corneal dystrophy in young athletes. Sudden cardiac Cessation of life is the leading cause of mortality among young athletes with an incidence of 1-2 per 100,000 athletes per annum. The majority of cases are caused by an underlying structural cardiac abnormality, most commonly Hypertrophic obstructive cardiomyopathy. More recently, the understanding of non-structural causes such as Long QT Syndrome and Brugada Syndrome (disorder) has grown and diagnostic criteria have been developed.  This review considers in particular the causes of Cessation of life affecting athletes below 35 years of age. In this age group the largest proportion of deaths are caused by diseases with Autosomal dominant inheritance such as Hypertrophic obstructive cardiomyopathy, Arrhythmogenic Right Ventricular Dysplasia, long QT-syndrome, and Marfan Syndrome.  Knowledge of sudden cardiac Cessation of life in young athletes is imperative for all physicians and allied health professionals.  In this article, we review several etiologies of sudden cardiac Cessation of life, including Hypertrophic obstructive cardiomyopathy, Arrhythmogenic Right Ventricular Dysplasia, Wolff-Parkinson-White Syndrome, Long QT Syndrome, Brugada Syndrome (disorder), and Commotio Cordis.  Sudden cardiac Cessation of life (Schnyder crystalline corneal dystrophy) in young athletes is generally caused by inherited cardiac disorders. The genetic abnormalities most associated with Schnyder crystalline corneal dystrophy are Hypertrophic obstructive cardiomyopathy, Arrhythmogenic Right Ventricular Dysplasia, Long QT Syndrome, Brugada Syndrome (disorder), and catecholaminergic polymorphic Ventricular Tachycardia by ECG Finding. The most common cause of sudden cardiac Cessation of life in athletes is Hypertrophic obstructive cardiomyopathy. Other reasons are congenital coronary artery anomalies, nivocarditis, dilatative cardiomyopathy, arrhythmogenic cardiomyopathy of the right ventricle, SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding), Mitral Valve Prolapse Syndrome, Aortic Valve Stenosis, Arteriosclerosis, Long QT Syndrome, and blunt impact to the chest. The congenital Long QT Syndrome (Congenital Long QT Syndrome) is caused by cardiac ion channel mutations, which predispose young individuals to sudden cardiac Cessation of life often related to exercise.  A group of relatively uncommon but important genetic cardiovascular diseases (GCVDs) are associated with increased risk for sudden cardiac Cessation of life during exercise, including Hypertrophic obstructive cardiomyopathy, long-QT syndrome, Marfan syndrome, and Arrhythmogenic Right Ventricular Dysplasia. Primary electrical disorders (such as the Long QT Syndrome) are rarely present in athletes but, so far, are a considerable reason for disqualification from sport activity.[SEP]Relations: SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding), susceptibility to has relations: disease_disease with SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding), disease_disease with SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding). Ventricular tachycardia has relations: disease_phenotype_positive with ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA 1, disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding), disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA 1, disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding), disease_phenotype_positive with Brugada Syndrome (disorder). Cardiomyopathy, Dilated has relations: disease_disease with Hypertrophic obstructive cardiomyopathy, disease_disease with Hypertrophic obstructive cardiomyopathy. Autosomal dominant inheritance has relations: disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA 1, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA 1. Hypertrophic cardiomyopathy has relations: disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with Cardiomyopathy, Dilated. Sudden cardiac Cessation of life has relations: disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA 1, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA 1, disease_phenotype_positive with Cardiomyopathy, Dilated.", "label": "yes"}
{"original_question": "Is protein M3/6 a dual specificity phosphatase?", "id": "converted_54", "sentence1": "Is protein M3/6 a dual specificity Phosphoric Monoester Hydrolases?", "sentence2": "Involvement of the Dual-Specificity Phosphatases M3/6 in c-Jun N-terminal kinase inactivation following Cerebral Infarction in the Rattus norvegicus hippocampus. The results revealed upregulation of Dual-Specificity Phosphatases M3/6 (DUSP8 gene gene) activity at 4\u00a0h 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. Phosphatases play a particularly important role in this respect, by tightly controlling MAPK phosphorylation and activation. M3/6 (DUSP8 gene gene) is a Dual-Specificity Phosphatases 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 phosphatases (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 gene gene) is one of the dual-specificity protein phosphatases with distinct specificity towards MAPK8 wt Allele. M3/6 is a Dual-Specificity Phosphatases 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 Mitogen-Activated Protein Kinases or MAPK8 wt Allele/SAPK and p38 MAP kinases when expressed in COS-7 cells. M3/6 is the first Phosphoric Monoester Hydrolases 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 Phosphatases M3/6  Dual-Specificity Phosphatases M3/6 (DUSP8 gene gene) M3/6 (DUSP8 gene gene) is a Dual-Specificity Phosphatases implicated in the dephosphorylation and inactivation of MAPK8 wt Allele  the M3/6 Dual-Specificity Phosphatases M3/6 (DUSP8 gene gene) is one of the dual-specificity protein phosphatases with distinct specificity towards MAPK8 wt Allele M3/6 is a Dual-Specificity Phosphatases 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 Phosphatases enhances the activation of MAPK8 wt Allele by arsenite. Indeed, expanded polyglutamine impaired the solubility of the dual-specificity MAPK8 wt Allele Phosphoric Monoester Hydrolases M3/6. Regulation of dual-specificity phosphatases M3/6 and hVH5 by Phorbol Esters. M3/6 (DUSP8 gene gene) is one of the dual-specificity protein phosphatases with distinct specificity towards MAPK8 wt Allele. M3/6 is a Dual-Specificity Phosphatases selective for MAPK8 wt Allele [7, 8] M3/6 (DUSP8 gene gene) 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 Phosphoric Monoester Hydrolases M3/6 M3/6 is a Dual-Specificity Phosphatases selective for MAPK8 wt Allele [7, 8] Regulation of dual-specificity phosphatases M3/6 and hVH5 by Phorbol Esters. Analysis of a delta-like domain. The results revealed upregulation of Dual-Specificity Phosphatases M3/6 (DUSP8 gene gene) activity at 4\u00a0h of reperfusion in Rattus norvegicus hippocampi Indeed, expanded polyglutamine impaired the solubility of the dual-specificity MAPK8 wt Allele Phosphoric Monoester Hydrolases 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 gene gene) signaling[SEP]", "label": "yes"}
{"original_question": "Are there focused databases from which you can retrieve gene expression data on renal disease?", "id": "converted_55", "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 Homo sapiens urinary peptides for use in diagnosis of Chronic Kidney Diseases[SEP]", "label": "yes"}
{"original_question": "Are there any DNMT3 proteins present in plants?", "id": "converted_56", "sentence1": "Are there any DNMT3 proteins present in plants?", "sentence2": "De novo DNA methylation in Arabidopsis sp. sp. thaliana <Plant allergen> 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]", "label": "yes"}
{"original_question": "Has vitamin D has been shown to reduce incidence of falls in older people in clinical trials?", "id": "converted_57", "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]", "label": "yes"}
{"original_question": "Has depression been shown to be a predictor of frailty?", "id": "converted_58", "sentence1": "Has Cancer patients and suicide and depression been shown to be a predictor of frailty?", "sentence2": "significant role of frailty as a predictor of Cancer patients and suicide and Cancer patients and suicide and 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. 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]", "label": "yes"}
{"original_question": "Is there any association between Jarid2 and miR-155 in Th17 cells?", "id": "converted_59", "sentence1": "Is there any association between JARID2 gene and miR-155 in Th17 Cells?", "sentence2": "JARID2 gene links MicroRNA and Chromatin in Th17 Cells. In this issue of Immunity, Escobar et\u00a0al. (2014) bring MicroRNAs and Chromatin together by showing how activation-induced miR-155 targets the Chromatin protein JARID2 gene to regulate proinflammatory cytokine production in T helper 17 Cells. miR-155 activates cytokine gene expression in Th17 Cells by regulating the DNA-Binding Proteins JARID2 gene to relieve polycomb-mediated repression. MIR155 gene was bound by Th17 \"U\" lymphocyte transcription factors and was highly expressed during Th17 \"U\" lymphocyte differentiation. miR-155-deficient Th17 and T regulatory (Treg) Cells expressed increased amounts of JARID2 gene, a DNA-Binding Proteins that recruits the Polycomb Repressive Complex 2 (Polycomb Repressive Complex 2) to Chromatin. Polycomb Repressive Complex 2 binding to Chromatin and H3K27 histone methylation was increased in miR-155-deficient Cells, coinciding with failure to express IL22 protein, human, interleukin-10, interleukin-9, and Cyclic AMP-Dependent Transcription Factor ATF-3. Defects in Th17 \"U\" lymphocyte cytokine expression and Treg \"U\" lymphocyte homeostasis in the absence of MIR155 gene could be partially suppressed by JARID2 gene deletion. Thus, miR-155 contributes to Th17 \"U\" lymphocyte function by suppressing the inhibitory effects of JARID2 gene. Thus, miR-155 contributes to Th17 \"U\" lymphocyte function by suppressing the inhibitory effects of JARID2 gene. Thus, miR-155 contributes to Th17 \"U\" lymphocyte function by suppressing the inhibitory effects of JARID2 gene. Defects in Th17 \"U\" lymphocyte cytokine expression and Treg \"U\" lymphocyte homeostasis in the absence of MIR155 gene could be partially suppressed by JARID2 gene deletion. Thus, miR-155 contributes to Th17 \"U\" lymphocyte function by suppressing the inhibitory effects of JARID2 gene. Thus, miR-155 contributes to Th17 \"U\" lymphocyte function by suppressing the inhibitory effects of JARID2 gene.[SEP]", "label": "yes"}
{"original_question": "Is it safe to take isotretinoin during pregnancy?", "id": "converted_60", "sentence1": "Is it safe to take isotretinoin during pregnancy?", "sentence2": "isotretinoin is a remarkably effective Pharmacologic Substance for severe, recalcitrant Acne Vulgaris 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 vulgaris. isotretinoin has revolutionized the management of Acne Vulgaris 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 Vulgaris. 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 Vulgaris 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 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 Vulgaris 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 Vulgaris 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 Vulgaris 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 Human Culture of 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 Heart 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%). Retinoic acid 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. Retinoic acid, 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 Vulgaris. 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: Vitamin A has relations: drug_drug with isotretinoin, drug_drug with isotretinoin. Ethanol has relations: drug_drug with isotretinoin, drug_drug with isotretinoin. Eczema has relations: drug_effect with isotretinoin, drug_effect with isotretinoin. isolated Cleft palate, isolated has relations: disease_protein with epidermal growth factor, disease_protein with epidermal growth factor. Fatigue has relations: drug_effect with isotretinoin, drug_effect with isotretinoin.", "label": "no"}
{"original_question": "Can DNA intercalators function as topoisomerase inhibitors?", "id": "converted_61", "sentence1": "Can DNA Intercalating Agents 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 DNA intercalator and PPP1R1A gene of Topoisomerase II II) Amsacrine, a DNA intercalator 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 DNA intercalator and Topoisomerase II II PPP1R1A gene. To determine whether the ability of amiloride to intercalate into DNA and to inhibit DNA Topoisomerases, Type I II 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 Topoisomerases, Type I II (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 DNA intercalator 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 DNA intercalator, 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 DNA intercalator. Amonafide is a DNA intercalator 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 DNA intercalator 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-Intercalating Agents as potential DNA ligands or Topoisomerase II inhibitors. It was found that 1) morpholinodoxorubicin, cyanomorpholinyldoxorubicin, and dactinomycin (but not doxorubicin) stimulated DNA Topoisomerases, Type I I-induced cleavage at specific DNA sites; 2) only doxorubicin and dactinomycin stimulated DNA cleavage by DNA Topoisomerases, Type I II; 3) at higher Pharmacologic Substance concentrations, DNA Intercalating Agents suppressed Enzyme [APC]-mediated DNA cleavage induced by DNA Topoisomerases, Type I 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 Intercalating Agents are not only inhibitors of DNA Topoisomerases, Type I II but act also on DNA Topoisomerases, Type I 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 (Topoisomerase II I/II inhibitors, DNA Intercalating Agents, and DNA alkylation agents) as predicted by its structure. Cytotoxicity of several classes of Antitumor DNA Intercalating Agents is thought to result from disturbance of DNA metabolism following trapping of the nuclear Enzyme [APC] DNA Topoisomerases, Type I II as a covalent complex on DNA. Most DNA Intercalating Agents 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 Topoisomerases, Type I II are DNA Intercalating Agents. Numerous Topoisomerase II I poisons including DNA minor groove binders such as Hoechst 33258 and DNA Intercalating Agents such as benzophenanthridine Alkaloids and indolocarbazole derivatives have been discovered and developed. The stabilization of cleavage intermediates by Intercalating Agents may have a common mechanism for DNA Topoisomerases, Type I I and DNA Topoisomerases, Type I II. 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-Intercalating Agents 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 Intercalating Agents 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-Intercalating Agents was assessed by a novel and convenient Topoisomerase II fluorescent assay. Structure-activity relationship of polypyridyl ruthenium(II) complexes as DNA Intercalating Agents, DNA photocleavage reagents, and DNA Topoisomerases, Type I 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 Intercalating Agents are not only inhibitors of DNA Topoisomerases, Type I II but act also on DNA Topoisomerases, Type I 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 Intercalating Agents mAMSA and mitoxantrone. Effects of the DNA Intercalating Agents amsacrine and elliptinium on Topoisomerase II II mediated DNA Genomic Orientation cleavage and Genomic Orientation passage. Most DNA Intercalating Agents 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 Intercalating Agents 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 Intercalating Agents, and Topoisomerase II inhibitors.  Our study indicates that Epoxy anthraquinone derivative may be a novel DNA Topoisomerases, Type I PPP1R1A gene that can be potentially used for treatment of Neuroblastoma or other Primary malignant neoplasm patients. Organic Intercalating Agents 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 Topoisomerases, Type I II in vitro, 4) promote the Topoisomerase II II-dependent cleavage of DNA, and 5) inhibit functions associated with DNA Topoisomerases, Type I II 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 Topoisomerases, Type I II in vitro and DNA Topoisomerases, Type I II-dependent cell functions in vivo. Many compounds capable of inhibiting DNA Topoisomerases, Type I II are DNA Intercalating Agents. 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 II\u03b1 and Topoisomerase II II\u03b2 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: Daunorubicin has relations: drug_drug with quinacrine, off_label_use with Neuroblastoma, drug_drug with quinacrine, off_label_use with Neuroblastoma. Doxorubicin has relations: indication with Neuroblastoma, indication with Neuroblastoma.", "label": "yes"}
{"original_question": "Do orphan and gene related CpG islands follow power-law-like distributions?", "id": "converted_62", "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": "Can valproic acid act as an activator of AMPK?", "id": "converted_63", "sentence1": "Can valproic acid act as an activator of AMP-Activated Protein Kinases?", "sentence2": "Here we demonstrate that valproic acid is a novel activator of AMP-activated protein kinase (AMP-Activated Protein Kinases), 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 AMP-Activated Protein Kinases.[SEP]", "label": "yes"}
{"original_question": "Is the Drosophila Translational Control Element (TCE) involved in spermatogenesis?", "id": "converted_64", "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 (Sch\u00e4fer 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]", "label": "yes"}
{"original_question": "Is low T3 syndrome a prognostic marker in patients with renal insufficiency?", "id": "converted_65", "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, cubic foot 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 cubic foot 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 FT3 levels are not predictive for mortality in a subgroup of stable Hodgkin Disease patients who could survive more than 12 months. Low cubic foot 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]", "label": "yes"}
{"original_question": "Does burning mouth syndrome preferentially affect post-mepopausal women?", "id": "converted_66", "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]", "label": "yes"}
{"original_question": "Can life style changes reduce oxidative stress", "id": "converted_67", "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: Metabolic Syndrome X X has relations: disease_disease with Metabolic Syndrome X, disease_disease with Metabolic Syndrome X.", "label": "yes"}
{"original_question": "Is oxidative stress affected by FOXO expression?", "id": "converted_68", "sentence1": "Is oxidative stress affected by FOXO expression?", "sentence2": "Forkhead-box class O (FOXO Family) TRANSCRIPTION FACTOR regulate mechanisms of cellular aging, including protein quality control, autophagy and defenses against oxidative stress. Statin-mediated upregulation of KL wt Allele expression and differential regulation of FOXO Family expression promote resistance to CsA-induced oxidative stress. FOXO Family expression suppressed the ROS-induced apoptosis in differentiated 3T3-L1 Cells via the expression of ROS-scavenging ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS. Differential expression of FOXO1 gene gene and FOXO3A protein, Homo sapiens confers resistance to oxidative cell death upon endometrial decidualization. We demonstrate that Homo sapiens endometrial stromal Cells become extraordinarily resistant to oxidative stress-induced apoptosis upon decidualization in response to cyclophosphamide/doxorubicin/methotrexate/procarbazine protocol and progesterone signaling. This differentiation process is associated with the induction of the forkhead transcription factor FOXO1 gene gene, which in turn increases the expression of the Mitochondrial Inheritance antioxidant manganese superoxide dismutase. Comparative analysis demonstrated that hydrogen peroxide, a source of free radicals, strongly induces FOXO3A protein, Homo sapiens mRNA and protein expression in undifferentiated Homo sapiens endometrial stromal Cells but not in decidualized Cells. These results suggest that the induction of FOXO1 gene gene may enhance the ability of decidualized Cells to prevent oxidative damage while the simultaneous repression of FOXO3A protein, Homo sapiens expression disables the signaling pathway responsible for oxidative cell death. The differential regulation of FOXO expression provides the Decidua with a robust system capable of coping with prolonged episodes of oxidative stress during pregnancy.[SEP]", "label": "yes"}
{"original_question": "Is the Dictyostelium discoideum proteome known?", "id": "converted_69", "sentence1": "Is the Dictyostelium discoideum proteome known?", "sentence2": "The Negative Proteome Database (neodymium pyrocatechin disulfonate) is populated with pair-wise protein Sequence - ParameterizedDataType comparisons between each of the following proteomes: Homo sapiens, House mice, Drosophila melanogaster, Caenorhabditis elegans, Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae, Dictyostelium discoideum, Chlamydomonus reinhardti, Escherichia coli K12, Arabidopsis thaliana <plant> <plant> and Methanoscarcina acetivorans. The Dictyostelium discoideum proteome--the SWISS-2DPAGE database of the multicellular aggregate (slug). Consequently, this genomic Sequence - ParameterizedDataType information can now be exploited to realize D. discoideum proteomics projects.  The Dictyostelium discoideum Genome - anatomical entity has been sequenced, assembled and annotated to a high degree of reliability. The parts-list of Proteins and RNA encoded by the six Chromosomes, Human, Pair 1 can now be accessed and analyzed.  The 34 Mb Genome - anatomical entity of Dictyostelium discoideum is carried on 6 Chromosomes, Human, Pair 1 and has been fully sequenced by an international consortium. The Sequence - ParameterizedDataType was assembled on the classical and physical maps that had been built up over the years and refined by HAPPY mapping. Annotation of the Sequence - ParameterizedDataType predicted about 12,000 Genes for Proteins of at least 50 Antifibrinolytic Antifibrinolytic amino acids in length. In this study, a quantitative comparative proteomics approach has been used to analyze the Dictyostelium discoideum mitochondrial proteome variations during vegetative growth, starvation and the early stages of development.  The secreted proteome profile of developing Dictyostelium discoideum cells. The present repertoire validates our purification method and paves the way for a future proteomics approach to study the dynamics of macropinocytosis. Proteomic analysis of a developmentally regulated Secretory Vesicles.[SEP]", "label": "yes"}
{"original_question": "Is single-cell analysis (SCA) possible in proteomics?", "id": "converted_70", "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]", "label": "no"}
{"original_question": "Is shotgun lipidomics the direct infusion of a lipid sample into a mass spectrometer?", "id": "converted_71", "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]", "label": "yes"}
{"original_question": "Is apixaban effective for treatment of acute venous thromboembolism?", "id": "converted_72", "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]", "label": "yes"}
{"original_question": "Is the tricarboxylic acid (TCA) cycle affected in inflammation?", "id": "converted_73", "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 succinate dehydrogenase (Succinates Dehydrogenase) 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 RC The Mitochondrial Inheritance respiratory chain (RC) and the Tricarboxylic Acids (Tricyclic Antidepressant [EPC]) cycle were explored in the Hmbs(-/-) mouse model. RC and Tricyclic Antidepressant [EPC] cycle were significantly affected in comparison to controls in CASP14 gene treated with phenobarbital with decreased activities of RC 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]", "label": "yes"}
{"original_question": "Are reduced-nicotine cigarettes effective for smoking cessation?", "id": "converted_74", "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 (\u223c1.2 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]", "label": "yes"}
{"original_question": "Is the Wnt protein modified by notum?", "id": "converted_75", "sentence1": "Is the Wnt protein modified by notum?", "sentence2": "NOTUM gene deacylates Wnt Proteins to suppress signalling activity. Kinetic and mass spectrometric analyses of NR4A2 protein, human show that NOTUM gene is a carboxylesterase that removes an essential palmitoleate moiety from Wnt Proteins and thus constitutes the first known extracellular protein deacylase. the Wnt PPP1R1A gene notum the WNT-PPP1R1A gene notum.[SEP]", "label": "yes"}
{"original_question": "Is ospemifene effective for treatment of dyspareunia?", "id": "converted_76", "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]\u2009=\u2009-37.5, 95% confidence interval [CI]\u2009=\u2009-41.83 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 =\u2009-0.89, 95% CI =\u2009-0.98 to -0.80, P = 0.00001), and Have Dyspareunia question (Spondylometaphyseal dysplasia =\u2009-0.37, 95% CI =\u2009-0.43 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]", "label": "yes"}
{"original_question": "Is pregabalin effective for treatment of patients with restless leg syndrome?", "id": "converted_77", "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 RLS 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 RLS/WED (Level A evidence).  In the group of Anticonvulsants [TC], only the trials performed with \u03b1\u2082\u03b4 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 RLS 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 RLS 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 RLS. 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 RLS symptoms in patients with moderate-to-severe idiopathic RLS 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 RLS, 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 RLS 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 RLS[SEP]Relations: Gabapentin enacarbil has relations: indication with Restless Legs Syndrome, drug_drug with pregabalin, indication with Restless Legs Syndrome, drug_drug with pregabalin. Pramipexole has relations: drug_drug with pregabalin, indication with Restless Legs Syndrome, drug_drug with pregabalin, indication with Restless Legs Syndrome. Gabapentin has relations: drug_drug with pregabalin, indication with Restless Legs Syndrome, drug_drug with pregabalin, indication with Restless Legs Syndrome. Tramadol has relations: drug_drug with pregabalin, drug_drug with pregabalin. Rotigotine has relations: drug_drug with pregabalin, indication with Restless Legs Syndrome, drug_drug with pregabalin, indication with Restless Legs Syndrome. Clonidine has relations: drug_drug with pregabalin, drug_drug with pregabalin. Codeine has relations: drug_drug with pregabalin, drug_drug with pregabalin. Ropinirole has relations: indication with Restless Legs Syndrome, drug_drug with pregabalin, indication with Restless Legs Syndrome, drug_drug with pregabalin. Oxycodone has relations: drug_drug with pregabalin, drug_drug with pregabalin.", "label": "yes"}
{"original_question": "Can zinc finger nucleases be used to combat disease?", "id": "converted_78", "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 ZFN technology, an analysis of current techniques and applications, and an examination of the ethical issues applicable to translational ZFN 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 (TALENs), 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 (TALENs) 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 (TALENs), 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]", "label": "yes"}
{"original_question": "Is RET the major gene involved in Hirschsprung disease?", "id": "converted_79", "sentence1": "Is ret unit of radiation dose the major Genes involved in HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1?", "sentence2": "The ret unit of radiation dose Proto-Oncogenes is the major Genes associated to HSCR with differential contributions of its rare and common, coding and noncoding Gene Mutation to the multifactorial nature of this pathology The ret unit of radiation dose Proto-Oncogenes is the major Genes for HSCR with differential contributions of its rare and common, coding and noncoding Gene Mutation to the multifactorial nature of this pathology The rearranged during transfection Genes (ret unit of radiation dose) is considered the major Genes in HSCR ret unit of radiation dose is the major Genes associated to HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR) with differential contributions of its rare and common, coding and noncoding Gene Mutation to the multifactorial nature of this pathology While all Mendelian modes of inheritance have been described in syndromic HSCR, isolated HSCR stands as a model for genetic disorders with complex patterns of inheritance. The High Affinity Nerve Growth Factor Receptor, Homo sapiens ret unit of radiation dose is the major Genes with both rare Open Reading Frames Gene Mutation and/or a frequent variant located in an Enhancer Elements, Genetic predisposing to the disease  The rearranged during transfection (ret unit of radiation dose) Proto-Oncogenes is the major susceptibility Genes for HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, and germline Gene Mutation in ret unit of radiation dose have been reported in up to 50% of the inherited forms of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 and in 15-20% of sporadic cases of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. The ret unit of radiation dose Proto-Oncogenes is the major Genes involved in the complex genetics of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR), or aganglionic megacolon, showing causative loss-of-function Gene Mutation in 15-30% of the sporadic cases. The major Genes for HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR) encodes the receptor tyrosine kinase ret unit of radiation dose. The ret unit of radiation dose Proto-Oncogenes is considered to be the major susceptibility Genes involved in HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1.  HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR), a developmental disorder characterized by the absence of enteric neurons in distal segments of the gut, shows a complex pattern of inheritance, with the ret unit of radiation dose protooncogene acting as a major Genes and additional susceptibility loci playing minor roles.  Traditional ret unit of radiation dose germline Gene Mutation account for a small subset of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 patients, but several studies have shown that there is a specific cdE cdE haplotype finding finding of ret unit of radiation dose associated with the sporadic forms of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. PURPOSE: The ret unit of radiation dose Proto-Oncogenes is considered to be the major susceptibility Genes involved in HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. The ret unit of radiation dose Proto-Oncogenes is the major Genes involved in the pathogenesis of Hirschsprung (HSCR), a complex genetic disease characterized by lack of Ganglia along variable lengths of the gut. While rare Variant (RVs) in the Open Reading Frames (Triglyceride storage disease with ichthyosis) of several genes involved in ENS development lead to disease, the association of common Variant (CVs) with HSCR has only been reported for ret unit of radiation dose (the major HSCR Genes) and NRG1 protein, Homo sapiens protein, Homo sapiens. The rearranged during transfection (ret unit of radiation dose) Proto-Oncogenes is the major susceptibility Genes for HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, and germline Gene Mutation in ret unit of radiation dose have been reported in up to 50% of the inherited forms of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 and in 15-20% of sporadic cases of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. The major Genes for HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR) encodes the receptor tyrosine kinase ret unit of radiation dose. In a study of 690 European- and 192 Chinese-descent probands and their parents or controls, we demonstrate the ubiquity of a >4-fold susceptibility from a C-->T allele (rs2435357: p = 3.9 x 10(-43) in European ancestry; p = 1.1 x 10(-21) in Chinese samples) that probably arose once within the intronic ret unit of radiation dose enhancer MCS+9.7. HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR), a developmental disorder characterized by the absence of enteric neurons in distal segments of the gut, shows a complex pattern of inheritance, with the ret unit of radiation dose protooncogene acting as a major Genes and additional susceptibility loci playing minor roles. BACKGROUND: The ret unit of radiation dose Genes encodes a High Affinity Nerve Growth Factor Receptor, Homo sapiens involved in different Homo sapiens neurocristopathies, such as specific Neuroendocrine Tumors and HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR). The first major susceptibility Genes for HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 is the ret unit of radiation dose Proto-Oncogenes on 10q11.2. The developmental abnormalities apparent in these CASP14 Genes, together with the observation that the major Body tissue affected in Multiple Endocrine Neoplasia Type 2a and HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 have a common origin in the embryonal neural crest, suggest that ret unit of radiation dose encodes a receptor for a developmental regulator involved in the genesis of a variety of neural crest derivatives, and in the organogenesis of the Both kidneys. ret unit of radiation dose is the major Genes involved in HSCR. Recent advances show that the ret unit of radiation dose Genes is a major Gene Locus involved in the pathogenesis of HSCR. Although with several genes involved in its pathogenesis, the major HSCR Genes is the ret unit of radiation dose Proto-Oncogenes. In this model, a major Genes, ret unit of radiation dose, is involved in most if not all cases of isolated (i.e., nonsyndromic) HSCR, in conjunction with other autosomal susceptibility loci under a multiplicative model. The ret unit of radiation dose Proto-Oncogenes is the major Genes involved in the pathogenesis of Hirschsprung (HSCR), a complex genetic disease characterized by lack of Ganglia along variable lengths of the gut The ret unit of radiation dose Proto-Oncogenes is the major Genes involved in the complex genetics of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR), or aganglionic megacolon, showing causative loss-of-function Gene Mutation in 15-30% of the sporadic cases The ret unit of radiation dose Proto-Oncogenes is considered to be the major susceptibility Genes involved in HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 Analysis of the ret unit of radiation dose Genes, the major Genes involved in HSCR susceptibility, revealed neither linkage nor Gene Mutation ret unit of radiation dose is the major Genes involved in HSCR Although with several genes involved in its pathogenesis, the major HSCR Genes is the ret unit of radiation dose Proto-Oncogenes While rare Variant (RVs) in the Open Reading Frames (Triglyceride storage disease with ichthyosis) of several genes involved in ENS development lead to disease, the association of common Variant (CVs) with HSCR has only been reported for ret unit of radiation dose (the major HSCR Genes) and NRG1 protein, Homo sapiens protein, Homo sapiens The rearranged during transfection (ret unit of radiation dose) Proto-Oncogenes is the major susceptibility Genes for HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, and germline Gene Mutation in ret unit of radiation dose have been reported in up to 50% of the inherited forms of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 and in 15-20% of sporadic cases of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 Recent advances show that the ret unit of radiation dose Genes is a major Gene Locus involved in the pathogenesis of HSCR In this model, a major Genes, ret unit of radiation dose, is involved in most if not all cases of isolated (i.e., nonsyndromic) HSCR, in conjunction with other autosomal susceptibility loci under a multiplicative model We report on mutation analysis of five genes involved in the receptor tyrosine kinase (ret unit of radiation dose) or the endothelin-signalling pathways in 28 sporadic Japanese patients with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 In addition to Gene Mutation in the ret unit of radiation dose and EDNRB protein, Homo sapiens protein, Homo sapiens genes, embryonic environmental factors and/or other genetic factors appear to be involved in the development of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 The ret unit of radiation dose Genes is the major HSCR Genes, although reduced penetrance of ret unit of radiation dose Gene Mutation and variable expression of HSCR phenotype indicates that more than one Genes is required[SEP]Relations: hirschsprung disease, susceptibility to has relations: disease_protein with EDNRB protein, Homo sapiens, disease_disease with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_protein with ret unit of radiation dose, disease_protein with EDNRB protein, Homo sapiens, disease_disease with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_protein with ret unit of radiation dose. multiple endocrine neoplasia has relations: disease_protein with ret unit of radiation dose, disease_protein with ret unit of radiation dose.", "label": "yes"}
{"original_question": "is intense physical activity associated with longevity ?", "id": "converted_80", "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]", "label": "yes"}
{"original_question": "Are cyclophilins proteins that bind to prolines?", "id": "converted_81", "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]", "label": "yes"}
{"original_question": "Can a given genotype exhibit opposite fitness effects (beneficial and detrimental) within the same environment?", "id": "converted_82", "sentence1": "Can a given genotype exhibit opposite fitness effects (beneficial and detrimental) within the same environment?", "sentence2": "Mutations 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 Gene Mutation were beneficial, deleterious or neutral at an intermediate growth rate (0.5\u2009h(-1)) and one changed from beneficial to deleterious within a 36\u2009min 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 Gene Mutation 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 Gene Mutation 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]", "label": "yes"}
{"original_question": "Has the protein SETMAR (Metnase) a transposase domain?", "id": "converted_83", "sentence1": "Has the Protein Info SETMAR gene (Metnase) a Transposase Superkingdom (taxonomic category)?", "sentence2": "Metnase (SETMAR gene gene) is a Parameterized Data Type - Set-Transposase fusion Protein Info that promotes nonhomologous end joining (Non-Homologous DNA End-Joining) repair in Homo sapiens. The Transposase Superkingdom (taxonomic category) Protein Info Metnase/SETMAR gene gene suppresses chromosomal translocations.  Metnase (also termed SETMAR gene gene) is a fusion of a histone methyltransferase and Transposase Protein Info that arose specifically in Primates.  the only intact SETMAR gene wt Allele Transposase gene exists within a chimeric Parameterized Data Type - Set-Transposase fusion Protein Info referred to as Metnase or SETMAR gene gene.  The Metnase Transposase has been remarkably conserved through evolution; Metnase (also known as SETMAR gene gene) is a Parameterized Data Type - Set and Transposase fusion Protein Info in Homo sapiens and plays a positive role in double-strand break (DSB) repair. While the Parameterized Data Type - Set Superkingdom (taxonomic category) possesses Histone-Lysine N-Methyltransferase activity, the Transposase Superkingdom (taxonomic category) is responsible for 5'-terminal inverted repeat (TIR)-specific binding, DNA looping, and DNA cleavage activities.  Metnase is a Gene Fusion Abnormality comprising a Parameterized Data Type - Set histone methyl transferase Superkingdom (taxonomic category) and a Transposase Superkingdom (taxonomic category) derived from the Mariner Transposase. ulated by the DNA repair component Metnase (also termed SETMAR gene gene). Metnase contains a Parameterized Data Type - Set histone methyltransferase and Transposase nuclease Superkingdom (taxonomic category) Metnase is a human Parameterized Data Type - Set and Transposase Superkingdom (taxonomic category) Protein Info  The human set and Transposase Superkingdom (taxonomic category) Protein Info Metnase  of Transposase-related sequences in Homo sapiens are Pseudogenes. We recently isolated and characterized a Parameterized Data Type - Set and Transposase Superkingdom (taxonomic category) Protein Info termed Metnase that promotes DNA double-strand break (DSB) repair by non-homologous end-joining (Non-Homologous DNA End-Joining). Both the Parameterized Data Type - Set and Transposase Superkingdom (taxonomic category) were required for its Non-Homologous DNA End-Joining activity. Metnase, also known as SETMAR gene gene, is a Parameterized Data Type - Set and Transposase fusion Protein Info with an undefined role in mammalian DNA repair. Biochemical characterization of a Parameterized Data Type - Set and Transposase fusion Protein Info, Metnase: i Metnase (SETMAR gene gene) is a Parameterized Data Type - Set and Transposase fusion Protein Info that promotes in vivo end joining activity and mediates genomic integration of foreign DNA.   This Transposase coding region is part of the SETMAR gene gene gene, in which a histone methylatransferase Parameterized Data Type - Set Superkingdom (taxonomic category) is fused to an SETMAR gene wt Allele Transposase Superkingdom (taxonomic category).  The SETMAR gene gene Protein Info, human preserves most of the activities of the ancestral SETMAR gene wt Allele Transposase. ere we investigate the activity of the SETMAR gene gene Protein Info, human, a highly expressed fusion between a histone H3 methylase and a mariner family Transposase. SETMAR gene gene, a new primate chimeric gene resulting from fusion of a Parameterized Data Type - Set histone methyltransferase gene to the Transposase gene of a mobile element. We identified a Protein Info, termed Metnase, that has a Parameterized Data Type - Set Superkingdom (taxonomic category) and a Transposase/nuclease Superkingdom (taxonomic category).  Metnase has a nuclease Superkingdom (taxonomic category) that shares Homologous Gene with the Transposase family. Metnase (also called SETMAR gene gene) is a Parameterized Data Type - Set and Transposase Superkingdom (taxonomic category) Protein Info that promotes both DNA double-strand break (DSB) repair and restart of stalled replication forks.[SEP]", "label": "yes"}
{"original_question": "Is nucleosome eviction ATP-dependent?", "id": "converted_84", "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 promotes transcription through nucleosome location location eviction Ino80 complex 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]", "label": "yes"}
{"original_question": "Is TREM2 associated with Alzheimer's disease in humans?", "id": "converted_85", "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 \u226465 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 \u03b54 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\u00d710(-10)).[SEP]", "label": "yes"}
{"original_question": "Have mutations in the Polycomb group been found in human diseases?", "id": "converted_86", "sentence1": "Have mutations in the Polycomb group been found in human diseases?", "sentence2": "We identify a novel Mutation Abnormality in PHC1 Genes Genes, a human orthologue of the Drosophila polyhomeotic member of polycomb group (Polycomb-Group Proteins), which significantly decreases PHC1 Genes Genes 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 \u03b3\u03b4 T-cell leukemia (Precursor T-Cell Lymphoblastic Leukemia-Lymphoma) occurrence in CASP14 Genes 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 Genes Genes 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 Genes provisionally named OTOFACIOCERVICAL SYNDROME 1. Gene expression experiments in CASP14 Genes embryo of positional candidate genes revealed that JARID2 Genes Genes 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 Genes amplification is associated with increased expression of corresponding mRNAs and Proteins. he ezh2 protein, human Genes 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) Genes from 10p11; Enhancer of Polycomb Homolog 1 has hitherto not been associated with Neoplasms.[SEP]Relations: neurofibromatosis has relations: disease_protein with Neurofibromatosis 1, disease_protein with Neurofibromatosis 1. ezh2 protein, human has relations: protein_protein with PHF1 protein, human, protein_protein with Putative Polycomb Group Protein ASXL1, protein_protein with AEBP2 protein, human, protein_protein with Enhancer of Polycomb Homolog 1, protein_protein with BMI1 protein, human, protein_protein with PHF1 protein, human, protein_protein with Putative Polycomb Group Protein ASXL1, protein_protein with AEBP2 protein, human, protein_protein with Enhancer of Polycomb Homolog 1, protein_protein with BMI1 protein, human. precursor lymphoblastic lymphoma/leukemia has relations: disease_protein with RUNX1 protein, human, disease_protein with RUNX1 protein, human. head and neck neoplasm has relations: disease_disease with Malignant Head and Neck Neoplasm, disease_disease with Malignant Head and Neck Neoplasm.", "label": "yes"}
{"original_question": "Is microRNA(miRNA) 29 involved in post-ischemic cardiac remodeling?", "id": "converted_87", "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 collagens, 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 collagens, 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]", "label": "yes"}
{"original_question": "Can sorafenib activate AMPK?", "id": "converted_88", "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]", "label": "yes"}
{"original_question": "Is Vortioxetine effective for treatment of depression?", "id": "converted_89", "sentence1": "Is Vortioxetine effective for treatment of Cancer patients and suicide and depression?", "sentence2": "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 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 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 Homo sapiens 5-HT3A and 5-HT7 receptor antagonist, 5-HT1B receptor partial Agonist, 5-HT1A 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-HT1A-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\u2009mg or 5\u2009mg 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\u2009mg/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 symptoms after 6 weeks of treatment.[SEP]Relations: anxiety disorder has relations: indication with Vortioxetine, indication with Vortioxetine. Duloxetine has relations: drug_drug with Vortioxetine, drug_drug with Vortioxetine. Dopamine has relations: drug_drug with Vortioxetine, drug_drug with Vortioxetine. Norepinephrine has relations: drug_drug with Vortioxetine, drug_drug with Vortioxetine. Vilazodone has relations: drug_drug with Vortioxetine, drug_drug with Vortioxetine. major depressive disorder has relations: indication with Vortioxetine, indication with Vortioxetine.", "label": "yes"}
{"original_question": "Is exome sequencing efficient for the detection of germline mutations?", "id": "converted_90", "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]", "label": "yes"}
{"original_question": "Is it feasible to determine the complete proteome of yeast?", "id": "converted_91", "sentence1": "Is it feasible to determine the complete proteome of Saccharomyces cerevisiae?", "sentence2": "or model organisms like Saccharomyces cerevisiae or Saccharomyces 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 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": "Are circRNAs associated with diseases and traits?", "id": "converted_92", "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 circular RNA are important for Disease regulation. Firstly, the interactions of circRNAs with Disease associated MicroRNAs were identified, following which the likelihood of a RNA, Circular being associated with a Disease was calculated Emerging evidence indicates that circRNAs might play important roles in atherosclerotic vascular Disease 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 circular RNA (RNA, Circular) with human diseases in two different ways. Firstly, the interactions of circRNAs with Disease associated MicroRNAs were identified, following which the likelihood of a RNA, Circular being associated with a Disease was calculated. Firstly, the interactions of circRNAs with Disease associated MicroRNAs were identified, following which the likelihood of a RNA, Circular 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: malignant colon neoplasm has relations: disease_disease with colorectal Primary malignant neoplasm, disease_disease with colorectal Primary malignant neoplasm.", "label": "yes"}
{"original_question": "Could the Menzerath-Altmann law be proved mathematically trivial in genomes?", "id": "converted_93", "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 \u223c 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 \u223c 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 \u223c 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]", "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_94", "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 Hematologic 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 Amyloid\u03b2 (A\u03b2) 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: gamma-Secretase complex has relations: cellcomp_protein with PSEN1 protein, Homo sapiens, cellcomp_protein with PSEN1 protein, Homo sapiens. Sorafenib has relations: indication with Liver carcinoma, indication with Liver carcinoma. NOTCH3 has relations: protein_protein with PSEN1 protein, Homo sapiens, disease_protein with Liver carcinoma, protein_protein with PSEN1 protein, Homo sapiens, disease_protein with Liver carcinoma. Cardiomyopathy, Dilated has relations: disease_protein with PSEN1 protein, Homo sapiens, disease_protein with PSEN1 protein, Homo sapiens.", "label": "yes"}
{"original_question": "Are there any functional differences between Mfd and its human Cocaine syndrome protein B (CSB) homolog?", "id": "converted_95", "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]", "label": "yes"}
{"original_question": "Is the yeast \u039cac1 transcription factor induced upon copper deficiency?", "id": "converted_96", "sentence1": "Is the Saccharomyces cerevisiae \u039cac1 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]", "label": "yes"}
{"original_question": "Have thyronamines  effects on fat tissue?", "id": "converted_97", "sentence1": "Have thyronamines  effects on fat tissue?", "sentence2": "In conclusion, trace amines and thyronamines are negative inotropic agents. Their in vivo administration induces effects opposite to those induced by Thyroid Hormones, including lowering of body temperature.[SEP]", "label": "no"}
{"original_question": "Is alemtuzumab effective for remission induction in patients diagnosed with T-cell prolymphocytic leukemia?", "id": "converted_98", "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-Cell Prolymphocytic Leukemia, which compares favorably to published data. Currently, the best treatment for T-Cell Prolymphocytic Leukemia 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-Cell Prolymphocytic Leukemia 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 alemtuzumab, 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-Cell Prolymphocytic Leukemia) 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-Cell Prolymphocytic Leukemia, 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: acute lymphoblastic/lymphocytic leukemia has relations: disease_disease with T-cell prolymphocytic leukemia, disease_disease with T-cell prolymphocytic leukemia.", "label": "yes"}
{"original_question": "Is there an association between TERT promoter mutation and survival of glioblastoma patients?", "id": "converted_99", "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 (\u226460 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]", "label": "yes"}
{"original_question": "Is bapineuzumab effective for treatment of patients with Alzheimer's disease?", "id": "converted_100", "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 A\u03b2 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 A\u03b2, and bapineuzumab, targeting amyloid plaques, prompted expert comments that Pharmacologic Substance discovery efforts in ALZHEIMER DISEASE, FAMILIAL, 1 should focus on soluble forms of A\u03b2 rather than fibrillar A\u03b2 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-A\u03b2 antibody bapineuzumab have demonstrated reduced Head>Brain PET-Pittsburg-B signals, suggesting the reduction of A\u03b2 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 A\u03b2 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 after bapineuzumab, and more rarely Head>Brain Microhemorrhages (especially in Apo E \u03b54 carriers), has raised concerns on the safety of these Antibodies, in vitro diagnostic directed against the N-terminus of the A\u03b2 peptide.   The most advanced of these immunological approaches is bapineuzumab, composed of humanized anti-A\u03b2 Monoclonal Antibodies, that has been tested in two Phase II trials, demonstrating to reduce A\u03b2 burden in the Head>Brain of cytarabine/daunorubicin protocol patients. However, the preliminary cognitive efficacy of bapineuzumab appears uncertain. The occurrence of Vasogenic Edema, 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-A\u03b2 monoclonal antibody, appears uncertain. Moreover, the occurrence of Vasogenic Edema and, more rarely, Head>Brain Microhemorrhages, especially in apolipoprotein E \u03f54 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 \u03b3-secretase inhibitor, raise the possibility that targeting A\u03b2 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, probably related to immunotherapy, but a subsequent MRI scan 38 days later demonstrated resolution of Vasogenic Edema. 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 A\u03b2 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 A\u03b2 burden in the Head>Brain of cytarabine/daunorubicin protocol patients. However, its preliminary cognitive efficacy appears uncertain, particularly in ApoE \u03b54 carriers, and Vasogenic Edema 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 - 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.  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 in 12 cases, which were significantly over represented in ApoE4 carriers.[SEP]Relations: bapineuzumab has relations: drug_drug with solanezumab, drug_drug with solanezumab. solanezumab has relations: drug_drug with bapineuzumab, drug_drug with bapineuzumab.", "label": "no"}
{"original_question": "Is desmin an intermediate filament protein involved in Dilated Cardiomyopathy (DCM)?", "id": "converted_101", "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 Gene Mutation in the CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human (CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1) Genes. Mutations 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 Gene Mutation 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 Gene Mutation 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 Gene Mutation 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. Cardiomyopathy, Dilated (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 Genes causes Abnormality of mitochondrial metabolism and apoptosis, resulting in Cardiomyopathies in CASP14 Genes. 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 Genes 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 Genes (CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1) causes 3',5'-dichloromethotrexate in a human family. Mice deficient in CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Protein Info, human, the muscle-specific member of the intermediate filament Genes 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 RNAs. Examination of families has identified so far eight Disease genes, namely the Dystrophin, TAFAZZIN Genes, 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 Genes. Mutations 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 Genes 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 Genes, the CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Genes, and the lamin A/C Genes. Cardiomyopathy, Dilated (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 Genes), 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 Genes screening, the molecular diagnosis can be provided for Dystrophin, Diacylglycerol, DNA, Mitochondrial, Actins and CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1 Genes 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 Chest>Heart failure in Homo sapiens and CASP14 Genes 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. muscle contraction has relations: bioprocess_protein with CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1, bioprocess_protein with CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1. myofibrillar myopathy 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. Myocardium has relations: anatomy_protein_present with CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1, anatomy_protein_present with CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1. cytoskeletal Protein Info binding has relations: molfunc_protein with CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1, molfunc_protein with CEREBELLAR ATAXIA, INTELLECTUAL DEVELOPMENTAL DISORDER, AND DYSEQUILIBRIUM SYNDROME 1.", "label": "yes"}
{"original_question": "Is lambrolizumab effective for treatment of patients with melanoma ?", "id": "converted_102", "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: melanocytic neoplasm has relations: disease_disease with Melanocytic neoplasm, disease_disease with Melanocytic neoplasm.", "label": "yes"}
{"original_question": "Is cadasil syndrome a hereditary disease?", "id": "converted_103", "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 Cerebrovascular accident, Abnormal behavior and Mental deterioration. Strokes 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: Retinal vasculopathy with cerebral Leukoencephalopathy and systemic manifestations has relations: disease_protein with TREX1 protein, human, disease_protein with TREX1 protein, human, disease_protein with TREX1 protein, human, disease_protein with TREX1 protein, human.", "label": "yes"}
{"original_question": "Is nintedanib effective for Idiopathic Pulmonary Fibrosis?", "id": "converted_104", "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 IPF, 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 IPF, 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 IPF patients treated with 150 mg nintedanib twice daily. In the INPULSIS-2 trial, the time to the first acute exacerbation significantly increased in IPF 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 IPF. nintedanib, an orally available, small-molecule Protein-Protein Tyrosine Kinase inhibitor (disposition) 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 IPF Disease progression. Consequently, nintedanib was given accelerated approval by the FDA in October 2014 for the treatment of IPF.  Most recently, pirfenidone and nintedanib, two compounds with pleiotropic anti-fibrotic properties, have been proven effective in reducing functional decline and Disease progression in IPF.  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(\u00ae)) is an orally available, small, multiple receptor Protein-Protein Tyrosine Kinase inhibitor (disposition) developed by Boehringer Ingelheim for the treatment of Idiopathic Pulmonary Fibrosis (IPF) and Primary malignant neoplasm. nintedanib received its first global approval in the US in October 2014 for the treatment of IPF. nintedanib has received a positive opinion from the European Medicines Agency's Committee for Pharmaceutical Preparations for Homo sapiens Use for the treatment of IPF, and for the second-line treatment in combination with docetaxel of locally advanced, metastatic or locally recurrent Non-Small Cell Lung Carcinoma of adenocarcinoma tumour histology.  This article summarizes the milestones in the development of nintedanib leading to this first approval for IPF. 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 (IPF). 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-Protein Tyrosine Kinase inhibitor (disposition) 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\ufffdmg twice daily had clinical benefits with an acceptable safety profile.METHODS: The INPULSIS\ufffd trials are replicate Phase III, randomized, double-blind, studies comparing the efficacy and safety of nintedanib 150\ufffdmg twice daily with placebo in patients with IPF.  nintedanib received its first global approval in the US in October 2014 for the treatment of IPF.  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(\ufffd)) is an orally available, small, multiple receptor Protein-Protein Tyrosine Kinase inhibitor (disposition) developed by Boehringer Ingelheim for the treatment of Idiopathic Pulmonary Fibrosis (IPF) and Primary malignant neoplasm. nintedanib received its first global approval in the US in October 2014 for the treatment of IPF.  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: indication with nintedanib, indication with nintedanib. Docetaxel has relations: drug_drug with nintedanib, drug_drug with nintedanib. nintedanib has relations: indication with Idiopathic Pulmonary Fibrosis, indication with Idiopathic Pulmonary Fibrosis. Pirfenidone has relations: drug_drug with nintedanib, indication with Idiopathic Pulmonary Fibrosis, drug_drug with nintedanib, indication with Idiopathic Pulmonary Fibrosis.", "label": "yes"}
{"original_question": "Is pesticide exposure associated with polyneuropathy?", "id": "converted_105", "sentence1": "Is pesticide exposure associated with Polyneuropathy?", "sentence2": "As the syndrome occurred after the acute Cholinergic Agents syndrome but before organophosphate-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 Phosphoric Acid Esters and Hydrocarbons, Chlorinated resulting in estrogenic effects and the promotion of organophosphate-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 polyneuropathies, affective disorders and suicide attempts.  These compounds cause four important neurotoxic effects in Homo sapiens: the Cholinergic Agents syndrome, the intermediate syndrome, organophosphate-induced delayed Polyneuropathy (OPIDP) and chronic organophosphate-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 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 organophosphate 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 extremities.  The two cases are presented here since organophosphate 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 organophosphate-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 insufficiency due to Muscle Weakness are common and patients often require respiratory support and delayed organophosphate induced Polyneuropathy. [Late onset Polyneuropathy due to exposure to Phosphoric Acid Esters].  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 organophosphate Insecticides, without adequate protection, have an increased risk of developing late onset neuropathy due to Phosphoric Acid Esters.  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 Organophosphate Pesticides, and the peak use coincides with the peak incidence of Guillain-Barre Syndrome. These results suggest that previously reported cases of organophosphate-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 organophosphate 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 organophosphate 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 Peripheral Nervous System Diseases, disease_disease with Peripheral Nervous System Diseases. peripheral nervous system disease has relations: disease_disease with Peripheral Nervous System Diseases, disease_disease with Peripheral Nervous System Diseases. Pesticides has relations: exposure_disease with Poisoning aspects, exposure_disease with Poisoning aspects.", "label": "yes"}
{"original_question": "Is there an association between borna virus and brain tumor?", "id": "converted_106", "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 cell.  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 neural cells. 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 cultures.  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 cell. 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]", "label": "no"}
{"original_question": "Does PU.1 (SPI1) affect NF-kB binding?", "id": "converted_107", "sentence1": "Does SPI1 wt Allele (SPI1) affect NF-kB 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-kB, AP-1, and Interferon Regulatory Factors (IRFs). Within 1217 bp of upstream sequence, 3 Site for NF-kB, 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 Spleen acupuncture point Spleen acupuncture point 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-kB site. Potential Regulatory Elements, Transcriptional, Transcription Factor AP-1, TFAP2A protein, human, AP3, NF-kB 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 (Sp1, AP-1, TFAP2A wt Allele, and NF-kB) 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-kappa B through a novel Ligand Binding Domain in a 17 kb upstream enhancer element.[SEP]", "label": "yes"}
{"original_question": "Does the majority of the mitochondrial genomes abide to the second parity rule (PR2)?", "id": "converted_108", "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 eubacteria. 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 eubacteria. 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 eubacteria 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]", "label": "no"}
{"original_question": "Is there an association between bruxism and reflux?", "id": "converted_109", "sentence1": "Is there an association between Bruxism and reflux?", "sentence2": "Sleep Bruxism is prevalent in Gastroesophageal reflux disease patients, and Gastroesophageal reflux disease is highly associated with SB. There was a statistical trend towards Tooth Wear progression being associated with gastric risk factors (p < 0.05).  This article presents a case report of a 27-year-old male smoker with Tooth Wear and dentin sensitivity caused by Gastroesophageal reflux disease associated with Bruxism.  The aim of this cross-over, randomized, single-blinded trial was to examine whether Intra-oesophageal acidification induces Sleep Bruxism (SB).  RMMA episodes including SB were induced by Esophageal acidification.  Chronic regurgitation of Gastric Acid in patients with Infantile Gastroesophageal Reflux disease may cause dental erosion, which can lead in combination with attrition or Bruxism to extensive loss of coronal tooth tissue. This clinical report describes treatment of severe Tooth Wear of a Infantile Gastroesophageal Reflux disease patient who is 54-year-old Turkish male patient. After his medical treatment, severe Tooth Wear, Bruxism and decreased vertical dimensions were determined.  Gastroesophageal reflux disease by itself or in combination with attrition, abrasion or Bruxism may be responsible for the loss. The association between Bruxism, feeding and smoking habits and Digestive System Disorders may lead to serious consequences to dental and related structures, involving dental alterations (wear, Fracture and cracks), periodontal signs (gingival recession and Tooth Mobility) and muscle-joint sensitivity, demanding a multidisciplinary treatment plan. 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.  The frequencies of RMMA, single short-burst, and clenching episodes were significantly higher during decreased Esophageal pH episodes than those during other times.  These results suggest that most jaw muscle activities, ie, RMMA, single short-burst, and clenching episodes, occur in relation to Infantile Gastroesophageal Reflux mainly in the supine position. Nocturnal Bruxism may be secondary to nocturnal Infantile Gastroesophageal Reflux, occurring via sleep arousal and often together with swallowing.[SEP]", "label": "yes"}
{"original_question": "Is paroxetine effective for treatment of premenstrual dysphoric disorder?", "id": "converted_110", "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 (Post-Traumatic Stress Disorder), 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-Stress Disorders, Traumatic, 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: Fluvoxamine has relations: indication with Obsessive-Compulsive Disorder, indication with Phobia, Social, indication with Obsessive-Compulsive Disorder, indication with Phobia, Social. Citalopram has relations: off_label_use with Obsessive-Compulsive Disorder, off_label_use with Obsessive-Compulsive Disorder. Paroxetine has relations: indication with Obsessive-Compulsive Disorder, indication with Phobia, Social, indication with Obsessive-Compulsive Disorder, indication with Phobia, Social. Fluoxetine has relations: indication with Obsessive-Compulsive Disorder, indication with Obsessive-Compulsive Disorder. Clomipramine has relations: indication with Obsessive-Compulsive Disorder, indication with Obsessive-Compulsive Disorder. Sertraline has relations: indication with Phobia, Social, indication with Obsessive-Compulsive Disorder, indication with Phobia, Social, indication with Obsessive-Compulsive Disorder.", "label": "yes"}
{"original_question": "Is endostatin a proangiogenic factor?", "id": "converted_111", "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 Angiostatin 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 cellular 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 angiogenic 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 Angiostatin and COL18A1 gene are two powerful inhibitors of angiogenesis in experimental models[SEP]", "label": "no"}
{"original_question": "Can botulism poisoning of a pregnant woman harm her fetus?", "id": "converted_112", "sentence1": "Can Botulism Poisoning aspects of a pregnant woman harm her Fetus in fetu?", "sentence2": "Two Botulism outbreaks were attributed to commercial ready-to-eat meat products and 3 to Food served in restaurants; several cases were attributed to non-Native home-prepared Food. Three affected pregnant women delivered healthy infants. Botulinum toxin is not expected to be present in systemic circulation following proper Intramuscular Route of Drug Administration or intradermal injection. Moreover, botulinum toxin type A, which has a high molecular weight, does not appear to cross the placenta. From the 38 pregnancies reported in the literature, including women who had Botulism Poisoning aspects during pregnancy, exposure to botulinum toxin type A does not appear to increase the risk of adverse outcome in the Fetus in fetu. From the 38 pregnancies reported in the literature, including women who had Botulism Poisoning aspects during pregnancy, exposure to botulinum toxin type A does not appear to increase the risk of adverse outcome in the Fetus in fetu.[SEP]", "label": "no"}
{"original_question": "Does a linker histone exist in the yeast genome?", "id": "converted_113", "sentence1": "Does a linker Histone antigen exist in the Saccharomyces cerevisiae genome?", "sentence2": "Hho1p is a bona fide linker Histone antigen In Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae, 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 or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae, 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 or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae 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 or Saccharomyces cerevisiae cerevisiae linker Histone antigen, Hho1p Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae encodes a single linker Histone antigen, Hho1p, with two globular domains.  The Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae linker Histone antigen Hho1p, with two globular domains, can simultaneously bind to two four-way junction DNA molecules Here, we show in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae, that the presence of Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae 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 or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae linker Histone antigen Hho1p is not essential for cell viability, and very little is known about its function in vivo.  Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae 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 or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae, 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 or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae linker Histone antigen-Hho1p maintains Chromatin Loop organization during ageing. Database Homologous Gene searching against the complete Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae 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 or Saccharomyces cerevisiae cerevisiae 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 or Saccharomyces cerevisiae cerevisiae Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae. Database Homologous Gene searching against the complete Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae 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 or Saccharomyces cerevisiae cerevisiae 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]", "label": "yes"}
{"original_question": "Can protein coding exons originate from ALU sequences?", "id": "converted_114", "sentence1": "Can protein coding Exons originate from ALU sequences?", "sentence2": "The Alu element 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]", "label": "yes"}
{"original_question": "Is there evidence that tomato juice lowers cholesterol levels?", "id": "converted_115", "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 \u00b1 15.8 to 51.7 \u00b1 14.8 mg/dL, P<0.001), and the ratio of total-C/High Density Lipoproteins-C (4.25 \u00b1 1.59 to 3.63 \u00b1 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 \u226510 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 Lipoprotein 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 \u226510 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 (\u22656.21 mmol/L), Low-Density Lipoproteins cholesterol (\u22654.14 mmol/L), and Glycosylated hemoglobin A (\u22656%), respectively.  In conclusion, women consuming \u226510 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 Lipoprotein 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 Lipoprotein 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]", "label": "yes"}
{"original_question": "Are there transposon-free regions in mammalian genomes?", "id": "converted_116", "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]", "label": "yes"}
{"original_question": "Are messenger RNA molecules epigenetically methylated?", "id": "converted_117", "sentence1": "Are messenger RNA molecules epigenetically methylated?", "sentence2": "The most abundant RNA, Messenger post-transcriptional ResponseLevel - ResponseLevel - modification is N-methyladenosine (m(6)A), which has broad roles in RNA biology. N-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 N6-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-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-methyladenosine (m(6)A) and 5-Methylcytosine (m(5)C).[SEP]", "label": "yes"}
{"original_question": "Is invasion and metastasis one of the hallmarks of cancer?", "id": "converted_118", "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]", "label": "yes"}
{"original_question": "Is progesterone effective for treatment of patients with traumatic brain injury based on clinical trial data?", "id": "converted_119", "sentence1": "Is Progesterone [EPC] effective for treatment of patients with traumatic Brain Injuries based on clinical trial data?", "sentence2": "BACKGROUND: Progesterone has been associated with robust positive effects in animal models of traumatic Brain Injuries (Traumatic Brain Injury) 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 [EPC], as compared with 50.5% with placebo. Mortality was similar in the two groups. No relevant safety differences were noted between Progesterone [EPC] and placebo. CONCLUSIONS: True primary (qualifier value) and secondary efficacy analyses showed no clinical benefit of Progesterone [EPC] in patients with severe Traumatic Brain Injury. 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 (Traumatic Brain Injury) is a major cause of death and Disability:Type:Pt:^Patient:Nom worldwide. Progesterone has been shown to improve neurologic outcome in multiple experimental models and two early-phase trials involving patients with Traumatic Brain Injury.  There was no significant difference between the Progesterone [EPC] group and the placebo group in the proportion of patients with a favorable outcome (relative benefit of Progesterone [EPC], 0.95; 95% confidence interval [NDUFB6 gene], 0.85 to 1.06; P=0.35). Phlebitis or Thrombophlebitis was more frequent in the Progesterone [EPC] 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 [EPC] over placebo in the improvement of outcomes in patients with acute Traumatic Brain Injury.  Numerous studies, however, show that Progesterone [EPC] 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 [EPC] 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 [EPC] may significantly improve neurologic outcome of patients suffering severe Traumatic Brain Injury up to 3 months after injury, especially those with 5\u2264GCS\u22648, providing a potential benefit to the treatment of acute severe Traumatic Brain Injury patients. Considering this Pharmacologic Substance had no significant side effects, so Progesterone [EPC] could be used in patients with severe Traumatic Brain Injury as a neuro-protective Pharmacologic Substance. While Progesterone [EPC] 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 [EPC] 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 [EPC] to be 0.77, 95% NDUFB6 gene 0.62 to 0.96. AUTHORS' CONCLUSIONS: Current clinical evidence from three small RCTs indicates Progesterone [EPC] may improve the neurologic outcome of patients suffering Traumatic Brain Injury. 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 [EPC], and Progesterone [EPC]-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 [EPC] and ergocalciferol together was significantly higher than that of Progesterone [EPC] 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 [EPC] was 0.77, 95% confidence interval (NDUFB6 gene) 0.62 to 0.96. AUTHORS' CONCLUSIONS: Current clinical evidence from three small RCTs indicates Progesterone [EPC] may improve the neurologic outcome of patients suffering Traumatic Brain Injury. This evidence is still insufficient and further multicentre randomised controlled trials are required. Clinical trials have shown that short-and long-term Progesterone [EPC] 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 [EPC] for patients with acute severe traumatic Brain Injuries: a randomized controlled trial. CONCLUSION: Our data suggest that acute severe Traumatic Brain Injury patients with administration of Progesterone [EPC] hold improved neurologic outcomes for up to 6 months. These results provide information important for further large and multicenter clinical trials on Progesterone [EPC] as a promising neuroprotective Pharmacologic Substance.  The Changing Functional Independence Measure scores in the Progesterone [EPC] 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 [EPC] 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 Traumatic Brain Injury patients with administration of Progesterone [EPC] hold improved neurologic outcomes for up to 6 months. These results provide information important for further large and multicenter clinical trials on Progesterone [EPC] as a promising neuroprotective Pharmacologic Substance.  These data, combined with the results of the previously published ProTECT trial, show Progesterone [EPC] to be safe and potentially efficacious in the treatment of Traumatic Brain Injury. 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 [EPC] 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 Injuries survivors who received Progesterone [EPC] were more likely to have a moderate to good outcome than those randomized to placebo. CONCLUSION: In this small study, Progesterone [EPC] 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 [EPC] 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 [EPC] 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 [EPC] for moderate-to-severe Traumatic Brain Injury in 1200 patients An industry-sponsored Phase III international trial is also under way, and planning for a trial using Progesterone [EPC] to treat pediatric Brain Injuries has begun More than two decades of pre-clinical research and two recent clinical trials have shown that Progesterone [EPC] (PROG) and its Metabolite exert beneficial effects after traumatic Brain Injuries (Traumatic Brain Injury) 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 [EPC] 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 Traumatic Brain Injury is inconclusive except that Corticosteroid ophthalmologic and otologic preparations are likely to be ineffective or harmful, and tranexamic acid, nimodipine and Progesterone [EPC] show a promising effect in bleeding trauma, Traumatic spinal subarachnoid hemorrhage, Traumatic Brain Injury or severe Traumatic Brain Injury. Laboratory data strongly show that Progesterone [EPC] treatment after Traumatic Brain Injury 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 [EPC] treatment after Traumatic Brain Injury.[SEP]Relations: Progesterone has relations: contraindication with Thrombophlebitis, contraindication with Thrombophlebitis. phlebitis has relations: disease_disease with Thrombophlebitis, disease_disease with Thrombophlebitis. Tranexamic acid has relations: contraindication with Thrombophlebitis, contraindication with Thrombophlebitis.", "label": "no"}
{"original_question": "Is there a role for the cylindromatosis tumor suppressor (CYLD) in lung cancer?", "id": "converted_120", "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-\u03baB survival signaling in Primary malignant neoplasm of lung cells increased expression of CYLD protein, human protein, human directly blocks TNFSF10 wt Allele-induced NF-\u03baB 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-\u03baB 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.", "label": "yes"}
{"original_question": "Can we detect DNA strand asymmetries using dinucleotide relative abundance \"genomic signatures\"?", "id": "converted_121", "sentence1": "Can we detect DNA strand asymmetries using Dinucleoside Phosphates relative abundance \"genomic signatures\"?", "sentence2": "comparing the heterogeneities of bacterial Genome with respect to strand-independent first- and second-order features, (i) G + C content and (ii) Dinucleoside Phosphates relative abundance, the concept of a genomic signature was introduced with the observation of species-type specific Dinucleotide Relative Abundance Profiles (DRAPs); dinucleotides were identified as the subsequences with the greatest bias in representation in a majority of Genome. Dinucleoside Phosphates relative abundance values (the genomic signature) The Dinucleoside Phosphates 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 Dinucleoside Phosphates frequencies to those expected under the assumption of stochastic equilibrium (thorough shuffling).  The Genome - anatomical entity signatures (Dinucleoside Phosphates relative abundance values) Early biochemical experiments measuring nearest neighbor frequencies established that the set of Dinucleoside Phosphates relative abundance values (Dinucleoside Phosphates biases) is a remarkably stable property of the DNA of an Organism. the set of Dinucleoside Phosphates biases constitutes a 'genomic signature' that can discriminate sequences from different organisms. the set of Dinucleoside Phosphates odds ratio (relative abundance) values constitute a signature of each DNA Genome - anatomical entity Dinucleotide relative abundance extremes: a genomic signature. The Dinucleoside Phosphates 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 Dinucleotide Relative Abundance Profiles (DRAPs); dinucleotides were identified as the subsequences with the greatest bias in representation in a majority of Genome. Comparisons within and between species sample sequences are based on the profile of Dinucleoside Phosphates 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 Dinucleoside Phosphates XY, both computed from the Sequence - ParameterizedDataType concatenated with its inverted complement). Dinucleotide relative abundances (i.e., Dinucleoside Phosphates representations normalized by the component nucleotide frequencies) are consonant with respect to the leading and lagging strands[SEP]", "label": "no"}
{"original_question": "Is there any relationship between histone ubiquitylation and splicing?", "id": "converted_122", "sentence1": "Is there any relationship between histone ubiquitylation and splicing?", "sentence2": "Histone H2b-specific deubiquitinase and demonstrate that H2B deubiquitination by USP49 gene gene is required for efficient cotranscriptional splicing of a large set of Exons. H2B monoubiquitylation (H2BK123ub1) marks Introns in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae H2B ubiquitination by facilitating splicing pre-mRNA splicing plays a critical role in Histone H2b ubiquitination unanticipated functional link between Histone H2b ubiquitination and pre-mRNA splicing[SEP]", "label": "yes"}
{"original_question": "Can SUMO affect calcium homeostasis?", "id": "converted_123", "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 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.  RIM1\u03b1 SUMOylation at lysine residue K502 facilitates\u00a0the clustering of CaV2.1 calcium channels and\u00a0enhances the Ca(2+) influx necessary for vesicular release, whereas non-SUMOylated RIM1\u03b1 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]", "label": "yes"}
{"original_question": "Have mutations in the GARS gene been identified to cause Charcot-Marie-Tooth Disease Type 2D (CMT2D)?", "id": "converted_124", "sentence1": "Have Gene Mutation in the GARS Genes 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 Genes 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 Gene Mutation in the GARS1 wt Allele Genes (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 Genes Genes (formerly RAB7A Genes wt Allele) (CMT2B), Prelamin-A/C (Charcot-Marie-Tooth Disease, Type 2B1), MED25 gene Genes (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 Genes Genes (CMT2I/J), GDAP1 gene Genes (CMT2H/K), Heat Shock Protein Beta-8 (Autosomal dominant Charcot-Marie-Tooth Disease type 2L), and AARS1 Genes (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) Genes 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 Gene Mutation in the Congenital Generalized Lipodystrophy Type 2 (BSCL2 Genes Genes) and in the GARS1 wt Allele encoding (GARS) genes.  We previously implicated Gene Mutation in the Genes 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 Gene Mutation in the Genes GARS, encoding glycyl tRNA synthetase (GlyRS).  Missense Gene Mutation in the GARS1 wt Allele (GARS) Genes 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 Gene Mutation have been identified in patients from each of the five studied families.[SEP]Relations: Charcot-Marie-Tooth Disease, axonal, Autosome recessive has relations: disease_disease with Charcot-Marie-Tooth Disease, disease_protein with GDAP1 gene, disease_disease with Charcot-Marie-Tooth Disease, disease_protein with GDAP1 gene, disease_disease with Charcot-Marie-Tooth Disease, disease_protein with GDAP1 gene, disease_disease with Charcot-Marie-Tooth Disease, disease_protein with GDAP1 gene. Charcot-Marie-Tooth Disease has relations: disease_protein with NEFL protein, human, disease_protein with MED25 gene, disease_protein with HSPB1 protein, human, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with KIF1B protein, human, disease_protein with Heat Shock Protein Beta-8, disease_protein with NEFL protein, human, disease_protein with MED25 gene, disease_protein with HSPB1 protein, human, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with KIF1B protein, human, disease_protein with Heat Shock Protein Beta-8, disease_protein with NEFL protein, human, disease_protein with MED25 gene, disease_protein with HSPB1 protein, human, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with KIF1B protein, human, disease_protein with Heat Shock Protein Beta-8, disease_protein with NEFL protein, human, disease_protein with MED25 gene, disease_protein with HSPB1 protein, human, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with KIF1B protein, human, disease_protein with Heat Shock Protein Beta-8, disease_protein with NEFL protein, human, disease_protein with MED25 gene, disease_protein with HSPB1 protein, human, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with KIF1B protein, human, disease_protein with Heat Shock Protein Beta-8, disease_protein with NEFL protein, human, disease_protein with MED25 gene, disease_protein with HSPB1 protein, human, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with KIF1B protein, human, disease_protein with Heat Shock Protein Beta-8, disease_protein with NEFL protein, human, disease_protein with MED25 gene, disease_protein with HSPB1 protein, human, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with KIF1B protein, human, disease_protein with Heat Shock Protein Beta-8, disease_protein with NEFL protein, human, disease_protein with MED25 gene, disease_protein with HSPB1 protein, human, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with KIF1B protein, human, disease_protein with Heat Shock Protein Beta-8. MED25 gene has relations: disease_protein with Charcot-Marie-Tooth Disease, disease_protein with Charcot-Marie-Tooth Disease. Optic Neuropathy has relations: disease_phenotype_positive with Charcot-Marie-Tooth Disease, disease_phenotype_positive with Charcot-Marie-Tooth Disease. neuronopathy, distal hereditary motor has relations: disease_disease with Charcot-Marie-Tooth Disease, disease_protein with HSPB1 protein, human, disease_protein with Heat Shock Protein Beta-8, disease_disease with Charcot-Marie-Tooth Disease, disease_protein with HSPB1 protein, human, disease_protein with Heat Shock Protein Beta-8. Autosome dominant Charcot-Marie-Tooth Disease type 2 has relations: disease_disease with Charcot-Marie-Tooth Disease, disease_disease with Charcot-Marie-Tooth Disease, disease_disease with Charcot-Marie-Tooth Disease, disease_disease with Charcot-Marie-Tooth Disease. GDAP1 gene has relations: disease_protein with Charcot-Marie-Tooth Disease, disease_protein with Charcot-Marie-Tooth Disease.", "label": "yes"}
{"original_question": "Does melanoma  occur in people of African origin ?", "id": "converted_125", "sentence1": "Does Melanocytic neoplasm  occur in people of African origin ?", "sentence2": "ALM is the most common type of Melanocytic neoplasm amongst Asians, Africans, 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 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 Africans. In a series of melanomas from black Africans (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 Africans 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 Africans, supporting a different pathogenesis of these tumors. Malignant Melanocytic neoplasm (Millimole per Liter) remains a pediatric rarity world-wide, but perhaps more so in black Africans. 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 Africans are predominantly located on the lower All All extremities Thus, our findings indicate that melanomas located on the lower All All extremities in black Africans 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 Africans. Africans 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 Melanoma to that of Anal Anal squamous cell carcinoma is larger than the corresponding ratio for Caucasians. ( Albino Africans, as compared with normally Pigmented Africans, seem to have a relatively small risk of getting cutaneous malignant melanomas 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 Africans. Eighteen cases of malignant Skin Specimen Source Code tumors seen at the University of Port Harcourt Teaching Hospital over 3 years (1984 to 1987) were analyzed for diagnoses, site of tumors, sex, and age. Seven patients (39%) had malignant melanomas 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 Neoplasms among Africans on the sole of the Lower extremity>Foot. Pathological features of twenty-one cases of 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 Neoplasms and 4.5% of all malignant Neoplasms, 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 Africans is resistant to Melanocytic neoplasm. This paper reports the incidence of this lesion in association with invasive malignant melanomas of the feet and hands of Black Africans. Follow-up data (over a 3-year period) and the histological appearances of Primary Lesion were studied and related in 40 Black patients with Melanocytic neoplasm. Malignant Melanocytic neoplasm of the Skin Specimen Source Code in Blacks in formidable and sinister tumour. The incidence of 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 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_protein with BRAF protein, human, disease_disease with Malignant neoplasm of Skin Specimen Source Code, disease_protein with BRAF protein, human, disease_disease with Malignant neoplasm of Skin Specimen Source Code. non-Cutaneous Melanoma has relations: disease_disease with Melanocytic neoplasm, disease_disease with Melanocytic neoplasm. Anal squamous cell carcinoma of floor of mouth has relations: disease_disease with Anal squamous cell carcinoma, disease_disease with Anal squamous cell carcinoma. anal canal Anal squamous cell carcinoma has relations: disease_disease with Anal squamous cell carcinoma, disease_disease with Anal squamous cell carcinoma. melanocytic neoplasm has relations: disease_disease with Melanocytic neoplasm, disease_disease with Melanocytic neoplasm.", "label": "yes"}
{"original_question": "Are people with blood group O protected against severe Malaria?", "id": "converted_126", "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]", "label": "yes"}
{"original_question": "Is there a crystal structure of the full-length of the flaviviridae NS5(Methyltransferase - RNA depended RNA Polymerase) ?", "id": "converted_127", "sentence1": "Is there a crystal structure of the full-length of the flaviviridae Noonan Syndrome 5(Methyltransferase - RNA depended RNA Polymerase) ?", "sentence2": "Flavivirus sp. Noonan Syndrome 5 harbors a CMTR1 gene (MTase) in its N-terminal \u2248 265 residues and an RNA-Directed RNA Polymerase (RNA-directed RNA polymerase activity) within the C-terminal part. One of the major interests and challenges in Noonan Syndrome 5 is to understand the interplay between RNA-directed RNA polymerase activity and MTase as a unique natural fusion protein in Viral Genome replication and cap formation. Here, we report the first crystal structure of the full-length Flavivirus sp. Noonan Syndrome 5 from Japanese encephalitis virus.  (DENV) nonstructural protein 5 (Noonan Syndrome 5) is composed of two globular domains separated by a 10-residue linker. The N-terminal Superkingdom (taxonomic category) participates in the synthesis of a mRNA cap 1 structure ((7Me)GpppA(2'OMe)) at the 5' end of the Viral Genome and possesses guanylyltransferase, guanine-N7-CMTR1 gene, and nucleoside-2'O-CMTR1 gene activities. The C-terminal Superkingdom (taxonomic category) is an RNA-Directed RNA Polymerase responsible for RNA, Viral synthesis. Although crystal structures of the two isolated domains have been obtained, there are no structural data for full-length Noonan Syndrome 5. It is also unclear whether the two Noonan Syndrome 5 domains interact with each other to form a stable structure in which the relative orientation of the two domains is fixed. To investigate the structure and dynamics of DENV type 3 Noonan Syndrome 5 in solution, we conducted small-angle X-ray scattering experiments with the full-length protein. Noonan Syndrome 5 was found to be monomeric and well-folded under the conditions tested. West Nile virus (West Nile viral infection) Noonan Syndrome 5 protein contains a CMTR1 gene (MTase) Superkingdom (taxonomic category) involved in RNA capping and an RNA-Directed RNA Polymerase (RdRp) Superkingdom (taxonomic category) essential for virus replication. Crystal structures of individual West Nile viral infection MTase and RdRp domains have been solved; however, the structure of full-length Noonan Syndrome 5 has not been determined. To gain more insight into the structure of Noonan Syndrome 5 and interactions between the MTase and RdRp domains, we generated a panel of seven monoclonal antibodies (mAbs) to the Noonan Syndrome 5 protein of West Nile viral infection (Kunjin strain) and mapped their Binding Sites using a series of truncated Noonan Syndrome 5 proteins and synthetic peptides. Binding sites of four mAbs (5D4, 4B6, 5C11 and 6A10) were mapped to residues 354-389 in the fingers subdomain of the RdRp. This is consistent with the ability of these mAbs to inhibit RdRp activity in vitro and suggests that this Geographic Locations represents a potential target for RdRp inhibitors. Using a series of synthetic peptides, we also identified a linear epitope (bound by Monoclonal Antibody [EPC] 5H1) that mapped to a 13 aa stretch surrounding residues 47 and 49 in the MTase Superkingdom (taxonomic category), a Geographic Locations predicted to interact with the palm subdomain of the RdRp. The failure of one Monoclonal Antibody [EPC] (7G6) to bind both N- and C-terminally truncated Noonan Syndrome 5 recombinants indicates that the immunoglobulin complex location recognizes a conformational epitope that requires the presence of residues in both the MTase and RdRp domains.[SEP]", "label": "yes"}
{"original_question": "Can venlafaxine block NET and SERT?", "id": "converted_128", "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 5-HT, whereas the high dose blocked the reuptake of both 5-HT and No evidence of. Moreover, an enhancement of serotonergic neurotransmission by venlafaxine was only achieved under conditions whereby the desensitization of the terminal 5-HT(1B) autoreceptor is appended to that of the somatodendritic 5-HT(1A) receptor.[SEP]Relations: Citalopram has relations: drug_drug with clomipramine, drug_drug with clomipramine. Venlafaxine has relations: drug_drug with clomipramine, drug_drug with clomipramine. Serotonin has relations: drug_drug with clomipramine, drug_drug with clomipramine. Paroxetine has relations: drug_drug with clomipramine, drug_drug with clomipramine. Desipramine has relations: drug_drug with clomipramine, drug_drug with clomipramine. Phenelzine has relations: drug_drug with clomipramine, drug_drug with clomipramine. Reboxetine has relations: drug_drug with clomipramine, drug_drug with clomipramine. Duloxetine has relations: drug_drug with clomipramine, drug_drug with clomipramine. Nomifensine has relations: drug_drug with clomipramine, drug_drug with clomipramine. Milnacipran has relations: drug_drug with clomipramine, drug_drug with clomipramine.", "label": "yes"}
{"original_question": "Can vitamin B1 deficiency cause encephalopathy?", "id": "converted_129", "sentence1": "Can vitamin B1 deficiency cause Encephalopathies?", "sentence2": "Wernicke Encephalopathy (WE) is a severe neurological syndrome caused by thiamine (vitamin B1) 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 nervous system disorder, which is caused by vitamin B1 deficiency Wernicke Encephalopathy (WE) is a potentially reversible yet serious neurological manifestation caused by vitamin B1(thiamine) deficiency Wernicke-Korsakoff Syndrome is caused by thiamine (vitamin B1) deficiency Both the Thyrotoxicosis and a catabolic state due to the Hyperemesis Gravidarum were thought to have induced a vitamin B1 deficiency, causing the Wernicke-Korsakoff Syndrome. Wernicke-Korsakoff Syndrome (or Wernicke-Korsakoff Encephalopathies) is a rarely diagnosed nervous system disorder, which is caused by vitamin B1 deficiency. Wernicke-Korsakoff Syndrome is caused by thiamine (vitamin B1) deficiency. Wernicke Encephalopathy is a nervous system disorder caused by thiamine (vitamin B1) deficiency characterized by Vertigo <invertebrate>, Cerebellar Ataxia, and mental confusion. Wernicke Encephalopathy (WE) is caused by thiamine (vitamin B1) deficiency and most commonly found in individuals with chronic Alcoholic Intoxication, Chronic and Malnutrition. Wernicke Encephalopathy (WE) is an acute neurological disease resulting from thiamine (vitamin B1) deficiency. Post-mortem findings demonstrate that thiamine (vitamin B1) deficiency sufficient to cause irreversible Traumatic AND/OR non-traumatic brain injury is not diagnosed ante mortem in 80-90% of these patients. Wernicke Encephalopathy is an acute neuropsychiatric disorder, due to thiamine (vitamin B1) deficiency. Wernicke Encephalopathy (WE) is a severe neurological syndrome caused by thiamine (vitamin B1) deficiency and clinically characterized by the sudden onset of mental status changes, Ocular abnormalities, and Cerebellar Ataxia. Wernicke Encephalopathy, a pathology caused by vitamin B1 (thiamin) deficiency, is often difficult to diagnose and can lead to severe cognitive sequels if left untreated. Wernicke Encephalopathy-Korsakoff syndrome (WE-KS) is common in alcoholics, caused by thiamine deficiency (diphtheria, tetanus toxoids and acellular pertussis vaccine; vitamin B1) and associated with Lesion to the Thalamic structure (thalidomide). Wernicke-Korsakoff Syndrome is caused by thiamine (vitamin B1) deficiency Thiamine Drug Class Drug Class (vitamin B1) deficiency, associated with a variety of conditions, including chronic Alcoholic Intoxication, Chronic and bariatric surgery for morbid obesity, can result in the nervous system disorder Wernicke&apos;s Encephalopathies (WE) Wernicke Encephalopathy is caused by Thiamine Drug Class Deficiency and can be recognized by severe neurological symptoms that are occasionally accompanied by systemic signs.  INTRODUCTION: Wernicke Encephalopathy, a pathology caused by vitamin B1 (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 (thiamine) and niacin (niacinamide) in an 80-year-old women, hospitalized for severe Sepsis (Invertebrate) caused by aspiration Pneumonia.  Acute Wernicke Encephalopathy (WE) is caused by profound vitamin B1 (thiamine) deficiency and commonly presents with the classic clinical triad of mental confusion, Cerebellar Ataxia, and ophthalmoplegia.  [Wernicke\u00b4s Encephalopathies and Polyneuropathy associated with vitamin B complex deficiency after a bariatric surgery]. BACKGROUND: Thiamine Drug Class Drug Class deficiency in patients who abuse alcohol can cause Wernicke Encephalopathy (WE).  Wernicke-Korsakoff Syndrome--a debilitating acute or subacute nervous system disorder-is caused by a deficiency in thiamine (vitamin B(1)).  Wernicke Encephalopathy is a serious neurological manifestation of vitamin B1 deficiency. Both the Thyrotoxicosis and a catabolic state due to the Hyperemesis Gravidarum were thought to have induced a vitamin B1 deficiency, causing the Wernicke-Korsakoff Syndrome. Wernicke-Korsakoff Syndrome is caused by thiamine (vitamin B1) deficiency. Wernicke-Korsakoff Syndrome (or Wernicke-Korsakoff Encephalopathies) is a rarely diagnosed nervous system disorder, which is caused by vitamin B1 deficiency. Wernicke Encephalopathy is a nervous system disorder caused by thiamine (vitamin B1) deficiency characterized by Vertigo <invertebrate>, Post-mortem findings demonstrate that thiamine (vitamin B1) 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 hydrochloride absorption in Homo sapiens caused by Malnutrition present in alcoholic patients or by the direct effects of ethanol on intestinal transport. Wernicke Encephalopathy is a serious neurologic disorder caused by vitamin-B1 or thiamine deficiency. Wernicke Encephalopathy results from thiamine (vitamin B1) deficiency. Common causes include Alcoholic Intoxication, Chronic and Stomach Diseases. Wernicke Encephalopathy is a nervous system disorder caused by thiamine (vitamin B1) deficiency characterized by Vertigo <invertebrate>, Cerebellar Ataxia, and mental confusion. Wernicke Encephalopathy (WE) is caused by thiamine (vitamin B1) deficiency and most commonly found in individuals with chronic Alcoholic Intoxication, Chronic and Malnutrition. Post-mortem findings demonstrate that thiamine (vitamin B1) deficiency sufficient to cause irreversible Traumatic AND/OR non-traumatic brain injury is not diagnosed ante mortem in 80-90% of these patients. Wernicke Encephalopathy, a pathology caused by vitamin B1 (thiamin) deficiency, is often difficult to diagnose and can lead to severe cognitive sequels if left untreated.[SEP]Relations: nervous system disorder has relations: disease_disease with Encephalopathies, disease_disease with Encephalopathies.", "label": "yes"}
{"original_question": "Are epigenetic modifications implicated in cardiovascular development and disease?", "id": "converted_130", "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 Diseases 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 Diseases 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 Diseases. 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 Diseases (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 Diseases. 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 Diseases. 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 Diseases setting. Epigenetics may represent one of the possible scientific explanations of the impact of such intrauterine risk factors for the subsequent development of Cardiovascular Diseases (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 Diseases. Emerging data suggest that these epigenetic modifications also impact on the development of Cardiovascular Diseases. Epigenetic alterations are associated with Inflammation and Cardiovascular Diseases in patients with Chronic Kidney Diseases. Emerging data suggest that these epigenetic modifications also impact on the development of Cardiovascular Diseases 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: inherited neurodegenerative disorder has relations: disease_disease with neurodegenerative Disease, disease_disease with neurodegenerative Disease. NKX2-5 gene has relations: cellcomp_protein with chromatin location, anatomy_protein_present with Chest>Heart, cellcomp_protein with chromatin location, anatomy_protein_present with Chest>Heart.", "label": "yes"}
{"original_question": "Can exosomes be detected in urine?", "id": "converted_131", "sentence1": "Can Exosomes be detected in 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 urine, they represent a precious biomedical tool.  Exosomes are Vesicle (morphologic abnormality) that are released from the Both kidneys into 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\u2009nm) 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 urine.  Urinary exosome-like Vesicle (morphologic abnormality) (ELVs) are a heterogenous mixture (diameter 40-200\u2009nm) 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 urine. Proteomic analysis of urinary Exosomes in cardiovascular and associated Kidney Diseases by two-dimensional electrophoresis and LC-MS/MS[SEP]", "label": "yes"}
{"original_question": "Is Kanzaki disease associated with deficiency in alpha-N-acetylgalactosaminidase?", "id": "converted_132", "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) 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 Schindler Disease, Type I (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 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 Schindler Disease, Type I 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) 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) 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]", "label": "yes"}
{"original_question": "Is Mycobacterium avium less susceptible to antibiotics than Mycobacterium tuberculosis?", "id": "converted_133", "sentence1": "Is Mycobacterium avium less susceptible to Antifungal Antibiotics, Topical than Mycobacterium Tuberculosis?", "sentence2": "The prevalence of cyclophosphamide/doxorubicin/mitomycin protocol lung Communicable Diseases in two inner city hospitals was four times higher than that of TB. Most patients with combined Communicable Diseases were clinically consistent with Mycobacterium Tuberculosis and responded to anti Mycobacterium Tuberculosis 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, 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 (TB) 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 (TB) 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 pulmonary Tuberculosis. From April 2001 to February 2002, 80 blood samples from patients who were suspected to have disseminated Mycobacterium Infections, 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 (TB) 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 (TB) 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 (TB) 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 (TB) 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 pulmonary Tuberculosis, disease_disease with pulmonary Tuberculosis. Rifabutin has relations: off_label_use with pulmonary Tuberculosis, off_label_use with pulmonary Tuberculosis. pulmonary Tuberculosis has relations: disease_disease with Tuberculosis, disease_disease with Tuberculosis.", "label": "yes"}
{"original_question": "Are there conserved noncoding elements identified between genomes of human and teleosts?", "id": "converted_134", "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 cartilaginous Fishes 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 cartilaginous Fishes 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]", "label": "yes"}
{"original_question": "Does cortical spreading depression appear in ischemic penumbra following ischemic stroke?", "id": "converted_135", "sentence1": "Does Adrenal Cortex spreading Cancer patients and suicide and depression appear in ischemic penumbra following ischemic stroke?", "sentence2": "During the subacute phase, the irreversible damage expands into the penumbra: multiple electrical and biological signals are triggered by periinfarct, spreading Cancer patients and suicide and Cancer patients and suicide and depression-like depolarizations leading to Hypoxia, CTCAE and stepwise increase in Lactic acid measurement. Experimental and clinical studies indicate that waves of Adrenal Cortex spreading depolarization (DIARRHEA 8, SECRETORY SODIUM, CONGENITAL) appearing in the ischemic penumbra contribute to secondary lesion growth. Analysis of Structure of middle cerebral artery occlusions (MCAOs) revealed a first DIARRHEA 8, SECRETORY SODIUM, CONGENITAL wave starting off during ischemic decline at the emerging core region, propagating concentrically over large portions of left Adrenal Cortex Diseases. Subsequent recurrent waves of DIARRHEA 8, SECRETORY SODIUM, CONGENITAL did not propagate concentrically but preferentially circled around the ischemic core. In the vicinity of the core region, CSDs were coupled to waves of predominantly vasoconstrictive Core-Binding Factor(LSF) responses, resulting in further decline of Core-Binding Factor in the entire inner penumbra and in expansion of the ischemic core. We conclude that CSDs and corresponding Core-Binding Factor responses follow a defined spatiotemporal order, and contribute to early evolution of ischemic territories. Astrocytes in the metabolically compromised ischemic penumbra-like area showed a long lasting swelling response to spontaneous spreading depolarizations despite rapid dendritic recovery in a photothrombotic occlusion model of focal stroke. Spontaneous spreading depolarizations (Symptom Distress Scale) occur in the penumbra surrounding ischemic core. These Symptom Distress Scale, often referred to as peri-infarct depolarizations, cause vasoconstriction and recruitment of the penumbra into the ischemic core in the critical first hours after focal ischemic stroke; however, the real-time spatiotemporal dynamics of SLC17A5 gene-induced injury to synaptic circuitry in the penumbra remain unknown. We propose that metabolic stress resulting from recurring Symptom Distress Scale facilitates acute injury at the level of Dendrites and Dendritic Spines in metabolically compromised Tissue Specimen Code, expediting penumbral recruitment into the ischemic core. Although the mechanism remains unknown, Symptom Distress Scale show delayed electrophysiological recovery within the ischemic penumbra. Spreading Cancer patients and suicide and Cancer patients and suicide and depression-like peri-infarct depolarizations not only characterize but also worsen penumbra conditions in Adrenal Cortex border zones of experimental focal ischemia. We conclude that in focal ischemia, transient peri-infarct depolarizations emerge not only in Adrenal Cortex but also in striatal gray matter, thereby demonstrating the existence of subcortical zones of ischemic penumbra. Spreading Cancer patients and suicide and Cancer patients and suicide and depression (SLC17A5 gene) has been demonstrated following focal ischemia, and the additional workload imposed by SLC17A5 gene on a Tissue Specimen Code already compromised by a marked reduction in blood flow may contribute to the evolution of irreversible damage in the ischemic penumbra. While the changes in the glucose-related metabolites persisted during recovery even in anterior portions of the Adrenal Cortex Diseases in both groups in the aftermath of the SLC17A5 gene, the magnitude of the changes was greater in the penumbra than in the normal Adrenal Cortex Diseases. SLC17A5 gene appears to impose an equivalent increase in energy demands in control and ischemic brain, but the ability of the penumbra to recover from the insult is compromised. Thus, increasing the energy imbalance in the penumbra after multiple Symptom Distress Scale may hasten the deterioration of the energy status of the Tissue Specimen Code and eventually contribute to Terminal (end postition) depolarization and cell Cessation of life, particularly in the penumbra. It is suggested that the limited survival of the penumbra is due to periinfarct depolarizations, which result in repeated episodes of Tissue Specimen Code Hypoxia, CTCAE, because the increased metabolic workload is not coupled to an adequate increase of collateral blood supply. Transient decreases of the apparent diffusion coefficient (ADC) of Water - Specimen Source Codes as measured by fast diffusion-weighted imaging (DWI) in the ischemic border zone are thought to reflect cellular swelling associated with spreading Cancer patients and suicide and Cancer patients and suicide and depression. Severely delayed recovery time after spreading Cancer patients and suicide and Cancer patients and suicide and depression is thought to represent the ischemic penumbra. One current but controversial hypothesis is that this penumbra Tissue Specimen Code often eventually dies because of the metabolic stress imposed by multiple Adrenal Cortex spreading Cancer patients and suicide and Cancer patients and suicide and depression (DIARRHEA 8, SECRETORY SODIUM, CONGENITAL) waves, that is, by ischemic depolarizations. After simulated infarction, the model displays the linear relation between final infarct size and the number of DIARRHEA 8, SECRETORY SODIUM, CONGENITAL waves traversing the penumbra that has been reported experimentally, although damage with each individual wave progresses nonlinearly with time. These findings support the hypothesis that DIARRHEA 8, SECRETORY SODIUM, CONGENITAL waves play an important causal role in the Cessation of life of ischemic penumbra Tissue Specimen Code. MCAO also triggers periodic periinfarction depolarizing waves (PIDs) in the ischemic penumbra, the Geographic state of salvage. Here, the effects of SLC17A5 gene at reduced flow conditions as encountered in the ischemic penumbra are examined. The experiments illustrate how peri-infarct depolarizations may detrimentally affect the penumbra. In the second series of experiments, periinfarct depolarizations (PIDs) were recorded with an Extracellular Dyskeratosis Congenita electrode at two locations in the ischemic penumbra for the initial 3 h following MCAO. In vivo two-photon microscopy of green fluorescent protein-expressing neurons in this penumbra-like area at risk revealed that Symptom Distress Scale were temporally correlated with rapid (<6 s) dendritic beading.[SEP]", "label": "yes"}
{"original_question": "Is phospholamban a regulatory/inhibitory protein of the Ca ATPase SERCA?", "id": "converted_136", "sentence1": "Is PLN gene a regulatory/inhibitory protein of the cyclophosphamide/doxorubicin protocol ATPase SERCA?", "sentence2": "The Membrane Proteins complex between the Sarcoplasmic Reticulum cyclophosphamide/doxorubicin protocol(2+)-ATPase (SERCA) and PLN gene (PLN) controls cyclophosphamide/doxorubicin protocol(2+) transport in Myocytes, Cardiac, thereby modulating Cardiac - anatomy qualifier contractility. \u03b2-Adrenergic-stimulated phosphorylation of PLN at Ser-16 enhances SERCA activity via an unknown mechanism. PLN gene (PLN) is a type II Membrane Proteins that inhibits the Sarcoplasmic Reticulum cyclophosphamide/doxorubicin protocol(2+)-ATPase (SERCA), thereby regulating calcium homeostasis in Cardiac - anatomy qualifier muscle. In Tissue Membrane Device, PLN forms pentamers that have been proposed to function either as a storage for active monomers or as ion channels. Regulation of the SERCA calcium pump by PLN gene (PLB1 gene) is largely due to interactions between their respective transmembrane domains. In spite of numerous Mutagenesis Procedure and kinetic studies, we still do not have a clear mechanistic picture of how PLB1 gene influences the calcium transport cycle of SERCA. Calcium transport across the Membrane Device of the Sarcoplasmic Reticulum (SNCG wt Allele) plays an important role in the regulation of Myocardium contraction and relaxation. The sarco(endo)plasmic reticulum cyclophosphamide/doxorubicin protocol(2+) ATPase (SERCA) 2a is responsible for cyclophosphamide/doxorubicin protocol(2+) up-take by this Cytoplasmic Cytoplasmic organelle and is inhibited in a reversible manner by PLN gene, another SNCG wt Allele Membrane Proteins. Thus, alleviation of PLN gene-mediated inhibition of SERCA2a is a potential therapeutic option for Congestive Congestive heart failure and Cardiomyopathies. PLN gene has been suggested to be a key regulator of Cardiac - anatomy qualifier Sarcoplasmic Reticulum (SNCG wt Allele) cyclophosphamide/doxorubicin protocol cycling and contractility and a potential therapeutic target in restoring the depressed cyclophosphamide/doxorubicin protocol cycling in failing hearts. In larger Mammals, a higher fraction of SERCA2a pumps are regulated by PLN gene, and this may influence therapeutic strategies to enhance Cardiac - anatomy qualifier contractility and functional Cardiac - anatomy qualifier reserve. PLN gene (PLB1 gene) inhibits the Sarcoplasmic Reticulum (SNCG wt Allele) cyclophosphamide/doxorubicin protocol(2+)-ATPase (SERCA), and this inhibition is relieved by cyclophosphamide/doxorubicin protocol(2+) calmodulin-dependent protein kinase II (calmodulin-dependent protein kinase II) phosphorylation These findings suggest that PLB1 gene is an important modulator of gastric antrum Smooth muscle (tissue) contractility by modulation of SNCG wt Allele cyclophosphamide/doxorubicin protocol(2+) release and calmodulin-dependent protein kinase II activity. The function of the SERCA pump is modulated by the endogenous molecules PLN gene (PLB1 gene) and sarcolipin (SLN gene gene), expressed in Cardiac - anatomy qualifier and Skeletal muscle structure. The mechanism of action of PLB1 gene on SERCA is well characterized, whereas that of SLN gene gene is only beginning to be understood.   PLN gene (PLB1 gene) is an inhibitor of the Sarcoplasmic Reticulum (SNCG wt Allele) Ca2+-ATPase (SERCA). These results show that alteration of the PLB1 gene:SERCA ratio can significantly modulate Smooth muscle (tissue) [Ca2+]i. PLN gene expressed in Cardiac - anatomy qualifier muscle and sarcolipin expressed in Specimen Source Codes - Skeletal muscle regulate SERCA activity. PLN gene (PLB1 gene) is a 24- to 27-kDa phosphoprotein that modulates activity of the sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA). Expression of PLB1 gene is reportedly limited to Cardiac - anatomy qualifier, slow-twitch skeletal and Smooth muscle (tissue) in which PLB1 gene is an important regulator of [Ca2+]i and contractility in these Muscle Tissue. Regulation of the sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA 2a) depends on the phosphorylation state of PLN gene (PLB1 gene). When PLB1 gene is phosphorylated, its inhibitory effect towards SERCA 2a is relieved, leading to an enhanced myocardial performance.   cyclophosphamide/doxorubicin protocol(2+) reuptake occurs via sarcoendoplasmic reticulum cyclophosphamide/doxorubicin protocol(2+) ATPase (SERCA) and is regulated by the inhibitory protein PLN gene (PLB1 gene) in many cell types. PLN gene (PLN) is a small integral Membrane Proteins, which binds and inhibits in a yet unknown fashion the cyclophosphamide/doxorubicin protocol(2+)-ATPase (SERCA) in the Sarcoplasmic Reticulum. PLN gene (PLN) is the endogenous inhibitor of the sarco(endo)plasmic reticulum cyclophosphamide/doxorubicin protocol(2+)-ATPase (SERCA), the integral Membrane Device enzyme responsible for 70\ufffd% of the removal of cyclophosphamide/doxorubicin protocol(2+) from the Cytoplasmic matrix, inducing Cardiac - anatomy qualifier muscle relaxation in Homo sapiens. PLN gene (PLB1 gene) is an integral Membrane Proteins regulating cyclophosphamide/doxorubicin protocol(2+) transport through inhibitory interaction with sarco(endo)plasmic reticulum calcium ATPase (SERCA). Phosphorylation by Cyclic AMP-Dependent Protein Kinases and dephosphorylation by Protein phosphatase modulate the inhibitory activity of PLN gene (PLN), the endogenous regulator of the sarco(endo)plasmic reticulum calcium cyclophosphamide/doxorubicin protocol(2+) ATPase (SERCA). Phosphorylation by Cyclic AMP-Dependent Protein Kinases and dephosphorylation by Protein phosphatase modulate the inhibitory activity of PLN gene (PLN), the endogenous regulator of the sarco(endo)plasmic reticulum calcium cyclophosphamide/doxorubicin protocol(2+) ATPase (SERCA) We used EPR spectroscopy to probe directly the interaction between PLN gene (PLB1 gene) and its regulatory target, the Sarcoplasmic Reticulum cyclophosphamide/doxorubicin protocol-ATPase (SERCA)[SEP]", "label": "yes"}
{"original_question": "Is Alpers disease inherited in an autosomal recessive mode?", "id": "converted_137", "sentence1": "Is Alpers disease inherited in an Autosomal recessive inheritance mode?", "sentence2": "Alpers-Huttenlocher syndrome (AHS) is a very rare Autosomal recessive inheritance disorder Alpers syndrome is an Autosomal recessive inheritance mitochondrial DNA depletion disorder that affects children and young adults Alpers Syndrome (disorder) 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 inheritance 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 inheritance disorder usually seen in infants and young children. Alpers syndrome is a rare Autosomal recessive inheritance hepatocerebral degenerative disorder. Alpers disease 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 disease 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: hepatobiliary disease has relations: disease_disease with Hepatobiliary Disorder, disease_disease with Hepatobiliary Disorder. Cerebral cortex has relations: anatomy_protein_present with POLG protein, human, anatomy_protein_present with POLG protein, human. Liver Failure has relations: disease_disease with Hepatobiliary Disorder, disease_disease with Hepatobiliary Disorder.", "label": "yes"}
{"original_question": "Is vemurafenib effective for hairy-cell leukemia?", "id": "converted_138", "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 \u00d7 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_protein with BRAF protein, human, drug_protein with BRAF protein, human. Dabrafenib has relations: drug_protein with BRAF protein, human, drug_protein with BRAF protein, human. hairy cell leukemia has relations: disease_protein with BRAF protein, human, disease_protein with BRAF protein, human.", "label": "yes"}
{"original_question": "Is there an association between TERT promoter mutation and survival of glioma patients?", "id": "converted_139", "sentence1": "Is there an association between TERT wt Allele promoter Mutation Abnormality and survival of glioma patients?", "sentence2": "Mutations lead to TERT wt Allele wt Allele upregulation and are associated with aggressive clinical behavior in Glioblastoma. Kaplan-Meier's survival analysis showed that TERT wt Allele wt Allele promoter Mutation Abnormality (P=0.037), Isocitrate Dehydrogenase (NAD+) (Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection) Mutation Abnormality (P<0.001), and 1p/19q codeletion (P<0.001) were associated with favorable overall survival (OS). In the subset of 116 Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection-mutated lower-grade Glioma lacking 1p/19q codeletion, 19 TERT wt Allele wt Allele promoter-mutated Neoplasms exhibited longer progression-free survival (PFS) (P=0.027) and OS (P=0.004). Consistent with this observation, in the subset of 97 Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection-mutated astrocytomas, 14 TERT wt Allele wt Allele promoter-mutated Neoplasms showed longer PFS (P=0.001) and OS (P=0.001). In contrast, among the subset of 74 Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection wild-type lower-grade Glioma with intact 1p/19q, TERT wt Allele wt Allele promoter Mutation Abnormality was associated with shorter PFS (P=0.001) and OS (P=0.001). Similarly, in the subset of 65 Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection wild-type astrocytomas, 16 TERT wt Allele wt Allele promoter-mutated Neoplasms exhibited unfavorable PFS (P=0.007) and OS (P=0.008). Our results indicate that when combined with Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection status, TERT wt Allele wt Allele promoter Mutation Abnormality contributes to prognostic subgroups of lower-grade astrocytic Neoplasms or 1p/19q intact lower-grade Glioma and this may further refine future molecular classification of lower-grade Glioma. RESULTS: TERTp-mut identified in 60.8% of Glioma (491 out of 807) was globally associated with poorer outcome (Hazard ratio (HR)=1.50).  TERT wt Allele wt Allele promoter Gene Mutation lead to high transcriptional activity under Hypoxia, CTCAE and temozolomide treatment and predict poor prognosis in Glioma. Patients with TERT wt Allele wt Allele promoter Gene Mutation had lower survival rates, even after adjusting for other known or potential risk factors, and the incidence of Mutation Abnormality was correlated with patient age. TERT wt Allele wt Allele promoter Gene Mutation maintained its ability of inducing high transcriptional activity even under hypoxic and TMZ treatment conditions, and the presence of Gene Mutation was associated with poor prognosis in glioma patients.  Patients whose Grade III-IV Glioma exhibit TERT wt Allele wt Allele promoter Gene Mutation alone predominately have primary GBMs associated with poor median OS (11.5 months). Patients whose Grade III-IV Glioma exhibit IDH1/2 Gene Mutation alone predominately have astrocytic morphologies and exhibit a median OS of 57 months while patients whose Neoplasms exhibit both TERT wt Allele wt Allele promoter and IDH1/2 Gene Mutation predominately exhibit oligodendroglial morphologies and exhibit median OS of 125 months. Patients with TERT wt Allele wt Allele promoter Gene Mutation had lower survival rates, even after adjusting for other known or potential risk factors, and the incidence of Mutation Abnormality was correlated with patient age.CONCLUSION: TERT wt Allele wt Allele promoter Gene Mutation were specific to Glioma.  We defined, based on TERTp-mut and Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection Mutation Abnormality status, four prognostic groups: (1) TERTp-mut and Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection-mut associated with 1p19q codeletion, overall survival (OS)>17 years; (2) TERTp-wt and Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection-mut, associated with TP53 wt Allele wt Allele Mutation Abnormality, OS=97.5 months; (3) TERTp-wt and Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection-wt, with no specific association, OS=31.6 months; (4) TERTp-mut and Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection-wt, associated with EGFR amplification, OS=15.4 months.  Mutations lead to TERT wt Allele wt Allele upregulation and are associated with aggressive clinical behavior in Glioblastoma.  In the subset of 116 Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection-mutated lower-grade Glioma lacking 1p/19q codeletion, 19 TERT wt Allele wt Allele promoter-mutated Neoplasms exhibited longer progression-free survival (PFS) (P=0.027) and OS (P=0.004).  The mean age at diagnosis was lowest (37 years) among patients who had Glioma with only Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection Gene Mutation and was highest (59 years) among patients who had Glioma with only TERT wt Allele wt Allele Gene Mutation. The molecular groups were independently associated with overall survival among patients with grade II or III Glioma but not among patients with grade IV Glioma. Mutations were detected in Glioma, but not in Meningioma, Pituitary Adenoma, cavernomas, intracranial metastases, normal brain tissue surgical material, or peripheral blood of glioma patients. Patients with TERT wt Allele wt Allele promoter Gene Mutation had lower survival rates, even after adjusting for other known or potential risk factors, and the incidence of Mutation Abnormality was correlated with patient age.[SEP]", "label": "yes"}
{"original_question": "Does ziconotide bind to N-type calcium channels?", "id": "converted_140", "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 Rattus norvegicus. 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 rat 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 rat model of spinal ischemia.[SEP]Relations: Mexiletine has relations: drug_drug with ziconotide, drug_drug with ziconotide. Duloxetine has relations: drug_drug with ziconotide, drug_drug with ziconotide. Serotonin has relations: drug_drug with ziconotide, drug_drug with ziconotide. Pregabalin has relations: drug_drug with ziconotide, drug_drug with ziconotide. Morphine has relations: drug_drug with ziconotide, drug_drug with ziconotide.", "label": "yes"}
{"original_question": "Is stop codon bypass possible?", "id": "converted_141", "sentence1": "Is Stop brand of fluoride codon bypass possible?", "sentence2": "In 1999, proof-of-concept for treating these disorders was obtained in a mouse model of Muscular Dystrophy, when administration of Antibiotics, Aminoglycoside restored protein translation by inducing the ribosome to bypass a Percutaneous transhepatic cholangiography. Aminoglycosides can bypass nonsense mutations and are the prototypic agents for translational bypass therapy (Tonation Breathing Technique). Expression of retroviral replication enzymes (Pol) requires a controlled translational recoding event to bypass the Stop brand of fluoride codon at the end of gag. This recoding event occurs either by direct suppression of termination via the Insert (object) of an Amino Acid [EPC] at the Stop brand of fluoride codon (readthrough) or by alteration of the mRNA reading frame (Frameshift Mutation function). Recent studies on translation termination in the yeast Saccharomyces cerevisiae have not only enabled the identification of the key components of the termination machinery, but have also revealed several regulatory mechanisms that might enable the controlled synthesis of C-terminally extended Polypeptides via Stop brand of fluoride-codon readthrough.  The effects of all possible single-base mutations in the codons flanking the Stop brand of fluoride indicated that 3' contexts of the form CAR-YYA confer leakiness and that the 3' context permits read through of UAA and UGA Stop brand of fluoride codons as well as UAG. As a first step to elucidate the mechanism(s) by which ribosomes bypass leaky Stop brand of fluoride codons in vivo, we have devised a system in which readthrough is coupled to the transient expression of Beta-glucuronidase (GUSB wt Allele) in tobacco protoplasts.[SEP]", "label": "yes"}
{"original_question": "Is the protein \u03b21-integrin recycled?", "id": "converted_142", "sentence1": "Is the protein \u03b21-integrin recycled?", "sentence2": "Pathways selectively regulating \u03b21-integrin recycling are implicated in cancer invasion and metastasis, integrin-positive early and recycling Endosomes  LPA-induced recycling of \u03b21 integrin, RCP-mediated recycling of Integrins  CycD1 overexpression increased \u03b21 integrin recycling  inhibition of autophagy slowed down the lysosomal degradation of internalized \u03b21 integrins and promoted its Membrane Device recycling recycling pathway for \u03b21-integrin  \u03b21 integrin recycling  \u03b21 integrin recycling  controlling \u03b21 integrin recycling to the plasma Membrane Device  integrin recycling pathway Distinct recycling of active and inactive \u03b21 integrins. Integrin functions are controlled by regulating their affinity for ligand, and by the efficient recycling of intact integrins through Endosomes.  \u03b21 integrins, resulting in their recycling to the Cell surface where they can be reused.[SEP]Relations: Membrane Device has relations: cellcomp_cellcomp with plasma Membrane Device, cellcomp_cellcomp with plasma Membrane Device. plasma Membrane Device has relations: cellcomp_cellcomp with Membrane Device, cellcomp_cellcomp with Membrane Device.", "label": "yes"}
{"original_question": "Are BBS mutations involved in syndromic Hirschsprung disease?", "id": "converted_143", "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_protein with ret unit of radiation dose, disease_protein with ret unit of radiation dose.", "label": "yes"}
{"original_question": "Is there any software for automated analysis of immuno-histochemistry images?", "id": "converted_144", "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]", "label": "yes"}
{"original_question": "Is TALEN being used on stem cells?", "id": "converted_145", "sentence1": "Is Transcription Activator-Like Effector Nucleases being used on Stem cells?", "sentence2": "Precise correction of the dystrophin Genes in duchenne muscular dystrophy patient induced pluripotent Stem cells by Transcription Activator-Like Effector Nucleases and CRISPR-Cas9. Genetic correction of patient-derived induced pluripotent Stem cells (iPSCs) by TALENs or CRISPR-Cas9 holds promise for DMD Genes 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 (Zinc Finger Nucleases)- or transcription activator-like effector nuclease (Transcription Activator-Like Effector Nucleases)-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 (Transcription Activator-Like Effector Nucleases)-mediated Genes editing in mouse embryonic Stem cells (mESCs) to produce CASP14 Genes with targeted Genes disruptions and Clinical act of insertion in two Genes, Y-Linked--SRY protein, Homo sapiens and UTY Genes. Transcription activator-like effector nuclease (Transcription Activator-Like Effector Nucleases)-mediated Genes correction in integration-free \u03b2-thalassemia induced pluripotent Stem cells. A Transcription Activator-Like Effector Nucleases 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 Transcription Activator-Like Effector Nucleases targeted Homo sapiens stem cell Clone Cells detected by whole-Genome - anatomical entity sequencing. Using CRISPR-Cas9 and Transcription Activator-Like Effector Nucleases 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 Transcription Activator-Like Effector Nucleases-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 Zinc Finger Nucleases and Transcription Activator-Like Effector Nucleases delivery. At all loci tested we obtained Homo sapiens embryonic stem cell (ESTERASE C) and induced pluripotent stem cell (iPSC) Clone Cells carrying transgenic cassettes solely at the Transcription Activator-Like Effector Nucleases-specified location. We report here the use of TALENs 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 (TALENs) have been successfully used to knock out endogenous genes in stem cell research. Here we report different methods to efficiently perform Transcription Activator-Like Effector Nucleases-mediated Genes 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 TALENs 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 TALENs 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 Transcription Activator-Like Effector Nucleases-mediated generation and genetic correction of disease-specific Homo sapiens induced pluripotent Stem cells. Baculoviral transduction facilitates Transcription Activator-Like Effector Nucleases-mediated targeted transgene integration and Cre/LoxP cassette exchange in Homo sapiens-induced pluripotent Stem cells. We used transcription activator-like effector nuclease (Transcription Activator-Like Effector Nucleases)-mediated Genes editing in mouse embryonic Stem cells (mESCs) to produce CASP14 Genes with targeted Genes disruptions and Clinical act of insertion in two Genes, Y-Linked--SRY protein, Homo sapiens and UTY Genes.  Using CRISPR-Cas9 and Transcription Activator-Like Effector Nucleases 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-Transcription Activator-Like Effector Nucleases as measured by the Surveyor assay.  TAT-Transcription Activator-Like Effector Nucleases protein-mediated Genes disruption was applicable in hiPSCs and represents a promising technique for Genes knockout in Stem cells. Here we engineered transcription activator-like effector nucleases (TALENs) for five distinct genomic loci. At all loci tested we obtained Homo sapiens embryonic stem cell (ESTERASE C) and induced pluripotent stem cell (iPSC) Clone Cells carrying transgenic cassettes solely at the Transcription Activator-Like Effector Nucleases-specified location. Seamless correction of the sickle cell disease Mutation Abnormality of the HBB Genes in Homo sapiens induced pluripotent Stem cells using TALENs. At all loci tested we obtained Homo sapiens embryonic stem cell (ESTERASE C) and induced pluripotent stem cell (iPSC) Clone Cells carrying transgenic cassettes solely at the Transcription Activator-Like Effector Nucleases-specified location. Our data suggest that TALENs 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]", "label": "yes"}
{"original_question": "Is there an association between bruxism and reflux", "id": "converted_146", "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 (Gastroesophageal reflux disease). However, no robust evidence supports the association between antimony and Gastroesophageal reflux disease. Sleep Bruxism is prevalent in Gastroesophageal reflux disease patients, and Gastroesophageal reflux disease 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 Gastroesophageal reflux disease 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 Gastroesophageal reflux disease 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]", "label": "yes"}
{"original_question": "Can a peptide aptamer be used as protein inhibitor?", "id": "converted_147", "sentence1": "Can a peptide aptamer be used as Protein Info inhibitor?", "sentence2": "Peptides aptamers of Rhombotin 2 (Lmo2) were previously used to successfully treat Lmo2-induced tumours in a mouse model of leukemia. Inhibition of mammalian cell proliferation by genetically selected peptide aptamers that functionally antagonize E2F activity. Accumulating work over the past decade has shown that peptide aptamer screening represents a valid strategy for inhibitor identification that can be applied to a variety of different targets.  . The target of one inhibitor peptide, 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-\u03b2 inhibitor, namely i) ligand traps, ii) Antisense Oligonucleotides, iii) receptor kinase inhibitors and iv) peptide aptamers.   A peptide aptamer (ID1/3-PA7) has been designed to prevent this interaction and thereby leading to the transcription of p16(INK4a). A peptide kinase inhibitor (IP(20)) was used as the aptameric peptide  Peptides aptamer mimicking RAD51-binding Superkingdom (taxonomic category) of BRCA2 gene gene inhibits DNA damage repair and survival in Trypanosoma brucei brucei brucei.  peptide 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 peptide 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 peptide 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 peptide-aptamer-based inhibitors of carboxypeptidase C E. he fusion peptide, 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 peptide of Thioredoxin 1 and ABAD-inhibiting peptide 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 peptide aptamer specifically suppressed receptor-mediated extrinsic apoptosis but not intrinsic pathway, which was recapitulated by the Antisense Oligonucleotides for CASP8AP2 wt Allele.  Peptides 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 peptide 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 Info binding has relations: molfunc_protein with microtubule-associated Protein Info 1B, molfunc_protein with microtubule-associated Protein Info 1B.", "label": "yes"}
{"original_question": "Are integrins part of the extracellular matrix?", "id": "converted_148", "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 \u03b21integrins, 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 \u03b15.  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 \u03b1v\u03b23 and \u03b1v\u03b25.  Integrin receptors connect the extracellular matrix to the cell cytoskeleton to provide essential forces and signals.   the integrin, TLN1 gene, and Microfilaments 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]", "label": "yes"}
{"original_question": "Is Calcium homeostasis important in cardiac physiology and pathophysiology?", "id": "converted_149", "sentence1": "Is Calcium homeostasis important in Cardiac - anatomy qualifier physiology and pathophysiology?", "sentence2": "Maintenance of cellular CALCIUM SUPPLEMENTS homeostasis is critical to regulating mitochondrial ATP production and Cardiac - anatomy qualifier contraction.  the Ca(2+) signal regulates the most important activities of the \"U\" lymphocyte, from the expression of Genes, to Chest>Heart and muscle contraction and other motility processes, to diverse metabolic pathways involved in the generation of \"U\" lymphocyte fuels Pharmacologic modification of cellular CALCIUM SUPPLEMENTS handling recently moved into focus as an alternative for prevention and treatment of ventricular tachyarrhythmias diabetic Rattus norvegicus displayed abnormal Cardiac - anatomy qualifier structure and systolic and diastolic dysfunction, and spermine (CASR gene agonist) could prevent or slow its progression. These results indicate that the CASR gene expression of Myocardium is reduced in the progress of 3',5'-dichloromethotrexate, and its potential mechanism is related to the impaired intracellular CALCIUM SUPPLEMENTS homeostasis. CALCIUM SUPPLEMENTS-sensing receptor (CASR gene) Na(+)/Ca(2+) exchanger (TLX2 gene) plays important roles in Cardiac - anatomy qualifier electrical activity and CALCIUM SUPPLEMENTS homeostasis. TLX2 gene current (I(TLX2 gene)) shows Transmural gradient across left ventricle in many species. Previous studies demonstrated that TLX2 gene expression was increased and Transmural gradient of I(TLX2 gene) was disrupted in failing Chest>Heart CALCIUM SUPPLEMENTS homeostasis, the key process underlying excitation-contraction coupling The results indicate the CALCIUM SUPPLEMENTS handling properties of hiPSC-derived Myocytes, Cardiac are relatively immature to hESC counterparts Our understanding of the Molecular processes which regulate Cardiac - anatomy qualifier function has grown immeasurably in recent years. Even with the advent of \u03b2-blockers, angiotensin inhibitors and CALCIUM SUPPLEMENTS modulating agents, Chest>Heart failure (Hydrops Fetalis) still remains a seriously debilitating and life-threatening condition. Here, we review the Molecular changes which occur in the Chest>Heart in response to increased load and the pathways which control Cardiac - anatomy qualifier hypertrophy, CALCIUM SUPPLEMENTS homeostasis, and immune activation during Hydrops Fetalis. Calcium-Sensing Receptor (CaSRs) are G-protein coupled receptors which maintain systemic CALCIUM SUPPLEMENTS homeostasis and participate in hormone secretion, activation of ion channels, \"U\" lymphocyte apoptosis, proliferation, and differentiation. CaSRs are associated with I/R injury and apoptosis in neonatal rat ventricular Myocytes, Cardiac via suppressing BCL2 gene and promoting caspase-3 expression. Important insights into the Molecular basis of Hypertrophic disorder of skin, unspecified cardiomyopathy and related diseases have been gained by studying families with inherited Cardiac - anatomy qualifier hypertrophy. Integrated clinical and genetic investigations have demonstrated that different genetic defects can give rise to the common phenotype of Cardiac - anatomy qualifier hypertrophy. Diverse pathways have been identified, implicating perturbations in force generation, force transmission, intracellular CALCIUM SUPPLEMENTS homeostasis, myocardial energetics, and Cardiac - anatomy qualifier metabolism in causing Disease HCLS1-Associated Protein X-1, Human as a regulator of contractility and CALCIUM SUPPLEMENTS cycling in the Chest>Heart. HCLS1-Associated Protein X-1, Human overexpression reduced sarcoplasmic reticulum Ca-ATPase (Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase 2) pump activity in isolated Myocytes, Cardiac and in vivo, leading to depressed Muscle Cells CALCIUM SUPPLEMENTS kinetics and mechanics. Thus, HCLS1-Associated Protein X-1, Human represents a regulatory mechanism in Cardiac - anatomy qualifier CALCIUM SUPPLEMENTS cycling and its responses to sympathetic stimulation, implicating its importance in CALCIUM SUPPLEMENTS homeostasis and \"U\" lymphocyte survival. CALCIUM SUPPLEMENTS ion are the most ubiquitous and versatile signaling molecules in eukaryotic Cells. Calcium homeostasis and signaling systems are crucial for both the normal growth of the budding yeast Saccharomyces cerevisiae and the intricate working of the Mammals Chest>Heart. this knowledge can be used to help treat relevant human diseases such as pathological Cardiac - anatomy qualifier hypertrophy and Chest>Heart failure With aging, the Chest>Heart develops Muscle Cells hypertrophy associated with impaired relaxation indices. To define the cellular basis of this adaptation, we examined the physiological changes that arise in CALCIUM SUPPLEMENTS handling in the aging Chest>Heart and contrasted the adaptations that occur following the imposition of a stimulus that alters CALCIUM SUPPLEMENTS homeostasis in a young and an old Chest>Heart alterations in the CALCIUM SUPPLEMENTS-handling machinery of the Cardiocyte - general anatomical term differ in the context of age and as such may predispose the older Chest>Heart to the development of a Hypertrophic disorder of skin, unspecified phenotype. The Cardiac - anatomy qualifier sodium-CALCIUM SUPPLEMENTS exchanger (SLC8A1 wt Allele) is a key sarcolemmal protein for the maintenance of CALCIUM SUPPLEMENTS homeostasis in the Chest>Heart.  Thus exchanger overexpression in CASP14 gene leads to abnormal CALCIUM SUPPLEMENTS handling and a decompensatory transition to Chest>Heart failure with stress Central to controlling intracellular CALCIUM SUPPLEMENTS concentration ([Ca(2+)](i)) are a number of Ca(2+) transporters and channels with the L-type Ca(2+) channel, Na(+)-Ca(2+) exchanger and Sarcoplasmic Reticulum Calcium-Transporting ATPases (SERCA) being of particular note in the Chest>Heart. This review concentrates on the regulation of [Ca(2+)](i) in Cardiac - anatomy qualifier muscle and the homeostatic mechanisms employed to ensure that the Chest>Heart can operate under steady-state conditions on a beat by beat basis. the tight regulation of SNCG wt Allele Ca(2+) content is also required to prevent the abnormal, spontaneous or diastolic release of Ca(2+) from the SNCG wt Allele. Such diastolic events are a major factor contributing to the genesis of Cardiac - anatomy qualifier arrhythmias in Disease situations and in recently identified familial mutations in the SNCG wt Allele Ca(2+) release channel (Ryanodine Receptor Calcium Release Channel, Ryanodine Receptor Calcium Release Channel complex location). Calcium channels have a unique functional role, because not only do they participate in this activity, they form the means by which electrical signals are converted to responses within the \"U\" lymphocyte. Calcium channels play an integral role in excitation in the Chest>Heart and shaping the Cardiac - anatomy qualifier action potential. In addition, CALCIUM SUPPLEMENTS influx through CALCIUM SUPPLEMENTS channels is responsible for initiating contraction. Abnormalities in CALCIUM SUPPLEMENTS homeostasis underlie Cardiac - anatomy qualifier arrhythmia, contractile dysfunction and Cardiac - anatomy qualifier remodelling.  Cardiac CALCIUM SUPPLEMENTS (Ca(2+)) handling subsumes the mechanisms maintaining the myocardial Ca(2+) homeostasis that contribute essentially to Cardiac - anatomy qualifier performance. Calcium is an important mediator in Cardiac - anatomy qualifier excitation and disorders in Cardiac - anatomy qualifier Ca(2+) homeostasis have great influence on the Cardiac - anatomy qualifier action potential. We review the physiology of the Cardiac - anatomy qualifier CALCIUM SUPPLEMENTS homeostasis, including the Cardiac - anatomy qualifier excitation contraction coupling and Muscle Cells CALCIUM SUPPLEMENTS cycling. We review the physiology of the Cardiac - anatomy qualifier CALCIUM SUPPLEMENTS homeostasis, including the Cardiac - anatomy qualifier excitation contraction coupling and Muscle Cells CALCIUM SUPPLEMENTS cycling Calcium is an important mediator in Cardiac - anatomy qualifier excitation and disorders in Cardiac - anatomy qualifier Ca(2+) homeostasis have great influence on the Cardiac - anatomy qualifier action potential The role of CALCIUM SUPPLEMENTS in Cardiac - anatomy qualifier and Muscle, Smooth, Vascular physiology was reviewed, highlighting the major mechanisms responsible for maintaining CALCIUM SUPPLEMENTS homeostasis in these Cells Energy metabolism and Ca(2+) handling serve critical roles in Cardiac - anatomy qualifier physiology and pathophysiology[SEP]Relations: Hypertrophic cardiomyopathy has relations: disease_phenotype_positive with Hypertrophic disorder of skin, unspecified cardiomyopathy, disease_phenotype_positive with Hypertrophic disorder of skin, unspecified cardiomyopathy. Congestive Chest>Heart failure has relations: disease_phenotype_positive with Hypertrophic disorder of skin, unspecified cardiomyopathy, disease_phenotype_positive with Hypertrophic disorder of skin, unspecified cardiomyopathy. Arrhythmia has relations: disease_phenotype_positive with Hypertrophic disorder of skin, unspecified cardiomyopathy, disease_phenotype_positive with Hypertrophic disorder of skin, unspecified cardiomyopathy.", "label": "yes"}
{"original_question": "Is the gene DUX4 epigenetically regulated in somatic cells?", "id": "converted_150", "sentence1": "Is the Genes 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 Genes 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. Muscular Dystrophy, Facioscapulohumeral (FSHD) 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 Genes 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 FSHD-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 FSHD 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 Genes 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 Genes 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 FSHD. Recent studies provide compelling evidence that a retrotransposed Genes 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 FSHD 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 Genes 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 Genes(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 Genes 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) Genes. DUX4L2 wt Allele expresses a TRANSCRIPTION FACTOR that plays a major role in the development of FSHD through the initiation of a large Genes 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, Muscular Dystrophy, Facioscapulohumeral (FSHD) is characterized by chromatin relaxation of the D4Z4 macrosatellite array on Chromosomes, Human, Pair 4 and expression of the D4Z4-encoded DUX4L2 wt Allele Genes 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]", "label": "yes"}
{"original_question": "Have hESC been tested for the treatment of age-related macular degeneration?", "id": "converted_151", "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 retinaldehyde pigment epithelium (Structure of retinaldehyde pigment epithelium), a monolayer of Cells vital to photoreceptor cell health. We discuss the various methods used to differentiate and purify Structure of retinaldehyde pigment epithelium from Human 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 retinaldehyde pigment epithelium (Structure of retinaldehyde pigment epithelium) and is the most common cause of Unspecified visual loss among the elderly. Stem-cell-based strategies, using Human Embryonic Stem Cells (hESCs) or Homo sapiens-induced pluripotent stem Cells (hiPSCs), may provide an abundant donor source for generating Structure of retinaldehyde pigment epithelium Cells in cell replacement therapies. This study contributes to our understanding of the utility of hESC/hiPSC-derived Structure of retinaldehyde pigment epithelium in Age related macular degeneration therapy. Two important early potential hESC applications are the use of retinaldehyde pigment epithelium (Structure of retinaldehyde pigment epithelium) for the treatment of age-related macular degeneration and Stargardt's disease's disease disease, an untreatable form of macular dystrophy that leads to early-onset Blindness. Human embryonic stem Cells (hESCs) are a promising source of retinaldehyde pigment epithelium (Structure of retinaldehyde pigment epithelium) 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 Human Embryonic Stem Cells (hESCs) and induced pluripotent stem Cells (iPSCs) is the generation of retinaldehyde pigmented epithelium (Structure of retinaldehyde pigment epithelium) 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 retinaldehyde pigment epithelium (Structure of retinaldehyde pigment epithelium) 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 Human Embryonic Stem Cells (hESCs) and induced pluripotent stem Cells (iPSCs) is the generation of retinaldehyde pigmented epithelium (Structure of retinaldehyde pigment epithelium) 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 retinaldehyde pigment epithelium (Structure of retinaldehyde pigment epithelium) for the treatment of age-related macular degeneration and Stargardt's disease's disease disease, an untreatable form of macular dystrophy that leads to early-onset Blindness. A potential application of Human Embryonic Stem Cells (hESCs) and induced pluripotent stem Cells (iPSCs) is the generation of retinaldehyde pigmented epithelium (Structure of retinaldehyde pigment epithelium) to treat age-related macular degeneration (Age related macular degeneration), a common but incurable retinaldehyde disease. Structure of retinaldehyde pigment epithelium Cells derived from hESCs (hESC-RPEs) and iPSCs (iPSC-RPEs) express essential Structure of retinaldehyde pigment epithelium markers and can rescue visual function in animal models. Two important early potential hESC applications are the use of retinaldehyde pigment epithelium (Structure of retinaldehyde pigment epithelium) for the treatment of age-related macular degeneration and Stargardt's disease's disease disease, an untreatable form of macular dystrophy that leads to early-onset Blindness. Here we show long-term functional rescue using hESC-derived Structure of retinaldehyde pigment epithelium in both the RCS Rattus norvegicus and Elov14 mouse, which are animal models of retinaldehyde degeneration and Stargardt's disease's disease, respectively.[SEP]Relations: retinaldehyde disease has relations: disease_disease with retinaldehyde degeneration, disease_disease with retinaldehyde degeneration. Retinal degeneration has relations: disease_phenotype_positive with retinaldehyde degeneration, disease_phenotype_positive with retinaldehyde degeneration.", "label": "yes"}
{"original_question": "Does d-tubocurarine (d-TC) induces irreversible inhibition of nicotinic acetylcholine receptor (nAChR) at the neuromuscular junction?", "id": "converted_152", "sentence1": "Does d-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 d-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, d-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 d-tubocurarine, pancuronium and vecuronium on different Protein Isoforms of Nicotinic Receptors At all three receptor types, d-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 d-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 d-tubocurarine (d-TC). Study of the reversal effect of NF 449 on Observation of Neuromuscular Block induced by d-tubocurarine.[SEP]Relations: Muscle Tissue tissue has relations: anatomy_protein_present with Complement Component C6, human, anatomy_protein_present with Complement Component C6, human.", "label": "no"}
{"original_question": "Is zyxin a focal adhesion protein?", "id": "converted_153", "sentence1": "Is ZYX gene a focal adhesion protein?", "sentence2": "ZYX gene from FAs 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 \u03b1-actinins are delayed in their maturation, exhibit altered morphology, have decreased amounts of Zyxin and VASP protein, human protein, human, and reduced adhesiveness to Extracellular Matrix one focal adhesion protein (ZYX gene) Zyxin is a focal adhesion protein that has been implicated in the modulation of cell adhesion and motility  focal adhesion proteins (vinculin, 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.  Zyxin concentrates at Focal Adhesions  ZYX gene, a focal adhesion protein, Focal adhesion proteins Zyxin and VCL protein, human 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. . Zyxin is a focal adhesion protein that responds to external mechanical forces; VCL protein, human 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  Zyxin 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 VASP protein, human, cellcomp_protein with VASP protein, human, cellcomp_protein with VASP protein, human, cellcomp_protein with VASP protein, human.", "label": "yes"}
{"original_question": "Could DNA (cytosine-5-)-methyltransferases serve as tumour markers?", "id": "converted_154", "sentence1": "Could DNA (cytosine-5-)-methyltransferases serve as tumour markers?", "sentence2": "Here, we report evidence of the overexpression of DNA methyltransferases 3B (DNMT3B protein, human gene protein, Homo sapiens gene) in invasive cervical Primary malignant neoplasm and of the inhibition of metastasis by DNMT3B protein, human gene protein, Homo sapiens 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 methyltransferase 1 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 (DNA Modification Methylases) 1 and 3b expression in Stomach Carcinoma (GC) treated by neoadjuvant chemotherapy. High DNMT1 wt Allele wt Allele and DNMT3b expression was found in 105/127 (83%) and 79/127 (62%) Carcinoma, respectively. Tumoral DNMT3b RNA, Messenger up-regulation was significantly correlated with hypermethylation of multiple tumor-related Genes (P=0.021). A regulator of de novo DNA methyltransferases DNA (Cytosine-5)-Methyltransferase 3A, Human and DNMT3B protein, human gene protein, Homo sapiens 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 DNA Modification Methylases 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 DNMT3a 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 wt Allele wt Allele and DNMT3a immunoexpression and salivary gland neoplasms development. DNA methylation, mediated by the combined action of three DNA methyltransferases (DNMT1 wt Allele wt Allele, DNA (Cytosine-5)-Methyltransferase 3A, Human, and DNMT3B protein, human gene protein, Homo sapiens 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 DNA (Cytosine-5)-Methyltransferase 3A, Human mutations was studied in 415 patients with acute myeloid leukemia (Leukemia, Myelocytic, Acute) younger than 60 years. The recent identification of DNA (Cytosine-5)-Methyltransferase 3A, Human mutations in de novo acute myeloid leukemia prompted us to determine their frequency, patterns and clinical impact in a cohort of 98 patients with either therapy-related or secondary acute myeloid leukemia developing from an antecedent Hematological Disease. DNA methyltransferases (DNMT1 wt Allele wt Allele and DNMT3b) 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 DNA (Cytosine-5)-Methyltransferase 3A, Human wt Allele, DNMT3B protein, human gene protein, Homo sapiens gene, and EZH2 protein, human protein, Homo sapiens in Neoplasms. DNA methyltransferase 1 (DNMT1 wt Allele wt Allele) 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 protein, human gene protein, Homo sapiens 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 over-expression. DNA methylation patterns in Genome - anatomical entity are maintained during replication by a DNA methyltransferase Dnmt1. 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 DNA Modification Methylases and clinical prognosis in adult patients with Acute leukemia (AL), the RNA, Messenger expressions of DNA Modification Methylases, 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 ensures Clonality transmission of lineage-specific DNA methylation patterns in a Mammals Genome - anatomical entity during replication. Overexpression of the major DNA methyltransferase Dnmt1 is cytotoxic and has been hypothesized to result in aberrant hypermethylation of Genes required for cell survival. DNA (cytosine-5-)-methyltransferase 1 (DNMT1 wt Allele wt Allele) 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 methyltransferase 1 (DNMT1 wt Allele wt Allele) protein expression during gastric carcinogenesis.[SEP]Relations: acute promyelocytic leukemia has relations: disease_protein with DNA (Cytosine-5)-Methyltransferase 3A, Human, disease_protein with DNA (Cytosine-5)-Methyltransferase 3A, Human. carcinoma has relations: disease_protein with DNMT3B protein, human gene, disease_disease with Primary malignant neoplasm, disease_protein with DNMT3B protein, human gene, disease_disease with Primary malignant neoplasm. DNA (cytosine-5-)-methyltransferase activity has relations: molfunc_protein with DNMT3B protein, human gene, molfunc_protein with DNA (Cytosine-5)-Methyltransferase 3A, Human, molfunc_protein with DNMT3B protein, human gene, molfunc_protein with DNA (Cytosine-5)-Methyltransferase 3A, Human, molfunc_protein with DNMT3B protein, human gene, molfunc_protein with DNA (Cytosine-5)-Methyltransferase 3A, Human, molfunc_protein with DNMT3B protein, human gene, molfunc_protein with DNA (Cytosine-5)-Methyltransferase 3A, Human. malignant giant cell tumor has relations: disease_disease with Primary malignant neoplasm, disease_disease with Primary malignant neoplasm. malignant germ cell tumor of cervix uteri has relations: disease_disease with cervical Primary malignant neoplasm, disease_disease with cervical Primary malignant neoplasm. transcription factor binding has relations: molfunc_protein with DNA (Cytosine-5)-Methyltransferase 3A, Human, molfunc_protein with DNA (Cytosine-5)-Methyltransferase 3A, Human.", "label": "yes"}
{"original_question": "Is phospholamban phosphorylated by Protein kinase A?", "id": "converted_155", "sentence1": "Is phospholamban phosphorylated by Protein kinase A?", "sentence2": "cAMP-dependent protein kinase (Cyclic AMP-Dependent Protein Kinases) phosphorylation of PLB1 gene phosphorylation of PLN gene gene, at either Ser(16) by Cyclic AMP-Dependent Protein Kinases  Activation of cardiac muscle Sarcoplasmic Reticulum Ca2+-ATPase (SERCA2a) by beta1-agonists involves cAMP- and Cyclic AMP-Dependent Protein Kinases-dependent phosphorylation of phospholamban (PLB1 gene), which relieves the inhibitory effects of PLB1 gene on SERCA2a.  phospholamban (PLB1 gene) is a Sarcoplasmic Reticulum (SR) protein that when phosphorylated at Ser16 by Cyclic AMP-Dependent Protein Kinases phosphorylation of PLB1 gene by the Ca2+-calmodulin-dependent protein kinase (CaMK) and cAMP-dependent protein kinase (Cyclic AMP-Dependent Protein Kinases).  cAMP-dependent protein kinase (Cyclic AMP-Dependent Protein Kinases)-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 Cyclic AMP-Dependent Protein Kinases reverses the inhibitory action of PLB1 gene. phosphorylation of both PLB1 gene residues (Ser16, Cyclic AMP-Dependent Protein Kinases site, and Thr17, calmodulin-dependent protein kinase II site)  Phosphorylation of Ser(16) by Cyclic AMP-Dependent Protein Kinases stabilization of the structure of PLB1 gene following phosphorylation of Ser(16) phospholamban (PLB1 gene) inhibits the Sarcoplasmic Reticulum (SR) Ca(2+)-ATPase, and this inhibition is relieved by cAMP-dependent protein kinase (Cyclic AMP-Dependent Protein Kinases)-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 SR function is regulated by phosphorylation of phospholamban (PLB1 gene), a SR protein phosphorylated by cAMP-dependent protein kinase (Cyclic AMP-Dependent Protein Kinases) 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 protein kinase A 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 protein kinase A (Cyclic AMP-Dependent Protein Kinases) 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]", "label": "yes"}
{"original_question": "Are there telemedicine applications for chronic pain management?", "id": "converted_156", "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]", "label": "yes"}
{"original_question": "Is paramyxovirus involved in human subacute thyroiditis?", "id": "converted_157", "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]", "label": "no"}
{"original_question": "Is there any link between the aurora B kinase and the polycomb protein ring1B?", "id": "converted_158", "sentence1": "Is there any link between the aurora B kinase and the polycomb protein ring1B?", "sentence2": "The aurora B kinase 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\u00a0cells. 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\u00a0cells. 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\u00a0cells.[SEP]", "label": "yes"}
{"original_question": "Is CD99 encoded by MIC2 gene?", "id": "converted_159", "sentence1": "Is CD99 antigen encoded by MIC2 Genes?", "sentence2": "We report 2 unusual cytogenetic findings in a pediatric Ewings sarcoma, an Insertion Mutation of the MIC2 Genes encoding CD99 antigen antigen 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 MIC2 Genes product - ParticipationType - ParticipationType (CD99 antigen antigen) and a Ewings sarcoma breakpoint region 1 (EWSR1 Genes Genes) Genes rearrangement CD99 antigen antigen, a Integral Membrane Proteins encoded by MIC2 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 antigen antigen is a 32-kDa transmembrane glycoprotein that is encoded by the MIC2 Genes The surgical specimens showed small round cell Specimen Source Codes - Specimen Source Codes - tumor with positive staining for MIC2 Genes product - ParticipationType - ParticipationType (CD99 antigen antigen) CD99 antigen antigen is a 32-kDa transmembrane glycoprotein that is encoded by the MIC2 Genes. The leukocyte surface molecule CD99 antigen antigen is an GINM1 Genes encoded by the ubiquitin-like protein conjugating enzyme activity/MIC2 Genes. Human CD99 antigen antigen, which is encoded by the mic2 Genes, is a ubiquitous 32 kDa Integral Membrane Proteins. Human CD99 antigen antigen is a 32-kDa cell surface protein that is encoded by the MIC2 Genes localized to the SLC52A2 Genes. The Neoplasms displayed intense immunoreactivity in a Tissue membrane pattern for CD99 antigen antigen, the Membrane Glycoproteins encoded by the MIC2 Genes. CD99 antigen antigen, a Integral Membrane Proteins encoded by MIC2 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 antigen antigen, the product - ParticipationType - ParticipationType of the MIC2 Genes, exhibits an erythroid-specific quantitative Genetic Polymorphism coregulated with the Genetic Polymorphism of the XG blood group Genes. CD99 antigen antigen, the product - ParticipationType - ParticipationType of the MIC2 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 MIC2 Genes product - ParticipationType - ParticipationType (CD99 antigen antigen; 32-kDa) of T Specimen Source Codes - Lymphocytes. Although considered a specific marker for Ewing's sarcoma of bone of bone/peripheral neuroectodermal tumour, the MIC2 Genes product - ParticipationType - ParticipationType (CD99 antigen antigen) has been immunolocalised in a variety of Homo sapiens tumours. MIC2, the Genes encoding the CD99 antigen antigen antigen, is found in the Pseudoautosomal Regions of both the X and Y chromosomes. Human CD99 antigen antigen is a 32-kDa cell surface protein that is encoded by the MIC2 Genes localized to the SLC52A2 Genes. The Neoplasms displayed intense immunoreactivity in a Tissue membrane pattern for CD99 antigen antigen, the Membrane Glycoproteins encoded by the MIC2 Genes. CD99 antigen antigen (MIC2) 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 MIC2/CD99 antigen antigen-positive Neoplasms of the Ewing family. The Ewing family of Neoplasms (EFT) is characterized by high MIC2/CD99 antigen antigen expression and specific EWS/ETS Genes rearrangements, resulting in different chimeric transcripts. The Neoplasms displayed intense immunoreactivity in a Tissue membrane pattern for CD99 antigen antigen, the Membrane Glycoproteins encoded by the MIC2 Genes. Monoclonal antibody (Monoclonal Antibody [EPC]) CD99 antigen antigen wt Allele, which was raised against Ewing's sarcoma of bone of bone cells, recognizes a cell-surface glycoprotein, p30/32MIC2, that is encoded by the MIC2 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 MIC2 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 Specimen Source Codes - Lymphocytes. Homology searches resulted in finding Homologous Sequences (totally about 40% Homologous Gene) in the Homo sapiens MIC2 Genes product - ParticipationType - ParticipationType (CD99 antigen antigen; 32-kDa) of T Specimen Source Codes - Lymphocytes. CD99 antigen antigen is a 32-kDa transmembrane glycoprotein that is encoded by the MIC2 Genes CD99 antigen antigen, a Integral Membrane Proteins encoded by MIC2 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 MIC2 Genes product - ParticipationType - ParticipationType (CD99 antigen antigen) We report 2 unusual cytogenetic findings in a pediatric Ewings sarcoma, an Insertion Mutation of the MIC2 Genes encoding CD99 antigen antigen from Xp to 10p and a submicroscopic deletion of the well-known Specimen Source Codes - Specimen Source Codes - tumor supressor Genes KLF6 MIC2, the Genes encoding the CD99 antigen antigen antigen, is found in the Pseudoautosomal Regions of both the X and Y chromosomes Immunohistochemical analysis showed weak to moderate and partial staining for MIC2 (CD99 antigen antigen) and Nephroblastoma, respectively Human CD99 antigen antigen, which is encoded by the mic2 Genes, is a ubiquitous 32 kDa Integral Membrane Proteins The leukocyte surface molecule CD99 antigen antigen is an GINM1 Genes encoded by the ubiquitin-like protein conjugating enzyme activity/MIC2 Genes The Neoplasms displayed intense immunoreactivity in a Tissue membrane pattern for CD99 antigen antigen, the Membrane Glycoproteins encoded by the MIC2 Genes Human CD99 antigen antigen is a 32-kDa cell surface protein that is encoded by the MIC2 Genes localized to the SLC52A2 Genes MIC2, the Genes encoding the CD99 antigen antigen antigen, is found in the Pseudoautosomal Regions of both the X and Y chromosomes CD99 antigen antigen, the product - ParticipationType - ParticipationType of the MIC2 Genes, exhibits an erythroid-specific quantitative Genetic Polymorphism co-regulated with the Xga blood group Genetic Polymorphism[SEP]Relations: EWSR1 Genes has relations: disease_protein with Ewings sarcoma, disease_protein with Ewings sarcoma. Ewings sarcoma has relations: disease_phenotype_positive with Ewings sarcoma, disease_protein with EWSR1 Genes, disease_phenotype_positive with Ewings sarcoma, disease_protein with EWSR1 Genes. Ewings sarcoma of bone has relations: disease_disease with Ewings sarcoma, disease_disease with Ewings sarcoma.", "label": "yes"}
{"original_question": "Has the fungus Ashbya gossypii got many nuclei that share cytoplasm?", "id": "converted_160", "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]", "label": "yes"}
{"original_question": "Is microRNA(miRNA) 30 involved in post-ischemic cardiac remodeling?", "id": "converted_161", "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 Chest>Heart disease 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: cognitive impairment - coarse facies - Chest>Heart defects - obesity - pulmonary involvement - short stature - skeletal dysplasia syndrome has relations: disease_disease with Chest>Heart disease, disease_disease with Chest>Heart disease.", "label": "yes"}
{"original_question": "Is statin use associated with improved outcomes after aneurysmal subarachnoid hemorrhage?", "id": "converted_162", "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 haemorrhage (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 haemorrhage. 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 haemorrhage 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 haemorrhage 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: cerebral infarction has relations: indication with simvastatin, indication with simvastatin. Atorvastatin has relations: drug_drug with simvastatin, drug_drug with simvastatin. Pravastatin has relations: drug_drug with simvastatin, drug_drug with simvastatin.", "label": "yes"}
{"original_question": "Does molindone affect body weight?", "id": "converted_163", "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 Gaining Weight question.  No agent demonstrated superior efficacy, and all were associated with side effects, including Gaining Weight question.  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 Gaining Weight question 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 Gaining Weight question. Olanzapine showed the greatest risk of Gaining Weight question 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. Weight gain 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 Gaining Weight question 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: Olanzapine has relations: drug_drug with clozapine, drug_drug with molindone, drug_drug with clozapine, drug_drug with molindone. Loxapine has relations: drug_drug with clozapine, drug_drug with molindone, drug_drug with clozapine, drug_drug with molindone. Thioridazine has relations: drug_drug with clozapine, drug_drug with molindone, drug_drug with clozapine, drug_drug with molindone. Ziprasidone has relations: drug_drug with clozapine, drug_drug with molindone, drug_drug with clozapine, drug_drug with molindone. Risperidone has relations: drug_drug with molindone, drug_drug with clozapine, drug_drug with molindone, drug_drug with clozapine. Chlorpromazine has relations: drug_drug with molindone, drug_drug with clozapine, drug_drug with molindone, drug_drug with clozapine. clozapine has relations: drug_drug with molindone, drug_drug with molindone. molindone has relations: drug_drug with clozapine, drug_drug with clozapine. Seizure has relations: drug_effect with clozapine, drug_effect with clozapine. Fluphenazine has relations: drug_drug with molindone, drug_drug with clozapine, drug_drug with molindone, drug_drug with clozapine. Sertindole has relations: drug_drug with molindone, drug_drug with clozapine, drug_drug with molindone, drug_drug with clozapine. Quetiapine has relations: drug_drug with clozapine, drug_drug with molindone, drug_drug with clozapine, drug_drug with molindone. Pimozide has relations: drug_drug with molindone, drug_drug with clozapine, drug_drug with molindone, drug_drug with clozapine.", "label": "yes"}
{"original_question": "Is the SDHAF2 gene  encoding a protein necessary for flavination of SDHA?", "id": "converted_164", "sentence1": "Is the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein gene  encoding a Protein Info necessary for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial?", "sentence2": "the gene 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 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 (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 gene, von Hippel-Lindau disease tumor suppressor gene (Von Hippel-Lindau Syndrome), neurofibromatosis type 1 tumor suppressor gene (Neurofibromatosis 1), Genes encoding the succinate dehydrogenase (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 gene 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 gene 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 (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 gene, von Hippel-Lindau disease tumor suppressor gene (Von Hippel-Lindau Syndrome), neurofibromatosis type 1 tumor suppressor gene (Neurofibromatosis 1), Genes encoding the succinate dehydrogenase (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 gene 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 gene 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 (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 (Succinate Dehydrogenase), and in Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, required for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial.  This gene 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.[SEP]Relations: neurofibromatosis has relations: disease_protein with Neurofibromatosis 1, disease_protein with Neurofibromatosis 1. mitochondrial electron transport, succinate to ubiquinone has relations: bioprocess_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, bioprocess_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, bioprocess_protein with Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, bioprocess_protein with SDHC Protein Info, human, bioprocess_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, bioprocess_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, bioprocess_protein with Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, bioprocess_protein with SDHC Protein Info, human. mitochondrial respiratory chain complex II, succinate dehydrogenase complex (ubiquinone) has relations: cellcomp_protein with SDHC Protein Info, human, cellcomp_protein with SDHB Protein Info, human, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, cellcomp_protein with SDHC Protein Info, human, cellcomp_protein with SDHB Protein Info, human, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, cellcomp_protein with SDHC Protein Info, human, cellcomp_protein with SDHB Protein Info, human, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, cellcomp_protein with SDHC Protein Info, human, cellcomp_protein with SDHB Protein Info, human, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial. von Hippel-Lindau disease has relations: disease_protein with Von Hippel-Lindau Syndrome, disease_protein with Von Hippel-Lindau Syndrome.", "label": "yes"}
{"original_question": "Could Arimidex (anastrozole) cause hot flashes?", "id": "converted_165", "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\u00a0%), and hot flashes were the second most common adverse event (7.9\u00a0%). 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 Toxic effect 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 Toxic effect, 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 Toxic effect of the selective aromatase inhibitor anastrozole (Arimidex), we conducted a phase II trial in 53 women with asymptomatic recurrent/persistent m\u00fcllerian cancer. Toxicity was modest (grade I) and infrequent, with the most common toxicities 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, hot flashes, and abdominal discomfort caused almost twice as many patients to prefer to continue with letrozole therapy than with anastrozole[SEP]Relations: Tamoxifen has relations: off_label_use with Malignant neoplasm of endometrium, off_label_use with Malignant neoplasm of endometrium. Anxiety Disorders disorder has relations: disease_disease with Anxiety Disorders, disease_protein with TTR protein, human, disease_disease with Anxiety Disorders, disease_protein with TTR protein, human. endometrium neoplasm has relations: disease_disease with Malignant neoplasm of endometrium, disease_disease with Malignant neoplasm of endometrium.", "label": "yes"}
{"original_question": "Are Alu elements transcribed?", "id": "converted_166", "sentence1": "Are Alu Elements transcribed?", "sentence2": "Alu RNAs in the Homo sapiens transcriptome Alu Elements can be transcribed in two different ways, by two independent polymerases 'Free Alu RNAs' are transcribed by Pol III from their own Promoter 'embedded Alu RNAs' are transcribed by RNA Polymerase II as part of protein- and non-protein-coding RNAs Recent studies have demonstrated that both free and embedded Alu RNAs play a major role in post transcriptional regulation of gene expression Alu RNAs transcribed from these Elements are present at low levels at normal cell growth but various stress conditions increase their abundance Alu RNAs 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 RNAs, 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 RNAs. 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 RNAs 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 RNAs' are transcribed by Pol III from their own Promoter, while 'embedded Alu RNAs' are transcribed by RNA Polymerase II as part of protein- and non-protein-coding RNAs We report enzymatic studies of the Protein Structure, Secondary of Alu RNAs 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]", "label": "yes"}
{"original_question": "Are chromomethylases present in animal genomes?", "id": "converted_167", "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]", "label": "no"}
{"original_question": "Is low T3 syndrome related with high BNP in cardiac patients?", "id": "converted_168", "sentence1": "Is low T3 thoracic segmental innervation syndrome related with high BNP in cardiac patients?", "sentence2": "BNP and cubic foot are independently associated with exercise capacity in severely compromised Hydrops Fetalis patients. fter adjustment for known confounders, N-Terminal Fragment Brain Natriuretic Protein, human was significantly associated with cubic foot and low-T3 thoracic segmental innervation thoracic segmental innervation syndrome. cubic foot (HR 0.58, 95%CI 0.34-0.98) and low-T3 thoracic segmental innervation thoracic segmental innervation syndrome (HR 3.0, 95%CI 1.4-6.3) were predictive for mortality after adjustment for N-Terminal Fragment Brain Natriuretic Protein, human levels and other Cardiovascular system prognostic variables. cubic foot and low-T3 thoracic segmental innervation thoracic segmental innervation syndrome are significantly related to N-Terminal Fragment Brain Natriuretic Protein, human in patients with Cardiovascular system disease, but are predictors of mortality independently of N-Terminal Fragment Brain Natriuretic Protein, human and other known Cardiovascular system risk parameters. Higher NT-pro BNP concentrations were related to lower total T3 thoracic segmental innervation thoracic segmental innervation concentrations (r = -0.294, p = 0.011) and to higher reverse T3 thoracic segmental innervation thoracic segmental innervation concentrations (r = 0.353, p = 0.002)[SEP]", "label": "yes"}
{"original_question": "Has overexpression of sirtuins been reported to increase lifespan in budding yeast (Saccharomyces cerevisiae)?", "id": "converted_169", "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]", "label": "yes"}
{"original_question": "Is TREM2 associated with Alzheimer's disease?", "id": "converted_170", "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 APOE\u03b54 We observed an enrichment of rare Variant across TREM2 Protein Info, human Protein Info, human in both cytarabine/daunorubicin protocol and Frontotemporal Presenile dementia patients compared to controls, most notably in the extracellular IgV-set Superkingdom (taxonomic category) None of the rare Variant individually reached significant association, but the frequency of p.R47H was increased ~ 3-fold in both cytarabine/daunorubicin protocol and Frontotemporal 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 dementia, and show that TREM2 Protein Info, human Protein Info, human Variant may play a role in Neurodegenerative Disorders 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 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 (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 (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 APOE \u025b4 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 \u03b54 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 Variant 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) 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 (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 Variant that increase cytarabine/daunorubicin protocol risk evidence suggests that rare genetic Variant 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 disease 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 disease The association of TREM2 Protein Info, human Protein Info, human Variant 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 Variant (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: anatomy_protein_present with Neocortex, anatomy_protein_present with Neocortex. Neocortex has relations: anatomy_protein_present with TREM2 Protein Info, human, anatomy_protein_present with TREM2 Protein Info, human.", "label": "yes"}
{"original_question": "Does the protein mTOR regulate autophagy?", "id": "converted_171", "sentence1": "Does the protein FRAP1 protein, human regulate autophagy?", "sentence2": "autophagy is negatively regulated by the mammalian target of sirolimus receptor (FRAP1 protein, human) Subjecting cells to starvation or sirolimus efficiently induces autophagy by inhibiting the MTOR signaling pathway triggering increased autophagic flux.  Several pathways, including FRAP1 protein, human, have been shown to regulate autophagy. these results provide insights into the mechanism by which hyperactivation of mechanistic target of sirolimus complex 1 promotes Malignant neoplasm of breast progression through increasing autophagy and Akt activation in vivo.  the canonical FRAP1 protein, human-controlled autophagy pathway FRAP1 protein, human inhibition severely impairs liver regeneration and increases autophagy after pH:LsCnc:Pt:Ser/Plas:Qn FRAP1 protein, human remains at a high level and inhibits autophagy. Proto-Oncogene Proteins c-akt is involved in granulosa cell autophagy regulation via FRAP1 protein, human signaling during Rattus norvegicus follicular development and Impatent structure. mammalian target of sirolimus (FRAP1 protein, human), a major negative regulator of autophagy. FRAP1 protein, human suppresses granulosa cell autophagy Mammals target of sirolimus (FRAP1 protein, human), a potent suppressor of autophagy, The FRAP1 protein, human signaling pathway integrates inputs from a variety of upstream stimuli to regulate diverse cellular processes including proliferation, growth, survival, motility, autophagy, protein synthesis and metabolism The activation of mammalian target of sirolimus (FRAP1 protein, human) signaling pathway blocks the effects of ghrelin-induced autophagy and apoptosis,  inducing apoptosis and autophagy via the FRAP1 protein, human signaling pathway  The FRAP1 protein, human gene regulates cell growth by controlling RNA, Messenger translation, ribosome biogenesis, autophagy, and metabolism.[SEP]", "label": "yes"}
{"original_question": "Has proteomics been used in the study of Pick's disease?", "id": "converted_172", "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 (Cerebrospinal Fluid) 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 Cerebrospinal Fluid 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]", "label": "yes"}
{"original_question": "Are there any urine biomarkers for bladder cancer diagnosis?", "id": "converted_173", "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]", "label": "yes"}
{"original_question": "Is signal transducer and activator of transcription-3 (STAT3) critical for tumor angiogenesis progression?", "id": "converted_174", "sentence1": "Is signal transducer and activator of transcription-3 (STAT3 protein, human) critical for tumor angiogenesis progression?", "sentence2": "(STAT3 protein, human protein, human) is critical for cancer progression by regulating Tumor cells, uncertain whether benign or malignant survival, proliferation, and angiogenesis. Herein, we investigated the regulation of STAT3 protein, human protein, human activation and the therapeutic effects of icaritin, a prenyl flavonoid derivative from Epimedium Genus, in renal cell carcinoma (Conventional (Clear Cell) Renal Cell Carcinoma).   Overall, these results suggest that icaritin strongly inhibits STAT3 protein, human protein, human activation and is a potentially effective therapeutic option for the treatment of renal cell carcinoma we have reviewed important signaling pathways that are closely related to radiosensitization, such as cell cycle arrest, tumor angiogenesis, Janus kinase/STAT3 protein, human protein, human signaling pathway and Mismatch repair Interleukin-27 signaling is mediated by the Janus kinase-STAT pathway via activation of STAT1 protein, human protein, human and STAT3 protein, human protein, human, which have tumor suppressive and oncogenic activities, respectively. Epithelial-mesenchymal transition (EMT) and angiogenesis are key processes in carcinogenesis. The inhibition of STAT3 protein, human protein, human activation had no effect on the development of the Epithelial phenotype. STAT3 protein, human protein, human plays a vital role in inducing and maintaining a pro-carcinogenic inflammatory microenvironment and is reported to be a critical mediator of the oncogenic effects of Epidermal Growth Factor Receptor mutations. STAT3 protein, human protein, human activation is mediated through Janus kinase family kinases  EESB treatment could significantly suppress the activation of several CRC-related pathways, including STAT3 protein, human protein, human, Mitogen-Activated Protein Kinases, and p38 signalings in Tumor tissue sample, and alter the expression of multiple critical target Genes such as BCL2 gene, BAX protein, human, Cyclin D1, Cyclin-Dependent Kinase 4, and oncoprotein oncoprotein p21. These molecular effects lead to the induction of Tumor cells, malignant apoptosis and inhibition of cell proliferation. Our findings demonstrate that antimony possesses a broad range of antitumor activities because of its ability to affect multiple Protoplasm targets Western immunoblotting analyses of Mus sp. lung tissues indicated significantly lower level of pSTAT3 and MCL1 gene in the carcinogen plus DMAPT group relative to the group treated with the carcinogen only. Given the evidence that STAT3 protein, human protein, human is activated in more than half of Malignant neoplasm of lung and it regulates Genes involved in cell proliferation, survival and angiogenesis, DMAPT is a promising agent for Primary malignant neoplasm of lung chemoprevention in subjects who are at high risk of developing this devastating disease. (STAT3 protein, human protein, human) is a latent Cytoplasmic transcription factor, originally discovered as a transducer of signal from Receptors, Cell Surface to the Cell Nucleus. It is activated by tyrosine phosphorylation at position 705 leading to its dimerization, nuclear translocation, DNA binding, and activation of gene transcription. Under normal physiological conditions, STAT3 protein, human protein, human activation is tightly regulated. However, compelling evidence suggests that STAT3 protein, human protein, human is constitutively activated in many Malignant Neoplasms and plays a pivotal role in tumor growth and metastasis. It regulates cellular proliferation, invasion, migration, and angiogenesis that are critical for cancer metastasis STAT3 protein, human protein, human) signaling pathway plays important roles in oncogenesis, angiogenesis, immunity, and Tumor cells, uncertain whether benign or malignant invasion. In the present study, we investigated the association of Recombinant Interleukin-1Phosphorylated STAT3 protein, human protein, human (pSTAT3) regulates many Genes that are necessarily expressed in cancer initiation, development, and progression, being involved in proliferation, anti-apoptosis, invasion, angiogenesis, and immune surveillance evasion[SEP]Relations: cell surface has relations: cellcomp_protein with Epidermal Growth Factor Receptor, cellcomp_protein with Epidermal Growth Factor Receptor. cytoplasm has relations: cellcomp_protein with STAT3 protein, human, cellcomp_protein with Epidermal Growth Factor Receptor, cellcomp_protein with STAT1 protein, human, cellcomp_protein with STAT3 protein, human, cellcomp_protein with Epidermal Growth Factor Receptor, cellcomp_protein with STAT1 protein, human. germ cell Cell Nucleus has relations: cellcomp_cellcomp with Cell Nucleus, cellcomp_cellcomp with Cell Nucleus.", "label": "yes"}
{"original_question": "Is sumoylation implicated in myogenesis?", "id": "converted_175", "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]", "label": "yes"}
{"original_question": "Is the Miller-Fisher syndrome considered to be a variant of Guillain-Barr\u00e9?", "id": "converted_176", "sentence1": "Is the Miller Fisher Syndrome considered to be a Variant of Guillain-Barr\u00e9?", "sentence2": "Miller Fisher syndrome is a Variant of Guillain-Barre syndrome characterized by the classic triad of ophthalmoplegia, Cerebellar Ataxia, and Absent reflex We are reporting a rare case of Miller-Fisher (Marfan Syndrome) Variant of Guillain-Barr\u00e9 syndrome (Guillain-Barre Syndrome) as the first manifestation of Lupus Erythematosus, Systemic in a 41-year-old female Miller Fisher Syndrome is defined as ophthalmoplegia, Cerebellar Ataxia and Absent reflex. Considered as a Variant of Guillain-Barr\u00e9 syndrome, it differs in its clinical presentation and by anti-GQ1b antibody positivity Guillain-Barr\u00e9 syndrome (Guillain-Barre Syndrome) and its Variant, Miller Fisher syndrome (Marfan Syndrome), exist as several clinical subtypes with different neurological features and presentations Using in vitro and in vivo models of the Guillain-Barr\u00e9 syndrome Variant, Miller Fisher syndrome, we have shown previously that anti-GQ1b ganglioside antibody antibody Antibodies, in vitro diagnostic target the presynaptic motor nerve terminal axon and surrounding perisynaptic Schwann cells, thereby mediating destructive injury through deposition of Complement Membrane Attack Complex. Miller Fisher syndrome is a Variant of Guillain-Barr\u00e9 syndrome, characterized by ophthalmoplegia, Cerebellar Ataxia and Absent reflex. Miller Fisher syndrome is a localized Variant of Guillain-Barr\u00e9 syndrome, characterized by ophthalmoplegia, Absent reflex and Cerebellar Ataxia. Miller Fisher syndrome, a Variant of Guillain-Barr\u00e9 syndrome, is associated with immunoglobulin G to GQ1b ganglioside antibody antibody. Miller Fisher syndrome (Marfan Syndrome), a Variant of Guillain-Barr\u00e9 syndrome, is a rare disorder typically characterized by a triad of Cerebellar Ataxia, Absent reflex, and ophthalmoplegia, which may have a highly variable clinical presentation. Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a Variant of Guillain-Barr\u00e9 syndrome and is characterized by the clinical triad of Cerebellar Ataxia, Absent reflex, and ophthalmoplegia. The objective of this study was to review the occurrence and clinical features of Guillain-Barr\u00e9 syndrome and its Variant, the Miller Fisher syndrome, during TNFalpha antagonist therapy. Miller Fisher Variant of Guillain-Barr\u00e9 syndrome masquerading as acute sphenoid sinusitis with orbital apex syndrome. Controversy exists concerning whether Miller Fisher syndrome (Marfan Syndrome) is the result of a predominantly axonal or demyelinating polyneuropathy and whether the Guillain-Barr\u00e9 syndrome Variant of acute Cerebellar Ataxia and Absent reflex without ophthalmoplegia, ataxic Guillain-Barr\u00e9 syndrome (atxGBS), has a distinct pathophysiology. Miller Fisher syndrome is characterised by the triad ophthalmoparesis, Cerebellar Ataxia and Absent reflex and is considered to be a Variant of Guillain-Barr\u00e9 syndrome; its differential diagnosis includes Wernicke&apos;s encephalopathy Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a Variant of Guillain-Barr\u00e9 syndrome and is characterized by the clinical triad of Cerebellar Ataxia, Absent reflex, and ophthalmoplegia Miller Fisher Syndrome is characterised by the clinical triad of ophthalmoplegia, Cerebellar Ataxia and Absent reflex and is considered a Variant form of Guillain-Barr\u00e9 syndrome The syndrome of Cerebellar Ataxia, Absent reflex and ophthalmoplegia, or Miller Fisher Syndrome, has been considered to be a Variant of Guillain-Barr\u00e9 syndrome with pathology restricted to the peripheral nervous system Miller Fisher Syndrome (Marfan Syndrome) is considered the most common Variant of Guillain-Barr\u00e9 syndrome (Guillain-Barre Syndrome) and is characterized by the clinical triad of ophthalmoplegia, Cerebellar Ataxia and Absent reflex Miller Fisher syndrome (Marfan Syndrome), characterized as Cerebellar Ataxia, Absent reflex and ophthalmoplegia, is generally considered as a Variant of Guillain-Barr\u00e9 syndrome (Guillain-Barre Syndrome) Miller Fisher Syndrome (Marfan Syndrome), which is characterized by ophthalmoplegia, Cerebellar Ataxia and tendon Absent reflex, is generally considered as a clinical Variant of Guillain-Barr\u00e9 Syndrome Miller Fisher Syndrome (Marfan Syndrome), a Variant of Guillain-Barr\u00e9 syndrome (Guillain-Barre Syndrome) is a self-limiting demyelinating disease of the peripheral nervous system BACKGROUND: Miller Fisher Syndrome is characterised by the clinical triad of ophthalmoplegia, Cerebellar Ataxia and Absent reflex and is considered a Variant form of Guillain-Barr\u00e9 syndrome.  BACKGROUND AND OBJECTIVE: Miller Fisher Syndrome (Marfan Syndrome) is considered the most common Variant of Guillain-Barr\u00e9 syndrome (Guillain-Barre Syndrome) and is characterized by the clinical triad of ophthalmoplegia, Cerebellar Ataxia and Absent reflex.  Miller Fisher syndrome is characterised by the triad ophthalmoparesis, Cerebellar Ataxia and Absent reflex and is considered to be a Variant of Guillain-Barr\u00e9 syndrome; its differential diagnosis includes Wernicke Encephalopathy.  A recent report described serum anti-GQ1b ganglioside antibody antibody Antibodies, in vitro diagnostic in Miller Fisher syndrome (Marfan Syndrome), a clinical Variant of Guillain-Barr\u00e9 syndrome (Guillain-Barre Syndrome). The syndrome of Cerebellar Ataxia, Absent reflex and ophthalmoplegia, or Miller Fisher Syndrome, has been considered to be a Variant of Guillain-Barr\u00e9 syndrome with pathology restricted to the peripheral nervous system. Guillain-Barr\u00e9 syndrome (Guillain-Barre Syndrome), an acute inflammatory polyneuropathy, is preceded in most cases by an infectious illness, and Campylobacter jejuni, a leading cause of acute gastroenteritis, is the most common antecedent to Guillain-Barre Syndrome and its ocular Variant, Miller Fisher syndrome (Marfan Syndrome). Miller Fisher Syndrome is characterised by the clinical triad of ophthalmoplegia, Cerebellar Ataxia and Absent reflex and is considered a Variant form of Guillain-Barr\u00e9 syndrome. Miller Fisher Syndrome is characterised by the clinical triad of ophthalmoplegia, Cerebellar Ataxia and Absent reflex and is considered a Variant form of Guillain-Barr\u00e9 syndrome.  The syndrome of Cerebellar Ataxia, Absent reflex and ophthalmoplegia, or Miller Fisher Syndrome, has been considered to be a Variant of Guillain-Barr\u00e9 syndrome with pathology restricted to the peripheral nervous system. A patient with Miller Fisher Syndrome and bilateral demyelinating optic neuropathy suggesting associated CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS pathology is presented. Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a Variant of Guillain-Barr\u00e9 syndrome and is characterized by the clinical triad of Cerebellar Ataxia,  Miller Fisher syndrome is an uncommon disease and it is a Variant of Guillain-Barre syndrome. Miller Fisher syndrome also has rarer variants. Miller Fisher syndrome is characterised by the triad ophthalmoparesis, Cerebellar Ataxia and Absent reflex and is considered to be a Variant of Guillain-Barr\u00e9 syndrome; its differential diagnosis includes Wernicke Encephalopathy. Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a Variant of Guillain-Barr\u00e9 syndrome and is characterized by the clinical triad of Cerebellar Ataxia, Absent reflex, and ophthalmoplegia. Data were separately analysed for Miller Fisher syndrome and other Guillain-Barr\u00e9 syndrome variants. Guillain-Barr\u00e9 syndrome variants alone (excluding Miller Fisher syndrome) accounted for 10.5% of total cases. The syndrome of Cerebellar Ataxia, Absent reflex and ophthalmoplegia, or Miller Fisher Syndrome, has been considered to be a Variant of Guillain-Barr\u00e9 syndrome with pathology restricted to the peripheral nervous system.[SEP]", "label": "yes"}
{"original_question": "Is Ctf4 involved in sister chromatid cohesion establishment?", "id": "converted_177", "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, Chl1 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 Chl1, but not of the other factors, causes a synthetic growth defect in Cells lacking Eco1. Distinct from acetylation defects, sister chromatid cohesion in ctf4\u0394 and chl1\u0394 Cells is not improved by removing Wapl Thus, Ctf4 and Chl1 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 Chl1 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 DDX11 gene, and the second containing MRC1 gene gene, CTF18, CHTF8 gene, and DSCC1 gene Our results suggest that Chl1 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 Chl1 and the pathway involving the acetylation of SMC3 wt Allele. Our results suggest that Chl1 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 Chl1 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 DDX11 gene are required for efficient sister chromatid cohesion in unperturbed mitotic Cells, and provide evidence that Chl1 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 Chl1 and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion. Thus, Ctf4 and Chl1 delineate an additional acetylation-independent pathway that might hold important clues as to the mechanism of sister chromatid cohesion establishment. Thus, Ctf4 and Chl1 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 Chl1 and the pathway involving the acetylation of SMC3 wt Allele Establishment of sister chromatid cohesion at the Saccharomyces cerevisiae replication fork.[SEP]", "label": "yes"}
{"original_question": "Are retroviruses used for gene therapy?", "id": "converted_178", "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 (HSCs) 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: Wiskott-Aldrich syndrome has relations: disease_protein with Wiskott-Aldrich Syndrome, disease_protein with Wiskott-Aldrich Syndrome.", "label": "yes"}
{"original_question": "Is there a phylogenetic analysis for HIV?", "id": "converted_179", "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 Variant 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 Gene 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]", "label": "yes"}
{"original_question": "Are there randomised controlled trials on sevoflurane?", "id": "converted_180", "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]", "label": "yes"}
{"original_question": "Can FOXOs modulate longevity?", "id": "converted_181", "sentence1": "Can FOXOs modulate longevity?", "sentence2": "Forkhead box O (FOXO) TRANSCRIPTION FACTOR have a conserved function in regulating metazoan lifespan. In contrast to FoxO1, FoxO3a 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) 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, 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 Family function in Mammals systems with the evolutionarily conserved role of FOXO Family 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 Family) 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 Family 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) 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.  In Homo sapiens, FOXO3A protein, human, as well as FOXO1 gene gene and -4, and their downstream effectors, could hold the key to counteracting ageing and common diseases. FOXO TRANSCRIPTION FACTOR have important roles in metabolism, cellular proliferation, stress tolerance, and aging.[SEP]", "label": "yes"}
{"original_question": "Is there an association between FGFR3 mutation and plagiocephaly?", "id": "converted_182", "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 Gene Mutation and Plagiocephaly. FGFR genes have important effects on bone development, and Gene Mutation 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, Gene Mutation 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. Mutations 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 Gene Mutation.  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 Gene Mutation 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 Gene Mutation 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 Gene Mutation 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: Plagiocephaly has relations: disease_phenotype_positive with CRANIOSYNOSTOSIS, TYPE 2, disease_phenotype_positive with CRANIOSYNOSTOSIS, TYPE 2. CRANIOSYNOSTOSIS, TYPE 2 Fontaine type has relations: disease_disease with CRANIOSYNOSTOSIS, TYPE 2, disease_disease with CRANIOSYNOSTOSIS, TYPE 2. apert syndrome has relations: disease_protein with FGFR3 protein, human, disease_protein with Fibroblast Growth Factor Receptor 2, disease_protein with FGFR1 protein, human, disease_protein with FGFR3 protein, human, disease_protein with Fibroblast Growth Factor Receptor 2, disease_protein with FGFR1 protein, human. Pfeiffer Syndrome has relations: disease_protein with FGFR1 protein, human, disease_protein with Fibroblast Growth Factor Receptor 2, disease_protein with FGFR1 protein, human, disease_protein with Fibroblast Growth Factor Receptor 2. FGFR3 protein, human has relations: protein_protein with Fibroblast Growth Factor Receptor 2, disease_protein with Achondroplasia, disease_protein with CRANIOSYNOSTOSIS, TYPE 2, protein_protein with Fibroblast Growth Factor Receptor 2, disease_protein with Achondroplasia, disease_protein with CRANIOSYNOSTOSIS, TYPE 2. Bicoronal synostosis has relations: disease_phenotype_positive with Pfeiffer Syndrome, disease_phenotype_positive with CRANIOSYNOSTOSIS, TYPE 2, disease_phenotype_positive with Pfeiffer Syndrome, disease_phenotype_positive with CRANIOSYNOSTOSIS, TYPE 2. Craniofacial dysostosis has relations: disease_phenotype_positive with Craniofacial dysostosis type 1, disease_phenotype_positive with Craniofacial dysostosis type 1. Unicoronal synostosis has relations: disease_phenotype_positive with CRANIOSYNOSTOSIS, TYPE 2, disease_phenotype_positive with CRANIOSYNOSTOSIS, TYPE 2. Achondroplasia has relations: disease_protein with FGFR3 protein, human, disease_protein with FGFR3 protein, human. Macrocephaly has relations: disease_phenotype_positive with CRANIOSYNOSTOSIS, TYPE 2, disease_phenotype_positive with Achondroplasia, disease_phenotype_positive with CRANIOSYNOSTOSIS, TYPE 2, disease_phenotype_positive with Achondroplasia. Anterior Plagiocephaly has relations: disease_phenotype_positive with CRANIOSYNOSTOSIS, TYPE 2, disease_phenotype_positive with CRANIOSYNOSTOSIS, TYPE 2.", "label": "yes"}
{"original_question": "Are CD44 variants (CD44v) associated with poor prognosis of metastasis?", "id": "converted_183", "sentence1": "Are CD44 Antigens Variant (CD44v) associated with poor prognosis of metastasis?", "sentence2": "CD44 Antigens Antigens Variant 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 B-cell chronic lymphocytic leukemia CD44 Antigens Antigens Variant 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 Tumor cells, malignant 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 cancer a number of variant forms of CD44 Antigens Antigens are frequently expressed, although these Variant are infrequently expressed in normal Specimen Source Codes - Tissue lung, and that the expression of CD44v6 is particularly associated with lymph node metastasis in Non-Small Cell Lung Carcinoma 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 Variant (CD44v) can promote the metastatic behaviour of cancer cells. 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: endometrioid Malignant adenomatous neoplasm has relations: disease_disease with Malignant adenomatous neoplasm, disease_disease with Malignant adenomatous neoplasm. colorectal Carcinoma has relations: disease_disease with Colon Carcinoma, disease_disease with Colon Carcinoma. Malignant adenomatous neoplasm has relations: disease_disease with Carcinoma, disease_disease with Carcinoma. Carcinoma has relations: disease_disease with Malignant adenomatous neoplasm, disease_disease with Breast Carcinoma, disease_disease with Malignant adenomatous neoplasm, disease_disease with Breast Carcinoma.", "label": "yes"}
{"original_question": "Is Bladder training an effective method to treat  urge incontinence ?", "id": "converted_184", "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 urine 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]", "label": "yes"}
{"original_question": "Do proton pump inhibitors affect thyroxine absorption?", "id": "converted_185", "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: Sucralfate has relations: drug_drug with pantoprazole, drug_drug with pantoprazole. Raloxifene has relations: drug_drug with pantoprazole, drug_drug with pantoprazole. Ferrous sulfate anhydrous has relations: drug_drug with pantoprazole, drug_drug with pantoprazole. Levothyroxine has relations: indication with Hypothyroidism, drug_drug with pantoprazole, indication with Hypothyroidism, drug_drug with pantoprazole.", "label": "yes"}
{"original_question": "Is PER3 required for CHK2 activation in human cells?", "id": "converted_186", "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 ammonium tetrathiomolybdate, protein_protein with ammonium tetrathiomolybdate.", "label": "yes"}
{"original_question": "Are there any clinical trials of the effect of evening primrose oil on postmenopausal symptoms ?", "id": "converted_187", "sentence1": "Are there any clinical trials of the effect of evening Primrose oil on postmenopausal symptoms ?", "sentence2": "To analyze whether the time (morning/evening) of administration of a fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether containing 60 mg of dry soy seed extract (glycine max) with 40% of total Isoflavones, Primrose oil and \u03b1-tocopherol modifies the effect on the Menopausal syndrome. The object of this study was to evaluate the effect of different doses of a fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether containing Isoflavones 60 mg, Primrose oil 440 mg and Vitamin E Drug Class 10 mg. (IOVE) on menopausal complaints. This was an open, multicentre, randomised, group comparative, efficacy and safety trial. Emphasis was placed on randomized, double-blind, placebo-controlled clinical trials, as these provide the best efficacy and safety data Nonprescription therapies reviewed include black cohosh, Angelica sinensis root extract, evening Primrose oil, physical activity, phytoestrogens, and red clover The effect of oral evening Primrose oil on menopausal hot flashes: a randomized clinical trial. The aim of this study was to compare the efficacy of evening Primula obconica preparation with placebo in improvement of menopausal hot flashes.   The application of oral evening Primrose oil compared with placebo for controlling hot flashes may decrease more the intensity of attacks  Our search identified 58 randomised controlled trials of which 11 involved the use of clonidine, six for Selective Serotonin Reuptake Inhibitors, four for gabapentin, seven for black cohosh, seven for red clover, 18 for phytoestrogens, two for ginseng, one for evening Primula obconica preparation, Single clinical trials have found no benefit for Angelica sinensis root extract, evening Primrose oil, Single clinical trials have found that Angelica sinensis root extract, evening Primrose oil, To evaluate the efficacy of gamma-linolenic acid provided by evening Primrose oil in treating hot flushes and sweating associated with the menopause. DESIGN: Randomised, double blind, placebo controlled study.[SEP]", "label": "yes"}
{"original_question": "Is acid alpha-glucosidase the enzyme that causes Pompe disease when mutant?", "id": "converted_188", "sentence1": "Is Ga language Genes 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 \u03b1-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 \u03b1-glucosidase (Ga language) Acid \u03b1-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 Ga language Genes. Generalized glycogen storage disease of infants is a lysosomal storage disease (Lysergic Acid Diethylamide) caused by a deficiency in the Lysosomal Enzyme [APC] Ga language Genes. Glycogen storage disease type II (GSDII; Generalized glycogen storage disease of infants or acid maltase deficiency) is an Autosomal Recessive Disorder caused by lysosomal Ga language Genes (AalphaGlu) deficiency and manifests predominantly as Skeletal Muscle Tissue weakness. Structural study on a Mutant Ga language Genes in silico combined with biochemical investigation is useful for understanding the molecular pathology of Generalized glycogen storage disease of infants. The nature of Mutant Ga language Genes (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 Gene Mutation in the Ga language Genes Genes. Glycogen storage disease type II (Generalized glycogen storage disease of infants) is inherited by autosomal recessive transmission and caused by a deficiency of Ga language Genes (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 Gene Mutation in the Genes that encodes Ga language Genes (Ga language). Demonstration of Ga language Genes 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 Ga language Genes Enzyme [APC] replacement therapy for Generalized glycogen storage disease of infants. Infantile Generalized glycogen storage disease of infants is caused by deficiency of lysosomal Ga language Genes. Determination of Ga language Genes 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 Ga language Genes, and promotes glycogen reduction in a transgenic mouse model of Generalized glycogen storage disease of infants Structural study on a Mutant Ga language Genes 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 Ga language Genes 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 Ga language Genes (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 Ga language Genes (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 Ga language Genes 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 lysosome Generalized glycogen storage disease of infants (Glycogen Storage Disease Type III) is caused by Gene Mutation in the Ga language Genes Genes Glycogen storage disease type II (Generalized glycogen storage disease of infants) is inherited by autosomal recessive transmission and caused by a deficiency of Ga language Genes (Ga language), resulting in impaired degradation and lysosomal accumulation of glycogen Glycogen stored in Skeletal but not in Cardiac - anatomy qualifier Muscle Tissue in Ga language Genes 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 Ga language Genes 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 Ga language Genes, 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] Ga language Genes.  Structural study on a Mutant Ga language Genes 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 Ga language Genes. Trials with recombinant Homo sapiens Ga language Genes 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] Ga language Genes. Due to virtual absence of Ga language Genes, 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] Ga language Genes. The nature of Mutant Ga language Genes (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 Gene Mutation in the Genes that encodes Ga language Genes (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 Ga language Genes. Glycogen-storage disease type II, Generalized glycogen storage disease of infants, is caused by the deficiency of acid alpha-D-glucosidase in lysosome. 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 Gene Mutation in the Genes that encodes Ga language Genes (Ga language). Structural study on a Mutant Ga language Genes 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 Ga language Genes Enzyme [APC] replacement therapy for Generalized glycogen storage disease of infants. Mutations 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] Ga language Genes. Infantile Generalized glycogen storage disease of infants is a fatal genetic Muscle Tissue disorder caused by a deficiency of Ga language Genes, a glycogen-degrading Lysosomal Enzyme [APC].[SEP]Relations: Ga language has relations: disease_protein with Cardiomyopathies, disease_protein with Cardiomyopathies.", "label": "yes"}
{"original_question": "Is the optogenetics tool ChR2 light-sensitive?", "id": "converted_189", "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]", "label": "yes"}
{"original_question": "Is autism one of the characteristics of Moebius syndrome?", "id": "converted_190", "sentence1": "Is autism one of the characteristics of Moebius syndrome 1?", "sentence2": "The diagnosis of Moebius syndrome 1 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 autism have been reported in some cases Mobius Syndrome is a rare Congenital Disorders usually defined as a combination of facial weakness with impairment of ocular abduction. A strong association of Mobius Syndrome with autism 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 autism. 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 1, Steinert disease, 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, Moebius syndrome 1 1, Hypopigmentation disorder of Ito, Neurofibromatosis 2, CHARGE Syndrome and HEADD syndrome. Seventeen children and young adults with Moebius syndrome 1 1 were examined with a view to finding symptoms of autism. Some 40% of the group showed all or many of the symptoms typical of Autistic Disorder Fifty-nine cases with infantile autism/Autistic Disorder were subclassified according to associated medical condition (fragile-X, TUBEROUS SCLEROSIS 2 (disorder), neurofibromatosis, hypo-melanosis of Ito, Moebius syndrome 1 1, Rett Syndrome, and a 'new' syndrome associated with a Extra unidentified structurally abnormal chromosome (disorder)). Autism Spectrum Disorders in children and adolescents with Mobius Syndrome. Mobius Syndrome and autism spectrum disorders--less frequently associated than formerly thought. A strong association of Mobius Syndrome with autism spectrum disorders (ASDs) has been suggested in earlier studies with heterogenous age groups. Autistic behaviour in Moebius syndrome 1 1. The high frequency of Autistic symptoms in Moebius syndrome 1 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 Mobius Syndrome. Mobius Syndrome and autism spectrum disorders--less frequently associated than formerly thought. Autistic behaviour in Moebius syndrome 1 1.[SEP]Relations: congenital nervous system disorder has relations: disease_disease with Smith-Lemli-Opitz Syndrome, disease_disease with Fragile X Syndrome, disease_disease with Williams Syndrome, disease_disease with Angelman Syndrome, disease_disease with Smith-Magenis syndrome, disease_disease with Smith-Lemli-Opitz Syndrome, disease_disease with Fragile X Syndrome, disease_disease with Williams Syndrome, disease_disease with Angelman Syndrome, disease_disease with Smith-Magenis syndrome. Iris hypopigmentation has relations: disease_phenotype_positive with Prader-Willi Syndrome, disease_phenotype_positive with Prader-Willi Syndrome. Intellectual disability has relations: disease_phenotype_negative with MYOTONIC DYSTROPHY 1, disease_phenotype_positive with CHARGE Syndrome, disease_phenotype_negative with NOONAN SYNDROME 3, disease_phenotype_positive with NOONAN SYNDROME 3, disease_phenotype_positive with Williams Syndrome, disease_phenotype_positive with Down Syndrome, disease_phenotype_positive with Smith-Magenis syndrome, disease_phenotype_positive with TUBEROUS SCLEROSIS 2 (disorder), disease_phenotype_negative with Prader-Willi Syndrome, disease_phenotype_positive with Familial aplasia of the vermis, disease_phenotype_positive with SOTOS SYNDROME 1, disease_phenotype_positive with Smith-Lemli-Opitz Syndrome, disease_phenotype_negative with MYOTONIC DYSTROPHY 1, disease_phenotype_positive with CHARGE Syndrome, disease_phenotype_negative with NOONAN SYNDROME 3, disease_phenotype_positive with NOONAN SYNDROME 3, disease_phenotype_positive with Williams Syndrome, disease_phenotype_positive with Down Syndrome, disease_phenotype_positive with Smith-Magenis syndrome, disease_phenotype_positive with TUBEROUS SCLEROSIS 2 (disorder), disease_phenotype_negative with Prader-Willi Syndrome, disease_phenotype_positive with Familial aplasia of the vermis, disease_phenotype_positive with SOTOS SYNDROME 1, disease_phenotype_positive with Smith-Lemli-Opitz Syndrome.", "label": "yes"}
{"original_question": "Is Sarcolipin a regulatory/inhibitory protein of the Calcium ATPase SERCA?", "id": "converted_191", "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 - anatomy qualifier atria. Our study documented that sarcolipin is a key regulator of SERCA2a in Both Cardiac - anatomy qualifier Both Cardiac - anatomy qualifier atria. Importantly, our data demonstrate the existence of distinct modulators for the SERCA pump in the Both Cardiac - anatomy qualifier Both Cardiac - anatomy qualifier 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]", "label": "yes"}
{"original_question": "Is the circadian clock involved in ribosome biogenesis?", "id": "converted_192", "sentence1": "Is the circadian clock involved in Ribosomes biogenesis?", "sentence2": "The circadian clock coordinates Ribosomes biogenesis. Here we show that the circadian clock exerts its function also through the regulation of Protein Biosynthesis. Namely, the circadian clock influences the temporal translation of a subset of mRNAs involved in Ribosomes biogenesis by controlling the transcription of translation initiation factors as well as the clock-dependent rhythmic activation of signaling pathways involved in their regulation. Moreover, the circadian oscillator directly regulates the transcription of Ribosomal Proteins mRNAs and ribosomal RNAs. Thus the circadian clock exerts a major role in coordinating transcription and translation steps underlying Ribosomes biogenesis. Namely, the circadian clock influences the temporal translation of a subset of mRNAs involved in Ribosomes biogenesis by controlling the transcription of translation initiation factors as well as the clock-dependent rhythmic activation of signaling pathways involved in their regulation The circadian clock coordinates Ribosomes biogenesis Here we show that the circadian clock exerts its function also through the regulation of Protein Biosynthesis Here we show that the circadian clock exerts its function also through the regulation of Protein Biosynthesis. Namely, the circadian clock influences the temporal translation of a subset of mRNAs involved in Ribosomes biogenesis by controlling the transcription of translation initiation factors as well as the clock-dependent rhythmic activation of signaling pathways involved in their regulation.[SEP]", "label": "yes"}
{"original_question": "Can mutations in Calmodulin cause ventricular fibrillation?", "id": "converted_193", "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 CALM1 gene encoding Calmodulin 1. 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 CALM1 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 1 (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 peptide modelled after the IQ domain.[SEP]", "label": "yes"}
{"original_question": "Is rivaroxaban metabolized in kidneys?", "id": "converted_194", "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 Renal Insufficiency, 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: Apixaban has relations: drug_drug with dabigatran etexilate, drug_drug with dabigatran etexilate. Edoxaban has relations: drug_drug with dabigatran etexilate, drug_drug with dabigatran etexilate. Dabigatran has relations: drug_drug with dabigatran etexilate, drug_drug with dabigatran etexilate. Betrixaban has relations: drug_drug with dabigatran etexilate, drug_drug with dabigatran etexilate. Rivaroxaban has relations: drug_drug with dabigatran etexilate, drug_drug with dabigatran etexilate.", "label": "yes"}
{"original_question": "Is Hirschsprung disease one of the characteristics of the Mowat-Wilson syndrome?", "id": "converted_195", "sentence1": "Is HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 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. The syndrome is characterized by typical Facial features, moderate-to-severe mental retardation, Epilepsy and variable congenital malformations, including HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, 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, SUSCEPTIBILITY TO, 1, and intellectual disabilities caused by Mutation Abnormality or Gene Deletion Abnormality of ZEB2 gene Mowat-Wilson syndrome is a genetic disease characterized by typical Facial features, HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 and multiple Congenital Abnormality 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, SUSCEPTIBILITY TO, 1 (HSCR)  The prevalence of Mowat-Wilson syndrome is currently unknown, but it seems that Mowat-Wilson syndrome is underdiagnosed, particularly in patients without HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. Mowat-Wilson syndrome is a mental retardation-multiple congenital anomaly syndrome characterized by a typical facies, developmental delay, Epilepsy, and variable congenital malformations, including HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, Urogenital Abnormalities, congenital heart disease, and Congenital absence of the corpus callosum. \"Mowat-Wilson\" syndrome with and without HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 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, SUSCEPTIBILITY TO, 1 or severe constipation, genitourinary anomaly, Congenital Heart Defects, Congenital absence of corpus callosum and Eye Specimen Source Code defects. We report a girl who had HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 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, SUSCEPTIBILITY TO, 1, anomalies of the corpus callosum, and genitourinary and cardiac malformations. BACKGROUND/PURPOSE: Patients with zinc finger homeo box 1B (ZEB2 wt Allele) Gene Mutation or Gene Deletion develop multiple congenital anomalies including HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, known as Mowat-Wilson syndrome (Muckle-Wells Syndrome). Severe clinical course of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 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 malformations including HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR), 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, SUSCEPTIBILITY TO, 1, Microcephaly (physical finding) and mental retardation. Mowat-Wilson syndrome is a genetic disease characterized by typical Facial features, HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 and multiple Congenital Abnormality. Supernumerary intestinal muscle coat in a patient with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1/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, SUSCEPTIBILITY TO, 1. Mowat-Wilson\" syndrome with and without HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 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, SUSCEPTIBILITY TO, 1, 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, SUSCEPTIBILITY TO, 1 (HSCR), 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 malformations, including HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, Urogenital Abnormalities, 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, SUSCEPTIBILITY TO, 1, 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, SUSCEPTIBILITY TO, 1 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, SUSCEPTIBILITY TO, 1, 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, SUSCEPTIBILITY TO, 1, 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, SUSCEPTIBILITY TO, 1, 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, SUSCEPTIBILITY TO, 1 (HSCR), 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, SUSCEPTIBILITY TO, 1, Microcephaly (physical finding) and mental retardation[SEP]Relations: Seizure has relations: disease_phenotype_positive with Mowat-Wilson syndrome, disease_phenotype_positive with Mowat-Wilson syndrome. Large earlobe has relations: disease_phenotype_positive with Mowat-Wilson syndrome, disease_phenotype_positive with Mowat-Wilson syndrome. Abnormality of the genital system has relations: disease_phenotype_positive with Mowat-Wilson syndrome, disease_phenotype_positive with Mowat-Wilson syndrome. ZEB2 has relations: disease_protein with Mowat-Wilson syndrome, disease_protein with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_protein with Mowat-Wilson syndrome, disease_protein with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. hirschsprung disease, susceptibility to has relations: disease_disease with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_disease with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. Intellectual disability has relations: disease_phenotype_positive with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_phenotype_positive with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. Frontal bossing has relations: disease_phenotype_positive with Mowat-Wilson syndrome, disease_phenotype_positive with Mowat-Wilson syndrome.", "label": "yes"}
{"original_question": "Is PLK2 involved in alpha-synuclein phosphorylation in the nervous system?", "id": "converted_196", "sentence1": "Is PLK2 gene involved in alpha-Synuclein phosphorylation in the nervous system?", "sentence2": "Polo-like kinase 2 (PLK2 gene gene) phosphorylates alpha-Synuclein at serine 129 in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS Here we submit evidence that PLK1 gene (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 inhibitors of PLK1 protein, human kinases inhibited alpha-Synuclein phosphorylation both in primary cortical cell cultures and in Mus sp. Head>Brain in vivo specific knockdown of PLK2 gene gene 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 gene gene plays a critical role in alpha-Synuclein phosphorylation in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS. These results indicate that PLK2 gene gene plays a critical role in alpha-Synuclein phosphorylation in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS. Here we submit evidence that PLK1 gene (PLK2 gene gene, also known as serum-inducible kinase or SNK) is a principle contributor to alpha-Synuclein phosphorylation at Ser-129 in Neurons. Polo-like kinase 2 (PLK2 gene gene) phosphorylates alpha-Synuclein at serine 129 in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS. PLK2 gene gene directly phosphorylates alpha-Synuclein 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 alpha-Synuclein (\u03b1-syn) phosphorylating PLK1 gene (PLK2 gene gene). Also, due to the dominant mode of \u03b1-syn and LRRK2 protein, human protein, human inheritance and based on current knowledge of LRRK2 protein, human protein, human and \u03b1-syn phosphorylation by PLK2 gene gene, inhibition of LRRK2 protein, human protein, human and PLK2 gene gene may constitute a potential therapy for Lugano Lymphoma Response Classification Progressive Disease by PET. To better understand the role of PLK2 gene gene in SNCA gene phosphorylation in vivo, we further evaluated the effect of PLK2 gene gene genetic knockdown and pharmacological inhibition on Phospho-\u03b1-Syn levels in different Head>Brain regions of PLK2 gene gene knockout (KELL NULL), heterozygous (Het) and wild-type (WT) mice. This PLK2 gene gene-mediated neuroprotective effect is also dependent on PLK2 gene gene activity and SNCA gene phosphorylation. PLK2 gene gene-mediated degradation of SNCA gene requires both phosphorylation at S129 and PLK2 gene gene/SNCA gene complex formation. Overexpression of only PLK2 gene gene increased phosphorylation of aggregated \u03b1-syn at S129, which likely is due to increased phosphorylation of soluble \u03b1-syn, which then was incorporated into aggregates. Here we submit evidence that PLK1 gene (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. Unlike other kinases reported to partially phosphorylate alpha-syn at Ser-129 in vitro, phosphorylation by PLK2 gene gene and PLK3 protein, human protein, human is quantitative ( inhibitors of PLK1 protein, human kinases inhibited alpha-Synuclein phosphorylation both in primary cortical cell cultures and in Mus sp. Head>Brain in vivo. These results indicate that PLK2 gene gene plays a critical role in alpha-Synuclein phosphorylation in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS inhibitors of PLK1 protein, human kinases inhibited alpha-Synuclein phosphorylation both in primary cortical cell cultures and in Mus sp. Head>Brain in vivo PLK2 gene gene directly phosphorylates alpha-Synuclein at Ser-129 in an in vitro biochemical assay To better understand the role of PLK2 gene gene in SNCA gene phosphorylation in vivo, we further evaluated the effect of PLK2 gene gene genetic knockdown and pharmacological inhibition on Phospho-\u03b1-Syn levels in different Head>Brain regions of PLK2 gene gene knockout (KELL NULL), heterozygous (Het) and wild-type (WT) mice Polo-like kinase-2 (Plk-2) has been implicated as the dominant kinase involved in the phosphorylation of SNCA gene 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.", "label": "yes"}
{"original_question": "Does GC content vary markedly within a given isochore?", "id": "converted_197", "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]", "label": "no"}
{"original_question": "Is tubulin acetylation involved in cell motility?", "id": "converted_198", "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 Microtubules (MT) acetylation/deacetylation, a process regulated by ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS as HDAC6 gene gene, a major Cytoplasmic \u03b1-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 Microtubules dynamics by decreasing the growth velocity of the Microtubules 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 Microtubules-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: cytoplasm has relations: cellcomp_protein with beta-adrenergic receptor kinase activity, cellcomp_protein with beta-adrenergic receptor kinase activity. TPPP has relations: cellcomp_protein with Microtubules, cellcomp_protein with Microtubules. beta-adrenergic receptor kinase activity has relations: molfunc_protein with beta-adrenergic receptor kinase activity, molfunc_protein with beta-adrenergic receptor kinase activity.", "label": "yes"}
{"original_question": "Can PLN mutations lead to dilated cardiomyopathy?", "id": "converted_199", "sentence1": "Can PLN Genes Gene Mutation lead to Cardiomyopathy, Dilated?", "sentence2": "A PLN Genes Genes founder Mutation Abnormality (43 cases) and LMNA Gene Mutation (19 cases, 16 different Gene Mutation) were most prevalent and often demonstrated a specific phenotype. PLN Genes Genes Mutation Abnormality R14del was identified in 12 (12 %) Arrhythmogenic Right Ventricular Dysplasia patients and in 39 (15 %) 3',5'-dichloromethotrexate patients The PLN Genes Genes 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) \u2192 Cys (R9C) and Arg(14) Gene Deletion Abnormality (R14del) Gene Mutation in PLN Genes Genes are associated with lethal Cardiomyopathy, Dilated 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. Mutations in the Genes encoding PLN Genes Genes have been associated with idiopathic Cardiomyopathy, Dilated; Mutations in the PLN Genes Genes Genes are a rare cause of Congestive Congestive heart failure, present almost exclusively in patients with Cardiomyopathy, Dilated etiology A missense Mutation Abnormality in PLN Genes Genes cytoplasmic domain (R9C) triggers Cardiomyopathy, Dilated in Homo sapiens, leading to Mortality, Premature. Complete Genetic and clinical analyses were performed in a family with familial Cardiomyopathy, Dilated due to the PLN Genes Genes-R14Del Mutation Abnormality. A candidate Genes approach resulted in identification of a heterozygous Gene Deletion Abnormality of arginine 14 in the Genes encoding phospholamban (PLN Genes Genes-R14Del) segregating with Cardiomyopathy, Dilated in the family pedigree. Mutation carriers suffered from familial Cardiomyopathy, Dilated associated with Cardiac Death between the ages of 26 and 50 years. a family with familial Cardiomyopathy, Dilated due to the PLN Genes Genes-R14Del Mutation Abnormality. For the phospholamban (PLN Genes Genes) 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 Genes Genes Gene Mutation, associated with either absence or sustained dephosphorylation of PLN Genes Genes, were linked to Cardiomyopathy, Dilated. Mutations in the Genes encoding PLN Genes Genes have been associated with Cardiomyopathy, Dilated characterized by early onset and the presence of lethal Ventricular arrhythmia. The identical PLN Genes Genes Mutation Abnormality can be associated with both mild and severe forms of Cardiomyopathy, Dilated. Additionally, PLN Genes Genes Gene Mutation should be considered in late onset Cardiomyopathies Through Genetic screening of Cardiomyopathy, Dilated patients, we identified a previously uncharacterized Gene Deletion Abnormality of arginine 14 (PLN Genes Genes-R14Del) in the coding region of the phospholamban (PLN Genes Genes) Genes in a large family with hereditary Congestive Congestive heart failure. No PLN Genes Genes Genes Mutation Abnormality was found in patients with 3',5'-dichloromethotrexate in Chengdu. This result indicated that PLN Genes Genes Genes Mutation Abnormality may not be a common cause for 3',5'-dichloromethotrexate in the Chinese population in Chengdu. none in PLN Genes Genes the recent discoveries of human PLN Genes Genes Gene Mutation leading to disease states. Strikingly, both individuals homozygous for L39stop developed Cardiomyopathy, Dilated and Congestive Congestive heart failure, requiring cardiac transplantation at ages 16 and 27. Homo sapiens lacking PLN Genes Genes develop lethal Cardiomyopathy, Dilated. Here we report that an inherited human Cardiomyopathy, Dilated with refractory congestive Congestive Congestive heart failure is caused by a dominant Arg --> Cys missense Mutation Abnormality at residue 9 (R9C) in phospholamban (PLN Genes Genes)[SEP]Relations: arrhythmogenic right ventricular dysplasia has relations: disease_protein with TTN protein, human, disease_protein with TTN protein, human. Sudden Cardiac Death has relations: disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated. Cardiomyopathy, Dilated has relations: disease_protein with TTN protein, human, disease_disease with familial Cardiomyopathy, Dilated, disease_protein with TTN protein, human, disease_disease with familial Cardiomyopathy, Dilated. Cardiomyopathy has relations: disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated. familial Cardiomyopathy, Dilated has relations: disease_protein with TTN protein, human, disease_disease with Cardiomyopathy, Dilated, disease_protein with TTN protein, human, disease_disease with Cardiomyopathy, Dilated. idiopathic Cardiomyopathies has relations: disease_disease with Cardiomyopathies, disease_disease with Cardiomyopathies. Congestive Congestive heart failure has relations: disease_phenotype_positive with familial Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with familial Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated. Ventricular arrhythmia has relations: disease_phenotype_positive with familial Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with familial Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated.", "label": "yes"}
{"original_question": "Is corpus callosum involved in the Mowat\u2013Wilson syndrome?", "id": "converted_200", "sentence1": "Is Structure of body of corpus callosum involved in the Mowat\u2013Wilson Book Syndrome?", "sentence2": "The Book Syndrome is characterized by typical Facial features, moderate-to-severe mental retardation, Epilepsy and variable congenital malformations, including HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, Abnormality of the genital system, congenital heart disease, Congenital absence of the Structure of body of Structure of body of corpus callosum, and Eye Specimen Source Code defects.  Mowat-Wilson Book Syndrome in a Fetus in fetu with antenatal diagnosis of short Structure of body of Structure of body of corpus callosum: advocacy for standard autopsy. It is mainly characterized by moderate-to-severe Intellectual Disability, Epilepsy, Facial dysmorphism and various malformations including HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 and Structure of body of Structure of body of corpus callosum teratologic.  The association of a Structure of body of Structure of body of corpus callosum hypoplasia with a histological HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 and a typical Facial gestalt allowed the guiding of genetic testing. Mowat-Wilson Book Syndrome (Muckle-Wells Syndrome) is a severe Intellectual Disability (ID)-distinctive Facial gestalt-multiple congenital anomaly Book Syndrome, commonly associating Microcephaly (physical finding), Epilepsy, Structure of body of Structure of body of corpus callosum Congenital absence, Conotruncal defect, urogenital malformations and HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR).  Mowat-Wilson Book Syndrome (Muckle-Wells Syndrome) is characterized by severe mental retardation with Seizures, specific Facial dysmorphism, HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, teratologic of the Structure of body of Structure of body of corpus callosum, and genitourinary and cardiac malformations. Mowat-Wilson Book Syndrome (Muckle-Wells Syndrome) is a genetic disease caused by heterozygous Gene Mutation or Gene Deletion of the ZEB2 gene and is characterized by distinctive Facial features, Epilepsy, moderate to severe Intellectual Disability, Structure of body of Structure of body of corpus callosum abnormalities and other congenital malformations. The striking Facial phenotype in addition to other features such as severely impaired speech, Muscle Muscle hypotonia, Microcephaly (physical finding), short stature, Seizures, Structure of body of Structure of body of corpus callosum Congenital absence, Congenital Heart Defects, Penile Penile hypospadias, and HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 are particularly important clues for the initial clinical diagnosis.  Mowat-Wilson Book Syndrome is a genetic disorder characterized by a distinct Facial appearance, moderate-to-severe mental retardation, Microcephaly (physical finding), Congenital absence of the Structure of body of Structure of body of corpus callosum, HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, congenital heart disease, and Abnormality of the genital system.  It is characterized by a distinctive Facial appearance in association with Intellectual Disability (ID) and variable other features including Congenital absence of the Structure of body of Structure of body of corpus callosum, Seizures, Congenital Heart Defects, Microcephaly (physical finding), short stature, Muscle Muscle hypotonia, and HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1.  Mowat-Wilson Book Syndrome (Muckle-Wells Syndrome) is an autosomal dominant Intellectual Disability Book Syndrome characterised by unique Facial features and Congenital Abnormality such as HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, Congenital Heart Defects, Structure of body of Structure of body of corpus callosum Congenital absence and urinary tract teratologic. Mowat-Wilson Book Syndrome (Muckle-Wells Syndrome) is a recently delineated mental retardation; a multiple congenital anomaly Book Syndrome characterised by a typical Facial gestalt, HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 or severe constipation, genitourinary anomaly, Congenital Heart Defects, Congenital absence of Structure of body of Structure of body of corpus callosum and Eye Specimen Source Code defects.  Agenesis or hypogenesis of the Structure of body of Structure of body of corpus callosum. The teratologic may include HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, heart defects, structural Eye Specimen Source Code teratologic including Microphthalmos, Congenital absence of the Structure of body of Structure of body of corpus callosum, and Urogenital Abnormalities.  Mowat-Wilson Book Syndrome (Muckle-Wells Syndrome; OMIM #235730) is a genetic condition caused by heterozygous Gene Mutation or Gene Deletion of the ZEB2 gene, and characterized by typical face, moderate-to-severe mental retardation, Epilepsy, HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, and multiple Congenital Abnormality, including Abnormality of the genital system (particularly Penile Penile hypospadias in males), Congenital Heart Defects, Congenital absence of the Structure of body of Structure of body of corpus callosum, and Eye Specimen Source Code defects. In 11 of the 28 patients with Agenesis of Structure of body of Structure of body of corpus callosum, the following diagnoses could be established: Mowat-Wilson Book Syndrome (n = 2), Walker-Warburg congenital muscular dystrophy (n = 1), oro-Facial-digital Book Syndrome type 1 (n = 1), and chromosomal rearrangements (n = 7), including a patient with an apparently balanced reciprocal translocation, which led to the disruption and a predicted loss of function in the FOXG1 wt Allele. Mowat-Wilson Book Syndrome (Muckle-Wells Syndrome) is a multiple congenital anomaly Book 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 malformations including HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR), genitourinary teratologic (in particular Penile Penile hypospadias in males), Congenital Heart Defects, Congenital absence of the Structure of body of Structure of body of corpus callosum and Eye Specimen Source Code teratologic. Mowat-Wilson Book Syndrome is a mental retardation-multiple congenital anomaly Book Syndrome characterized by a typical facies, developmental delay, Epilepsy, and variable congenital malformations, including HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, Urogenital Abnormalities, congenital heart disease, and Congenital absence of the Structure of body of Structure of body of corpus callosum.  Mowat-Wilson Book Syndrome (Muckle-Wells Syndrome) is a recently delineated mental retardation (Mitral Valve Insufficiency)-multiple congenital anomaly Book Syndrome, characterized by typical facies, severe Mitral Valve Insufficiency, Epilepsy, and variable congenital malformations, including HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR), Abnormality of the genital system, congenital heart disease (altretamine/cisplatin/cyclophosphamide protocol), and Congenital absence of the Structure of body of Structure of body of corpus callosum (Agenesis of Structure of body of Structure of body of corpus callosum).  Medical issues in our cohort of patients included Seizures (75%) with no predeliction for any particular seizure type; Congenital absence of the Structure of body of Structure of body of corpus callosum (60% of our patients studied); Congenital Heart Defects (75%), particularly involving the pulmonary arteries and/or valves; Penile Penile hypospadias (55% of males); severely impaired or absent speech (100% of individuals over 1 year of age) with relatively spared receptive language; and HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (50%) or Chronic constipation (25%).  Mowat-Wilson Book Syndrome (Muckle-Wells Syndrome) is a mental retardation Book Syndrome associated with distinctive Facial features, Microcephaly (physical finding), Epilepsy, and a variable spectrum of Congenital Abnormality, including HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR), Congenital absence of the Structure of body of Structure of body of corpus callosum, genitourinary abnormalities, and congenital heart disease. Agenesis of Structure of body of Structure of body of corpus callosum is found in 40% of the cases of Mowat-Wilson Book Syndrome (Muckle-Wells Syndrome), a polytopic embryonic defect including a distinctive Facial gestalt, severe mental retardation, Epilepsy and postnatal Microcephaly (physical finding) as constant features.  However, analysis of Muckle-Wells Syndrome should be considered in the differential diagnosis of Agenesis of Structure of body of Structure of body of corpus callosum, especially when the Facial features raise the possibility of Muckle-Wells Syndrome. Frameshift Mutation function of the zinc finger homeo box 1 B gene in syndromic Structure of body of Structure of body of corpus callosum Congenital absence (Mowat-Wilson Book Syndrome). We report a girl who had HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 in association with distinct Facial appearance, Microcephaly (physical finding), Congenital absence of the Structure of body of Structure of body of corpus callosum and mental retardation (Mowat-Wilson Book Syndrome). Congenital teratologic, including HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR), congenital heart disease, Penile Penile hypospadias, genitourinary teratologic, Congenital absence of the Structure of body of Structure of body of corpus callosum, and short stature are common.[SEP]Relations: Seizure has relations: disease_phenotype_positive with Mowat-Wilson Book Syndrome, disease_phenotype_positive with Mowat-Wilson Book Syndrome. Large earlobe has relations: disease_phenotype_positive with Mowat-Wilson Book Syndrome, disease_phenotype_positive with Mowat-Wilson Book Syndrome. Abnormality of the genital system has relations: disease_phenotype_positive with Mowat-Wilson Book Syndrome, disease_phenotype_positive with Mowat-Wilson Book Syndrome. ZEB2 has relations: anatomy_protein_present with Structure of body of corpus callosum, disease_protein with Mowat-Wilson Book Syndrome, disease_protein with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, anatomy_protein_present with Structure of body of corpus callosum, disease_protein with Mowat-Wilson Book Syndrome, disease_protein with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. hirschsprung disease, susceptibility to has relations: disease_disease with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_disease with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. Agenesis of Structure of body of corpus callosum has relations: disease_phenotype_positive with Mowat-Wilson Book Syndrome, disease_phenotype_positive with Mowat-Wilson Book Syndrome. Intellectual disability has relations: disease_phenotype_positive with Microphthalmos, disease_phenotype_positive with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_phenotype_positive with Microphthalmos, disease_phenotype_positive with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. Frontal bossing has relations: disease_phenotype_positive with Mowat-Wilson Book Syndrome, disease_phenotype_positive with Mowat-Wilson Book Syndrome.", "label": "yes"}
{"original_question": "Can NXY-059 be used for treatment of acute ischemic stroke patients?", "id": "converted_201", "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]", "label": "no"}
{"original_question": "Is flibanserin effetive for Hypoactive Sexual Desire Disorder?", "id": "converted_202", "sentence1": "Is flibanserin effetive for Hypoactive Sexual Desire Disorder?", "sentence2": "Mechanism of action of flibanserin, a multifunctional Serotonin Agonists 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 Agonists 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: indication with Hypoactive Sexual Desire Disorder, indication with Hypoactive Sexual Desire Disorder. Serotonin has relations: drug_drug with flibanserin, drug_drug with flibanserin. Hypoactive Sexual Desire Disorder has relations: indication with flibanserin, indication with flibanserin.", "label": "yes"}
{"original_question": "Is recommended the use of perioperative treatment with thyroid hormone therapy in patients undergoing coronary artery bypass grafting?", "id": "converted_203", "sentence1": "Is recommended the use of perioperative treatment with thyroid hormone therapy in patients undergoing coronary artery bypass grafting?", "sentence2": "Short duration postoperative iv T(3) therapy increases cardiac index and does not alter mortality. We conclude that although widespread interest has been shown on the use of Thyroid Hormones in the perioperative period, and the effect of cardiopulmonary bypass on thyroid hormone metabolism widely studied, there is no substantial evidence to justify routine use of Thyroid Hormones in patients undergoing coronary artery bypass grafting. There is no clear evidence at this point to support thyroid hormone replacement in the latter patients, and it may be potentially harmful. Rather, we hold that T3 thoracic segmental innervation thoracic segmental innervation treatment of various surgical and other patients with nonthyroidal illness should be deferred until proof of its therapeutic efficacy is demonstrated. Perioperative administration of liothyronine increased cardiac output slightly and decreased systemic vascular resistance, but it had no effect on operative outcome. Routine use after coronary surgery is thus not recommended. Although mild effects on myocardial performance may exist, we cannot recommend at this time the routine use of intravenous T(3) as an inotropic agent in patients undergoing coronary artery bypass graft surgery. Raising serum liothyronine concentrations in patients undergoing coronary-artery bypass surgery increases cardiac output and lowers systemic vascular resistance, but does not change outcome or alter the need for standard postoperative therapy. Thus, there seems to be no sound justification for a routine use of T3 thoracic segmental innervation thoracic segmental innervation in patients undergoing open-heart procedures.[SEP]", "label": "no"}
{"original_question": "Is protein CXCR4 used as a prognostic marker of cancer?", "id": "converted_204", "sentence1": "Is protein C-X-C motif chemokine 12 receptor activity used as a prognostic marker of Primary malignant neoplasm?", "sentence2": "Aberrant overexpression of C-X-C motif chemokine 12 receptor activity is associated with worse overall survival, Malignant adenomatous neoplasm histology, distant metastasis, lymph node involvement in Non-Small Cell Lung Carcinoma. C-X-C motif chemokine 12 receptor activity belongs to a family of G protein-coupled cell surface receptors and has been proved to a prognostic marker in a various Neoplasms, including esophageal squamous cell Primary malignant neoplasm.  The CXCR3 gene (C-X-C motif chemokine 12 receptor activity) has been found to be a prognostic marker in various types of Primary malignant neoplasm, being involved in chemotaxis, stemness and drug resistance.  The chemokine receptor C-X-C motif chemokine 12 receptor activity that has been shown to be implicated in ANOPHTHALMIA AND PULMONARY HYPOPLASIA tumorigenicity and Aggressive behavior could serve as a prognostic marker for survival after a curative-intent surgery and was associated with the pattern of tumour recurrence (distant versus local relapse). XCR4 promotes tumor growth, angiogenesis and metastasis, and is a prognostic marker in a number of different types of Neoplasms. C-X-C motif chemokine 12 receptor activity has been identified as a prognostic marker for acute myeloid leukemia (Leukemia, Myelocytic, Acute) and other Malignant Neoplasms.  The chemokine receptor C-X-C motif chemokine 12 receptor activity has been found to be a prognostic marker in various types of Primary malignant neoplasm, including breast Primary malignant neoplasm.  Upregulated expression of C-X-C chemokine receptor 4 is an independent prognostic predictor for patients with gastric Primary malignant neoplasm. detection of C-X-C motif chemokine 12 receptor activity expression will be helpful for predicting prognosis for patients with gastric Primary malignant neoplasm. The chemokine receptor C-X-C motif chemokine 12 receptor activity is a marker of metastatic disease. High C-X-C motif chemokine 12 receptor activity level in Primary malignant neoplasm specimens independently predicts a poor outcome for patients with node-positive breast Primary malignant neoplasm. Univariate and multivariate analyses demonstrated that the high levels of nuclear C-X-C motif chemokine 12 receptor activity and Chemokine Chemokine CXCL12 expression in Hepatocyte were significantly better prognostic factors for overall and hepatic disease-free survival in patients with LAMB1 gene. The chemokine receptor C-X-C motif chemokine 12 receptor activity has been implicated in Malignant neoplasm of soft tissue development and has been found to be a prognostic marker for poor clinical outcome.  high C-X-C motif chemokine 12 receptor activity expression is correlated to shorter DFS and could be used as a prognostic marker in order to stratify Melanocytic neoplasm patients at higher progression risk.[SEP]Relations: C-X-C motif chemokine 12 receptor activity has relations: molfunc_protein with C-X-C motif chemokine 12 receptor activity, molfunc_protein with C-X-C motif chemokine 12 receptor activity. melanocytic neoplasm has relations: disease_disease with Melanocytic neoplasm, disease_disease with Melanocytic neoplasm. malignant soft tissue neoplasm has relations: disease_disease with Primary malignant neoplasm, disease_disease with Primary malignant neoplasm.", "label": "yes"}
{"original_question": "Is transcapillary  albumin escape altered in diabetic patients?", "id": "converted_205", "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]", "label": "yes"}
{"original_question": "Are conserved noncoding elements associated with developmental genes?", "id": "converted_206", "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 gene expression, and their enrichment in gene 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 gene development, result in neurocristopathies via the alteration of tissue- or stage-specific long-distance regulation of gene 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 gene 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 gene and PAX6 gene gene, 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]", "label": "yes"}
{"original_question": "Is myasthenia gravis associated with osteoporosis?", "id": "converted_207", "sentence1": "Is Myasthenia Gravis associated with Encounter due to family history of osteoporosis?", "sentence2": "We performed cisplatin/etoposide protocol in 4 patients with generalized MG 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 MG 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 (MG) 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 MG 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 Fracture (aromatic hydrocarbon receptor 0.99 [95 % CI, 0.31-3.14]) compared with MG 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 (MG) 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 (MG) 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: Prednisolone has relations: off_label_use with Myasthenia Gravis, contraindication with Encounter due to family history of osteoporosis, off_label_use with Myasthenia Gravis, contraindication with Encounter due to family history of osteoporosis. aryl hydrocarbon receptor complex has relations: cellcomp_protein with aromatic hydrocarbon receptor, cellcomp_protein with aromatic hydrocarbon receptor. Muscle weakness has relations: disease_phenotype_positive with Myasthenia Gravis, disease_phenotype_positive with Myasthenia Gravis.", "label": "yes"}
{"original_question": "Does a selective sweep increase genetic variation?", "id": "converted_208", "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 allele 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 mtDNA 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]", "label": "no"}
{"original_question": "Is indicated the use of antioxidant supplements in patients at risk for coronary artery disease?", "id": "converted_209", "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 B VITAMINS [VA 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 \u03b1-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 \u00b5mol/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. Coenzyme Q10 supplementation at a dosage of 150 mg appears to decrease the inflammatory marker Recombinant Interleukin-6 in patients with cyclophosphamide/dacarbazine/doxorubicin protocol.  Coenzyme Q10 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 system disease 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: Selenium has relations: exposure_disease with coronary artery disease, exposure_disease with coronary artery disease.", "label": "no"}
{"original_question": "Is there evidence to suggest that triiodothyronine has neuroprotective properties in traumatic brain injury?", "id": "converted_210", "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 (1.2\u03bcg/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-\u03baB (NF-\u03baB). 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: glial cell-derived neurotrophic factor receptor binding has relations: molfunc_protein with Glial Cell Line-Derived Neurotrophic Factor, molfunc_protein with Glial Cell Line-Derived Neurotrophic Factor. CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS has relations: anatomy_protein_present with brain-derived neurotrophic factor, anatomy_protein_present with brain-derived neurotrophic factor.", "label": "yes"}
{"original_question": "Is Lysine-specific demethylase 1 (LSD1) a critical regulator of hematopoiesis?", "id": "converted_211", "sentence1": "Is KDM1A gene (KDM1A wt Allele) a critical regulator of hematopoiesis?", "sentence2": "KDM1A protein, human (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 KDM1A gene 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 Lysine-Specific Demethylase 7A 1 (KDM1A wt Allele), RE1 silencing transcription factor corepressor (RCOR1 gene), Histone Deacetylase (HDAC1 gene gene), and histone deacetylase 2 in Acute Erythroblastic Leukemia and Leukemia, T-Cell 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. KDM1A protein, human (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: T-cell leukemia has relations: disease_protein with TAL1 protein, human, disease_protein with TAL1 protein, human.", "label": "yes"}
{"original_question": "Is K-63 linked protein ubiquitination related to proteasomal degradation?", "id": "converted_212", "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 nuclear factor kappaB (NF-kappa B) through IkappaB Kinase beta (IKKbeta), but a negative role in the noncanonical pathway that activates NF-kappa B 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-kappa B 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-triphosphate receptor 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]", "label": "no"}
{"original_question": "Could transcription factors act as cell-cell signalling molecules?", "id": "converted_213", "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]", "label": "yes"}
{"original_question": "is pharmacological treatment of subclinical hypothyroidism effective in reducing cardiovascular events?", "id": "converted_214", "sentence1": "is pharmacological treatment of subclinical hypothyroidism effective in reducing Cardiovascular system events?", "sentence2": "The decision to treat elderly people is still an unresolved clinical challenge--first, due to a lack of appropriately powered randomized controlled trials of L-T4 in sHT patients, examining Cardiovascular system hard endpoints in various classes of age; and second, because of the negative effects of possible overtreatment. The lack of specific randomized trials enrolling either old or very old subjects, aimed at evaluate the efficacy of hormonal replacement on overall survival and Cardiovascular system risk reduction along with the negative effects of possible over-treatment, makes the decision to treat older people a still unresolved clinical challenge In patients with type 2 DM, the presence of SH serves as an additional risk factor for endothelial dysfunction. Treatment of Supracervical hysterectomy with levothyroxine was associated with fewer Myocardial Ischemia events in younger individuals, but this was not evident in older people. Subclinical hyperthyroidism seems to be a risk factor of developing major Cardiovascular system events, especially Cerebrovascular accident in older adults from the general population with normal left ventricular function. Supracervical hysterectomy appears to influence the postoperative outcome for patients by increasing the development of postoperative atrial fibrillation. However, it is still unproven whether preoperative thyroxine replacement therapy for patients with Supracervical hysterectomy might prevent postoperative atrial fibrillation after CABG. In Congestive heart failure patients Thyrotropin:-:Pt:Ser/Plas:- levels even slightly above normal range are independently associated with a greater likelihood of heart failure progression. In current RCTs, levothyroxine replacement therapy for subclinical hypothyroidism did not result in improved survival or decreased Cardiovascular system morbidity. Data on health-related quality of life and symptoms did not demonstrate significant differences between intervention groups. However, the actual effectiveness of Thyroid Hormones substitution in reducing the risk of Cardiovascular system events remains to be elucidated. In conclusion, the multiplicity and the possible reversibility of subclinical hypothyroidism-associated Cardiovascular system abnormalities suggest that the decision to treat a patient should depend on the presence of risk factors, rather than on a Thyrotropin:-:Pt:Ser/Plas:- threshold.  However, whether SH confers a high risk for Cardiovascular system disease, and whether LT4 therapy has a long-term benefit that clearly outweighs the risks of overzealous treatment in these individuals, remain topics of controversy.[SEP]Relations: Levothyroxine has relations: contraindication with Cardiovascular system disease, contraindication with Cardiovascular system disease.", "label": "no"}
{"original_question": "Could Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) cause sudden cardiac death?", "id": "converted_215", "sentence1": "Could Catecholaminergic Polymorphic Ventricular Tachycardia (Polymorphic catecholergic ventricular tachycardia) cause sudden cardiac death?", "sentence2": "Two siblings died suddenly at the ages of 9 and 10\u00a0years 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\u00b194 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 (disorder) (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 (disorder) (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 Gene Mutation that destabilize cardiac ryanodine receptor Ca(2+) release channels. Sudden cardiac death is incompletely prevented by conventional drug therapy with \u03b2-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 (disorder), 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 (disorder) (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 Sudden Cardiac 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 Gene Mutation 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 (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 (disorder), 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 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 cardiomyopathy (Arrhythmogenic Right Ventricular Dysplasia) 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: Ventricular tachycardia has relations: disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Brugada Syndrome (disorder). arrhythmogenic right ventricular dysplasia has relations: disease_protein with Ryanodine Receptor 2, disease_protein with Ryanodine Receptor 2. Arrhythmia has relations: disease_phenotype_positive with Sudden Cardiac Arrest, disease_phenotype_positive with Sudden Cardiac Arrest. Long QT Syndrome has relations: disease_protein with Ryanodine Receptor 2, disease_protein with Ryanodine Receptor 2, disease_protein with Ryanodine Receptor 2, disease_protein with Ryanodine Receptor 2. catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding has relations: disease_disease with Long QT Syndrome, disease_protein with Ryanodine Receptor 2, disease_disease with Long QT Syndrome, disease_protein with Ryanodine Receptor 2. Ventricular arrhythmia has relations: disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Long QT Syndrome. Sudden cardiac death has relations: disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with Brugada Syndrome (disorder). Chest>Heart Disease has relations: disease_disease with Chest>Heart failure, disease_disease with Chest>Heart failure, disease_disease with Chest>Heart failure, disease_disease with Chest>Heart failure. Congestive Chest>Heart failure has relations: disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with Long QT Syndrome.", "label": "yes"}
{"original_question": "Are histone deacetylase (HDAC) inhibitors good candidates to control metastasis of solid tumors?", "id": "converted_216", "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: Sodium tetradecyl sulfate has relations: contraindication with Primary malignant neoplasm, contraindication with Primary malignant neoplasm.", "label": "yes"}
{"original_question": "Is muscle lim protein (MLP) involved in cardiomyopathies?", "id": "converted_217", "sentence1": "Is Muscle Tissue lim Protein Info (MARCKSL1 Genes) involved in cardiomyopathies?", "sentence2": "Muscle LIM Protein Info (MARCKSL1 Genes) has been proposed to be a central player in the pathogenesis of Chest>Heart Muscle Tissue disease. In line with this notion, the homozygous loss of MARCKSL1 Genes results in Cardiac - anatomy qualifier hypertrophy and Cardiomyopathy, Dilated. Moreover, MARCKSL1 Genes 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 Genes) null CASP14 Genes are often used as a model for human Cardiomyopathy, Dilated. A lack of MARCKSL1 Genes leads to an age-dependent impairment of excitation-contraction coupling with resulting contractile dysfunction and secondary fibrosis. Loss of murine MARCKSL1 Genes results in Cardiomyopathy, Dilated, and Gene Mutation in human MARCKSL1 Genes lead to Cardiac - anatomy qualifier hypertrophy, indicating a critical role for MARCKSL1 Genes in maintaining normal Cardiac - anatomy qualifier function. Our data indicate that MARCKSL1 Genes contributes to Muscle Tissue stiffness and is necessary for maximum work and power generation. Interestingly, MARCKSL1 Genes was also found to be down-regulated in Homo sapiens with Chest>Heart failure (Zolk et al. Circulation 101:2674-2677, 2000) and MARCKSL1 Genes Gene Mutation 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; Kn\u00f6ll et al. \"U\" lymphocyte 111:943-955, 2002; Kn\u00f6ll et al. Circ Res 106:695-704, 2010; Mohapatra et al. Mol Genet Metab 80:207-215, 2003). MARCKSL1 Genes soon became an important model for experimental cardiology when it was first demonstrated that MARCKSL1 Genes deficiency leads to Myocardial hypertrophy followed by a Cardiomyopathy, Dilated and Chest>Heart failure phenotype (Arber et al. \"U\" lymphocyte 88:393-403, 1997).  Previous studies have shown an association between CSRP3 Genes Genes missense Gene Mutation 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 Genes Genes Gene Mutation.  We used a newly designed monoclonal antibody CAL CAL to show that cysteine and glycine-rich Protein Info 3 (MARCKSL1 Genes), the Protein Info encoded by CSRP3 Genes Genes, 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 Genes's mutated forms seems to be destabilized in the Chest>Heart of Hypertrophic Cardiomyopathy patients harbouring a CSRP3 Genes Genes missense Mutation Abnormality. Muscle LIM Protein Info (MARCKSL1 Genes) is a Cytoskeletal Proteins located at the Z line of sarcomeres. Mutations in the human MARCKSL1 Genes Genes 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 Genes) is a Cytoskeleton LIM-only Protein Info expressed in Skeletal Muscle Tissue structure. Mutations in human MARCKSL1 Genes are associated with cardiomyopathy; TTN-encoded titin, CSRP3 Genes Genes-encoded cysteine and glycine-rich Protein Info 3, 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 disorder of skin, unspecified cardiomyopathy (Hypertrophic Cardiomyopathy).  Approximately 4.1% of unrelated patients had Hypertrophic Cardiomyopathy-associated MARCKSL1 Genes or 2,2,2',4'-tetrachloroacetophenone Gene Mutation. MARCKSL1 Genes/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 Abnormality. The precise role of W4R-MARCKSL1 Genes in the pathogenesis of either 3',5'-dichloromethotrexate or Hypertrophic Cardiomyopathy warrants further investigation. MARCKSL1 Genes (Muscle Tissue-LIM-Protein Info) deficient CASP14 Genes 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 cysteine and glycine-rich Protein Info 3 (MARCKSL1 Genes) in CASP14 Genes consistently leads to Cardiomyopathy, Dilated (3',5'-dichloromethotrexate) after one or more months.  In summary, young MLPKO CASP14 Genes revealed substantial alterations in passive myocardial properties and relaxation time, but not in most systolic characteristics. These results indicate that the progression to Chest>Heart failure in the MLPKO model may be driven by diastolic myocardial dysfunction and abnormal passive properties rather than Systolic dysfunction. Mice lacking the cysteine and glycine-rich Protein Info 3 (MARCKSL1 Genes) develop morphological and clinical signs resembling human Cardiomyopathy, Dilated and Chest>Heart failure. Our results show that the absence of MARCKSL1 Genes 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 Chest>Heart failure. Previous work has shown that Gene Mutation in cysteine and glycine-rich Protein Info 3 (MARCKSL1 Genes) can cause Hypertrophic disorder of skin, unspecified 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 Genes and of the (C58G) Mutant MARCKSL1 Genes that causes Hypertrophic disorder of skin, unspecified cardiomyopathy. The molecular basis for Hypertrophic Cardiomyopathy-causing Gene Mutation in the MARCKSL1 Genes Genes might therefore be an alteration in the equilibrium of interactions of the ternary complex MARCKSL1 Genes-N-RAP-alpha-Actinin. Muscle LIM Protein Info (MARCKSL1 Genes) 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 Genes-deficient mouse has been described; these CASP14 Genes develop Cardiomyopathy, Dilated and Chest>Heart failure. We identified a patient with 3',5'-dichloromethotrexate and Endocardial Fibroelastosis, having a Mutation Abnormality in MARCKSL1 Genes with the residue lysine 69 substituted by arginine (K69R).  MARCKSL1 Genes-knockout CASP14 Genes develop a marked Cardiac - anatomy qualifier hypertrophy reaction and Cardiomyopathy, Dilated (3',5'-dichloromethotrexate). MARCKSL1 Genes is therefore a candidate Genes for heritable forms of Hypertrophic disorder of skin, unspecified cardiomyopathy (Hypertrophic Cardiomyopathy) and 3',5'-dichloromethotrexate in Homo sapiens. Family studies revealed cosegregation of clinically affected individuals with the respective Gene Mutation in MARCKSL1 Genes. CONCLUSION: Here, we present evidence that Gene Mutation in the CRP3/MARCKSL1 Genes Genes can cause Hypertrophic Cardiomyopathy. The Skeletal cysteine and glycine-rich Protein Info 3 1 (FHL1 Genes) is highly expressed in Skeletal and Cardiac - anatomy qualifier Muscle Tissue, and its expression is downregulated significantly in dilated human cardiomyopathy.  Targeted disruption of cysteine and glycine-rich Protein Info 3 (MARCKSL1 Genes) has previously been shown to result in Cardiomyopathy, Dilated with many of the clinical signs of Chest>Heart failure, although the effects of MARCKSL1 Genes disruption on passive ventricular mechanics and Muscle Cells architecture are not known. These results suggest that the disruption of the Cytoskeletal Proteins MARCKSL1 Genes 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.  Mutations in cysteine and glycine-rich Protein Info 3 (CSRP3 Genes Genes), the Genes encoding MARCKSL1 Genes, 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 Genes) has been proposed to be a central player in the pathogenesis of Chest>Heart Muscle Tissue disease. Previous work has shown that Gene Mutation in cysteine and glycine-rich Protein Info 3 (MARCKSL1 Genes) can cause Hypertrophic disorder of skin, unspecified cardiomyopathy (Hypertrophic Cardiomyopathy)[SEP]Relations: MARCKSL1 has relations: cellcomp_protein with Microtubules associated with cytoplasmic filaments, anatomy_protein_present with Chest>Heart, cellcomp_protein with Microtubules associated with cytoplasmic filaments, anatomy_protein_present with Chest>Heart. Hypertrophic cardiomyopathy has relations: disease_phenotype_positive with Hypertrophic disorder of skin, unspecified cardiomyopathy, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Hypertrophic disorder of skin, unspecified cardiomyopathy, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Hypertrophic disorder of skin, unspecified cardiomyopathy, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Hypertrophic disorder of skin, unspecified cardiomyopathy, disease_phenotype_positive with Cardiomyopathy, Dilated. Cardiomyopathy has relations: disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Hypertrophic disorder of skin, unspecified cardiomyopathy, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Hypertrophic disorder of skin, unspecified cardiomyopathy. Cardiomyopathy, Dilated has relations: disease_disease with Hypertrophic disorder of skin, unspecified cardiomyopathy, disease_disease with Hypertrophic disorder of skin, unspecified cardiomyopathy. Congestive Chest>Heart failure has relations: disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Hypertrophic disorder of skin, unspecified cardiomyopathy, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Hypertrophic disorder of skin, unspecified cardiomyopathy. Cardiomyocyte hypertrophy has relations: disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated.", "label": "yes"}
{"original_question": "Have 5q35 microdeletions been implicated in Sotos syndrome development?", "id": "converted_218", "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: Intellectual disability has relations: disease_phenotype_positive with SOTOS SYNDROME 1, disease_phenotype_positive with SOTOS SYNDROME 1. SOTOS SYNDROME 1 has relations: disease_protein with NSD1 protein, Homo sapiens, disease_protein with NSD1 protein, Homo sapiens. Abnormality of the dentition has relations: disease_phenotype_positive with SOTOS SYNDROME 1, disease_phenotype_positive with SOTOS SYNDROME 1. Macrocephaly has relations: disease_phenotype_positive with SOTOS SYNDROME 1, disease_phenotype_positive with SOTOS SYNDROME 1.", "label": "yes"}
{"original_question": "Is metabolic syndrome related with cardiovascular disease?", "id": "converted_219", "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.", "label": "yes"}
{"original_question": "Are defects in recombination repair involved in carcinogenesis?", "id": "converted_220", "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: malignant colon neoplasm has relations: disease_disease with colorectal Primary malignant neoplasm, disease_disease with colorectal Primary malignant neoplasm.", "label": "yes"}
{"original_question": "Are seizures among the neurological symptoms of incontinentia pigmenti?", "id": "converted_221", "sentence1": "Are Seizures among the neurological symptoms of IKBKG Genes?", "sentence2": "High-dose glucocorticoid therapy in the management of Seizures in neonatal IKBKG Genes Bloch Sulzberger syndrome is an X-linked dominant disorder resulting from a Mutation Abnormality of IKBKG. This disorder has a classic dermatologic presentation, but neurologic involvement, with Seizures and cortical infarction, can arise shortly after birth Some children with IKBKG Genes 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-\u03baB) 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 coma 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 IKBKG Genes. High-dose glucocorticoid therapy in the management of Seizures in neonatal IKBKG Genes: 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 IKBKG Genes A rare cause of neonatal seizure: IKBKG Genes. Here, we describe the clinical, electrographic, and neuroradiologic effect of systemic glucocorticoid therapy in a neonate with IKBKG Genes manifesting an Epileptic encephalopathy. Bloch Sulzberger syndrome presenting as Seizures. Neonatal Seizures in two sisters with IKBKG Genes.[SEP]Relations: Seizure has relations: disease_phenotype_positive with IKBKG Genes, disease_phenotype_positive with IKBKG Genes. Intellectual disability has relations: disease_phenotype_positive with IKBKG Genes, disease_phenotype_positive with IKBKG Genes. IKBKG has relations: disease_protein with IKBKG Genes, disease_protein with IKBKG Genes.", "label": "yes"}
{"original_question": "Is there a genome-wide technique for the detection of R-loop formation?", "id": "converted_222", "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]", "label": "yes"}
{"original_question": "Can bioprinting use human cells?", "id": "converted_223", "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]", "label": "yes"}
{"original_question": "Is transcription-associated mutagenesis (TAM) related to gene expression levels?", "id": "converted_224", "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]", "label": "yes"}
{"original_question": "Is there a pharmacogenetic test for trastuzumab?", "id": "converted_225", "sentence1": "Is there a pharmacogenetic test for trastuzumab?", "sentence2": "The clinical need for novel approaches to improve drug therapy derives from the high rate of adverse reactions to drugs and their lack of efficacy in many individuals that may be predicted by pharmacogenetic testing. the assessment of the epidermal growth factor receptor 2, human (HER-2-neu peptide vaccine-neu peptide vaccine) expression for trastuzumab therapy of Malignant neoplasm of breast erbB-2 Receptor positive Malignant neoplasm of breast and the use of the drug Herceptin The dependence on gene copy number or expression levels of erbB-2 Receptor and epidermal growth factor receptor (Epidermal Growth Factor Receptor) for therapeutic efficacy of trastuzumab and cetuximab (Erbitux), respectively, supports the importance of selecting suitable patient populations based on their pharmacogenetic profile. to explore informed consent issues surrounding the use of the drug Herceptin, widely cited as an example of a novel approach to drug development called pharmacogenetics. Drawing on qualitative semi-structured interviews with 25 UK-based Malignant neoplasm of breast specialists, this paper explores Herceptin's disputed epistemological status, as an example of pharmacogenetics or as something out of the ordinary in terms of clinical practice. There have been several success stories in the field of pharmacogenetics in recent years, including the analysis of erbB-2 Receptor amplification for trastuzumab selection in Malignant neoplasm of breast Trastuzumab is standard of care in the treatment of epidermal growth factor receptor 2, human (HER)-2\u207a early and advanced Malignant neoplasm of breast. HER-2-neu peptide vaccine-neu peptide vaccine overexpression as a predictor of response to trastuzumab Pharmacogenomic analysis aspires to identify individuals with specific genetic characteristics in order to predict a positive response or reduce a negative response to a therapeutic modality. Assays are available to detect the erbB-2 Receptor protein receptor or copies of the erbB-2 Receptor gene sequence to determine eligibility for Herceptin treatment or Adriamycin treatment in node positive patients, respectively. Determining the erbB-2 Receptor status of breast carcinomas is a prerequisite for the use of the monoclonal antibody trastuzumab (Herceptin), which has recently been licensed for the treatment of Metastatic Neoplasm. Laboratory testing of erbB-2 Receptor/neu in Breast Carcinoma has become vital to patient care following the approval of trastuzumab as the first therapy to target the erbB-2 Receptor/neu oncoprotein. Immunohistochemical (IHC) analysis was performed with use of a diagnostic test for the assessment of erbB-2 Receptor overexpression, the HercepTest. To test for HER-2-neu peptide vaccine-neu peptide vaccine/neu overexpression in patients with Non-Hodgkin's lymphoma of bone and the possible role of the recombinant monoclonal anti-HER-2-neu peptide vaccine-neu peptide vaccine/neu antibody trastuzumab (Herceptin) in the treatment of Non-Hodgkin's lymphoma of bone. To evaluate concordance between local and central laboratory erbB-2 Receptor testing results in patients from the North Central Cancer Treatment Group (NCCTG) N9831 adjuvant trial of trastuzumab. These findings support the importance of using high-volume, experienced laboratories for erbB-2 Receptor testing to improve the process of selecting patients likely to benefit from trastuzumab therapy. we measured trastuzumab levels in the serum and in Cerebrospinal Fluid of metastatic Malignant neoplasm of breast patients with brain metastases receiving trastuzumab for erbB-2 Receptor-overexpressing metastatic Malignant neoplasm of breast. In a pilot study, metastatic Malignant neoplasm of breast patients with brain metastases and erbB-2 Receptor-overexpressing tumors (HercepTest; Dako, Copenhagen, Denmark) were included. Monitoring of trastuzumab levels in the serum and Cerebrospinal Fluid may enable individualized therapy strategies in metastatic Malignant neoplasm of breast patients with brain metastases, and lead to a better understanding of trastuzumab pharmacokinetics in the Cerebrospinal Fluid and serum. Biotin-labeled trastuzumab (BiotHER) can be used to test for erbB-2 Receptor by immunohistochemistry. The results support a role for BiotHER testing in better tailoring trastuzumab-based treatments in patients with advanced erbB-2 Receptor-amplified breast cancers. response to anti-epidermal growth factor receptor 2, human 2 (erbB-2 Receptor) therapy trastuzumab.[SEP]Relations: Cetuximab has relations: drug_protein with Epidermal Growth Factor Receptor, drug_protein with Epidermal Growth Factor Receptor.", "label": "yes"}
{"original_question": "Do carmustine wafers improve survival of glioblastoma patients?", "id": "converted_226", "sentence1": "Do carmustine Oral Wafer improve survival of glioblastoma patients?", "sentence2": "At recurrence, treatment options include repeat surgery (with or without Gliadel wafer placement), reirradiation or systemic therapy.  DISCUSSION: Carmustine Oral Wafer for primary HGG surgery in accordance with the NICE TA121 were associated with a median survival of 15.3 months; this is improved compared with previously reported randomised trials. Multimodal treatment with carmustine Oral Wafer, radical radiotherapy and concomitant temozolomide was associated with improved survival. Gliadel wafer is a new approach to the treatment of glioblastoma, which involves controlled release delivery of carmustine from biodegradable polymer Oral Wafer. It has shown promising results and provides a silver lining for glioblastoma patients. For patient with and without Gliadel, median and 1-year RFS were 12.9 months and 52% vs. 14 months and 42%, respectively (p = 0.89). According to pathology, Gliadel did not influence OS of patients with Grade III or glioblastoma CONCLUSION: In patients with high-grade Glioma, adding Gliadel before performing a Stupp protocol did not improve survival. Randomized phase III trials have shown significant improvement of survival 1, 2, and 3 years after implantation of 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) Oral Wafer for patients with newly diagnosed Malignant Glioma.  CONCLUSIONS: The combination of aggressive resection, Gliadel wafer implantation, and GKS in addition to standard fractionated RT in selected patients resulted in increased local control and increased survival compared with a historical control group treated with surgery and involved-field RT alone. OBJECT: Gliadel (BCNU) wafer and concomitant temozolomide (TMZ) therapy, when used individually as adjuvant therapies, extend survival from that achieved by resection and radiation therapy (XRT) for Glioblastoma Multiforme (Glomerular Basement Membrane).  BACKGROUND: Gliadel (polifeprosan 20 20 20 with carmustine [BCNU] implant) is commonly used for local delivery of BCNU to high-grade Glioma after resection and is associated with increased survival. temozolomide administered according to this protocol produced a median survival benefit of 2 months in Glioblastoma, and carmustine a similar benefit in high-grade Glioma. Analysis of a large trial by Westphal and colleagues (n = 240) showed a 29% risk reduction (P = 0.03) in the BCNU wafer-treated group over the course of the 30-month trial. Median survival of patients treated with BCNU Oral Wafer was 13.8 months vs 11.6 months in placebo-treated patients (P = 0.017) with a hazard ratio of 0.73 (P = 0.018), representing a 27% significant risk reduction. This survival advantage was maintained at 1, 2, and 3 years and was statistically significant (P = 0.01) at 3 years. CONCLUSION: Malignant glioma patients treated with BCNU Oral Wafer at the time of initial surgery in combination with radiation therapy demonstrated a survival advantage at 2 and 3 years follow-up compared with placebo. OBJECTIVE: Recently a randomized placebo-controlled phase III trial of biodegradable Polymers containing carmustine has demonstrated a significant survival benefit for patients treated with local chemotherapy.  CONCLUSION: In this subgroup analysis of a phase III trial population both the clinical progression and radiological progression were significantly delayed in patients treated with local chemotherapy, resulting in an increased survival time. A previous placebo-controlled trial has shown that biodegradable 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) Oral Wafer (Gliadel Oral Wafer) prolong survival in patients with recurrent Glioblastoma Multiforme. A previously completed phase 3 trial, also placebo controlled, in 32 patients with newly diagnosed Malignant Glioma also demonstrated a survival benefit in those patients treated with BCNU Oral Wafer. Median survival in the intent-to-treat group was 13.9 months for the BCNU wafer-treated group and 11.6 months for the placebo-treated group (log-rank P -value stratified by country = 0.03), with a 29% reduction in the risk of death in the treatment group. When adjusted for factors affecting survival, the treatment effect remained positive with a risk reduction of 28% ( P = 0.03).  Controlled release delivery of carmustine from biodegradable polymer Oral Wafer was approved as an adjunct to surgical resection in the treatment of recurrent Glioblastoma Multiforme after it was shown in clinical trials to be well tolerated and effective.  Clinical trials have demonstrated significant improvements in survival and quality of life for patients after complete tumour resection and BCNU wafer implantation. BCNU Oral Wafer are an effective means of increasing survival and quality of life in patients diagnosed with Malignant Glioma, and are a valuable addition to the overall multimodal treatment strategy for these Neoplasms. CONCLUSIONS: Carmustine wafer with concurrent TMZ and radiation followed by rotational chemotherapy is a well tolerated, effective therapy, and has a survival benefit compared with radiation alone. Median overall survival in 14 studies of newly-diagnosed patients suggested a modest improvement versus resection followed by Stupp protocol or resection with BCNU Oral Wafer, with an acceptable and manageable safety profile. The efficacy of carmustine Oral Wafer for older patients with Glioblastoma Multiforme: prolonging survival. DISCUSSION: Older patients with Glomerular Basement Membrane may benefit from carmustine Oral Wafer. The survival for older patients who received carmustine Oral Wafer is significantly longer than matched patients who did not receive carmustine Oral Wafer. For glioblastoma patients who received \u226590% resection in the BCNU wafer study, median survival increased for BCNU wafer versus placebo (14.5 versus 12.4\u00a0months, respectively; P\u2009=\u20090.02), but no survival increase was found for <90% resection (11.7 versus 10.6\u00a0months, respectively; P\u2009=\u20090.98). A wafer impregnated with carmustine, for use as an implant after surgical removal of recurrent Glomerular Basement Membrane showed a prolongation in the median survival time of only 2 mo, from 20 to 28 wk in a study with a total of 222 patients.  No clear survival benefit associated with wafer implantation was identified. In three of the trials, patients with Glomerular Basement Membrane who received carmustine Oral Wafer had significantly longer median survival than patients who did not receive Oral Wafer.  TMZ and carmustine (BCNU) biodegradable wafer (Gliadel) are the only adjuvant chemotherapies that have improved survival in randomised GB clinical trials .  The carmustine implant wafer was demonstrated to improve survival in blinded placebo-controlled trials in selected patients with newly diagnosed or recurrent Malignant Glioma, with little increased risk of adverse events.  For patients undergoing repeat resection for Malignant Glioma, a randomized, blinded, placebo-controlled trial demonstrated a median survival for 110 patients who received carmustine Polymers of 31 weeks compared with 23 weeks for 122 patients who only received placebo Polymers. Median survival was improved from 11.6 to 13.9 months (P = 0.03), with a 29% reduction in the risk of death. When patients with Glioblastoma Multiforme alone were analyzed, the median survival improved from 11.4 to 13.5 months, but this improvement was not statistically significant.  OBJECT: Locoregional chemotherapy with carmustine Oral Wafer, positioned at surgery and followed by radiation therapy, has been shown to prolong survival in patients with newly diagnosed glioblastoma, as has concomitant radiochemotherapy with temozolomide. Following the resection of newly diagnosed or recurrent Glioblastoma, local implantation of carmustine-impregnated biodegradable Oral Wafer (Gliadel) in the resection cavity constitutes an adjuvant therapy that can improve the possibilities of survival. The carmustine implant wafer was demonstrated to improve survival in blinded placebo-controlled trials in selected patients with newly diagnosed or recurrent Malignant Glioma, with little increased risk of adverse events. However, patients with carmustine Oral Wafer demonstrated prolonged survival as compared to patients without Oral Wafer. The median survival for patients with carmustine Oral Wafer was 8.7 months, while median survival for patients without Oral Wafer was 5.5 months (P=0.007). Likewise, in subgroup analysis, patients older than 70 years (P=0.0003) and 75 years (P=0.04) who had carmustine Oral Wafer had significantly longer survival than matched patients without Oral Wafer. Implantation of carmustine Oral Wafer did not significantly improve progression-free survival In three of the trials, patients with Glomerular Basement Membrane who received carmustine Oral Wafer had significantly longer median survival than patients who did not receive Oral Wafer A previous placebo-controlled trial has shown that biodegradable 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) Oral Wafer (Gliadel Oral Wafer) prolong survival in patients with recurrent Glioblastoma Multiforme A previously completed phase 3 trial, also placebo controlled, in 32 patients with newly diagnosed Malignant Glioma also demonstrated a survival benefit in those patients treated with BCNU Oral Wafer Following the resection of newly diagnosed or recurrent Glioblastoma, local implantation of carmustine-impregnated biodegradable Oral Wafer (Gliadel) in the resection cavity constitutes an adjuvant therapy that can improve the possibilities of survival Multimodal treatment with carmustine Oral Wafer, radical radiotherapy and concomitant temozolomide was associated with improved survival The carmustine implant wafer was demonstrated to improve survival in blinded placebo-controlled trials in selected patients with newly diagnosed or recurrent Malignant Glioma, with little increased risk of adverse events TMZ and carmustine (BCNU) biodegradable wafer (Gliadel) are the only adjuvant chemotherapies that have improved survival in randomised GB clinical trials[SEP]Relations: Carmustine has relations: indication with Malignant Glioma, drug_drug with temozolomide, indication with Malignant Glioma, drug_drug with temozolomide.", "label": "yes"}
{"original_question": "Is Dicer part of the RISC loading complex?", "id": "converted_227", "sentence1": "Is DICER1 protein, human part of the RNA-Induced Silencing Complex loading complex?", "sentence2": "DICER1 protein, human is a component of the protein machinery (the RNA Induced Silencing Complex [RNA-Induced Silencing Complex]) which is involved in catalyzing the formation of mature MicroRNAs from their precursors in the process of microRNA biogenesis. RNA-induced silencing complex (RNA-Induced Silencing Complex) Proteins Cyclophosphamide/Doxorubicin/Prednisone/Tamoxifen regimen (Cyclophosphamide/Doxorubicin/Prednisone/Tamoxifen regimen (PACT)), TARBP2P1 gene, and DICER1 protein, human are SRA binding nuclear receptor coregulators. The cytoplasmic RNA-induced silencing complex (RNA-Induced Silencing Complex) contains dsRNA binding proteins, including protein kinase RNA activator (Cyclophosphamide/Doxorubicin/Prednisone/Tamoxifen regimen (Cyclophosphamide/Doxorubicin/Prednisone/Tamoxifen regimen (PACT))), transactivation response RNA-Binding Proteins (TARBP2P1 gene), and DICER1 protein, human, that process pre-MicroRNAs into mature MicroRNAs (miRNAs) that target specific mRNA species for regulation.   Although the major RNAi pathway proteins are found in most subcellular compartments, the miRNA- and siRNA-loaded EIF2C2 protein, human populations co-sediment almost exclusively with the rER membranes, together with the RNA-Induced Silencing Complex loading complex (ITGA9 wt Allele) factors DICER1 protein, human, Thrombocytopenia-Absent Radius Syndrome RNA-Binding Proteins (TARBP2P1 gene) and protein activator of the interferon-induced protein kinase (Cyclophosphamide/Doxorubicin/Prednisone/Tamoxifen regimen (Cyclophosphamide/Doxorubicin/Prednisone/Tamoxifen regimen (PACT))). RNA interference (RNAi) is mediated by RNA, Small Interfering (siRNAs), which are liberated from double-stranded (ds)RNA precursors by DICER1 protein, human and guide the RNA-induced silencing complex (RNA-Induced Silencing Complex) to targets. . DICER1 protein, human, an RNase III enzyme, plays a central role in the RNAi pathway by cleaving precursors of both of these classes of RNAs to form mature siRNAs and miRNAs, which are then loaded into the RNA-induced silencing complex (RNA-Induced Silencing Complex).  Canonical siRNAs are 21 Nucleotides (nt) in length and are loaded to the RNA Induced Silencing Complex when introduced into the Cells, while longer siRNA Molecule are first processed by endogenous DICER1 protein, human and thus termed DICER1 protein, human-substrate siRNA (DsiRNA).[SEP]", "label": "yes"}
{"original_question": "Is hypersensitivity to DNA crosslinking agents a hallmark of Fanconi anemia?", "id": "converted_228", "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, cancer/leukemia susceptibility and cellular Emotional Emotional hypersensitivity to DNA crosslinking agents, such as cisplatin. Fanconi anemia (doxorubicin/fluorouracil protocol) is an inherited Chromosomes recessive syndrome characterized by cellular Emotional Emotional hypersensitivity to DNA crosslinking agents and Bone marrow hypocellularity, which cause Aplastic Anemia, and an increased incidence of Primary malignant neoplasm. Features of Chromosomes aberrations, Emotional Emotional hypersensitivity to DNA crosslinking agents, and predisposition to Primary malignant neoplasm have suggested a fundamental anomaly of DNA repair in Fanconi anemia. Fanconi anemia (doxorubicin/fluorouracil protocol) is one of several genetic diseases with characteristic cellular 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 cellular 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, cancer predisposition and Emotional Emotional hypersensitivity to DNA crosslinking agents. Fanconi anemia (doxorubicin/fluorouracil protocol) is a heterogeneous Disease associated with a Bone marrow hypocellularity, cancer predisposition and Emotional Emotional hypersensitivity to DNA crosslinking agents. Fanconi anemia (doxorubicin/fluorouracil protocol) is an inherited disorder characterized by defective DNA repair and cellular sensitivity to DNA crosslinking agents. Fanconi anemia (doxorubicin/fluorouracil protocol) is an inherited Disease characterized by Bone marrow hypocellularity, increased cancer 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 cancer types, including head and neck squamous cell carcinomas (Squamous cell carcinoma of the head and neck), 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, cellular 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 cellular 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 cancer 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, cancer or leukemia susceptibility, and cellular 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 cellular 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 cellular 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 cellular 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 cellular 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 Primary malignant neoplasm have suggested a fundamental anomaly of DNA repair in Fanconi anemia Fanconi anemia (doxorubicin/fluorouracil protocol) is an inherited Chromosomes recessive syndrome characterized by cellular Emotional Emotional hypersensitivity to DNA crosslinking agents and Bone marrow hypocellularity, which cause Aplastic Anemia, and an increased incidence of Primary malignant neoplasm Genetic or epigenetic inactivation of the pathway formed by the FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) Proteins occurs in several cancer types, including head and neck squamous cell carcinomas (Squamous cell carcinoma of the head and neck), rendering the affected Neoplasms potentially hypersensitive to DNA crosslinking agents Fanconi anemia (doxorubicin/fluorouracil protocol) is a Homo sapiens autosomal disorder characterized by cancer susceptibility and cellular 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, cancer or leukemia susceptibility, and cellular 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_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_disease with Fanconi anemia, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_disease with Fanconi anemia, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_disease with Fanconi anemia, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_disease with Fanconi anemia. Bloom syndrome has relations: disease_protein with Bloom Syndrome, disease_protein with Bloom Syndrome. chromosome has relations: cellcomp_protein with Bloom Syndrome, cellcomp_protein with Bloom Syndrome. Bone marrow hypocellularity has relations: phenotype_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, phenotype_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2.", "label": "yes"}
{"original_question": "Have C12orf65 mutations been associated with axonal neuropathy and optic atrophy?", "id": "converted_229", "sentence1": "Have MTRFR Genes Gene Mutation been associated with axonal Neuropathy and Optic Atrophy 1?", "sentence2": "Novel MTRFR Genes Gene Mutation 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. Mutations in MFN2 Genes have been found to cause dominant forms of Hereditary motor and sensory Neuropathy with Optic Atrophy 1 (disorder). Phosphoribosylpyrophosphate synthetase-I Gene Mutation cause X-linked Hereditary motor and sensory Neuropathy with Optic Atrophy 1 (disorder), but until now, Gene Mutation 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 Gene Mutation 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 Gene Mutation 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 Gene Mutation 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 Gene Mutation 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 Gene Mutation 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 Gene Mutation 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\u2009T>A (c.282+2\u2009T>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 Gene Mutation 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 Gene Mutation in seven affected individuals originating from two consanguineous families.[SEP]Relations: peripheral nervous system disease has relations: disease_disease with Peripheral Nervous System Diseases, disease_disease with Peripheral Nervous System Diseases. Optic atrophy has relations: disease_phenotype_positive with Leigh Disease, disease_phenotype_positive with Optic Atrophy 1, disease_phenotype_positive with Leigh Disease, disease_phenotype_positive with Optic Atrophy 1. axonal Neuropathy has relations: disease_disease with Peripheral Nervous System Diseases, disease_disease with Peripheral Nervous System Diseases.", "label": "yes"}
{"original_question": "Is cystatin C or cystatin 3 used as a biomarker of kidney function?", "id": "converted_230", "sentence1": "Is CST3 gene or cystatin 3 used as a biomarker of kidney function?", "sentence2": "to explore the effect of ageing on renal function with CST3 gene as the marker of glomerular filtration rate (GFR) in the general population without Vascular Diseases or Diabetes Mellitus. Cystatin C, a more specific kidney function biomarker, was also elevated at 24 h after CLP. This study evaluated FGF-23 as well as traditional markers of Kidney Diseases, namely urine albumin-to-creatine/creatine/creatinine ratio (UACR) and creatine/creatine/creatinine-CST3 gene estimated GFR (eGFRCrCyC), as risk factors for Blighia sapida in elderly individuals.  he primary predictor was estimated GFR (Epidermal Growth Factor Receptor) calculated using serum CST3 gene (Epidermal Growth Factor Receptor(cys)). A number of recent reports have suggested that the CST3 gene/creatine/creatine/creatinine (CysC/Cr) ratio might be a useful biomarker of renal function in pediatric patients. The CKD-EPI equation using CST3 gene was the most precise method of renal function evaluation in patients with Neurogenic Urinary Bladder. Serum CST3 gene (CysC) is an endogenous marker of kidney function. The Urinary tract content of CysC reflects tubular epithelial dysfunction whereas that of LCN2 wt Allele also characterizes Tubular atrophy. Estimated kidney function based on serum CST3 gene  : Several formulas for glomerular filtration rate (GFR) estimation, based on Creatinine measurement, serum (procedure) or CST3 gene, have been proposed.  he highest and lowest Epidermal Growth Factor Receptor levels corresponded to the CST3 gene-based and MDRD-4 equations, respectively.  The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) recently proposed an equation to estimate GFR in subjects without Liver Cirrhosis using both Creatinine measurement, serum (procedure) and CST3 gene levels. Emerging evidence has shown that CST3 gene may improve classification of glomerular filtration rate for defining chronic Kidney Diseases in certain clinical populations and assist in understanding the complications of chronic Kidney Diseases prostaglandin R2 D-isomerase (BTP) and CST3 gene (CysC) are novel biomarkers of renal function.  Cystatin C could improve chronic Kidney Diseases (CKD) classification in HIV-infected women relative to Creatinine measurement, serum (procedure).  iohexol clearance and CST3 gene formulae identify a greater proportion of patients with a GFR <60 mL/min/1.73 m(2), which also predicts the development of Blighia sapida.  Cystatin C was recently reported to be an endogenous surrogate of kidney function, and a high level of CST3 gene is reported to be a strong predictor of CVD; Studies that have simultaneously compared measured GFR and estimated GFR (using endogenous filtration markers such as creatine/creatine/creatinine, or newer ones such as CST3 gene or \u03b2-trace protein)[SEP]Relations: Kidney Diseases has relations: disease_disease with chronic Kidney Diseases, disease_disease with chronic Kidney Diseases.", "label": "yes"}
{"original_question": "Can fetal aneuploidy be detected with non-invasive prenatal testing?", "id": "converted_231", "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]", "label": "yes"}
{"original_question": "Is dichlorphenamide effective for periodic paralysis?", "id": "converted_232", "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]", "label": "yes"}
{"original_question": "Is nivolumab used for treatment of Non\u2013Small-Cell Lung Cancer?", "id": "converted_233", "sentence1": "Is nivolumab used for treatment of Non\u2013Small-Cell Lung Cancer?", "sentence2": "BACKGROUND: Patients with advanced squamous-cell non-small-cell Primary malignant neoplasm of lung (Non-Small Cell Lung Carcinoma) 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 Non-Small Cell Lung Carcinoma, 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 (Non-Small Cell Lung Carcinoma) receiving nivolumab in this trial.PATIENTS AND METHODS: Patients (N = 129) with heavily pretreated advanced Non-Small Cell Lung Carcinoma 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 Non-Small Cell Lung Carcinoma. Randomized clinical trials with nivolumab in advanced Non-Small Cell Lung Carcinoma 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 Primary malignant neoplasm of lung, reported at the World Conference on Lung Cancer in Sydney, Australia. Recently, many trials addressed the role of such therapies for metastatic Non-Small Cell Lung Carcinoma 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 Primary malignant neoplasm of lung, 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 Primary malignant neoplasm of lung, Conventional (Clear Cell) Renal Cell Carcinoma, Malignant Head and Neck Neoplasm, 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 Primary malignant neoplasm of lung. These data support the assessment of nivolumab in randomised, controlled, phase 3 studies of first-line and second-line treatment.[SEP]Relations: Pembrolizumab has relations: drug_drug with nivolumab, indication with Primary malignant neoplasm of lung, drug_drug with nivolumab, indication with Primary malignant neoplasm of lung. Tremelimumab has relations: drug_drug with nivolumab, drug_drug with nivolumab. Docetaxel has relations: indication with Primary malignant neoplasm of lung, indication with Primary malignant neoplasm of lung. nivolumab has relations: indication with Primary malignant neoplasm of lung, indication with Primary malignant neoplasm of lung. Ipilimumab has relations: drug_drug with nivolumab, drug_drug with nivolumab. melanocytic neoplasm has relations: disease_disease with Melanocytic neoplasm, disease_disease with Melanocytic neoplasm.", "label": "yes"}
{"original_question": "Does  thyroid hormone receptor beta1 affect insulin secretion?", "id": "converted_234", "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]", "label": "no"}
{"original_question": "Does replication timing affect the rate of somatic mutations?", "id": "converted_235", "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 yeast 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 Saccharomyces 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 yeast. 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: malignant giant cell tumor has relations: disease_disease with Primary malignant neoplasm, disease_disease with Primary malignant neoplasm.", "label": "yes"}
{"original_question": "Is NOD1 activated in inflammation?", "id": "converted_236", "sentence1": "Is NOD1 activated in Inflammation?", "sentence2": "NOD1 gene and NOD2 gene control Bacterial infections and Inflammation The Nod proteins NOD1 gene and NOD2 gene 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 gene represent central players in the control of immune responses to Bacterial infections and Inflammation. The innate immune receptor NOD1 gene protects the Intestines 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 intestinal Epithelial Cells barrier due to Chemicals induced injury as manifested by increased surface epithelial apoptosis early on during Chemicals induced Colitis and increased intestinal permeability. The increased intestinal permeability is associated with enhanced inflammatory cytokine production and Epithelial Cells 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 Intestines 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 Polymorphisms 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, 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 gene regulation of Inflammation in the Salmonella Colitis model CASP14 gene deficient for both NOD1 gene and NOD2 gene 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 gene 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 gene. 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 Signaling in Communicable Diseases and Inflammation NOD1 engagement generates an inflammatory response via activation of NF\u03baB 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-\u03baB-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 gene have different functions in controlling Inflammation, and that Protoplasm NOD1 gene-NOD2 gene 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 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 gene, 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 (NF\u03baB).  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 gene 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 intestinal 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 intestinal mucosal Inflammation. NOD1 activation triggers Inflammation, In contrast to enhanced leptin mRNA by Van der Woude syndrome and TNF\u03b1, 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-\u03baB, 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 activation on Inflammation and the Therapeutic Insulin signalling pathway was also assessed. Interferon-gamma (IFN gamma), which is a potent pro-inflammatory cytokine in intestinal 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: Nitric Oxide has relations: exposure_disease with Asthma, exposure_disease with Asthma. Intestines has relations: anatomy_protein_present with aromatic hydrocarbon receptor, anatomy_protein_present with aromatic hydrocarbon receptor. SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding), susceptibility to has relations: disease_disease with SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding), disease_disease with SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding). aryl hydrocarbon receptor complex has relations: cellcomp_protein with aromatic hydrocarbon receptor, cellcomp_protein with aromatic hydrocarbon receptor. Inflammatory abnormality of the Eye Specimen Source Code has relations: disease_phenotype_positive with Uveitis, disease_phenotype_positive with Uveitis. coronary artery has relations: anatomy_protein_present with aromatic hydrocarbon receptor, anatomy_protein_present with aromatic hydrocarbon receptor.", "label": "yes"}
{"original_question": "Does magnesium sulfate improve outcomes of subarachnoid hemorrhage patients?", "id": "converted_237", "sentence1": "Does Magnesium supplements, alimentary tract and metabolism sulfate improve outcomes of Subarachnoid Hemorrhage patients?", "sentence2": "CONCLUSION: Patients assigned a higher serum Magnesium supplements, alimentary tract and metabolism concentration had a reduced incidence of Vasospasm as seen by angiography, but the difference was not statistically significant. Clinically significant outcomes were not different between groups. 158 patients (26\u00b72%) had poor outcome in the Magnesium supplements, alimentary tract and metabolism group compared with 151 (25\u00b73%) in the placebo group (risk ratio [RR] 1\u00b703, 95% CI 0\u00b785-1\u00b725). Our updated meta-analysis of seven randomised trials involving 2047 patients shows that Magnesium supplements, alimentary tract and metabolism is not superior to placebo for reduction of poor outcome after aneurysmal subarachnoid haemorrhage (RR 0\u00b796, 95% CI 0\u00b786-1\u00b708). INTERPRETATION: Intravenous Magnesium supplements, alimentary tract and metabolism sulphate does not improve clinical outcome after aneurysmal subarachnoid haemorrhage, therefore routine administration of Magnesium supplements, alimentary tract and metabolism cannot be recommended.  There is a tendency in the Magnesium supplements, alimentary tract and metabolism group to have better outcomes.  Due to inconsistently reported benefits and the occurrence of side effects, phase II data suggested that intravenous Magnesium supplements, alimentary tract and metabolism for Yakut language provided either no overall net benefit or uncertain trade-offs. Benefit was likewise not supported in the single phase III clinical trial. tatistically significant clinical benefits could not be demonstrated for the other drugs (clazosentan, Hydroxymethylglutaryl-CoA Reductase Inhibitors, and Magnesium supplements, alimentary tract and metabolism). CONCLUSIONS: Insufficient evidence is available to support the use of the triple-H therapy, clazosentan, Hydroxymethylglutaryl-CoA Reductase Inhibitors, or Magnesium supplements, alimentary tract and metabolism sulfate for the prevention of Cerebral hemisphere structure (body structure) Vasospasm following Subarachnoid Hemorrhage.  Magnesium sulfate decreased the rate of Cerebral hemisphere structure (body structure) infarction, but not of Noninfiltrating Intraductal Carcinoma or poor functional outcome. Regarding outcome, a beneficial effect of Magnesium supplements, alimentary tract and metabolism sulfate on outcome can not be ruled out because of sample size limitations. CONCLUSIONS: The present findings do not lend support to a beneficial effect of Magnesium supplements, alimentary tract and metabolism sulphate infusion on delayed Cerebral hemisphere structure (body structure) infarction. The reduction in Noninfiltrating Intraductal Carcinoma and improvement in the clinical outcomes of aneurysmal Yakut language patients following Magnesium supplements, alimentary tract and metabolism sulphate infusion observed in previous pilot studies are not confirmed, although a beneficial effect cannot be ruled out because of sample size limitation. Favorable outcome (Good recovery and moderate disability, as defined by Glasgow Outcome Scale) was achieved in 20 of 30 (67%) patients receiving Magnesium supplements, alimentary tract and metabolism sulfate infusion and 16 of 30 (53%) patients receiving placebo treatment, p = 0.292, odds ratio 1.750, 95% CI 0.616-4.974. Similarly, the pooled odds ratio for favorable outcome is 1.598, 95% CI 1.074-2.377, statistically significant.  RESULTS: The worst clinical outcomes at 6 months were seen in MgSO(4) group patients, with mean plasma Magnesium supplements, alimentary tract and metabolism concentrations in the fourth quartile, and in placebo group patients, with mean such concentrations in the third and fourth quartiles. CONCLUSIONS: No evidence was found to suggest that a higher mean plasma Magnesium supplements, alimentary tract and metabolism concentration improves clinical outcomes. On the contrary, we found an association between high plasma Magnesium supplements, alimentary tract and metabolism concentration and worse clinical outcomes. The proportions of patients with a favorable outcome at 6 months (Extended Glasgow Outcome Scale 5 to 8) were similar, 64% in the Magnesium supplements, alimentary tract and metabolism sulfate group and 63% in the saline group (OR, 1.0; 95% CI, 0.7 to 1.6). Secondary outcome analyses (modified Rankin Scale, Barthel Index, Short Form 36, and clinical Vasospasm) also showed no significant differences between the 2 groups.  CONCLUSIONS: The results do not support a clinical benefit of intravenous Magnesium supplements, alimentary tract and metabolism sulfate infusion over placebo infusion in patients with acute aneurysmal Subarachnoid Hemorrhage. Magnesium infusion reduced the risk of poor outcome and delayed Cerebral hemisphere structure (body structure) ischemia (Noninfiltrating Intraductal Carcinoma): the relative risk was 0.62 (95% confidence interval (CI) 0.46-0.83) and 0.73 (95% CI 0.53-1.00), respectively.  CONCLUSION: The meta-analysis suggests that intravenous Magnesium supplements, alimentary tract and metabolism therapy reduces the risk of Noninfiltrating Intraductal Carcinoma and poor outcome after aneurysmal Yakut language.  The incidence of delayed ischemic infarction was significantly lower in Magnesium supplements, alimentary tract and metabolism-treated patients (22% vs. 51%; p = .002); 34 of 54 Magnesium supplements, alimentary tract and metabolism patients and 27 of 53 control patients reached good outcome (p = .209). BACKGROUND: A meta-analysis of current data suggests that Magnesium supplements, alimentary tract and metabolism sulfate infusion improves the outcome after aneurysmal Subarachnoid Hemorrhage through a reduction in delayed ischemic neurological deficit.  These data imply that intravenous Magnesium supplements, alimentary tract and metabolism therapy, besides a supposed beneficial effect on outcome, also provides pain relief for Yakut language patients, for whom it might also improve functional outcome. Preliminary evidence has suggested that Magnesium supplements, alimentary tract and metabolism sulfate infusion reduces delayed ischemic neurological deficit and improves clinical outcome after aneurysmal Subarachnoid Hemorrhage.  In a phase II randomized clinical trial of 283 patients, Magnesium supplements, alimentary tract and metabolism treatment reduced the risk of Noninfiltrating Intraductal Carcinoma by 34% and of poor outcome by 23%. BACKGROUND: Recent studies suggest that high-dose MgSO4 therapy is safe and reduces the incidence of DIND and subsequent poor outcome after Yakut language.  On-treatment analysis showed a significantly better outcome after 3 months (P = .017) and a trend toward better outcome after 1 year (P = .083).   CONCLUSIONS: High-dose MgSO4 therapy might be efficient as a prophylactic adjacent therapy after Yakut language to reduce the risk for poor outcome.  There was no significant difference in mortality rate at discharge (p = 0.328). A trend toward improved outcome as measured by the modifed Rankin Scale (p = 0.084), but not the Glasgow Outcome Scale (p = 1.0), was seen in the MgSO4 treated group. CONCLUSIONS: Analysis of the results suggests that MgSO4 infusion may have a role in Cerebral hemisphere structure (body structure) Vasospasm prophylaxis if therapy is initiated within 48 hours of Aneurysm, Ruptured. There was, however, no difference between groups in functional recovery or Glasgow Outcome Scale score.  Patients receiving MgSO4 tended to have fewer Neurologic Deficits, better functional recovery and an improved score in Genomics Outcome Scale.  CONCLUSIONS: MgSO4 infusion after aneurysmal Yakut language is well tolerated and may be useful in producing better outcome. CONCLUSION: Magnesium did not seem to interfere in Vasospasm frequency but apparently acted favorably in decreasing morbidity and length of hospital stay. None of the patients died; no X-Ray Computed Tomography evidence of ischemic infarction was present; and most had good outcomes (Genomics Outcome Scale 5 in 10 patients; Genomics Outcome Scale 4 in 8 patients). At that time, 18 patients in the treatment group and 6 in the placebo group had an excellent outcome (risk ratio, 3.4; 95% CI, 1.3 to 8.9). CONCLUSIONS: This study suggests that Magnesium supplements, alimentary tract and metabolism reduces Noninfiltrating Intraductal Carcinoma and subsequent poor outcome, but the results are not yet definitive.  We observed a trend in which a higher percentage of patients obtained Genomics Outcome Scale scores of 4 or 5 in the group treated with MgSO4, but the trend did not reach a statistically significant level.  Magnesium sulfate treatment improves outcome in patients with Subarachnoid Hemorrhage: a meta-analysis study. BACKGROUND AND PURPOSE: Pilot clinical trials using Magnesium supplements, alimentary tract and metabolism sulfate in patients with acute aneurysmal Subarachnoid Hemorrhage have reported trends toward improvement in clinical outcomes. Preliminary evidence has suggested that Magnesium supplements, alimentary tract and metabolism sulfate infusion reduces delayed ischemic neurological deficit and improves clinical outcome after aneurysmal Subarachnoid Hemorrhage. Our results indicate that although there was reduced likelihood of a poor outcome for patients treated with Magnesium supplements, alimentary tract and metabolism sulfate after Yakut language, patient mortality was not improved. CONCLUSION: Administration of intra-arterial Magnesium supplements, alimentary tract and metabolism sulfate in combination with nicardipine was well tolerated in patients with Subarachnoid Hemorrhage and Cerebral hemisphere structure (body structure) Vasospasm without a significant change in cisplatin/doxorubicin/mitomycin protocol and ICP. Current evidence does not support the prophylactic use of Magnesium supplements, alimentary tract and metabolism sulfate in aneurysmal Subarachnoid Hemorrhage Preliminary evidence has suggested that Magnesium supplements, alimentary tract and metabolism sulfate infusion reduces delayed ischemic neurological deficit and improves clinical outcome after aneurysmal Subarachnoid Hemorrhage A meta-analysis of current data suggests that Magnesium supplements, alimentary tract and metabolism sulfate infusion improves the outcome after aneurysmal Subarachnoid Hemorrhage through a reduction in delayed ischemic neurological deficit Despite the publication of several randomized controlled studies, there is still much debate on whether Magnesium supplements, alimentary tract and metabolism sulfate improves outcome in patients with aneurysmal Subarachnoid Hemorrhage Magnesium supplements, alimentary tract and metabolism sulfate is a neuroprotective agent that might improve outcome after aneurysmal subarachnoid haemorrhage by reducing the occurrence or improving the outcome of delayed Cerebral hemisphere structure (body structure) ischaemia[SEP]Relations: Nicardipine has relations: contraindication with Cerebral hemisphere structure (body structure) infarction, contraindication with Cerebral hemisphere structure (body structure) infarction.", "label": "no"}
{"original_question": "Are there plasma membrane receptors for thyroid hormones?", "id": "converted_238", "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 \u03b1v\u03b23 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]", "label": "yes"}
{"original_question": "Does Rad9 interact with Aft1 in S.cerevisiae?", "id": "converted_239", "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 Saccharomyces 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 \u223c2% 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 Saccharomyces 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]", "label": "yes"}
{"original_question": "Are there any desmins present in plants?", "id": "converted_240", "sentence1": "Are there any desmins present in plants?", "sentence2": "Inherited Gene Mutation 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. Mutations 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.  Mutations 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 Gene Mutation 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]", "label": "no"}
{"original_question": "Are viruses involved in the etiology of human subacute thyroiditis?", "id": "converted_241", "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]", "label": "yes"}
{"original_question": "Is miR-126 involved in heart failure?", "id": "converted_242", "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]", "label": "yes"}
{"original_question": "Does resveratrol reduce cardiac remodeling?", "id": "converted_243", "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]", "label": "yes"}
{"original_question": "Is there a role for transcription factories in genome organization?", "id": "converted_244", "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]", "label": "yes"}
{"original_question": "Do selenoproteins and selenium play a role in prostate cancer prevention?", "id": "converted_245", "sentence1": "Do Selenoproteins and Selenium supplement 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 supplement 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 supplement metabolism are regulated at multiple levels in Pelvis>Prostate cells In a low-Selenium supplement 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 supplement 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 supplement 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 supplement 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 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 supplement 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 Benign Prostatic 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\u2009=\u20090.67, P\u2009=\u20090.02)[SEP]Relations: SELENOP has relations: disease_protein with Pelvis>Prostate Primary malignant neoplasm, disease_protein with Pelvis>Prostate Primary malignant neoplasm. Selenium has relations: exposure_disease with Pelvis>Prostate Primary malignant neoplasm, exposure_disease with Pelvis>Prostate Primary malignant neoplasm. Pelvis>Prostate gland has relations: anatomy_protein_present with Pachyonychia Congenita, anatomy_protein_present with Pachyonychia Congenita.", "label": "no"}
{"original_question": "Has protein citrullination been implicated in rheumatoid arthritis?", "id": "converted_246", "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, 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, in vitro diagnostic (acetyl 4-aminosalicylic acid) form against citrullinated antigens are formed.[SEP]Relations: Rheumatoid factor positive has relations: disease_phenotype_positive with rheumatoid arthritis, disease_phenotype_positive with rheumatoid arthritis. Rheumatoid Arthritis has relations: disease_phenotype_positive with rheumatoid arthritis, disease_phenotype_positive with rheumatoid arthritis. Anti-citrullinated protein antibody positivity has relations: disease_phenotype_positive with rheumatoid arthritis, disease_phenotype_positive with rheumatoid arthritis.", "label": "yes"}
{"original_question": "Do R-loops tend to form at sites of DNA replication?", "id": "converted_247", "sentence1": "Do R-Loop Structures 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-Loop Structures stabilized in the absence of Pancreatic ribonuclease HI. We propose that the organized structure of the R-loop 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, 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 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-Loop Structures 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-Loop Structures is discussed. We propose that downstream of a replication block, RNA at R-Loop Structures 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-Loop Structures 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 RNAs and template DNA, leading to stable DNA-RNA hybrids (R-loop) formation. Strikingly, we found that attenuation of replication strongly suppresses R-loop-mediated DNA rearrangements in both E. coli and HeLa Cells. More importantly, we then show that R-loop formation causes DNA replication Orthopedic Fork stalling, and that this in fact underlies the effects of R loops on genomic stabilit R-loop-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 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-Loop Structures already formed in the \"U\" lymphocyte, and by which, the bad effects of R-Loop Structures on DNA replication, TAF1 Gene Mutation and homologous recombination can be regulated. Here we propose that physiological R-loop 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-Loop Structures 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 dysregulation at CpG island promoter-origins might contribute to the phenotype of DNA replication abnormalities and loss of Genome - anatomical entity integrity detected in cancer Cells. We show that RNA:DNA hybrids (R-Loop Structures) form at Site of transcription/replication collisions and that ribonuclease H1 functions to suppress Chronic Fatigue Syndrome instability. R-Loop Structures and initiation of DNA replication in human Cells: a missing link? Stable RNA-DNA hybrids (R-Loop Structures) prime the initiation of replication in Escherichia coli 2 2 Cells. We propose that downstream of a replication block, RNA at R-Loop Structures 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-Loop Structures) 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 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. This scenario builds on the connection between transcription and replication in human Cells and suggests that R-loop dysregulation at CpG island promoter-origins might contribute to the phenotype of DNA replication abnormalities and loss of Genome - anatomical entity integrity detected in cancer Cells. The multiple cleavage Site on the R-loop 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-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-Loop Structures. Our results suggest that TOP1 protein, human execute this function by suppressing the formation of DNA-RNA hybrids during transcription, these so-called R-Loop Structures interfering with the progression of replication forks. Critical role of R-Loop Structures 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-Loop Structures is discussed. Competition between the RNA transcript and the nontemplate DNA strand during R-loop formation in vitro: a nick can serve as a strong R-loop initiation site. More importantly, we then show that R-loop 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 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. Previous studies have shown that the newly synthesized primers form a stable and persistent RNA-DNA hybrid, a R-loop, 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-Loop Structures stabilized in the absence of Pancreatic ribonuclease HI.[SEP]", "label": "yes"}
{"original_question": "Is selenium deficiency involved in autoimmune thyroid disease?", "id": "converted_248", "sentence1": "Is Selenium supplement deficiency involved in autoimmune Thyroid Diseases?", "sentence2": "In areas with severe Selenium supplement deficiency higher incidence of Thyroiditis has been reported due to a decreased activity of Selenium supplement-dependent glutathione peroxidase Enzyme [APC] within THYROID DIAGNOSTIC RADIOPHARMACEUTICALS cells Of 30 patients in the Selenium supplement 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 supplement treated group versus 10.1% (P < 0.95) in the placebo-treated group Selenium substitution has a significant impact on inflammatory activity in THYROID DIAGNOSTIC RADIOPHARMACEUTICALS-specific autoimmune disease Serum Selenium supplement is low in newly diagnosed Graves Disease S-Se was lower in patients with GD than in controls (mean (SD), GD: 89\u00b79\u00a0\u03bcg/l (18\u00b74); controls: 98\u00b78\u00a0\u03bcg/l (19\u00b77), P\u00a0<\u00a00\u00b701) 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 supplement supply and overt autoimmune Thyroid Diseases, especially GD Selenium deficiency is likely to constitute a risk factor for a feedforward derangement of the immune system-THYROID DIAGNOSTIC RADIOPHARMACEUTICALS interaction, while Selenium supplement supplementation appears to dampen the self-amplifying nature of this derailed interaction The recent recognition that the essential trace element Selenium supplement is incorporated as selenocysteine in all three deiodinases has decisively confirmed the clear-cut link between Selenium supplement and THYROID DIAGNOSTIC RADIOPHARMACEUTICALS function. It has additionally been established that the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS contains more Selenium supplement than any other Tissue Specimen Code and that Selenium supplement deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune Thyroid Diseases Maintenance of \"selenostasis\" via optimal intake not only aids preservation of general health but also contributes substantially to the prevention of Thyroid Diseases Low birth weight, Iodine, Homeopathic preparation excess and deficiency, Selenium supplement deficiency, parity, oral contraceptive use, reproductive span, fetal microchimerism, stress, seasonal variation, Allergy Specialty, smoking, radiation damage to the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS 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 supplement than any other Tissue Specimen Code and that Selenium supplement deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune Thyroid Diseases. Selenium deficiency may play an important role in the initiation and progression of autoimmune Thyroid Diseases. [Selenium deficiency in Celiac Disease: risk of autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS diseases]. Low birth weight, Iodine, Homeopathic preparation excess and deficiency, Selenium supplement deficiency, parity, oral contraceptive use, reproductive span, fetal microchimerism, stress, seasonal variation, Allergy Specialty, smoking, radiation damage to the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS 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 supplement-deficient patients with autoimmune Thyroid Diseases benefit from Selenium supplement supplementation, although the data are conflicting and many parameters must still be defined. Our observation supports the postulated link between inadequate Selenium supplement supply and overt autoimmune Thyroid Diseases, especially GD. Selenium deficiency in Celiac Disease: risk of autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS diseases]. Selenoproteins contain the essential trace element Selenium supplement whose deficiency leads to major disorders including Primary malignant neoplasm, male reproductive system failure, or autoimmune Thyroid Diseases. It has additionally been established that the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS contains more Selenium supplement than any other Tissue Specimen Code and that Selenium supplement deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune Thyroid Diseases. EVIDENCE SYNTHESIS: Evidence in support of Selenium supplement supplementation in Autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS disease is evaluated, the results herein presented demonstrating the potential effectiveness of Selenium supplement in reducing the antithyroid peroxidase titer and improving the echostructure in the ultrasound examination. Some investigators suggest that Selenium supplement may be a useful adjunctive treatment for autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS diseases, such as Hashimoto and Graves Disease. Therefore, even mild Selenium supplement deficiency may contribute to the development and maintenance of autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS diseases. Some clinical studies have demonstrated that Selenium supplement-deficient patients with autoimmune Thyroid Diseases benefit from Selenium supplement supplementation, although the data are conflicting and many parameters must still be defined. Some clinical studies have demonstrated that Selenium supplement-deficient patients with autoimmune Thyroid Diseases benefit from Selenium supplement 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 supplement It has additionally been established that the THYROID DIAGNOSTIC RADIOPHARMACEUTICALS contains more Selenium supplement than any other Tissue Specimen Code and that Selenium supplement deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune Thyroid Diseases. Therefore, even mild Selenium supplement deficiency may contribute to the development and maintenance of autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS diseases Some investigators suggest that Selenium supplement may be a useful adjunctive treatment for autoimmune THYROID DIAGNOSTIC RADIOPHARMACEUTICALS diseases, such as Hashimoto and Graves Disease[SEP]Relations: Graves disease has relations: disease_disease with autoimmune Thyroid Diseases, disease_disease with autoimmune Thyroid Diseases.", "label": "yes"}
{"original_question": "Is it safe to use Abatacept during pregnancy?", "id": "converted_249", "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: azathioprine has relations: drug_drug with Abatacept, drug_drug with Abatacept. Methotrexate has relations: drug_drug with Abatacept, drug_drug with azathioprine, drug_drug with Abatacept, drug_drug with azathioprine. Leflunomide has relations: drug_drug with azathioprine, drug_drug with Abatacept, drug_drug with azathioprine, drug_drug with Abatacept. Cyclosporine has relations: drug_drug with Abatacept, drug_drug with azathioprine, drug_drug with Abatacept, drug_drug with azathioprine. Cyclophosphamide has relations: drug_drug with azathioprine, drug_drug with Abatacept, drug_drug with azathioprine, drug_drug with Abatacept. Anakinra has relations: drug_drug with azathioprine, drug_drug with Abatacept, drug_drug with azathioprine, drug_drug with Abatacept. Abatacept has relations: drug_drug with azathioprine, drug_drug with azathioprine. Sulfasalazine has relations: drug_drug with azathioprine, drug_drug with Abatacept, drug_drug with azathioprine, drug_drug with Abatacept. Prednisolone has relations: drug_drug with Abatacept, drug_drug with azathioprine, drug_drug with Abatacept, drug_drug with azathioprine. Chloroquine has relations: drug_drug with Abatacept, drug_drug with azathioprine, drug_drug with Abatacept, drug_drug with azathioprine. Rituximab has relations: drug_drug with azathioprine, drug_drug with Abatacept, drug_drug with azathioprine, drug_drug with Abatacept. Tocilizumab has relations: drug_drug with azathioprine, drug_drug with Abatacept, drug_drug with azathioprine, drug_drug with Abatacept.", "label": "no"}
{"original_question": "Is STAT3 involved in EIF2AK2-dependent suppression of autophagy?", "id": "converted_250", "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 eIF2\u03b1 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 eIF2\u03b1 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 eIF2\u03b1 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: eukaryotic translation initiation factor 2 complex has relations: cellcomp_protein with Eukaryotic Translation Initiation Factor 2 Subunit 1, cellcomp_protein with Eukaryotic Translation Initiation Factor 2 Subunit 1. germ cell Cell Nucleus has relations: cellcomp_cellcomp with Cell Nucleus, cellcomp_cellcomp with Cell Nucleus. EIF2AK2 gene has relations: protein_protein with STAT3 protein, human, protein_protein with Eukaryotic Translation Initiation Factor 2 Subunit 1, cellcomp_protein with Cell Nucleus, protein_protein with STAT3 protein, human, protein_protein with Eukaryotic Translation Initiation Factor 2 Subunit 1, cellcomp_protein with Cell Nucleus. SH2 Domain binding has relations: molfunc_protein with JAK2 protein, human, molfunc_protein with JAK2 protein, human.", "label": "yes"}
{"original_question": "Are CTCF and BORIS involved in genome regulation and cancer?", "id": "converted_251", "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 Tumor 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.", "label": "yes"}
{"original_question": "Are Sidekick proteins members of the immunoglobulin superfamily?", "id": "converted_252", "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]", "label": "yes"}
{"original_question": "Have mutations in the ZEB2 gene been found in any human syndrome?", "id": "converted_253", "sentence1": "Have Gene Mutation in the ZEB2 Genes been found in any Homo sapiens 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) Genes Mowat-Wilson 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. owat-Wilson syndrome (Muckle-Wells Syndrome) is a genetic disease caused by heterozygous Gene Mutation or Gene Deletion of the ZEB2 Genes Muckle-Wells Syndrome is caused by de novo heterozygous Gene Mutation in the ZEB2 Genes The cause of Muckle-Wells Syndrome is a de novo Mutation Abnormality in the ZEB2 Genes owat-Wilson syndrome (Muckle-Wells Syndrome) is a genetic disease caused by heterozygous Gene Mutation or Gene Deletion of the ZEB2 Genes Muckle-Wells Syndrome have a heterozygous loss-of-function Mutation Abnormality in the zinc finger E-box protein 2 (ZEB2) Genes, also called SLC9A3R2 Genes (Zinc Finger E-box Binding Homeobox 2) and ZFHX1B,  Homo sapiens Mowat-Wilson syndrome, we suggest that Gene Deletion Abnormality of ZEB2, is responsible for most of the effects of the Mutation Abnormality Mutations at the hZeb2 locus cause Mowat-Wilson syndrome (Muckle-Wells Syndrome) Mowat-Wilson syndrome and a Mutation Abnormality in ZEB2 owat-Wilson syndrome (Muckle-Wells Syndrome) is caused by a heterozygous Mutation Abnormality or Gene Deletion Abnormality of the ZEB2 Genes The syndrome is caused by Gene Mutation or Gene Deletion of the ZEB2 Genes owat-Wilson syndrome (Muckle-Wells Syndrome) is an autosomal dominant intellectual disability syndrome single-copy ZEB2 Genes Gene Deletion Abnormality at 2q22.3 consistent with Mowat-Wilson syndrome Mowat-Wilson syndrome, confirmed by molecular analysis as a heterozygous Gene Deletion Abnormality of the ZEB2 Genes. Gene Deletion Abnormality encompassing ZEB2, the Genes responsible for the Mowat-Wilson syndrome  Six patients had Gene Deletion in the ZEB2 Genes ZEB2 Genes analysis for Mowat-Wilson syndrome Mowat-Wilson syndrome (Muckle-Wells Syndrome) like appearance was noted. The disease is caused by Mutation Abnormality or Gene Deletion Abnormality of ZEB2 Genes owat-Wilson syndrome (Muckle-Wells Syndrome; Online Mendelian Inheritance In Man #235730) is a genetic condition caused by heterozygous Gene Mutation or Gene Deletion of the ZEB2 Genes owat-Wilson syndrome (Muckle-Wells Syndrome) is an autosomal dominant developmental disorder with mental retardation and variable multiple Congenital Abnormality due to Gene Mutation of the ZEB2 (ZFHX1B)  Muckle-Wells Syndrome is caused by heterozygous Gene Mutation or Gene Deletion in the Zinc finger E-box-binding homeobox 2 Genes, ZEB2, previously called ZFHX1B (SLC9A3R2 Genes) owat-Wilson syndrome (Muckle-Wells Syndrome) is a multiple congenital anomaly-mental retardation complex caused by Gene Mutation in the Zinc Finger Homeobox 1 B Genes (ZFHX1B) the ZEB2 wt Allele, which is known to be involved in the Mowat-Wilson syndrom de novo heterozygous Gene Mutation or Gene Deletion of the ZEB2 wt Allele located at 2q22 owat-Wilson syndrome (Muckle-Wells Syndrome) is a recently delineated mental retardation (Mitral Valve Insufficiency)-multiple congenital anomaly syndrome FHX1B Gene Mutation in patients with Mowat-Wilson syndrome Mutations leading to haploinsufficiency of the ZEB2 wt Allele Mutation Abnormality in the ZEB2 wt Allele associated with an atypical Mowat-Wilson syndrome phenotype ZFHX1B Mutation Abnormality associated with a mild Mowat-Wilson syndrome Patients with zinc finger homeo box 1B (ZFHX1B) Gene Mutation or Gene Deletion develop multiple congenital anomalies including HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, known as Mowat-Wilson syndrome (Muckle-Wells Syndrome) Heterozygous Gene Mutation or Gene Deletion involving the Genes ZFHX1B (previously SLC9A3R2 Genes) [Online Mendelian Inheritance In Man 605802] have recently been found to cause Muckle-Wells Syndrome  ZFHX1B Gene Deletion, splice site or truncating Gene Mutation were detected in all 28 patients classified as typical Muckle-Wells Syndrome Mowat-Wilson syndrome with Gene Deletion Abnormality/Mutation Abnormality in the zinc finger homeo box 1B Genes (ZFHX1B)  Gene Mutation in the zinc finger homeo box 1B Genes, ZFHX1B (SLC9A3R2 Genes) ZEB2 wt Allele transcripts during Mus sp. and Homo sapiens development supports the various clinical manifestations of the \"Mowat-Wilson\" syndrome  ZFHX1B Gene Mutation 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 syndrome syndrome is the result of heterozygous Gene Deletion or truncating Gene Mutation of the ZFHX1B (SLC9A3R2 Genes) Genes humans with Zfhx1b Gene Mutation (Mowat-Wilson syndrome syndrome occurs as a result of heterozygous Gene Mutation or Gene Deletion in the zinc finger E-box-binding homeobox 2 Genes, ZEB2, previously called ZFHX1B (SLC9A3R2 Genes) owat-Wilson syndrome (Muckle-Wells Syndrome) is a recently delineated mental retardation; Mowat-Wilson syndrome is a congenital syndrome caused by a defect of the transcriptional repressor ZFHX1B (SLC9A3R2 Genes) Mowat-Wilson syndrome patients, and all siblings had the same E87X nonsense Mutation Abnormality in ZFHX1B[SEP]Relations: ZEB2 has relations: disease_protein with Mowat-Wilson syndrome, disease_protein with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_protein with Mowat-Wilson syndrome, disease_protein with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. hirschsprung disease, susceptibility to has relations: disease_disease with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_disease with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. Intellectual disability has relations: disease_phenotype_positive with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_phenotype_positive with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1.", "label": "yes"}
{"original_question": "Are the Fanconi anemia genes a part of the same signalling pathway?", "id": "converted_254", "sentence1": "Are the FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) Genes a part of the same signalling pathway?", "sentence2": "Mutations 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 Gene Mutation 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 Gene Mutation 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 Gene Mutation 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_disease with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_disease with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_disease with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_disease with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder).", "label": "yes"}
{"original_question": "Are there clinical trials using stem cells for the treatment of cardiac disease?", "id": "converted_255", "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 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 allergens trials have demonstrated the ability to improve cardiac function by transfer of Hematopoietic Scanning Transmission Electron Microscopy Procedures Cells into the Myocardium, and early Homo sapiens studies have demonstrated the feasibility and safety of this approach.[SEP]Relations: Chest>Heart disease has relations: disease_disease with Cardiomyopathies, disease_disease with Chest>Heart failure, disease_disease with Cardiovascular Diseases, disease_disease with Cardiomyopathies, disease_disease with Chest>Heart failure, disease_disease with Cardiovascular Diseases.", "label": "yes"}
{"original_question": "Is DNA methylation an epigenetic modification of chromatin related to gene expression?", "id": "converted_256", "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]", "label": "yes"}
{"original_question": "Is Growth factor independence 1b (GFI1B) important for hematopoiesis?", "id": "converted_257", "sentence1": "Is Growth factor independence 1b (GFI1B) important for Hematopoiesis?", "sentence2": "Growth Factor Independence (Gfi) TRANSCRIPTION FACTOR 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 protein, human GFI1 and GFI1B control the loss of Endothelium identity of hemogenic endothelium during hematopoietic commitment  Taken together, our findings demonstrate a critical and specific role of the GFI1 TRANSCRIPTION FACTOR 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 protein, human, a known repressor of erythroid differentiation This reversible modulation of Endothelium-haematopoietic state is accomplished by targeting key haematopoietic TRANSCRIPTION FACTOR for downregulation, including RUNX1 protein, human, GATA1 wt Allele, Gfi1B, IKZF1 Genes, and PU.1 Zinc Finger Protein GFI1 wt Allele, Human and GFI1B protein, human: key regulators of Hematopoiesis we review how Zinc Finger Protein GFI1 wt Allele, Human and its paralogue GFI1B protein, human control the development of Blood Cells, discuss how changes in Zinc Finger Protein GFI1 wt Allele, Human and GFI1B protein, human 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 Genes disruption of GFI1B in CASP14 Genes 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 FACTOR that play a critical role in Hematopoiesis (MECOM wt Allele and GFI1B protein, human loci) Transcription factors play essential roles in both normal and malignant Hematopoiesis. This is the case for the Growth Factor [APC] independent 1b (GFI1B) 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 locus. In GFI1B-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 Genes activation and bind multiple TRANSCRIPTION FACTOR and co-repressors Our findings indicate that GFI1B 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 GFI1 wt Allele and Gfi-1b are homologous transcriptional repressors involved in diverse developmental contexts, including Hematopoiesis and oncogenesis GFI1B protein, human:green fluorescent protein knock-in CASP14 Genes reveal a dynamic expression pattern of GFI1B protein, human during Hematopoiesis that is largely complementary to Zinc Finger Protein GFI1 wt Allele, Human We found highly dynamic expression patterns of GFI1B protein, human in Erythroid Cells, megakaryocytes, and their Stem cells (MEPS) where Zinc Finger Protein GFI1 wt Allele, Human is not detected. Vice versa, GFI1B protein, human 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 Zinc Finger Protein GFI1 wt Allele, Human is expressed, suggesting a complementary regulation of both loci during Hematopoiesis Zinc Finger Protein GFI1 wt Allele, Human and GFI1B protein, human act equivalently in haematopoiesis our findings show that an intact SNAG domain is essential for all functions of Zinc Finger Protein GFI1 wt Allele, Human and that GFI1B protein, human can replace Zinc Finger Protein GFI1 wt Allele, Human functionally in haematopoiesis GFI1 wt Allele oncoproteins in Hematopoiesis Recent Genes targeting experiments and mutational screening in Homo sapiens have revealed an essential role for GFI1 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 Megakaryocytes 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 Genes 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 Genes 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 Megakaryocytes development Growth factor independence 1b (GFI1B) 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 protein, human:green fluorescent protein knock-in CASP14 Genes reveal a dynamic expression pattern of GFI1B protein, human during Hematopoiesis that is largely complementary to Zinc Finger Protein GFI1 wt Allele, Human. Zinc Finger Protein GFI1 wt Allele, Human and GFI1B protein, human: key regulators of Hematopoiesis. We show that gfi1aa and gfi1b are expressed in the primitive and definitive sites of Hematopoiesis in Zebrafish. Targeted Genes disruption of GFI1B in CASP14 Genes 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. Growth factor-independence 1b (GFI1B protein, human) is a zinc finger transcription factor essential for erythroid and Megakaryocytic development. GFI1B protein, human (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) and of mixed-Lineage leukemia translocated to chromosome 3 protein (MLLT3 wt Allele wt Allele), which are crucial regulators of erythrocyte and Megakaryocytes 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) Genes 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 Genes conditionally deficient for the transcription Growth factor independence 1b (GFI1B protein, human) show a significant expansion of functional Hematopoietic stem cells in the bone marrow and blood. Growth factor-independence 1b (GFI1B protein, human) 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) Genes 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 Genes conditionally deficient for the transcription Growth factor independence 1b (GFI1B protein, human) show a significant expansion of functional Hematopoietic stem cells in the bone marrow and blood[SEP]", "label": "yes"}
{"original_question": "Has Revlimid been approved by the US Food and Drug Administration?", "id": "converted_258", "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]", "label": "yes"}
{"original_question": "Has single guide RNA been used on human cells?", "id": "converted_259", "sentence1": "Has single guide RNA been used on Human cells?", "sentence2": "We used a library containing 73,000 sgRNAs to generate knockout collections and performed screens in two human cell lines. Here we engineer this system to enable RNA-guided genome regulation in Human cells by tethering transcriptional activation domains either directly to a nuclease-null CRISPR-Associated Protein 9 or to an aptamer-modified single guide RNA (sgRNA). The type II CRISPR/Cas system from Streptococcus pyogenes and its simplified derivative, the Cas9/single guide RNA (sgRNA) system, have emerged as potent new tools for targeted gene knockout in Bacteria, Saccharomyces cerevisiae, Drosophila <Drosophila <fruit fly, genus>, genus>, Zebrafish and Human cells. Here we engineer this system to enable RNA-guided genome regulation in Human cells by tethering transcriptional activation domains either directly to a nuclease-null CRISPR-Associated Protein 9 or to an aptamer-modified single guide RNA (sgRNA).  Using synthetic single RNA guides, Cas9 can be reprogrammed to create specific double-stranded DNA breaks in the Genome of a variety of Organism, ranging from Human cells to Bacteria, and thus constitutes a powerful tool for genetic engineering.  Here we engineer this system to enable RNA-guided genome regulation in Human cells by tethering transcriptional activation domains either directly to a nuclease-null CRISPR-Associated Protein 9 or to an aptamer-modified single guide RNA (sgRNA).[SEP]", "label": "yes"}
{"original_question": "Is Fibroblast Growth Factor 23 a phosphaturic hormone?", "id": "converted_260", "sentence1": "Is Fibroblast Growth Factor 23 a phosphaturic hormone?", "sentence2": "PTH wt Allele wt Allele can induce skeletal synthesis of another potent phosphaturic hormone, FGF23 gene (FGF23),   Recombinant Fibroblast Growth Factor 1 23 (FGF23) is a phosphaturic hormone that has recently been identified as a CKD-related factor affecting CRS.   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. FGF23 gene (FGF23), a phosphaturic hormone and regulator of 1,25(OH)2 vitamin D3 (1,25VitD3).  fibroblast growth factor-23 (FGF23), a bone-derived phosphaturic hormone.  the phosphaturic hormone FGF23 gene (FGF23) 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) have come to the forefront in terms of directing new models explaining mineral metabolism serum levels of a phosphaturic hormone, FGF23 gene (Fgf23),[SEP]", "label": "yes"}
{"original_question": "Is amoxicillin used for treatment of malnutrition in children?", "id": "converted_261", "sentence1": "Is amoxicillin used for treatment of Malnutrition in children?", "sentence2": "Another RCT did not show superiority of ceftriaxone over amoxicilllin for these same outcomes, but adressed Systolic anterior movement of mitral valve children with and without complications (p\u200a=\u200a0.27). Another RCT showed no difference between amoxicillin and Trimethoprim-Sulfamethoxazole Combination efficacies for Pneumonia in underweight, but not Systolic anterior movement of mitral valve. Our meta-analysis of 12 pooled susceptibility-studies for all types of bacterial isolates, including 2767 stricly Systolic anterior movement of mitral valve children, favoured amoxicillin over Trimethoprim-Sulfamethoxazole Combination for susceptibility medians: 42% (IQR 27-55%) vs 22% (IQR 17-23%) and population-weighted-means 52.9% (range 23-57%) vs 35.4% (range 6.7-42%).  Susceptibility-studies favour amoxicillin over Trimethoprim-Sulfamethoxazole Combination.  Oral amoxicillin for 5\u00a0days was as effective as intramuscular ceftriaxone for 2\u00a0days (1 RCT). For uncomplicated Systolic anterior movement of mitral valve, amoxicillin showed no benefit over placebo (1 retrospective study).  Children who took amoxicillin and de-worming had 95% (plant-type hypersensitive response\u200a=\u200a1.95, 95%-NDUFB6 gene\u200a=\u200a1.17, 3.23) and 74% (plant-type hypersensitive response\u200a=\u200a1.74, 95%-NDUFB6 gene\u200a=\u200a1.07, 2.83) more probability to recover from Systolic anterior movement of mitral valve as compared to those who didn't take them. METHODS: In this randomized, double-blind, placebo-controlled trial, we randomly assigned Malawian children, 6 to 59 months of age, with severe acute Malnutrition to receive amoxicillin, cefdinir, or placebo for 7 days in addition to ready-to-use therapeutic food for the outpatient treatment of uncomplicated severe acute Malnutrition.  In the amoxicillin, cefdinir, and placebo groups, 88.7%, 90.9%, and 85.1% of the children recovered, respectively (relative risk of treatment failure with placebo vs. amoxicillin, 1.32; 95% confidence interval [NDUFB6 gene], 1.04 to 1.68; relative risk with placebo vs. cefdinir, 1.64; 95% NDUFB6 gene, 1.27 to 2.11). The mortality rates for the three groups were 4.8%, 4.1%, and 7.4%, respectively (relative risk of death with placebo vs. amoxicillin, 1.55; 95% NDUFB6 gene, 1.07 to 2.24; relative risk with placebo vs. cefdinir, 1.80; 95% NDUFB6 gene, 1.22 to 2.64). Evaluation of the routine use of amoxicillin as part of the home-based treatment of severe acute Malnutrition. OBJECTIVE: To determine whether the inclusion of amoxicillin correlates with better recovery rates in the home-based treatment of severe acute Malnutrition with ready-to-use therapeutic food. The standard protocol group received a 7-day course of amoxicillin at the onset of treatment. RESULTS: Four hundred and ninety-eight children were treated according to the standard protocol with amoxicillin, and 1955 were treated under the alternate protocol without Antifungal Antibiotics, Topical.  The recovery rate for children who received amoxicillin was worse at 4 weeks (40%vs. 71%) but similar after up to 12 weeks of therapy (84%vs. 86%), compared to the children treated without Antifungal Antibiotics, Topical. CONCLUSIONS: This review of two therapeutic feeding programmes suggests that children with severe acute Malnutrition who were treated without amoxicillin did not have an inferior rate of recovery. Treatment of severe Malnutrition with 2-day intramuscular ceftriaxone vs 5-day amoxicillin. To determine whether the inclusion of amoxicillin correlates with better recovery rates in the home-based treatment of severe acute Malnutrition with ready-to-use therapeutic food. Evaluation of the routine use of amoxicillin as part of the home-based treatment of severe acute Malnutrition OBJECTIVE: To determine whether the inclusion of amoxicillin correlates with better recovery rates in the home-based treatment of severe acute Malnutrition with ready-to-use therapeutic food. METHODS: This retrospective cohort study compared data from the treatment of two groups of children in Malawi aged 6-59 months with uncomplicated severe acute Malnutrition.  The recovery rate for children who received amoxicillin was worse at 4 weeks (40%vs. 71%) but similar after up to 12 weeks of therapy (84%vs. 86%), compared to the children treated without Antifungal Antibiotics, Topical. Regression modelling indicated that this difference at 4 weeks was most strongly associated with the receipt of amoxicillin. CONCLUSIONS: This review of two therapeutic feeding programmes suggests that children with severe acute Malnutrition who were treated without amoxicillin did not have an inferior rate of recovery.  CONCLUSIONS: This review of two therapeutic feeding programmes suggests that children with severe acute Malnutrition who were treated without amoxicillin did not have an inferior rate of recovery.[SEP]", "label": "yes"}
{"original_question": "Is it possible to purify pseudopodia to be used for proteomic analysis?", "id": "converted_262", "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 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: neuronal Cell body of neuron has relations: cellcomp_cellcomp with Cell body of neuron, cellcomp_cellcomp with Cell body of neuron.", "label": "yes"}
{"original_question": "Is  farnesoid X receptor (FXR) a nuclear receptor?", "id": "converted_263", "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 colon adenocarcinomas 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-\u03b2-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 (FXR\u03b1) 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]", "label": "yes"}
{"original_question": "Are DNA helicases involved in progeroid syndromes?", "id": "converted_264", "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-gene 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. WRN was originally identified as a gene responsible for Werner Syndrome (WS; \"Progeria of Adults\"). The WRN gene product has RecQ-type helicase domains in the central region of the Protein Info.[SEP]", "label": "yes"}
{"original_question": "Is there association of matrix metalloproteinases with behaviour of pituitary adenomas?", "id": "converted_265", "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 prolactin-secreting pituitary adenoma 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 Metalloproteinases-9).  We found no correlation of Matrix Metalloproteinases-9 expression and tumour invasion. 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 Metalloproteinases-9 expression did not differ between noninvasive Neoplasms and normal pituitary gland, or between different sized Prolactinoma. Matrix Metalloproteinases-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 Metalloproteinases-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 Metalloproteinases-9 (P = 0.01). Pituitary carcinoma were significantly more likely to be Matrix Metalloproteinases-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 Metalloproteinases-9 expression (P<0.05). In summary, we have shown the presence of Matrix Metalloproteinases-9 expression in some invasive and recurrent pituitary Adenoma, and in the majority of pituitary carcinoma. The mechanisms whereby Matrix Metalloproteinases-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 MMP1 protein, Homo sapiens, -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 Metalloproteinases-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 Metalloproteinases-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 Metalloproteinases-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 Metalloproteinases-9 have associations with invasiveness of pituitary Adenoma, they are lack of specificity.[SEP]", "label": "yes"}
{"original_question": "Is Vitamin D deficiency in pregnant women associated with gestational diabetes?", "id": "converted_266", "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 Gestational Diabetes. Accumulating evidence links vitamin D deficiency with abnormal glucose metabolism, and epidemiological studies have shown that women who develop Gestational Diabetes are more likely to be vitamin D deficient This review discusses the prevalence, risk factors, and outcomes of Gestational Diabetes 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 Gestational Diabetes 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 mellitus [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 mellitus, Association between vitamin D insufficiency and the risk for gestational diabetes mellitus 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 Gestational Diabetes. 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 Gestational Diabetes. 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 \u03b2-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 mellitus, 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 Gestational Diabetes. The aim of the study is evaluating the associations of FokI vitamin D receptor (VDR) Genetic Polymorphism with gestational diabetes mellitus (Gestational Diabetes), and its relations with postpartum metabolic syndrome. Our results indicate a meaningful association between FokI VDR genotypes and an increase risk of Gestational Diabetes 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 Gestational Diabetes 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 Gestational Diabetes. These results suggested that rates of vitamin D deficiency are higher among women with IGT/Gestational Diabetes, 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 mellitus 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 Gestational Diabetes 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 mellitus, 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: Cholecalciferol has relations: drug_drug with ergocalciferol, drug_drug with ergocalciferol. Ergocalciferol has relations: drug_drug with ergocalciferol, drug_drug with ergocalciferol. 25-Hydroxyvitamin D3 Measurement has relations: exposure_exposure with ergocalciferol, exposure_exposure with ergocalciferol.", "label": "yes"}
{"original_question": "Does Chromatin Immunoprecipitation (ChIP) show a bias for highly expressed loci?", "id": "converted_267", "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]", "label": "yes"}
{"original_question": "Is clathrin involved in E-cadherin endocytosis?", "id": "converted_268", "sentence1": "Is clathrin involved in CDH1 gene endocytosis?", "sentence2": "We demonstrated that MGAT2 gene induced a stabilizing effect on CDH1 gene at the Cellular Membrane by inducing a delay in the turnover rate of the Protein Info, contributing for the formation of stable and functional adherens-junctions, and further preventing clathrin-dependent CDH1 gene endocytosis. Conversely, GnT-V promotes the destabilization of CDH1 gene, leading to its mislocalization and unstable adherens-junctions with impairment of cell-cell adhesion. Here we show that CDH1 gene polarity is controlled by the polarized regulation of clathrin- and Dynamin GTPase-mediated endocytosis. We delineate a pathway that controls the initiation of CDH1 gene endocytosis through the regulation of AP2 and clathrin coat recruitment by CDH1 gene. Clathrin dependent endocytosis of CDH1 gene is regulated by the Arf6GAP isoform UNC45A wt Allele CDH1 gene is a central component of the adherens junction in Epithelial Cells and continuously undergoes endocytosis via Clathrin-Coated Vesicles and/or Caveolae depending on the cell type. Collectively, UNC45A wt Allele likely represents a key Arf6GAP in clathrin dependent endocytosis of CDH1 gene in Madin Darby Canine Kidney Cells. Consistent with these observations, we found that selective uncoupling of CTNND1 wt Allele from CDH1 gene by [AA000] INTRODUCTION of Amino Acid Substitution in the CTNND1 wt Allele-binding site increased the level of CDH1 gene endocytosis. The increased endocytosis was clathrin-dependent, because it was blocked by expression of a dominant-negative form of Dynamin GTPase or by hypertonic shock. We found that in this experimental system CDH1 gene entered a transferrin-negative compartment before transport to the early endosomal compartment, where it merged with classical clathrin-mediated uptake pathways.[SEP]", "label": "yes"}
{"original_question": "Does splicing occur co-transcriptionally?", "id": "converted_269", "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]", "label": "yes"}
{"original_question": "Are there clinical trials on stem cells in multiple sclerosis", "id": "converted_270", "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 human clinical trials Homo sapiens 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 human 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: Rheumatoid arthritis has relations: disease_phenotype_positive with Rheumatoid Arthritis, disease_phenotype_positive with Rheumatoid Arthritis.", "label": "yes"}
{"original_question": "Are piRNAs involved in gene silencing?", "id": "converted_271", "sentence1": "Are piRNAs involved in gene silencing?", "sentence2": "In Drosophila <basidiomycetes> <basidiomycetes> ovaries, the nuclear Piwi 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 Piwi complex (molecular entity) that functions downstream of Piwi 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. Piwi 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, PIWIL1 gene-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 Piwi-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 PIWIL1 gene 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 piwi-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 PIWIL1 gene 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 Piwi pathway to the Argonaute pathway in gene regulation PIWIL1 gene-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 Piwi-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 PIWIL1 gene 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 Piwi 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]", "label": "yes"}
{"original_question": "Can RG7112 inhibit MDM2?", "id": "converted_272", "sentence1": "Can RG7112 inhibit MDM2 protein, human?", "sentence2": "To assess the influence of the TP53 wt Allele regulatory pathway further, we studied the effect of RG7112, a small molecule MDM2 protein, human protein, Homo sapiens Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) that activates TP53 wt Allele by preventing its interaction with MDM2 protein, human protein, Homo sapiens, on normal megakaryocytopoiesis and platelet production. RG7112 (2g) is the first clinical small-molecule MDM2 protein, human protein, Homo sapiens Inhibitor designed to occupy the TP53 wt Allele-binding pocket of MDM2 protein, human protein, Homo sapiens. Effect of the MDM2 protein, human 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, human protein, Homo sapiens-amplified, well-differentiated or dedifferentiated liposarcoma: an exploratory proof-of-mechanism study. We report a proof-of-mechanism study of RG7112, a small-molecule MDM2 protein, human 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, human protein, Homo sapiens-amplified liposarcoma who were eligible for resection. To assess the influence of the TP53 wt Allele regulatory pathway further, we studied the effect of RG7112, a small molecule MDM2 protein, human protein, Homo sapiens Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) that activates TP53 wt Allele by preventing its interaction with MDM2 protein, human protein, Homo sapiens, on normal megakaryocytopoiesis and platelet production. Discovery of RG7112: A Small-Molecule MDM2 protein, human protein, Homo sapiens Inhibitor in Clinical Development. RG7112 was the first small-molecule TP53 wt Allele-MDM2 protein, human protein, Homo sapiens Inhibitor in clinical development. RG7112 binds MDM2 protein, human protein, Homo sapiens with high affinity (K(D) ~ 11 nmol/L), blocking its interactions with TP53 wt Allele in vitro. RG7112 is a selective inhibitor of TP53 wt Allele-MDM2 protein, human 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. The effects of RG7112 and Peg-IFN\u03b1 2a on Myeloproliferative disease progenitor cells were dependent on blocking TP53 wt Allele-MDM2 protein, human protein, Homo sapiens interactions and activating the TP53 wt Allele pathway, thereby increasing Myeloproliferative disease CD34(+) cell apoptosis The orally bioavailable MDM2 protein, human protein, Homo sapiens Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) RG7112 and pegylated interferon \u03b1 2a target JAK2V617F-positive progenitor and Stem cells Initial testing of the MDM2 protein, human protein, Homo sapiens Inhibitor RG7112 by the Pediatric Preclinical Testing Program In this issue of Blood, Lu et al describe the cooperation between an orally bioavailable Mus sp. double minute 2 (MDM2 protein, human protein, Homo sapiens) Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) (RG7112) and the pegylated interferon \u03b1 (Peg-IFN\u03b1 2a) to target JAK2V617F hematopoietic progenitors and Stem cells MDM2 protein, human 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. Activation of TP53 wt Allele by the MDM2 protein, human protein, Homo sapiens Inhibitor RG7112 impairs thrombopoiesis. The orally bioavailable MDM2 protein, human protein, Homo sapiens Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) RG7112 and pegylated interferon \u03b1 2a target JAK2V617F-positive progenitor and Stem cells. Initial testing of the MDM2 protein, human protein, Homo sapiens Inhibitor RG7112 by the Pediatric Preclinical Testing Program. The primary endpoint was to assess markers of RG7112-dependent MDM2 protein, human protein, Homo sapiens inhibition and P53 pathway activation (P53, oncoprotein p21, MDM2 protein, human protein, Homo sapiens, MKI67 gene, GDF15 protein, Homo sapiens [GDF15 wt Allele], and apoptosis).  RG7112 is a selective inhibitor of TP53 wt Allele-MDM2 protein, human 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. However, the hydrophobic protein-protein interaction surface represents a significant challenge for the development of small-molecule inhibitors with desirable pharmacological profiles. RG7112 was the first small-molecule TP53 wt Allele-MDM2 protein, human protein, Homo sapiens Inhibitor in clinical development. Treatment with low doses of RG7112, an orally available small-molecule inhibitor of TP53 wt Allele-MDM2 protein, human protein, Homo sapiens, both alone and combined with pegylated interferon \u03b1 2a (Peg-IFN\u03b1 2a), significantly decreased Myeloproliferative disease colony-forming unit-granulocyte macrophage and burst-forming unit-erythroid numbers and preferentially eliminated the total number of JAKV617F(+) Myeloproliferative disease Hematopoietic Stem cells. The effects of RG7112 and Peg-IFN\u03b1 2a on Myeloproliferative disease progenitor cells were dependent on blocking TP53 wt Allele-MDM2 protein, human protein, Homo sapiens interactions and activating the TP53 wt Allele pathway, thereby increasing Myeloproliferative disease CD34(+) cell apoptosis. RG7112 (2g) is the first clinical small-molecule MDM2 protein, human protein, Homo sapiens Inhibitor designed to occupy the TP53 wt Allele-binding pocket of MDM2 protein, human 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.[SEP]", "label": "yes"}
{"original_question": "Are there any specific antidotes for dabigatran?", "id": "converted_273", "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\u00ae), rivaroxaban (Xarelto\u00ae) and apixaban (Eliquis\u00ae), 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: hepatobiliary disease has relations: disease_disease with Hepatobiliary Disorder, disease_disease with Hepatobiliary Disorder. Rivaroxaban has relations: contraindication with Hepatobiliary Disorder, contraindication with Hepatobiliary Disorder. Warfarin has relations: contraindication with Cerebral Hemorrhage, contraindication with Hepatobiliary Disorder, contraindication with Cerebral Hemorrhage, contraindication with Hepatobiliary Disorder.", "label": "no"}
{"original_question": "Are there any Decision support systems for chronic pain management ?", "id": "converted_274", "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]", "label": "yes"}
{"original_question": "Does amiodarone affect thyroid hormone receptors in the myocardium?", "id": "converted_275", "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]", "label": "yes"}
{"original_question": "Does thyroid hormone affect cardiac remodeling?", "id": "converted_276", "sentence1": "Does Thyroid Hormones affect Cardiac - anatomy qualifier remodeling?", "sentence2": "The aim of this brief paper is to highlight new developments in understanding the cardioprotective role of Thyroid Hormones in reverting regulatory networks involved in adverse Cardiac - anatomy qualifier remodeling. Thyroid Hormone Receptor (TR\u03b11) is shown to be critical for the maturation of Myocytes, Cardiac and for the cellular response to stress. TR\u03b11 is altered during post ischemic Cardiac - anatomy qualifier remodeling but the physiological significance of this response is not fully understood.  Anterior Myocardial Infarction induces downregulation of Thyroid Hormones signaling and pharmacological inhibition of TR\u03b11 further depresses post-ischemic Cardiac - anatomy qualifier function. These findings reveal crucial roles for DIO3 gene in Chest>Heart function and remodeling, which may have pathophysiologic implications for Homo sapiens restrictive cardiomyopathy. Tyrosine 3-Monooxygenase, Homo sapiens administration after Anterior Myocardial Infarction prevented Tissue Specimen Code Hypothyroidism and resulted in decreased beta-MHC expression, increased wall thickening and normalized wallstress, while stretch-induced p38 MAPK activation was increased. We conclude that Diabetes Mellitus exacerbates post-ischemic Cardiac - anatomy qualifier remodeling and that Tissue Specimen Code Hypothyroidism may be involved in this response. Thyroid hormone can favorably remodel the diabetic myocardium after acute Myocardial Infarction. It has been previously shown that regulators of physiological growth such as Thyroid Hormones (Tyrosine 3-Monooxygenase, Homo sapiens) can favorably remodel the post ischaemic myocardium. Acute Myocardial Infarction in diabetic Rattus norvegicus results in Tyrosine 3-Monooxygenase, Homo sapiens receptor down-regulation with important physiological consequences. Tyrosine 3-Monooxygenase, Homo sapiens treatment prevents this response and improves Cardiac - anatomy qualifier hemodynamics. Tyrosine 3-Monooxygenase, Homo sapiens affects Cardiac - anatomy qualifier remodeling by limiting Reperfusion Injury, and, at later states, by inducing distinct changes in Cardiac - anatomy qualifier chamber geometry in a time-dependent manner. Furthermore, administration of Tyrosine 3-Monooxygenase, Homo sapiens can convert pathologic to physiologic hypertrophy. These effects are the result of favorable cellular remodeling. Thyroid hormone (Tyrosine 3-Monooxygenase, Homo sapiens) is critical in Cardiac - anatomy qualifier cell differentiation (regulating Contractile Proteins and cell geometry) and this effect could be potentially exploited therapeutically in reversing the process of de-differentiation which underlies postischemic Cardiac - anatomy qualifier remodeling.  Tyrosine 3-Monooxygenase, Homo sapiens treatment partially reverses Cardiac - anatomy qualifier dysfunction in Rattus norvegicus with old Myocardial Infarction by favorably changing Cardiac - anatomy qualifier chamber geometry and expression of myosin isoforms. Thyroid hormone, unlike current treatments, appears to be a paradigm of therapeutic intervention which aims at restoring Cardiac - anatomy qualifier geometry and may prove new effective treatment for Chest>Heart failure. Changes in Thyroid Hormones (Tyrosine 3-Monooxygenase, Homo sapiens)-Tyrosine 3-Monooxygenase, Homo sapiens receptors (threonine-tRNA ligase activity) axis occur in the course of post-Infarction Cardiac - anatomy qualifier remodeling and seem to contribute to Cardiac - anatomy qualifier fetal phenotype. Tyrosine 3-Monooxygenase, Homo sapiens can \"rebuild\" the post-infarcted Chest>Heart by preventing the fetal-like pattern of Contractile Proteins expression, normalizing wall tension, and optimizing Cardiac - anatomy qualifier chamber geometry.  Tyrosine 3-Monooxygenase, Homo sapiens, apart from its \"classical\" actions on Cardiac - anatomy qualifier contractility and Chest>Heart rhythm, appears to regulate various Protoplasm signaling pathways related to stress responses and Cardiac - anatomy qualifier remodelling. More importantly, experimental and clinical studies demonstrate that Tyrosine 3-Monooxygenase, Homo sapiens can limit ischaemic injury, attenuate Cardiac - anatomy qualifier remodeling and improve Cardiac - anatomy qualifier hemodynamics.  Thyroid hormone attenuates Cardiac - anatomy qualifier remodeling and improves hemodynamics early after acute Myocardial Infarction in Rattus norvegicus. Thyroid hormone administration early after Infarction attenuates Cardiac - anatomy qualifier remodeling and significantly improves Myocardial performance. It has previously been shown that Thyroid Hormones can reverse Cardiac - anatomy qualifier remodeling in failing hearts by reducing Myocardial wall stress due to the unique changes induced in Cardiac - anatomy qualifier myocyte shape.[SEP]Relations: tyrosine 3-monooxygenase activity has relations: molfunc_protein with Tyrosine 3-Monooxygenase, Homo sapiens, molfunc_protein with Tyrosine 3-Monooxygenase, Homo sapiens.", "label": "yes"}
{"original_question": "Are there any HCV replication inhibitors available?", "id": "converted_277", "sentence1": "Are there any HCV replication inhibitors available?", "sentence2": "We report here the discovery of the first small-molecule HCV infectivity inhibitor, GS-563253, also called HCV infectivity inhibitor 1 (HCV II-1).  Resistance to Mericitabine (Prodrugs of HCV NS5B polymerase inhibitor PSI 6130) is rare and conferred by the NS5B S282T Mutation Abnormality. We tested the ability of NA808 to inhibit SPT's enzymatic activity in FLR3-1 replicon cells The SPT inhibitor NA808 prevents replication of HCV genotypes 1a, 1b, 2a, 3a, and 4a in cultured hepatocytes and in CASP14 gene with humanized livers. Vaniprevir (phase III clinical trials) and MK 5172 (phase II clinical trials) are two potent antiviral compounds that target NS3/4A protease treatment for hepatitis C virus (HCV) infection has been significantly improved with the approval of the first two HCV NS3/4A protease inhibitors, telaprevir (incivek) and boceprevir (Victrelis).  Combination therapy with telaprevir and BMS-788329 (NS5A inhibitor) reduced serum HCV RNA to undetectable levels. The presence of an NS3-V36A telaprevir resistance Mutation Abnormality resulted in poor response to telaprevir monotherapy but showed significant HCV reduction when telaprevir was combined with BMS-788329. However, a BMS-788329-resistant strain emerged at low frequency. Communicable Diseases with a BMS-788329-resistant NS5A-L31V Mutation Abnormality rapidly resulted in gain of an additional NS5A-Y93A Mutation Abnormality that conferred telaprevir resistance during combination therapy HCV NS5A replication complex inhibitors, exemplified by Daclatasvir (BMS-790052), represent a new class of DAA ACH-806 (or GS-9132) is a novel, small-molecule inhibitor specific for hepatitis C virus (HCV).  Telaprevir and boceprevir are the first two Retroviral Retroviral protease inhibitor (Pulmonary Valve Insufficiency) DAAs to be approved for combination therapy with PEG-IFN-SA (PEG-IFN) and ribavirin (RBV).  symmetrical bidentate structure of the NS5A inhibitor BMS-790052, a series of new monodentate molecules were designed In vitro, boceprevir is more active than telaprevir against the HCV G3 NS3/4A enzyme in cell-based and biochemical assays and against G3 isolates in replicon assays Alisporivir is the most advanced host-targeting antiviral in clinical development. Alisporivir blocks HCV replication by neutralizing the peptidyl-prolyl isomerase activity of the abundant host cytosolic protein, Peptidyl-Prolyl Cis-Trans Isomerase A, human Interestingly, the NS5A inhibitor daclatasvir (BMS-790052) caused a decrease in serum HCV RNA levels by about two orders of magnitude within 6 h of administration[SEP]", "label": "yes"}
{"original_question": "Is miR-21 related to carcinogenesis?", "id": "converted_278", "sentence1": "Is MLXIP gene-21 related to carcinogenesis?", "sentence2": "MLXIP gene-21* and MLXIP gene-203 were significantly dysregulated (P < 0.05) in PTC Body tissue with BRAFV600E. Expressions of MicroRNAs in Papillary thyroid carcinoma and their associations with the BRAFV600E mutation. Levels of miRNA-21 (MLXIP gene-21) 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) MLXIP gene-21 and MLXIP gene-106a compared with patients who had benign gastric diseases (both P < .001). MLXIP gene-21 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 MLXIP gene-21 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 MLXIP gene-21 over-expression extended to the distant non-neoplastic mucosa (p<0.001). Here we hypothesize that over-expression of MLXIP gene-155 and MLXIP gene-21, two inflammation-related MicroRNAs that target core Mismatch Repair Proteins, may constitute a pre-neoplastic event for the development of MSI Irritable Bowel Syndrome-CRCs. After administration, we determined the expressions of MLXIP gene-21, 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 (Nf\u03bab1), 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 MLXIP gene-21. Consistently with Programmed Cell Death Protein 4 downregulation, MLXIP gene-21 was upregulated in neoplastic by comparison with nonneoplastic tissue samples. Expression of MLXIP gene-21 (p=0.027), MicroRNA 181b (p=0.002), and MLXIP gene-146b (p=0.021) in Tumor tissue sample and MLXIP gene-21 (p=0.003) in noncancerous tissue were associated with patients' overall survival. We analyzed the expression of nine MicroRNAs (MLXIP gene-21, 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 MicroRNAs (the increase being 4.2-fold for MLXIP gene-21, 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 MicroRNAs 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, MLXIP gene-21 and MLXIP gene-155. Results: Medullary carcinoma of thyroid and CCH were both characterized by a significant overexpression of the whole set of MicroRNAs (the increase being 4.2-fold for MLXIP gene-21, 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-MicroRNAs MLXIP gene-21 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. MLXIP gene-21, MLXIP gene-106a and MLXIP gene-17), tumor suppressor MLXIP gene (e.g. MLXIP gene-101, MLXIP gene-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 MLXIP gene-21 were differentially expressed in Cerebrospinal Fluid samples from patients with gliomas, 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 MLXIP gene-21 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 MicroRNAs were related to various Malignant Neoplasms (e.g., MLXIP gene-125b, Liver carcinoma; MLXIP gene-21, leukemia; MLXIP gene-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 MicroRNAs (e.g., MLXIP gene-34a, MLXIP gene-21) 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 MLXIP gene-21 and MLXIP gene-206, the expression levels of all MicroRNAs significantly changed during the progression of CaP. In addition, diet and carcinogen exposure modulated a number of microRNAs (MLXIP gene-16, MLXIP gene-19b, MLXIP gene-21, miR26b, miR27b, MLXIP gene-93, and MLXIP gene-203) linked to canonical oncogenic signaling pathways. RESULTS: Elevated MLXIP gene-21 (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-\u03baB targets MLXIP gene-16 and MLXIP gene-21 in Malignant neoplasm of Abdomen>Stomach: involvement of Prostaglandin E Receptor. Expression of MLXIP gene-21, 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 MicroRNAs have previously been identified as being overexpressed in MCF-7 Breast cancer Cells, with MLXIP gene-21 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 MicroRNAs, MLXIP gene-21 was the only one that increased 6 folds in high-LET IR-promoted Mus sp. Abdomen>Liver Neoplasms when compared with that in the non-irradiated Abdomen>Liver Body tissue. We also showed that MLXIP gene-21 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 MLXIP gene-21, these Cells became tumorigenesis in nude CASP14 gene. METHODS: We used this combined ISH/IHC assay to study a subset of cancer-associated MicroRNAs, including MicroRNAs frequently detected at low (MLXIP gene-34a and MLXIP gene-126) and high (MLXIP gene-21 and MLXIP gene-155) levels, in a panel of Breast, colorectal, Chest>Lung, Abdomen>Pancreas, and Pelvis>Prostate Carcinoma. The MLXIP gene-15a, MLXIP gene-16, MLXIP gene-143, MLXIP gene-155, and MLXIP gene-21 were upregulated in M059K, and the modulation of these MicroRNAs fluctuated in M059J Cells in a time-dependent manner. Aberrantly increased expression of MLXIP gene-21 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 MLXIP gene-21 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, MLXIP gene-21, MLXIP gene-223, 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 MLXIP gene-21 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. MLXIP gene-21, 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 Chest>Lung Neoplasms relative to normal Lung. In CASP14 gene treated with VC and given indole-3-carbinol in the diet, levels of MLXIP gene-21, 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 MLXIP gene-21 indicated that phosphatase and tensin homolog, programmed cell death 4 and rich protein with Kazal Motifs are potential targets for the oncogenic effect of MLXIP gene-21 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 Abdomen+Pelvis>Colon cancer in addition to previously examined MLXIP gene-21 expression. CONCLUSIONS: IRS and MLXIP gene-21 expression are independent predictors of Abdomen+Pelvis>Colon cancer prognosis and may provide a clinically useful tool to identify high-risk patients. The most highly expressed MicroRNAs in Malignant neoplasm of Abdomen>Stomach Body tissue were MLXIP gene-20b, MLXIP gene-20a, MLXIP gene-17, MLXIP gene-106a, MLXIP gene-18a, MLXIP gene-21, 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 MicroRNAs 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, MLXIP gene-21 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 MLXIP gene-21, a candidate oncogenic miRNA). RESULTS: Several microRNAs were differentially expressed in Ovarian Serous Adenocarcinoma compared with normal ovarian Body tissue, including MLXIP gene-21, MLXIP gene-125a, MLXIP gene-125b, MLXIP gene-100, MLXIP gene-145, MLXIP gene-16, and MLXIP gene-99a, which were each differentially expressed in >16 patients. Selected for validation were MLXIP gene-20a, MLXIP gene-21, MLXIP gene-106a, MicroRNA 181b, and MLXIP gene-203, and all 5 were enriched in Neoplasms from the validation cohort (P < .001). Higher MLXIP gene-21 expression was present in Adenoma (P = .006) and in Neoplasms with more advanced TNM staging (P < .001). In situ hybridization demonstrated MLXIP gene-21 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, MicroRNA 16, and MIR21 gene) and also used in silico methods to test pharmacologic microRNA effects more broadly. Changing the cellular levels of let-7i, MicroRNA 16, and MIR21 gene affected the potencies of a number of the anticancer agents by up to 4-fold. The effect was most prominent with MIR21 gene, with 10 of 28 cell-compound pairs showing significant shifts in growth-inhibitory activity. Varying MIR21 gene 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 MIR21 gene, show highly significant correlations with numerous anticancer agents. Conversely, expression of other MicroRNAs was detected at varying levels predominantly within luminal epithelial Cells in normal tissue; expression of MLXIP gene-21 was frequently increased, whereas that of let-7a was decreased in Tumor Cells, malignant. We describe a novel EMT-specific microRNA signature that includes induction of MLXIP gene-21, a candidate oncogenic microRNA associated with carcinogenesis. Notable was the high expression of MLXIP gene-21 and MLXIP gene-205. Recently, microRNAs (MicroRNAs) have emerged as key actors in carcinogenesis and we demonstrated that microRNA-21 (MLXIP gene-21), oncomiR is expressed early during Posterior interventricular branch of right coronary artery. These results indicated that MLXIP gene-21 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 MLXIP gene-21 overexpression extended to the distant non-neoplastic mucosa (P < 0.001). Ectopic overexpression of MLXIP gene-21 promoted Proto-Oncogene Proteins c-akt activation and phosphorylation of EZH2 protein, human protein, Homo sapiens, whereas inhibiting MLXIP gene-21 by transfecting the Cells with anti-MLXIP gene-21 inhibited Proto-Oncogene Proteins c-akt activation and EZH2 protein, human protein, Homo sapiens phosphorylation. Programmed Cell Death Protein 4 nuclear down-regulation (which parallels MLXIP gene-21 up-regulation) is involved in the molecular pathway of Irritable Bowel Syndrome-associated carcinogenesis. The expression levels of MLXIP gene-21 (p = 0.027), MicroRNA 181b (p = 0.002) and MLXIP gene-146b (p = 0.021) in Tumor tissue sample and MLXIP gene-21 (p = 0.003) in noncancerous tissue were associated with overall survival of patients. OBJECTIVE: As an important oncogenic miRNA, MLXIP gene-21 has been reported to play crucial roles in Glioblastoma Multiforme (Glomerular Basement Membrane) carcinogenesis. We further analyzed the expression of microRNA-21 (MLXIP gene-21), an oncogenic noncoding RNA involved in oncogenic ras Oncogene signaling, by quantitative reverse-transcription polymerase chain reaction and in situ hybridization. MicroRNA-21 (MLXIP gene-21) plays crucial roles in carcinogenesis and is considered as one of the most studied oncomiRNAs. Although microRNA-21 (MLXIP gene-21) 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 (MLXIP gene-21) is a key oncomiR in carcinogenesis and is significantly elevated in Multiple Myeloma (Millimole per Liter). MicroRNA 21 (MLXIP gene-21) has been implicated in various aspects of carcinogenesis. Conversely, pAkt and MLXIP gene-21 expression was significantly up-regulated in the whole spectrum of preneoplastic/neoplastic lesions considered. Several MicroRNAs (e.g., MLXIP gene-34a, MLXIP gene-21) 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 MLXIP gene-21 and MLXIP gene-206, the expression levels of all MicroRNAs significantly changed during the progression of CaP. MicroRNA 21 (MLXIP gene-21) is overexpressed in virtually all types of Carcinoma and various types of Hematologic Neoplasms. As expected, MLXIP gene-21 expression was significantly upregulated in preneoplastic/neoplastic samples, consistent with Programmed Cell Death Protein 4 downregulation. Furthermore, MLXIP gene-21 levels in the primary tumours correlated with Disease stage:Find:Pt:^Patient:Ord (P\u2009<\u20090.0001). We found that MLXIP gene-16 and MLXIP gene-21 were upregulated upon nicotine stimulation, transfection with anti-MLXIP gene-16 or anti-MLXIP gene-21 significantly abrogated cell proliferation. MicroRNA-21 (MLXIP gene-21) is a unique miRNA in that it is overexpressed in most tumour types analysed so far. Although altered expressions of MLXIP gene-21 and MLXIP gene-34a were manifested within cancer Cells, those of MLXIP gene-126 and MLXIP gene-155 were predominantly confined to Endothelial Cells and immune Cells, respectively. However, the function of MLXIP gene-21 in Osteosarcoma of bone is still unclear. In sodium copper chlorophyllin patients, we found elevated MLXIP gene-21 and reduced MLXIP gene-375 expression levels in cancerous compared with noncancerous tissue. MLXIP gene-21, 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 Chest>Lung Neoplasms relative to normal Lung. Precancerous Adenoma also frequently showed MLXIP gene-21 up-regulation. Higher MLXIP gene-21 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 MLXIP gene-21 as the top-up-regulated species. Several MicroRNAs have been recently reported to be involved in modulation of Glioma development, especially some upregulated MicroRNAs, such as microRNA-21 (MLXIP gene-21), which has been found to function as an Oncogenes in cultured Glioblastoma Multiforme multiforme Cells. OBJECTIVE: MicroRNA-21 (MLXIP gene-21) is one of the MicroRNAs 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\u201121) induced upregulation of Protein Sprouty Homolog 2             and PTEN protein, human protein, Homo sapiens which underscores the importance of MIR21 gene in Protein Sprouty Homolog 2-associated tumorigenesis             of the Abdomen+Pelvis>Colon. The microRNA MLXIP gene-21, a known oncogenic miRNA, was found to be upregulated in Papillary and clear cell Carcinoma. Since microRNA-21 (MLXIP gene-21) may contribute to tumorigenesis and chemoresistance in many cancer types, we aimed to investigate its efficacy in TCCs. Several MicroRNAs have been recently reported to be involved in modulation of Glioma development, especially some up-regulated MicroRNAs, such as microRNA-21 (MLXIP gene-21), 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 MicroRNAs (MLXIP gene-21 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 (MLXIP gene-21) 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 (MLXIP gene-21 and MIR221 wt Allele) to the malignant phenotype was determined by inhibiting these MicroRNAs using Antisense Oligonucleotides. The microRNA-21(MLXIP gene-21) 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 MLXIP gene-21 (ASO-21) and/or MLXIP gene-155 (ASO-155) in NK-cell lymphoma lines overexpressing one or both of these MicroRNAs. In this study, microRNA (miRNA) expression profiling of 28 cases of never-smoker Primary malignant neoplasm of Chest>Lung identified aberrantly expressed MicroRNAs, which were much fewer than in Chest>Lung Malignant Neoplasms of smokers and included MicroRNAs previously identified (e.g., up-regulated MLXIP gene-21) and unidentified (e.g., down-regulated MLXIP gene-138) in those smoker cases. The oncogenic miRNA, microRNA-21 (MLXIP gene-21), was found to be upregulated in Carcinoma of larynx Body tissue. OBJECTIVE: To better understand microRNA MLXIP gene-21 function in carcinogenesis, we analyzed MLXIP gene-21 expression patterns in different stages of Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum development using in situ hybridization (ISH). Of these MicroRNAs, MLXIP gene-21 appears to be important in tumorigenesis given its up-regulation in almost all types of Homo sapiens cancer examined. The microRNA-21 gene (MIR21 gene) 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 MLXIP gene-21 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 MicroRNAs, a panel of 91 cancer-derived cell lines was analyzed for sequence variations in 15 MicroRNAs 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, MLXIP gene-145, MLXIP gene-26a-1, and MLXIP gene-21).[SEP]Relations: NDRG2 gene has relations: disease_protein with Malignant neoplasm of colon and/or rectum, disease_protein with Malignant neoplasm of colon and/or rectum. malignant germ cell tumor of cervix uteri has relations: disease_disease with Malignant tumor of cervix, disease_disease with Malignant tumor of cervix. Chest>Lung has relations: anatomy_protein_present with EZH2 protein, human, anatomy_protein_present with TGM2 protein, human, anatomy_protein_present with NDRG2 gene, anatomy_protein_present with PTEN protein, human, anatomy_protein_present with plant-type hypersensitive response, anatomy_protein_present with Programmed Cell Death Protein 4, anatomy_protein_present with EZH2 protein, human, anatomy_protein_present with TGM2 protein, human, anatomy_protein_present with NDRG2 gene, anatomy_protein_present with PTEN protein, human, anatomy_protein_present with plant-type hypersensitive response, anatomy_protein_present with Programmed Cell Death Protein 4. carcinoma has relations: disease_disease with Carcinoma of larynx, disease_protein with PTEN protein, human, disease_disease with Malignant adenomatous neoplasm, disease_disease with Carcinoma of larynx, disease_protein with PTEN protein, human, disease_disease with Malignant adenomatous neoplasm. Chest>Lung neoplasm has relations: disease_disease with Primary malignant neoplasm of Chest>Lung, disease_protein with PTEN protein, human, disease_protein with Programmed Cell Death Protein 4, disease_disease with Primary malignant neoplasm of Chest>Lung, disease_protein with PTEN protein, human, disease_protein with Programmed Cell Death Protein 4. bone Osteosarcoma of bone has relations: disease_disease with Osteosarcoma of bone, disease_protein with EZH2 protein, human, disease_disease with Osteosarcoma of bone, disease_protein with EZH2 protein, human. MIR122 has relations: disease_protein with Liver carcinoma, disease_protein with Liver carcinoma. malignant Abdomen+Pelvis>Colon neoplasm has relations: disease_protein with NDRG2 gene, disease_disease with Malignant neoplasm of colon and/or rectum, disease_protein with NDRG2 gene, disease_disease with Malignant neoplasm of colon and/or rectum. adenoma has relations: disease_disease with Liver carcinoma, disease_disease with Liver carcinoma. Abdomen>Liver neoplasm has relations: disease_disease with Liver carcinoma, disease_disease with Liver carcinoma.", "label": "yes"}
{"original_question": "Are thyroid hormone receptor alpha1 mutations  implicated in thyroid hormone resistance syndrome?", "id": "converted_279", "sentence1": "Are Thyroid Hormones receptor alpha1 mutations  implicated in Thyroid Hormones resistance syndrome?", "sentence2": "Gene Mutation in Homo sapiens TR\u03b11 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]", "label": "yes"}
{"original_question": "Is PLK2 involved in alpha-synuclein phosphorylation in Parkinson disease?", "id": "converted_280", "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.  \u03b1-Synuclein increased PLK2 gene gene levels and GSK-3\u03b2 activity and increased the levels of phosphorylated \u03b1-Synuclein and Tau 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: No Lewy bodies has relations: disease_phenotype_positive with PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE, disease_phenotype_positive with PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE. 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_phenotype_negative with No Lewy bodies, disease_disease with PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE, disease_phenotype_negative with No Lewy bodies, disease_disease with PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE.", "label": "yes"}
{"original_question": "Is there evidence for somatic mosaicism in Tuberous Sclerosis?", "id": "converted_281", "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 2 (disorder) confirmed by molecular genetic analysis This is the first case of germline mosaicism in TUBEROUS SCLEROSIS 2 (disorder) proven by molecular genetic analysis and also the first example of female germline mosaicism for a characterized Autosome dominant gene Mutation Abnormality apparently not associated with somatic mosaicism. Mutation screening by RT-PCR and direct sequencing of the TSC2 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 TSC2 alleles present in the affected subjects showed that the Mutation Abnormality had been inherited from the mother.[SEP]", "label": "yes"}
{"original_question": "Does smoking increase risk for glioblastoma?", "id": "converted_282", "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: GSTP1 gene has relations: disease_protein with Glioma, disease_protein with Glioma. GSTM3 gene has relations: protein_protein with GSTM1 protein, human, protein_protein with GSTM1 protein, human. NAD(P)H dehydrogenase (quinone) activity has relations: molfunc_protein with NAD(P)H dehydrogenase (quinone) 1, human, molfunc_protein with NAD(P)H dehydrogenase (quinone) 1, human.", "label": "no"}
{"original_question": "Is Wnt16b secreted in response to chemotherapy?", "id": "converted_283", "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": "Do DNA double-strand breaks play a causal role in carcinogenesis?", "id": "converted_284", "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 Cells (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 Homo sapiens 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 cancer Cells, 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 TP53 gene 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]", "label": "yes"}
{"original_question": "Do conserved noncoding elements co-occur with matrix-attachment regions?", "id": "converted_285", "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 MDFAttributeType - 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]", "label": "yes"}
{"original_question": "Are Drosophila ultraconserved elements candidate ncRNAs?", "id": "converted_286", "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 \u226580 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": "Does surgery for ovarian endometriomas improve fertility?", "id": "converted_287", "sentence1": "Does surgery for ovarian endometriomas improve fertility?", "sentence2": "CONCLUSION: Endometrioma 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 ovarian Chocolate cyst of ovary 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]", "label": "yes"}
{"original_question": "Are ACTA1 (alpha actin) and NEB (nebulin) genes related to nemaline myopathy?", "id": "converted_288", "sentence1": "Are ACTA1 Genes (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 Specimen Source Codes - Skeletal Muscle Tissue fibers. To date, ACTA1 Genes Genes, mitotic nuclear membrane disassembly, TPM3 protein, human protein, human, TPM2 Genes Genes, TNNT1 gene Genes, and CFL2 Genes Genes have been found to cause Nuclear medicine procedure. Nemaline myopathy (Nuclear medicine procedure) is the most common congenital myopathy and is caused by Gene Mutation in various genes including mitotic nuclear membrane disassembly (nebulin), TPM2 Genes Genes (beta-Tropomyosin), TPM3 protein, human protein, human (gamma-Tropomyosin), and ACTA1 Genes Genes (skeletal alpha-Actin). 20-25% of Nuclear medicine procedure cases carry ACTA1 Genes Genes defects and these particular Gene Mutation 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. Mutations in six genes have been reported to cause Nuclear medicine procedure: Nebulin (mitotic nuclear membrane disassembly Pelin 1999), alpha-Specimen Source Codes - Skeletal Muscle Tissue actin (ACTA1 Genes Genes Nowak 1999), alpha-slow tropomyosin (TPM3 protein, human protein, human Laing 1995), beta-Tropomyosin (TPM2 Genes Genes Donner 2002), slow Troponin T Assay (TNNT1 gene Genes Johnston 2000) and Cofilin 2 (CFL2 Genes Genes Agrawal 2007). The majority of cases are due to Mutation Abnormality in mitotic nuclear membrane disassembly and ACTA1 Genes Genes.  Nemaline myopathy is a heterogenous form of congenital myopathy characterised by a variable spectrum of clinical features, predominated in the severe form by profound Muscle Tissue 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: Specimen Source Codes - Skeletal Muscle Tissue actin (ACTA1 Genes Genes), 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 Specimen Source Codes - Skeletal Muscle Tissue.  Most Actin-Accumulation Myopathy patients have Gene Mutation in the nebulin (mitotic nuclear membrane disassembly) or Specimen Source Codes - Skeletal Muscle Tissue alpha-Actin (ACTA1 Genes Genes) 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) Genes showed a consistent pattern of selective Muscle Tissue involvement corresponding to clinical severity. Patients with Actin-Accumulation Myopathy secondary to Gene Mutation in the Specimen Source Codes - Skeletal Muscle Tissue alpha-Actin (ACTA1 Genes Genes) Genes 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 Specimen Source Codes - 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 Genes Genes), alpha- and beta-Tropomyosin (TPM3 protein, human protein, human and TPM2 Genes Genes), Troponin T Assay (TNNT1 gene Genes), and nebulin (mitotic nuclear membrane disassembly).  Nemaline myopathy is a structural congenital myopathy which may show both Autosomal dominant multiple pterygium syndrome and autosomal recessive inheritance patterns. Mutations in three different genes have been identified as the cause of Actin-Accumulation Myopathy: the Genes for slow Tropomyosin Alpha-1 Chain, human 3 (TPM3 protein, human protein, human) at 1q22-23, the nebulin Genes (mitotic nuclear membrane disassembly) at 2q21.1-q22, and the actin Genes (ACTA1 Genes Genes) 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 Specimen Source Codes - Skeletal Muscle Tissue alpha-Actin (ACTA1 Genes Genes) on Chromosomes, Human, Pair 1 1q42.  Nemaline myopathy (Nuclear medicine procedure) is the most common congenital myopathy and is caused by Gene Mutation in various genes including mitotic nuclear membrane disassembly (nebulin), TPM2 Genes Genes (beta-Tropomyosin), TPM3 protein, human protein, human (gamma-Tropomyosin), and ACTA1 Genes Genes (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 Specimen Source Codes - Skeletal Muscle Tissue alpha-Actin (ACTA1 Genes Genes) 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 Genes Genes), nebulin (mitotic nuclear membrane disassembly), beta-tropomysin (TPM2 Genes Genes) and Troponin T Assay (TNNT1 gene Genes). Most Actin-Accumulation Myopathy patients have Gene Mutation in the nebulin (mitotic nuclear membrane disassembly) or Specimen Source Codes - Skeletal Muscle Tissue alpha-Actin (ACTA1 Genes Genes) genes. Severe forms of Actin-Accumulation Myopathy may be caused by Mutation Abnormality of a number of different genes: Specimen Source Codes - Skeletal Muscle Tissue actin (ACTA1 Genes Genes), 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 Specimen Source Codes - 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 Genes Genes), nebulin (mitotic nuclear membrane disassembly), beta-tropomysin (TPM2 Genes Genes) and Troponin T Assay (TNNT1 gene Genes). 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 Specimen Source Codes - Skeletal Muscle Tissue alpha-Actin (ACTA1 Genes Genes) on Chromosomes, Human, Pair 1 1q42. Mutations in three different genes have been identified as the cause of Actin-Accumulation Myopathy: the Genes for slow Tropomyosin Alpha-1 Chain, human 3 (TPM3 protein, human protein, human) at 1q22-23, the nebulin Genes (mitotic nuclear membrane disassembly) at 2q21.1-q22, and the actin Genes (ACTA1 Genes Genes) at 1q42. Most Actin-Accumulation Myopathy patients have Gene Mutation in the nebulin (mitotic nuclear membrane disassembly) or Specimen Source Codes - Skeletal Muscle Tissue alpha-Actin (ACTA1 Genes Genes) 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 Genes Genes), nebulin (mitotic nuclear membrane disassembly), beta-tropomysin (TPM2 Genes Genes) and Troponin T Assay (TNNT1 gene Genes) 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 Specimen Source Codes - Skeletal Muscle Tissue alpha-Actin (ACTA1 Genes Genes) on Chromosomes, Human, Pair 1 1q42 Nemaline myopathy (Nuclear medicine procedure) is the most common congenital myopathy and is caused by Gene Mutation in various genes including mitotic nuclear membrane disassembly (nebulin), TPM2 Genes Genes (beta-Tropomyosin), TPM3 protein, human protein, human (gamma-Tropomyosin), and ACTA1 Genes Genes (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 Genes Genes), nebulin (mitotic nuclear membrane disassembly), beta-tropomysin (TPM2 Genes Genes) and Troponin T Assay (TNNT1 gene Genes) Nemaline myopathy (Nuclear medicine procedure) is the most common congenital myopathy and is caused by Gene Mutation in various genes including mitotic nuclear membrane disassembly (nebulin), TPM2 Genes Genes (beta-Tropomyosin), TPM3 protein, human protein, human (gamma-Tropomyosin), and ACTA1 Genes Genes (skeletal alpha-Actin) Mutations in three different genes have been identified as the cause of Actin-Accumulation Myopathy: the Genes for slow Tropomyosin Alpha-1 Chain, human 3 (TPM3 protein, human protein, human) at 1q22-23, the nebulin Genes (mitotic nuclear membrane disassembly) at 2q21.1-q22, and the actin Genes (ACTA1 Genes Genes) 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 Specimen Source Codes - Skeletal Muscle Tissue alpha-Actin (ACTA1 Genes Genes) on Chromosomes, Human, Pair 1 1q42 Most Actin-Accumulation Myopathy patients have Gene Mutation in the nebulin (mitotic nuclear membrane disassembly) or Specimen Source Codes - Skeletal Muscle Tissue alpha-Actin (ACTA1 Genes Genes) genes Severe forms of Actin-Accumulation Myopathy may be caused by Mutation Abnormality of a number of different genes: Specimen Source Codes - Skeletal Muscle Tissue actin (ACTA1 Genes Genes), 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 Specimen Source Codes - Skeletal Muscle Tissue[SEP]Relations: Respiratory insufficiency has relations: disease_phenotype_positive with Actin-Accumulation Myopathy, disease_phenotype_positive with Actin-Accumulation Myopathy. alpha-actinopathy has relations: disease_disease with Actin-Accumulation Myopathy, disease_disease with Actin-Accumulation Myopathy. Muscle Tissue tissue has relations: anatomy_protein_present with mitotic nuclear membrane disassembly, anatomy_protein_present with TPM3 protein, human, anatomy_protein_present with TNNT1 gene, anatomy_protein_present with mitotic nuclear membrane disassembly, anatomy_protein_present with TPM3 protein, human, anatomy_protein_present with TNNT1 gene. TNNT1 gene has relations: disease_protein with Actin-Accumulation Myopathy, protein_protein with TPM3 protein, human, disease_protein with Actin-Accumulation Myopathy, protein_protein with TPM3 protein, human. Myopathy has relations: disease_phenotype_positive with Actin-Accumulation Myopathy, disease_phenotype_positive with Actin-Accumulation Myopathy. congenital myopathy has relations: disease_protein with TPM3 protein, human, disease_disease with Actin-Accumulation Myopathy, disease_protein with TPM3 protein, human, disease_disease with Actin-Accumulation Myopathy. Actin-Accumulation Myopathy has relations: disease_protein with mitotic nuclear membrane disassembly, disease_protein with TPM3 protein, human, disease_protein with TNNT1 gene, disease_protein with mitotic nuclear membrane disassembly, disease_protein with TPM3 protein, human, disease_protein with TNNT1 gene.", "label": "yes"}
{"original_question": "Could RG7112 be used as cancer therapy?", "id": "converted_289", "sentence1": "Could RG7112 be used as Primary malignant neoplasm therapy?", "sentence2": "RG7112 is a potent and selective member of the nutlin family of MDM2 protein, human 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 Neoplasm 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 Primary malignant neoplasm patients. MDM2 protein, human 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 Primary malignant neoplasm 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 Primary malignant neoplasm patients. RG7112 is a selective inhibitor of TP53 wt Allele-MDM2 protein, human protein, Homo sapiens binding that frees TP53 wt Allele from negative control, activating the TP53 wt Allele pathway in Primary malignant neoplasm cells leading to cell cycle arrest and apoptosis. In Primary malignant neoplasm cells 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 Primary malignant neoplasm cells 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 Primary malignant neoplasm cells 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 Primary malignant neoplasm patients RG7112 is a selective inhibitor of TP53 wt Allele-MDM2 protein, human protein, Homo sapiens binding that frees TP53 wt Allele from negative control, activating the TP53 wt Allele pathway in Primary malignant neoplasm cells leading to cell cycle arrest and apoptosis MDM2 protein, human 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 Primary malignant neoplasm models In Primary malignant neoplasm cells 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, human 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, human protein, Homo sapiens-amplified liposarcoma who were eligible for resection BACKGROUND: RG7112 is a selective inhibitor of TP53 wt Allele-MDM2 protein, human protein, Homo sapiens binding that frees TP53 wt Allele from negative control, activating the TP53 wt Allele pathway in Primary malignant neoplasm cells 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 Primary malignant neoplasm cells 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, human 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, human 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, human protein, Homo sapiens binding that can reactivate TP53 wt Allele in Primary malignant neoplasm cells may offer an effective approach for Primary malignant neoplasm therapy. Treatment of Primary malignant neoplasm cells 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, human protein, Homo sapiens complex revealed that the small molecule binds in the TP53 wt Allele pocket of MDM2 protein, human protein, Homo sapiens, mimicking the interactions of critical TP53 wt Allele amino acid residues. Treatment of Primary malignant neoplasm cells 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, human protein, Homo sapiens inhibitor designed to occupy the TP53 wt Allele-binding pocket of MDM2 protein, human protein, Homo sapiens. In Primary malignant neoplasm cells 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 \u00b5M). Thus, inhibitors of TP53 wt Allele-MDM2 protein, human protein, Homo sapiens binding that can reactivate TP53 wt Allele in Primary malignant neoplasm cells may offer an effective approach for Primary malignant neoplasm therapy. RG7112 is a potent and selective member of the nutlin family of MDM2 protein, human protein, Homo sapiens antagonists currently in phase I clinical studies. In Primary malignant neoplasm cells 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, human protein, Homo sapiens interaction may represent a novel approach to Primary malignant neoplasm treatment. RG7112 (2g) is the first clinical small-molecule MDM2 protein, human protein, Homo sapiens inhibitor designed to occupy the TP53 wt Allele-binding pocket of MDM2 protein, human 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 \u00b5M). 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 Neoplasm expressing wild-type TP53 wt Allele. RG7112 induced tumor regressions in Solid Neoplasm 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, human protein, Homo sapiens binding that frees TP53 wt Allele from negative control, activating the TP53 wt Allele pathway in Primary malignant neoplasm cells 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: malignant giant cell tumor has relations: disease_disease with Primary malignant neoplasm, disease_disease with Primary malignant neoplasm.", "label": "yes"}
{"original_question": "Does thyroid hormone affect cardiac remodeling ?", "id": "converted_290", "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]", "label": "yes"}
{"original_question": "Is armodafinil used for treatment of insomnia?", "id": "converted_291", "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(\u00ae), 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 Sleep Apnea, Obstructive (OSA), shift work disorder (SWD), or Narcolepsy 1.  armodafinil represents an option for long-term treatment of patients with ES associated with treated OSA, 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 OSA 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 OSA.  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 OSA/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 OSA, 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 OSA/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: Narcolepsy 1 has relations: indication with armodafinil, indication with armodafinil. armodafinil has relations: indication with Narcolepsy 1, indication with Narcolepsy 1. Amphetamine has relations: indication with Narcolepsy 1, drug_drug with armodafinil, indication with Narcolepsy 1, drug_drug with armodafinil. Modafinil has relations: indication with Narcolepsy 1, indication with Narcolepsy 1. Melatonin has relations: drug_drug with armodafinil, drug_drug with armodafinil.", "label": "no"}
{"original_question": "Are there currently applications of deep learning in genomics?", "id": "converted_292", "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]", "label": "yes"}
{"original_question": "Are CpG islands located close to housekeeping genes?", "id": "converted_293", "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 Regions, Genetic 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 sequences. 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]", "label": "yes"}
{"original_question": "Have microRNAs been implicated in pharmacogenomics?", "id": "converted_294", "sentence1": "Have microRNAs been implicated in pharmacogenomics?", "sentence2": "A major discovery is the ability of MicroRNAs to determine the efficacy of drugs, which has given rise to the field of 'miRNA pharmacogenomics' through 'Pharmaco-miRs'. MicroRNAs 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 MicroRNAs 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 MicroRNAs. 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 MicroRNAs in pharmacogenomics, we have examined the potential regulation by MicroRNAs 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 MicroRNAs. 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 MicroRNAs 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. Genetic Polymorphism 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 MicroRNAs. 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 microRNA effects more broadly. n silico comparison of drug potencies with microRNA 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 microRNA 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, microRNA expression profiles may provide a critical link for understanding mechanisms involved in chemosensitivity and chemoresistance. This study reports on MicroRNAs implicated in Serotonin Reuptake Inhibitor [EPC] sensitivity of LCLs. these MicroRNAs as tentative Serotonin Reuptake Inhibitor [EPC] response biomarkers awaits validation with lymphocyte samples of major depression patients.[SEP]", "label": "yes"}
{"original_question": "Is nicotinamide effective for skin cancer prevention?", "id": "converted_295", "sentence1": "Is Nicotinamide Assay effective for Malignant neoplasm of skin prevention?", "sentence2": "Nicotinamide (Vitamins B3) 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 Assay group than in the placebo group (P=0.02). Similar differences were found between the Nicotinamide Assay group and the placebo group with respect to new basal-cell carcinomas (20% [95% NDUFB6 gene, -6 to 39]lower rate with Nicotinamide Assay, 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 Assay 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 Assay was safe and effective in reducing the rates of new Skin carcinoma and Actinic keratosis in high-risk patients. Nicotinamide 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 Assay, 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 Assay significantly reduces premalignant Actinic keratosis, and may reduce new non-melanoma skin cancers.  Nicotinamide (Vitamins B3) prevents UV-induced immunosuppression and carcinogenesis in CASP14 gene, and solar-simulated (ss) UV-induced immunosuppression in Homo sapiens. These results show that Nicotinamide Assay enhances two different pathways for repair of UV-induced photolesions, supporting Nicotinamide Assay'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 Assay 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 Assay was discontinued.CONCLUSIONS: Oral Nicotinamide Assay was safe and effective in reducing the rates of new Skin carcinoma and Actinic keratosis in high-risk patients.  Nicotinamide (Vitamins B3) 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 Assay twice daily or placebo for 12 months.  Similar differences were found between the Nicotinamide Assay group and the placebo group with respect to new basal-cell carcinomas (20% [95% NDUFB6 gene, -6 to 39]lower rate with Nicotinamide Assay, P=0.12) and new squamous-cell carcinomas (30% [95% NDUFB6 gene, 0 to 51] lower rate, P=0.05).  Oral Nicotinamide Assay was safe and effective in reducing the rates of new Skin carcinoma and Actinic keratosis in high-risk patients. Nicotinamide has shown potential as a safe and effective intervention for the prevention of malignant and premalignant skin lesions. Nicotinamide, which protected against both Ultraviolet B therapy and UVA, is a promising agent for Malignant neoplasm of skin prevention.[SEP]Relations: skin carcinoma has relations: disease_disease with Malignant neoplasm of skin, disease_disease with Malignant neoplasm of skin.", "label": "yes"}
{"original_question": "Do Parkinson's disease patients experience stridor?", "id": "converted_296", "sentence1": "Do Parkinson 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 Disease and severe Laryngospasm. The Laryngospasm 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 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 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.  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. RESULT: Only 12 previously reported cases of Stridor in Parkinsons Disease patients were identified. This case emphasises the importance of recognising different causes of Stridor in Parkinsons Disease patients, as this affects management. OBJECTIVES: (1) To present a rare case of Stridor secondary to prolonged laryngospasm in a patient with Parkinsons Disease, and (2) to review the literature on Stridor in Parkinsons Disease. METHODS: We report a 73-year-old Parkinsons 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 Disease, and (2) to review the literature on Stridor in Parkinson Disease.[SEP]", "label": "yes"}
{"original_question": "Is there an association between serum interleukin-6 concentrations and outcomes of stroke patients?", "id": "converted_297", "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 (C-reactive protein), Recombinant Interleukin-6, tumour necrosis factor-alpha and Intercellular adhesion molecule 1.[SEP]", "label": "yes"}
{"original_question": "Could bioprinting be used in regenerative medicine against bone disease?", "id": "converted_298", "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]", "label": "yes"}
{"original_question": "Is macroautophagy a selective degradation process?", "id": "converted_299", "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 Genes, a phosphatidylinositol 3-phosphate-binding Protein Info, is central to the selective elimination of aggregated Proteins. We propose that WDFY3 Genes 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 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's 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 Recombinant 70-kD Heat-Shock Protein (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 Genes Genes 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 Genes is not required for other types of selective autophagy or for nonspecific macroautophagy. However, in contrast to the core autophagy genes such as ATG5 Genes and ATG7 Genes, expression of ulk1 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 Protein Info, Homo sapiens, 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 neuron 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 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 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: heat shock Protein Info binding has relations: molfunc_protein with BAG Family Molecular Chaperone Regulator 3, human, molfunc_protein with BAG Family Molecular Chaperone Regulator 3, human, molfunc_protein with BAG Family Molecular Chaperone Regulator 3, human, molfunc_protein with BAG Family Molecular Chaperone Regulator 3, human, molfunc_protein with BAG Family Molecular Chaperone Regulator 3, human, molfunc_protein with BAG Family Molecular Chaperone Regulator 3, human. chaperone-mediated autophagy has relations: bioprocess_protein with BAG Family Molecular Chaperone Regulator 3, human, bioprocess_protein with BAG Family Molecular Chaperone Regulator 3, human. Cytoplasm has relations: cellcomp_protein with BAG Family Molecular Chaperone Regulator 3, human, cellcomp_protein with Heat Shock Protein Beta-8, cellcomp_protein with BAG Family Molecular Chaperone Regulator 3, human, cellcomp_protein with Heat Shock Protein Beta-8, cellcomp_protein with BAG Family Molecular Chaperone Regulator 3, human, cellcomp_protein with Heat Shock Protein Beta-8, cellcomp_protein with BAG Family Molecular Chaperone Regulator 3, human, cellcomp_protein with Heat Shock Protein Beta-8. autophagosome has relations: cellcomp_cellcomp with Vacuole, cellcomp_cellcomp with Vacuole. autosomal recessive PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE has relations: disease_disease with PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE, disease_disease with PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE.", "label": "yes"}
{"original_question": "Is there any link between conserved noncoding elements and alternative splicing in vertebrates?", "id": "converted_300", "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]", "label": "yes"}
{"original_question": "Is muscle regeneration possible in mdx mice with the use of induced mesenchymal stem cells?", "id": "converted_301", "sentence1": "Is muscle regeneration possible in mdx CASP14 gene with the use of induced mesenchymal stem Cells?", "sentence2": "Purified iMSCs displayed fibroblast-like morphology, formed three-dimensional spheroid structures, and expressed characteristic Mesenchymal Stem Cells surface markers such as Integrin Beta-1, human, CD33 antigen antigen, 5'-NUCLEOTIDASE, Thy-1 Membrane Glycoprotein, human, and Endoglin, human. Moreover, iMSCs were capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplanting iMSC Cells to tibialis anterior skeletal Muscle Tissue in mdx CASP14 gene lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal Dystrophin expression levels were restored This study demonstrates the therapeutic potential of purified iMSCs in Specimen Source Codes - Skeletal muscle regeneration in mdx CASP14 gene Vascular Endothelial Growth Factor Receptor 2, human+ adipose-derived mesenchymal stem Cells differentiate into Specimen Source Codes - Skeletal muscle satellite Cells and ameliorate Muscular Dystrophy in mdx CASP14 gene Within mdx CASP14 gene, an animal model of Muscular Dystrophy, Duchenne, adipose tissue-derived Vascular Endothelial Growth Factor Receptor 2, human(+) cyclic nucleotide-gated mechanosensitive ion channel activity (AD-cyclic nucleotide-gated mechanosensitive ion channel activity) homed to and differentiated into Cells that repaired injured Muscle Tissue. This repair correlated with reconstitution of Dystrophin expression on the damaged fibers Vascular Endothelial Growth Factor Receptor 2, human(+) AD-MSC transplants may repair Muscular Dystrophy This study demonstrates the therapeutic potential of purified iMSCs in Specimen Source Codes - Skeletal muscle regeneration in mdx CASP14 gene, and suggests that iPSCs are a viable alternate source for deriving cyclic nucleotide-gated mechanosensitive ion channel activity as needed. Transplanting iMSC Cells to tibialis anterior skeletal Muscle Tissue in mdx CASP14 gene lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal Dystrophin expression levels were restored This study demonstrates the therapeutic potential of purified iMSCs in Specimen Source Codes - Skeletal muscle regeneration in mdx CASP14 gene, and suggests that iPSCs are a viable alternate source for deriving cyclic nucleotide-gated mechanosensitive ion channel activity as needed[SEP]Relations: Muscle Tissue has relations: anatomy_protein_present with Muscular Dystrophy, Duchenne, anatomy_protein_present with Muscular Dystrophy, Duchenne. Duchenne Muscular Dystrophy has relations: disease_protein with Muscular Dystrophy, Duchenne, disease_protein with Muscular Dystrophy, Duchenne.", "label": "yes"}
{"original_question": "Is the SDHAF2 gene encoding a protein necessary for flavination of SDHA?", "id": "converted_302", "sentence1": "Is the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein gene 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 gene (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 gene, von Hippel-Lindau disease tumor suppressor gene (Von Hippel-Lindau Syndrome), neurofibromatosis type 1 tumor suppressor gene (Neurofibromatosis 1), Genes encoding the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein gene (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 gene 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 gene and MAX tumor suppressor Genes. the gene 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 gene, von Hippel-Lindau disease tumor suppressor gene (Von Hippel-Lindau Syndrome), neurofibromatosis type 1 tumor suppressor gene (Neurofibromatosis 1), Genes encoding the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein gene (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 gene 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 gene 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 gene (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 gene, von Hippel-Lindau disease tumor suppressor gene (Von Hippel-Lindau Syndrome), neurofibromatosis type 1 tumor suppressor gene (Neurofibromatosis 1), Genes encoding the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein gene (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 gene 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 gene 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 gene (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 gene (Succinate Dehydrogenase), and in Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, required for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial.  This gene 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 gene, von Hippel-Lindau disease tumor suppressor gene (Von Hippel-Lindau Syndrome), neurofibromatosis type 1 tumor suppressor gene (Neurofibromatosis 1), Genes encoding the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein gene (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 gene 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 gene 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 gene (Succinate Dehydrogenase), and in Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, required for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial.[SEP]Relations: neurofibromatosis has relations: disease_protein with Neurofibromatosis 1, disease_protein with Neurofibromatosis 1. mitochondrial electron transport, succinate to ubiquinone has relations: bioprocess_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, bioprocess_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, bioprocess_protein with Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, bioprocess_protein with SDHC Protein Info, human, bioprocess_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, bioprocess_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, bioprocess_protein with Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, bioprocess_protein with SDHC Protein Info, human. mitochondrial respiratory chain complex II, SDHAF2 gene complex (ubiquinone) has relations: cellcomp_protein with SDHC Protein Info, human, cellcomp_protein with SDHB Protein Info, human, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, cellcomp_protein with SDHC Protein Info, human, cellcomp_protein with SDHB Protein Info, human, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, cellcomp_protein with SDHC Protein Info, human, cellcomp_protein with SDHB Protein Info, human, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, cellcomp_protein with SDHC Protein Info, human, cellcomp_protein with SDHB Protein Info, human, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial. von Hippel-Lindau disease has relations: disease_protein with Von Hippel-Lindau Syndrome, disease_protein with Von Hippel-Lindau Syndrome.", "label": "yes"}
{"original_question": "Is zolpidem an antibiotic?", "id": "converted_303", "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: Desoxycorticosterone acetate has relations: drug_protein with taurochenodeoxycholate 6alpha-hydroxylase activity, drug_protein with taurochenodeoxycholate 6alpha-hydroxylase activity. Zolpidem has relations: drug_protein with taurochenodeoxycholate 6alpha-hydroxylase activity, drug_protein with taurochenodeoxycholate 6alpha-hydroxylase activity. Clonazepam has relations: drug_protein with taurochenodeoxycholate 6alpha-hydroxylase activity, drug_protein with taurochenodeoxycholate 6alpha-hydroxylase activity. Benzodiazepine has relations: drug_protein with taurochenodeoxycholate 6alpha-hydroxylase activity, drug_protein with taurochenodeoxycholate 6alpha-hydroxylase activity, drug_protein with taurochenodeoxycholate 6alpha-hydroxylase activity, drug_protein with taurochenodeoxycholate 6alpha-hydroxylase activity. Isoniazid has relations: drug_protein with taurochenodeoxycholate 6alpha-hydroxylase activity, drug_protein with taurochenodeoxycholate 6alpha-hydroxylase activity.", "label": "no"}
{"original_question": "Can desvenlafaxine be used at a dose of 50mg/day?", "id": "converted_304", "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]", "label": "yes"}
{"original_question": "Can ferric carboxymaltose be used to treat anemia in inflammatory bowel disease patients?", "id": "converted_305", "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\u00a0% 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 Diseases, 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 Diseases, 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 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 Diseases) 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 Diseases (CKD) 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 complex 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 Diseases (CKD) 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 Diseases (CKD) and those undergoing hemodialysis (Hodgkin Disease)[SEP]Relations: Phenylpropanolamine has relations: contraindication with INFLAMMATORY BOWEL DISEASE 2, contraindication with INFLAMMATORY BOWEL DISEASE 2.", "label": "yes"}
{"original_question": "Is there any association of the chromosomal region harboring the gene ITIH3 with schizophrenia?", "id": "converted_306", "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 \u00d7 10(-9)), ANK3 gene gene (rs10994359, P = 2.5 \u00d7 10(-8)) and the ITIH3 gene gene-ITIH4 region (rs2239547, P = 7.8 \u00d7 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: TENM4 gene has relations: disease_protein with Bipolar Disorder Type 2, disease_protein with SCHIZOPHRENIA 2 (disorder), disease_protein with Bipolar Disorder Type 2, disease_protein with SCHIZOPHRENIA 2 (disorder). GLT8D1 gene has relations: protein_protein with TCF7L2 protein, human, protein_protein with TCF7L2 protein, human. CACNA1C gene has relations: protein_protein with CACNB2 gene, disease_protein with Bipolar Disorder Type 2, disease_protein with SCHIZOPHRENIA 2 (disorder), protein_protein with CACNB2 gene, disease_protein with Bipolar Disorder Type 2, disease_protein with SCHIZOPHRENIA 2 (disorder). Bipolar Disorder Type 2 has relations: disease_protein with CSMD1 protein, human, disease_protein with TENM4 gene, disease_protein with CACNA1C gene, disease_protein with TCF7L2 protein, human, disease_protein with CACNB2 gene, disease_protein with SYNE1 gene, disease_protein with CSMD1 protein, human, disease_protein with TENM4 gene, disease_protein with CACNA1C gene, disease_protein with TCF7L2 protein, human, disease_protein with CACNB2 gene, disease_protein with SYNE1 gene. SYNE1 gene has relations: disease_protein with Bipolar Disorder Type 2, disease_protein with Bipolar Disorder Type 2. SDCCAG8 gene has relations: disease_protein with SCHIZOPHRENIA 2 (disorder), disease_protein with SCHIZOPHRENIA 2 (disorder). CACNB2 gene has relations: disease_protein with Bipolar Disorder Type 2, disease_protein with SCHIZOPHRENIA 2 (disorder), protein_protein with CACNA1C gene, disease_protein with Bipolar Disorder Type 2, disease_protein with SCHIZOPHRENIA 2 (disorder), protein_protein with CACNA1C gene. CNNM2 gene has relations: disease_protein with SCHIZOPHRENIA 2 (disorder), disease_protein with SCHIZOPHRENIA 2 (disorder).", "label": "yes"}
{"original_question": "Is the regulation of Vsr endonuclease independent of the growth phase of bacteria?", "id": "converted_307", "sentence1": "Is the regulation of vsr endonuclease independent of the growth phase of bacteria?", "sentence2": "Growth phase-dependent regulation of vsr endonuclease vsr endonuclease levels are growth phase dependent. Growth phase-dependent regulation of vsr endonuclease may contribute to 5-Methylcytosine mutational hot spots in Escherichia coli. Using rabbit allergenic extract allergenic extract polyclonal antibodies, we have shown that the Dcm cytosine methylase of Escherichia coli is maintained at a constant level during cell growth, while vsr endonuclease levels are growth phase dependent. vsr endonuclease, which initiates very short patch repair, has been hypothesized to regulate mutation in stationary-phase cells. The efficiency of the two pathways changes during the bacterial life cycle; Mismatch Repair is more efficient during exponential growth and Vital signs, smoking and pain scale repair is more efficient during the stationary phase. Overexpression of Vsr does dramatically increase the stationary-phase reversion of a Lac- frameshift allele, but the absence of Vsr has no effect. Using rabbit allergenic extract allergenic extract polyclonal antibodies, we have shown that the Dcm cytosine methylase of Escherichia coli is maintained at a constant level during cell growth, while vsr endonuclease levels are growth phase dependent The efficiency of the two pathways changes during the bacterial life cycle; Mismatch Repair is more efficient during exponential growth and Vital signs, smoking and pain scale repair is more efficient during the stationary phase vsr endonuclease, which initiates very short patch repair, has been hypothesized to regulate mutation in stationary-phase cells[SEP]", "label": "no"}
{"original_question": "Are there interactomes available for POU5F1 and SOX2?", "id": "converted_308", "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 (hESCs) 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 hESCs, 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 POU5F1 protein, human, protein_protein with SOX2 protein, human, protein_protein with POU5F1 protein, human, protein_protein with SOX2 protein, human.", "label": "yes"}
{"original_question": "Is Rheumatoid Arthritis related to myopathy?", "id": "converted_309", "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 areflexia Myopathy and Neuropathy in Rheumatoid Arthritis with Rheumatoid Arthritis (RA) have clinical or subclinical evidence of peripheral Neuropathy or Myopathy The study reveals an increased prevalence of neurogenic but not myogenic changes in patients with RA compared with controls[SEP]Relations: Hydroxychloroquine has relations: indication with Rheumatoid Arthritis, indication with Rheumatoid Arthritis. Chloroquine has relations: indication with Rheumatoid Arthritis, indication with Rheumatoid Arthritis. peripheral nervous system disease has relations: disease_disease with peripheral Neuropathy, disease_disease with peripheral Neuropathy. Rheumatoid arthritis has relations: disease_phenotype_positive with Rheumatoid Arthritis, disease_phenotype_positive with Rheumatoid Arthritis.", "label": "yes"}
{"original_question": "Is EZH2 associated with prostate cancer?", "id": "converted_310", "sentence1": "Is ezh2 protein, human 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 gene 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 Metalloproteinases-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 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, human 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, human protein, Homo sapiens promoter Collectively, our data indicate a Polycomb Repressive Complex 2 dependent mechanism in ID4 protein, human 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, human 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 PIN. 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, human 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 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, human 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, human protein, Homo sapiens, and RING1 gene 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 (\u03b12-integrin, \u03b16-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: RING1 gene has relations: protein_protein with BMI1 protein, human, protein_protein with BMI1 protein, human. ezh2 protein, human has relations: protein_protein with DNMT3B protein, human, disease_protein with Pelvis>Prostate Primary malignant neoplasm, disease_protein with Breast Primary malignant neoplasm, protein_protein with BMI1 protein, human, protein_protein with DNMT3B protein, human, disease_protein with Pelvis>Prostate Primary malignant neoplasm, disease_protein with Breast Primary malignant neoplasm, protein_protein with BMI1 protein, human. secondary malignant neoplasm has relations: disease_disease with Primary malignant neoplasm, disease_disease with Primary malignant neoplasm.", "label": "yes"}
{"original_question": "Is there any cross-talk between the Wnt and the Akt pathways?", "id": "converted_311", "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/\u03b2-catenin, PKA/CREB, and inhibition of RhoA/ROCK that substantially increase human \u03b2-cell proliferation while maintaining the \u03b2-cell phenotype. The cross-talk role of Wnt/\u03b2-catenin and 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt signaling pathway, with GSK-3\u03b2 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, GSK3\u03b2, 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 GSK3\u03b2, 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 \u03b2-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 \u03b2-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/\u03b2-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 TGF\u03b21 and WNT3A gene lead to increased accumulation of \u03b2-catenin, phosphorylation of AKT and p44/42 MAPK.[SEP]Relations: CTNNB1 has relations: protein_protein with PTEN protein, human, disease_protein with Medulloblastoma, protein_protein with PTEN protein, human, disease_protein with Medulloblastoma. cytoplasm has relations: cellcomp_protein with PTEN protein, human, cellcomp_protein with PTEN protein, human. Medulloblastoma has relations: disease_phenotype_positive with Medulloblastoma, disease_phenotype_positive with Medulloblastoma.", "label": "yes"}
{"original_question": "Has the protein GFP been used in transgenesis for live protein imaging?", "id": "converted_312", "sentence1": "Has the protein Green Fluorescent Proteins 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 protein (Green Fluorescent Proteins) Animals, Transgenic animal allergen extracts. founders were found to be Animals, Transgenic for Green Fluorescent Proteins. Green Fluorescent Proteins 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 protein (Green Fluorescent Proteins) or red fluorescent protein (Zinc-Finger Protein Zinc-Finger Protein RFP), is an extremely important research tool in \"U\" lymphocyte and developmental biology. Green Fluorescent Proteins-Animals, Transgenic animal allergen extracts for in vivo imaging: Rattus norvegicus, Family Leporidae (organism), and pigs. We have further extended the techniques of genetic engineering to Rattus norvegicus, Family Leporidae (organism), and pigs, and have created corresponding Green Fluorescent Proteins-Animals, Transgenic animal allergen extracts. The results revealed that the 3.6-Green Fluorescent Proteins Animals, Transgenic animal allergen extracts 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 Animals, Transgenic pigs. green fluorescent protein (Green Fluorescent Proteins) as reporter of the vector system were consistently expressed in Animals, Transgenic animal allergen extracts. The ability to specify the expression levels of exogenous Genes inserted in the Genome of Animals, Transgenic animal allergen extracts is critical for the success of a wide variety of experimental manipulations.  Welfare assessment in Animals, Transgenic pigs expressing green fluorescent protein (Green Fluorescent Proteins). Animals, Transgenic animal allergen extracts expressing Green Fluorescent Proteins with wildtype animal allergen extracts along various stages of post natal development Production of Animals, Transgenic chickens expressing a tetracycline-inducible Green Fluorescent Proteins gene. Animals, Transgenic animal allergen extracts can be readily created to express fluorescently tagged proteins or reporters These findings suggest that mhc2dab:Green Fluorescent Proteins and cd45:DsRed Animals, 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 Green Fluorescent Proteins-positive. Lentiviral vectors containing the green fluorescent protein gene have been successfully used to select Animals, Transgenic embryos before transfer to a surrogate mother Typically Transgenes are generated by placing a promoter upstream of a Green Fluorescent Proteins 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 protein Animals, Transgenic rat in the adult rat brain. This problem has been lessened by the availability of Animals, Transgenic animal allergen extracts that express \"reporter\" Genes, such as green fluorescent protein (Green Fluorescent Proteins)  full-length Green Fluorescent Proteins fusion proteins was examined, in Animals, Transgenic animal allergen extracts,  Two stable Animals, Transgenic lines express Green Fluorescent Proteins prior to hair-bundle formation we generated two Animals, Transgenic pigs by somatic \"U\" lymphocyte nuclear transfer (SCNT) that express green fluorescent protein (Green Fluorescent Proteins) driven by cytomegalovirus (CMV). Fluorescent proteins such as the green fluorescent protein (Green Fluorescent Proteins) have widely been used in Animals, Transgenic animal allergen extracts as Genes, Reporter.  Green Fluorescent Protein (Green Fluorescent Proteins) is used extensively as a reporter for transgene expression in Drosophila <basidiomycetes> <basidiomycetes> and other Organism.[SEP]", "label": "yes"}
{"original_question": "Is the Snord116 cluster associated with the Prader-Willi syndrome?", "id": "converted_313", "sentence1": "Is the Snord116 cluster associated with the Prader-Willi syndrome?", "sentence2": "All three Gene Deletion included SNORD116, but only two encompassed parts of small nuclear ribonucleoprotein-associated protein N gene, implicating SNORD116 as the major contributor to the Prader-Willi phenotype. Our case adds further information about genotype-phenotype correlation and supports the hypothesis that SNORD116 plays a major role in the pathogenesis of Prader-Willi syndrome These results demonstrate that the AS candidate drug topotecan acts predominantly through stabilizing R loops and chromatin decondensation at the paternally expressed Partial Wave Spectroscopic Microscopy Snord116 Gene Locus. Our study holds promise for targeted therapies to the Snord116 Gene Locus for both AS and Partial Wave Spectroscopic Microscopy. Prader-Willi syndrome (Partial Wave Spectroscopic Microscopy) is caused by the loss of RNA expression from an imprinted region on chromosome 15 that includes small nuclear ribonucleoprotein-associated protein N, SNORD115, and SNORD116.  Recently published data strongly suggest a role for the paternally expressed small nucleolar RNA (snoRNA) cluster, SNORD116, in Partial Wave Spectroscopic Microscopy etiology. Whereas loss of function of the SNORD116 Genes appears to be responsible for the major features of Partial Wave Spectroscopic Microscopy, the role of the other Genes is less clear.  Recent data suggest that snoRNA Snord116 is important for the pathogenesis of Prader-Willi syndrome (Partial Wave Spectroscopic Microscopy) characterized by Hyperphagia and BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20. The current study was conducted to assess a potential Cells link between Snord116 and phenotypes of Partial Wave Spectroscopic Microscopy.  The imprinted Snurf-Snrpn chromosomal domain contains two large arrays of tandemly repeated, paternally expressed box C/D small-nucleolar RNA (snoRNA) Genes: the SNORD115 (H/MBII-52) and SNORD116 (H/MBII-85) gene clusters believed to play key roles in the fine-tuning of serotonin receptor (5-HT2C) pre-mRNA processing and in the etiology of the Prader-Willi Syndrome (Partial Wave Spectroscopic Microscopy), respectively There are multiple imprinted Genes in this region, the loss of which contribute to the complete phenotype of Prader-Willi syndrome. However, absence of a small nucleolar organizing RNA gene, SNORD116, seems to reproduce many of the clinical features. Both kits should be made available for accurate characterization of Partial Wave Spectroscopic Microscopy/AS deletion subtypes as well as evaluating for IC and SNORD116 microdeletions. There are multiple imprinted Genes in this region, the loss of which contribute to the complete phenotype of Prader-Willi syndrome. However, absence of a small nucleolar organizing RNA gene, SNORD116, seems to reproduce many of the clinical features.  Although the SNORD116 gene cluster has become a prime candidate for Partial Wave Spectroscopic Microscopy, it cannot be excluded that other paternally expressed Genes in the Region of chromosome 15q11q13 contribute to the full phenotype. In addition, recently published data provide strong evidence in support of a role for the snoRNA SNORD116 cluster (HBII-85) in Partial Wave Spectroscopic Microscopy etiology. Identification and characterization of this case provide unequivocal evidence for a critical role for the SNORD116 snoRNA molecules in Partial Wave Spectroscopic Microscopy pathogenesis.[SEP]Relations: Prader-Willi syndrome has relations: disease_protein with small nuclear ribonucleoprotein-associated protein N, disease_protein with small nuclear ribonucleoprotein-associated protein N. small nuclear ribonucleoprotein-associated protein N has relations: disease_protein with Prader-Willi syndrome, disease_protein with Prader-Willi syndrome. small nuclear ribonucleoprotein complex has relations: cellcomp_protein with small nuclear ribonucleoprotein-associated protein N, cellcomp_protein with small nuclear ribonucleoprotein-associated protein N.", "label": "yes"}
{"original_question": "Is poly (ADP- ribosylation) involved in transcriptional control?", "id": "converted_314", "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 (TIPARP gene; 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 (Parp-1) 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 Parp-1 is required to maintain transcriptional regulation of a wide variety of Genes on a genome-wide scale TIPARP gene 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 TIPARP gene 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]", "label": "yes"}
{"original_question": "Is nimodipine recommended for prevention of vasospasm in aneurysmal subarachnoid hemorrhage patients?", "id": "converted_315", "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 infarctions 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]", "label": "yes"}
{"original_question": "Is lenvatinib effective for thyroid cancer?", "id": "converted_316", "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 carcinoma 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 Malignant epithelial neoplasm 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 carcinoma 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 \ufffd, 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: Sorafenib has relations: drug_protein with ret unit of radiation dose, drug_protein with stem cell factor receptor activity, drug_protein with ret unit of radiation dose, drug_protein with stem cell factor receptor activity. Lenvatinib has relations: drug_protein with stem cell factor receptor activity, drug_protein with ret unit of radiation dose, drug_protein with stem cell factor receptor activity, drug_protein with ret unit of radiation dose. stem cell factor receptor activity has relations: molfunc_protein with stem cell factor receptor activity, molfunc_protein with stem cell factor receptor activity. medullary thyroid gland carcinoma has relations: disease_protein with ret unit of radiation dose, disease_protein with ret unit of radiation dose. Vandetanib has relations: drug_protein with ret unit of radiation dose, drug_protein with ret unit of radiation dose. Cabozantinib has relations: drug_protein with ret unit of radiation dose, drug_protein with ret unit of radiation dose. thyroid gland carcinoma has relations: disease_disease with Malignant neoplasm of thyroid, disease_protein with ret unit of radiation dose, disease_disease with Malignant neoplasm of thyroid, disease_protein with ret unit of radiation dose.", "label": "yes"}
{"original_question": "Was tamoxifen tested for treatment of glioma patients?", "id": "converted_317", "sentence1": "Was tamoxifen tested for treatment of Glioma patients?", "sentence2": "Tamoxifen might have a role in the initial treatment of high-grade gliomas and should be studied in future Phase II trials building on the newly established platform of concurrent chemoradiotherapy. The addition of high-dose tamoxifen to standard radiotherapy does not improve the survival of patients with diffuse intrinsic pontine Glioma. In this study, in which tamoxifen was used in conjunction with radiotherapy, progression free survival was shown to be less good when compared with historical data HR = 3.1 (CI: 1.7-5.7). The addition of high-dose tamoxifen, although well tolerated, confers no clinical benefit to patients treated with diffuse intrinsic pontine Glioma treated with standard radiotherapy. CONCLUSIONS: Carboplatin and high dose tamoxifen has similar response rates to other regimens for recurrent Malignant Glioma and are probably equivalent to those found using tamoxifen as monotherapy.  CONCLUSIONS: Pegylated liposomal doxorubicin administered alone or in combination with tamoxifen is safe and moderately effective in patients with recurrent high-grade Glioma. Protein kinase C (Paroxysmal kinesigenic choreoathetosis) inhibitors such as high-dose tamoxifen and hypericin also have been used in the treatment of Malignant Glioma.  Considering these facts, polyethylene-glycol-liposomal doxorubicin with and without tamoxifen was evaluated within two sequential Phase II trials performed at our institution.  In a parallel phase-II-study investigating post-operative treatment with tamoxifen (Immunoreceptor Tyrosine-Based Activation Motif), carboplatin and radiation therapy for Glioblastoma, 16 of 49 patients (33%) showed multifocal recurrence, which developed after a mean of 46 weeks, raising the question of an association with therapy. Radiation therapy and high-dose tamoxifen in the treatment of patients with diffuse brainstem gliomas: results of a Brazilian cooperative study. Brainstem Glioma Cooperative Group. PURPOSE: The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem gliomas in a multicenter trial. CONCLUSION: This treatment combination produced no significant change in the overall poor prognosis of these patients. Most Neoplasms responded initially to treatment but recurred as the study progressed. A minority of patients seemed to benefit from the extended use of TX.  Tamoxifen, a Protein Kinase C inhibitor when administered in high dosages, is currently being used as an adjuvant in the treatment of patients with Malignant Glioma. We present a patient with a recurrent malignant Glioma who was continued on high dose tamoxifen despite radiologic documented doubling of the Specimen Source Codes - Specimen Source Codes - tumor size and who eventually showed a delayed response to this agent nine months after initiation of treatment. The combination of oral tamoxifen (120 to 240 mg/m2/day) and subcutaneous interferon-alpha [6 x 10(6) U three times per week] was associated with significant Neurotoxicity Syndromes in this group of recurrent Glioma patients, resulting in early study closure. A phase I study of high-dose tamoxifen for the treatment of refractory Malignant Glioma of childhood. Phase I clinical trial assessing temozolomide and tamoxifen with concomitant radiotherapy for treatment of high-grade Glioma. Prolonged treatment with Biological Factors for malignant Glioma: a case study with high dose tamoxifen. Tamoxifen as a potential treatment of Glioma. We tested the efficacy and Toxic effect of the combination of high-dose tamoxifen and Deprecated Interferon alpha in Serum or Plasma in adults with recurrent Glioma in a phase II trial.  PURPOSE: The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem gliomas in a multicenter trial.  We tested the efficacy and Toxic effect of the combination of high-dose tamoxifen and Deprecated Interferon alpha in Serum or Plasma in adults with recurrent Glioma in a phase II trial. The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem gliomas in a multicenter trial. The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem gliomas in a multicenter trial. We tested the efficacy and Toxic effect of the combination of high-dose tamoxifen and Deprecated Interferon alpha in Serum or Plasma in adults with recurrent Glioma in a phase II trial. Eligible patients had radiographically measurable recurrent gliomas of any grade after initial radiation therapy. Thyroid function was suppressed to reduce Insulin-Like Growth Factor I levels in Glioma patients and high-dose tamoxifen administered.  propylthiouracil was used to induce chemical hypothyroidism in 22 patients with recurrent Glioma. Activity against recurrent gliomas has been reported for both tamoxifen and Deprecated Interferon alpha in Serum or Plasma, agents that have more acceptable Toxic effect profiles and that can be administered in an outpatient setting. We tested the efficacy and Toxic effect of the combination of high-dose tamoxifen and Deprecated Interferon alpha in Serum or Plasma in adults with recurrent Glioma in a phase II trial. Thyroid function was suppressed to reduce Insulin-Like Growth Factor I levels in Glioma patients and high-dose tamoxifen administered. Radiation therapy and high-dose tamoxifen in the treatment of patients with diffuse brainstem gliomas: results of a Brazilian cooperative study. We tested the efficacy and Toxic effect of the combination of high-dose tamoxifen and Deprecated Interferon alpha in Serum or Plasma in adults with recurrent Glioma in a phase II trial. The subsequent in vitro testing of the Specimen Source Codes - Specimen Source Codes - tumor that was removed after the recurrence of Specimen Source Codes - Specimen Source Codes - tumor (22 months after the initiation of tamoxifen) revealed loss of sensitivity to tamoxifen. The combination of oral tamoxifen (120 to 240 mg/m2/day) and subcutaneous interferon-alpha [6 x 10(6) U three times per week] was associated with significant Neurotoxicity Syndromes in this group of recurrent Glioma patients, resulting in early study closure.[SEP]Relations: malignant Glioma has relations: disease_disease with Glioma, disease_disease with Glioma. Carboplatin has relations: drug_drug with propylthiouracil, drug_drug with propylthiouracil. Temozolomide has relations: drug_drug with propylthiouracil, drug_drug with propylthiouracil. Doxorubicin has relations: drug_drug with propylthiouracil, drug_drug with propylthiouracil. Hypericin has relations: drug_drug with propylthiouracil, drug_drug with propylthiouracil.", "label": "yes"}
{"original_question": "Are there any animal models for Niemann-Pick C1 disease?", "id": "converted_318", "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 (GFAP) 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]", "label": "yes"}
{"original_question": "Does HER2 under-expression lead to favorable response to trastuzumab?", "id": "converted_319", "sentence1": "Does HER2 under-expression lead to favorable response to trastuzumab?", "sentence2": "over-expression of HER2 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 HER2-overexpressing Malignant neoplasm of Breast: trastuzumab, trastuzumab has demonstrated clinical activity in several types of HER2-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 HER2-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) is an important target for the treatment of the Breast cancers in which it is overexpressed. However, no approved anti-ERBB2 wt Allele therapy is available for the majority of Malignant neoplasm of Breast patients, who express ERBB2 wt Allele at low levels (with scores of 1+ or 2+/fluorescence in situ hybridization-negative). The humanized anti-HER2 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 gene products, and evaluates the overexpression status of the ERBB2 wt Allele protein in determining eligibility for the trastuzumab (HerceptinR, Genentech, San Francisco, cyclophosphamide/doxorubicin protocol, USA) therapy.[SEP]Relations: HER2 positive Breast carcinoma has relations: indication with trastuzumab, indication with trastuzumab.", "label": "no"}
{"original_question": "Is the PTPN22 gene a biomarker for rheumatoid arthritis?", "id": "converted_320", "sentence1": "Is the PTPN22 gene Genes a biomarker for rheumatoid arthritis?", "sentence2": "TPN22 is a Protein Tyrosine Phosphatase and functions as a damper of transcription-coupled nucleotide-excision repair signals. A C-to-T single nucleotide polymorphism (Single Nucleotide Polymorphism) located at position 1858 of human PTPN22 gene Genes 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 21 single-nucleotide polymorphisms (SNPs) that have previously been associated with Rheumatoid Arthritis, including PTPN22 gene Genes, TRAF1-C5 Locus Locus, CTLA4 wt Allele wt Allele, PADI4 protein, human protein, human, STAT4 protein, human protein, human, FCRL3 gene Genes, Recombinant Secondary Lymphoid-Tissue Chemokine, MMEL1-TNFRSF14, CDK6 protein, human protein, human, Protein Kinase C-theta, KIF5A gene Genes-PIP4K2C, IL2RB protein, human protein, human, TNFAIP3 gene Genes, IL10-1082G/A and REL Protein Protein he Human leukocyte antigen complex Gene Locus, particularly human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal, is its strongest genetic risk determinant across ethnicities. Several other genes, including PTPN22 gene Genes and PADI4 protein, human protein, human, show modest association with Rheumatoid Arthritis.  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 Genes, TRAF1-C5 Locus Locus, PADI4 protein, human protein, human, STAT4 protein, human protein, human.  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 Disease Gene 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 Genes plays an outstanding role. ssociation of the PTPN22 gene Genes Genes (-1123G > C) polymorphism with rheumatoid arthritis in Chinese patients Eight markers (ie, rs1160542 (LAF4 protein, human), rs1678542 (KIF5A gene Genes), rs2476601 (PTPN22 gene Genes), rs3087243 (CTLA4 wt Allele wt Allele), rs4810485 (CD40 protein, human protein, human), rs5029937 (6q23), rs10760130 (TRAF1/C5) and rs7574865 (STAT4 protein, human protein, 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 histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal, PTPN22 gene Genes, STAT4 protein, human protein, human, TRAF1/C5, OLIG3/TNFAIP3 gene Genes, CD40 protein, human protein, human, Recombinant Secondary Lymphoid-Tissue Chemokine, MMEL1-TNFRSF14, CDK6 protein, human protein, human, Protein Kinase C-theta, IL2RB protein, human protein, human, and KIF5A gene Genes-PIP4K2C.  This study investigated five confirmed rheumatoid arthritis (Rheumatoid Arthritis) susceptibility genes/loci (human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal, PTPN22 gene Genes, STAT4 protein, human protein, human, OLIG3/TNFAIP3 gene Genes and TRAF1/C5) for association with susceptibility and severity in an inception cohort 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 Genes Genes polymorphism, C5/TRAF1 genes region polymorphism and TNFAIP3 gene Genes-OLIG3 genes region polymorphism(s) are among newly identified and already confirmed genetic risk factors As well as the major susceptibility Genes human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal, recent genome-wide and candidate-Genes studies reported additional evidence for association of single nucleotide polymorphism (Single Nucleotide Polymorphism) markers in the PTPN22 gene Genes, STAT4 protein, human protein, human, OLIG3/TNFAIP3 gene Genes and TRAF1/C5 loci 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 Genes, TRAF1/C5, TNFAIP3 gene Genes, and STAT4 protein, human protein, human) have been consistently reported, whereas others have been observed less systematically 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 Genes Genes in populations of European ancestry and PADI4 protein, human protein, human Genes in populations of Asian ancestry, revealing the presence of genetic heterogeneity in Rheumatoid Arthritis.  In conclusion, we have confirmed that PTPN22 gene Genes 620W Alleles is associated with Tunisian Rheumatoid Arthritis but does not constitute a factor influencing clinical manifestations.  After adjusting for smoking and reproductive factors, PTPN22 gene Genes was associated with Rheumatoid Arthritis risk among Caucasian women in these cohorts We found strong evidence of an association of PTPN22 gene Genes with the development of anti-citrulline antibody-positive Rheumatoid Arthritis (odds ratio [OR] 1.49; P=.00002), using previously untested Genus Eira samples. Although human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal is the main Rheumatoid Arthritis Genes, it accounts for only part of the familial risk for Rheumatoid Arthritis. human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal 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, human protein, human, SLC22A4 Genes Genes, RUNX1 protein, human protein, human, and PTPN22 gene Genes. the level of PTPN22 gene Genes.6 in peripheral blood correlates with Disease activity of rheumatoid arthritis PTPN22 gene Genes, PADI-4, and cytotoxic T-lymphocyte antigen 4 have been associated with risk for rheumatoid arthritis (Rheumatoid Arthritis) progression from undifferentiated arthritis to rheumatoid arthritis: the effect of the PTPN22 gene Genes 1858T-Alleles In this Dutch cohort of UA-patients, the PTPN22 gene Genes 1858T Alleles does not markedly improve individual decision-making to predict Rheumatoid Arthritis-development challenges in identifying Genetic Polymorphism that influence the susceptibility to rheumatoid arthritis are the same as those faced in most complex diseases Recently a number of convincing Candidate Disease Gene have begun to emerge and an update has been provided for three of these: PTPN22 gene Genes[SEP]Relations: Arginine has relations: drug_protein with SLC22A4 Genes, drug_protein with SLC22A4 Genes. SLC22A4 Genes has relations: disease_protein with rheumatoid arthritis, disease_protein with rheumatoid arthritis. protein kinase C activity has relations: molfunc_protein with Protein Kinase C-theta, molfunc_protein with Protein Kinase C-theta. Rheumatoid arthritis has relations: disease_phenotype_positive with rheumatoid arthritis, disease_phenotype_positive with rheumatoid arthritis. TNFAIP3 gene has relations: disease_protein with rheumatoid arthritis, disease_protein with rheumatoid arthritis. PTPN22 gene has relations: disease_protein with rheumatoid arthritis, disease_protein with rheumatoid arthritis.", "label": "yes"}
{"original_question": "Can administration of the thyrotropin releasing hormone reduce fatigue in cancer patients?", "id": "converted_321", "sentence1": "Can administration of the thyrotropin releasing hormone reduce Fatigue in cancer patients?", "sentence2": "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 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 Thyrotropin-Releasing Hormone, human as a treatment for cyclophosphamide/fluorouracil. 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).  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 Thyrotropin-Releasing Hormone, human therapeutics to treat cyclophosphamide/fluorouracil. Thyrotropin-releasing hormone can relieve cancer-related Fatigue: hypothesis and preliminary observations. Global assessment using both subjective and objective parameters showed that Thyrotropin-Releasing Hormone, human exerted clear anti-Fatigue effects in four of the six Thyrotropin-Releasing Hormone, human treatments.  These initial findings support the proposal that Thyrotropin-Releasing Hormone, human can ameliorate cancer-related Fatigue.[SEP]", "label": "yes"}
{"original_question": "Is curcumin a phytochemical?", "id": "converted_322", "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 (Multidrug Resistance-Associated Proteins), such as P-Glycoprotein Activity (P-Glycoprotein), breast cancer resistance protein (ABCG2 wt Allele) and multidrug resistance-associated proteins 1 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]", "label": "yes"}
{"original_question": "Is Fanconi anemia presented as a genetically and clinically heterogeneous disease entity?", "id": "converted_323", "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 inheritance 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 inheritance 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 inheritance disorder characterized clinically by Congenital Abnormality, progressive Bone marrow hypocellularity, and a predisposition to Primary malignant neoplasm. 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 inheritance 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 inheritance 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 cancer 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 cancer 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 inheritance 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, cancer 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 Primary malignant neoplasm. 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 (FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) wt Allele to FAH). 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 malformations and predisposition to Leukemia, Myelocytic, Acute. Fanconi Genus Anemia is genetically heterogeneous, with at least eight complementation groups of doxorubicin/fluorouracil protocol (FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) wt Allele to FAD2). Fanconi Genus Anemia (doxorubicin/fluorouracil protocol), an Autosomal recessive inheritance 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 inheritance 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 Hematological 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 Abnormality, Aplastic Anemia, and cancer 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 Primary malignant neoplasm Fanconi Genus Anemia (doxorubicin/fluorouracil protocol) is a rare Autosomal recessive inheritance Disease characterized by progressive Pancytopenia, congenital malformations, 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 malformations, progressive Pancytopenia and predisposition to both Hematologic Neoplasms and solid tumors Fanconi Genus Anemia is a genetically heterogeneous chromosomal instability syndrome, characterized by multiple congenital anomalies, progressive Bone marrow hypocellularity, and a predisposition to Primary malignant neoplasm[SEP]Relations: Fanconi Genus Anemia complementation group has relations: disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_protein with fanconi Genus Anemia complementation group g, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP C, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP E, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_protein with fanconi Genus Anemia complementation group g, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP C, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP E, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_protein with fanconi Genus Anemia complementation group g, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP C, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP E, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_protein with fanconi Genus Anemia complementation group g, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP C, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP E, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_protein with fanconi Genus Anemia complementation group g, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP C, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP E, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_protein with fanconi Genus Anemia complementation group g, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP C, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP E, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_protein with fanconi Genus Anemia complementation group g, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP C, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP E, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_protein with fanconi Genus Anemia complementation group g, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP C, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP E, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_protein with fanconi Genus Anemia complementation group g, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP C, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP E, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_protein with fanconi Genus Anemia complementation group g, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP C, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP E. Fanconi Genus Anemia has relations: disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_protein with fanconi Genus Anemia complementation group g, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP E, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP C, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_protein with fanconi Genus Anemia complementation group g, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP E, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP C. Bone marrow hypocellularity has relations: phenotype_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP E, phenotype_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, phenotype_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP C, phenotype_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), phenotype_protein with fanconi Genus Anemia complementation group g, phenotype_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP E, phenotype_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, phenotype_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP C, phenotype_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), phenotype_protein with fanconi Genus Anemia complementation group g.", "label": "yes"}
{"original_question": "Is there evidence for de novo genesis of enhancers in vertebrates?", "id": "converted_324", "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]", "label": "yes"}
{"original_question": "Is TNNI3K a cardiac-specific protein?", "id": "converted_325", "sentence1": "Is TNNI3K Genes a Cardiac - anatomy qualifier-specific protein?", "sentence2": "cardiomyocyte-specific kinase TNNI3K Genes Genes  We report that Cardiac - anatomy qualifier troponin I-interacting kinase (TNNI3K Genes Genes), a cardiomyocyte-specific kinase, TNNI3K Genes Genes, a Cardiac - anatomy qualifier-specific kinase,   The Cardiac - anatomy qualifier troponin I-interacting kinase (TNNI3K Genes Genes), a novel Cardiac - anatomy qualifier specific kinase, is associated with cardiomyocyte hypertrophy Homo sapiens Cardiac - anatomy qualifier troponin I-interacting kinase (TNNI3K Genes Genes) 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 Genes Genes, a Cardiac - anatomy qualifier-specific MAPKKK, promotes Cardiac - anatomy qualifier dysfunctio Cardiac troponin I-interacting kinase (TNNI3K Genes Genes) is a Cardiac - anatomy qualifier-specific kinase whose biological function remains largely unknown  Cardiac troponin I-interacting kinase (TNNI3K Genes Genes) is a novel Cardiac - anatomy qualifier-specific kinase Genes  a novel Cardiac - anatomy qualifier-specific kinase Genes (TNNI3K Genes Genes),  TNNI3K Genes Genes is a novel Cardiac - anatomy qualifier troponin I-interacting kinase Genes and its overexpression may promote Cardiac - anatomy qualifier myogenesis,  TNNI3K Genes Genes 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 Genes Genes for its interaction with Cardiac - anatomy qualifier troponin I, is both a unique expression and Chest>Heart-enriched Genes Molecular cloning of Cardiac - anatomy qualifier troponin I-interacting kinase (TNNI3K Genes Genes), 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 Genes Genes is highly expressed in Chest>Heart, but is undetectable in other Body tissue. Immunohistochemical analysis predominantly localized TNNI3K Genes Genes in the nucleus of Myocytes, Cardiac.[SEP]Relations: TNNI3K Genes has relations: anatomy_protein_present with Chest>Heart, anatomy_protein_present with Chest>Heart.", "label": "yes"}
{"original_question": "Is factor XI deficient in Hemophilia C?", "id": "converted_326", "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 Hereditary Factor XI Deficiency or hemophilia C) 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 hemophilia C Factor XI deficiency (Hemophilia C) Factor XI deficiency, also called hemophilia C,[SEP]", "label": "yes"}
{"original_question": "Are EDNRB mutations involved in the development of Hirschsprung disease?", "id": "converted_327", "sentence1": "Are EDNRB protein, human Gene Mutation involved in the development of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1?", "sentence2": "QTL analysis identifies a modifier Gene Locus of aganglionosis in the rat model of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 carrying Ednrb(sl) Gene Mutation As reported previously, when the same null Mutation Abnormality of the Ednrb Genes, 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, SUSCEPTIBILITY TO, 1, but not hearing impairment in Rattus norvegicus carrying Ednrb(sl) Gene Mutation In this study, we found that the null Mutation Abnormality of the Ednrb Genes, thought indispensable for enteric Neurons development, is insufficient to result in HSCR Disease when bred onto a different genetic background in Rattus norvegicus carrying Ednrb(sl) Gene Mutation. New roles of EDNRB protein, human protein, human and EDN3 Genes Genes in the pathogenesis of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. The aim of this study was to evaluate the implication of the EDN3 Genes Genes and EDNRB protein, human protein, human genes in a series of patients with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 from Spain and determinate their mutational spectrum. A De Novo novel Mutation Abnormality of the EDNRB protein, human protein, human Genes in a Taiwanese boy with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 Although Gene Mutation in eight different genes (EDNRB protein, human protein, human, EDN3 Genes Genes, ECE1 Genes Genes, SOX10, ret unit of radiation dose, Glial Cell Line-Derived Neurotrophic Factor, CX3CL1 Genes, SLC9A3R2 Genes) 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 HSCR. Mutations in genes of the Proto-Oncogene Proteins c-ret and endothelin receptor B (EDNRB protein, human protein, human) signaling pathways have been shown to be associated in HSCR patients.  Interactions between SOX10 Transcription Factor and EdnrB modulate penetrance and severity of aganglionosis in the Sox10Dom mouse model of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 Molecular genetic analyses have revealed that interactions between Gene Mutation in the genes encoding the Proto-Oncogene Proteins c-ret and the endothelin receptor type B (EDNRB protein, human protein, human) are central to the genesis of HSCR 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, SUSCEPTIBILITY TO, 1 Thus, genetic interaction between Gene Mutation 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 Genes Genes and HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 type II. Analysis of the ret unit of radiation dose, Glial Cell Line-Derived Neurotrophic Factor, EDN3 Genes Genes, and EDNRB protein, human protein, human genes in patients with intestinal neuronal dysplasia and HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 wo susceptibility genes have been recently identified in HSCR, namely the ret unit of radiation dose proto-oncogene and the Receptor, Endothelin B, Type 2 (EDNRB protein, human protein, human) Genes. We conclude that Ednrb loss only in Neural Crest Cells is sufficient to produce the Hirschsprungs Disease phenotype observed with genomic Ednrb Gene Mutation EDNRB protein, human protein, human Gene Mutation were detected in 2 of the 13 short-segment Hodgkin Disease The Gene Mutation of EDNRB protein, human protein, human Genes and EDN-3 Genes are found in the short-segment Hodgkin Disease of sporadic Hirschsprung Disease in Chinese population, which suggests that the EDNRB protein, human protein, human Genes and EDN-3 Genes play important roles in the pathogenesis of Hodgkin Disease Functional characterization of three Gene Mutation of the Receptor, Endothelin B, Type 2 Genes in patients with Hirschsprung Disease Hirschsprung Disease (HSCR) 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 Genes and its ligand, Neuroglia derived neutrophic factor (Glial Cell Line-Derived Neurotrophic Factor), Sox 10, Endothelin-3 (EDN3 Genes Genes) and its receptor B (EDNRB protein, human protein, human). EDNRB protein, human protein, human Gene Mutation are found in 5% of familial or sporadic HSCR Enteric aganglionosis in HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 has been linked to genes coding for endothelin-3 (EDN3 Genes Genes) and the Receptor, Endothelin B, Type 2 (EDNRB protein, human protein, human) To date, three genes have been identified as susceptibility genes for Hirschsprung Disease (HSCR), the ret unit of radiation dose proto-oncogene, the endothelin-B receptor Genes (EDNRB protein, human protein, human) and the endothelin-3 Genes (EDN3 Genes Genes) Our data indicate that ret unit of radiation dose and EDNRB protein, human protein, human Gene Mutation have a role in the aetiology of some sporadically occurring HSCR Mutations of the endothelin-B receptor and endothelin-3 genes in Hirschsprung Disease The endothelin-B receptor Genes (EDNRB protein, human protein, human) and the endothelin-3 Genes (EDN3 Genes Genes) have recently been recognized as susceptibility genes for Hirschsprung 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 Gene Mutation appear to be associated with short-segment Hodgkin Disease, in contrast to ret unit of radiation dose Gene Mutation, which are found mainly in Long-segment aganglionosis In addition to Gene Mutation 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, SUSCEPTIBILITY TO, 1. Heterozygous endothelin receptor B (EDNRB protein, human protein, human) Gene Mutation in isolated HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. QTL analysis identifies a modifier Gene Locus of aganglionosis in the rat model of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 carrying Ednrb(sl) Gene Mutation. Homozygous Gene Mutation in the endothelin-B receptor Genes (EDNRB protein, human protein, human) on 13q22 have been identified in Homo sapiens and CASP14 Genes with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 type 3 (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 2). A De Novo novel Mutation Abnormality of the EDNRB protein, human protein, human Genes in a Taiwanese boy with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. Hitherto however, homozygosity for EDNRB protein, human protein, human Gene Mutation accounted for the HSCR-Waardenburg syndrome (Werner Syndrome) association. These data might suggest that EDNRB protein, human protein, human Gene Mutation could be dosage sensitive: heterozygosity would predispose to isolated HSCR with incomplete penetrance, while homozygosity would result in more complex neurocristopathies associating HSCR and Werner Syndrome features. Highly recurrent ret unit of radiation dose Gene Mutation and novel Gene Mutation in genes of the High Affinity Nerve Growth Factor Receptor, human and endothelin receptor B pathways in Chinese patients with sporadic HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. Mutations in genes encoding the Proto-Oncogene Proteins c-ret and endothelin receptor type B (EDNRB protein, human protein, human) are involved in HSCR 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 HSCR-associated. Several missense Gene Mutation of the endothelin-B receptor (EDNRB protein, human protein, human) associated with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 have recently been identified. These findings indicate that these missense Gene Mutation result in loss of function of EDNRB protein, human protein, human, and may provide the molecular pathological basis of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 in some individuals. Manifestation of the Disease has been linked to Gene Mutation 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 Gene Mutation 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, SUSCEPTIBILITY TO, 1 In this study, we investigated whether germline Gene Mutation of endothelin receptor B (EDNRB protein, human protein, human), a Genes involved in HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR), could also predispose for Melanocytic neoplasm (Millimole per Liter) However, the similarity between the distal Aganglionosis, Colonic in HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 and that due to EDN3 Genes Genes or EDNRB protein, human protein, human Gene Mutation 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, SUSCEPTIBILITY TO, 1 phenotype Our data strongly suggest that EDNRB protein, human protein, human is involved in predisposition for two different multigenic disorders, HSCR and Melanocytic neoplasm.[SEP]Relations: Melanocytic neoplasm has relations: disease_protein with ret unit of radiation dose, disease_protein with ret unit of radiation dose. EDNRB protein, human has relations: disease_protein with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, protein_protein with EDN3 Genes, disease_protein with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, protein_protein with EDN3 Genes. HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 has relations: disease_protein with ret unit of radiation dose, disease_protein with Glial Cell Line-Derived Neurotrophic Factor, disease_protein with ECE1 Genes, disease_protein with EDNRB protein, human, disease_protein with EDN3 Genes, disease_protein with ret unit of radiation dose, disease_protein with Glial Cell Line-Derived Neurotrophic Factor, disease_protein with ECE1 Genes, disease_protein with EDNRB protein, human, disease_protein with EDN3 Genes, disease_protein with ret unit of radiation dose, disease_protein with Glial Cell Line-Derived Neurotrophic Factor, disease_protein with ECE1 Genes, disease_protein with EDNRB protein, human, disease_protein with EDN3 Genes, disease_protein with ret unit of radiation dose, disease_protein with Glial Cell Line-Derived Neurotrophic Factor, disease_protein with ECE1 Genes, disease_protein with EDNRB protein, human, disease_protein with EDN3 Genes, disease_protein with ret unit of radiation dose, disease_protein with Glial Cell Line-Derived Neurotrophic Factor, disease_protein with ECE1 Genes, disease_protein with EDNRB protein, human, disease_protein with EDN3 Genes, disease_protein with ret unit of radiation dose, disease_protein with Glial Cell Line-Derived Neurotrophic Factor, disease_protein with ECE1 Genes, disease_protein with EDNRB protein, human, disease_protein with EDN3 Genes. hirschsprung Disease, susceptibility to has relations: disease_protein with EDNRB protein, human, disease_protein with Glial Cell Line-Derived Neurotrophic Factor, disease_disease with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_protein with EDN3 Genes, disease_protein with ret unit of radiation dose, disease_protein with EDNRB protein, human, disease_protein with Glial Cell Line-Derived Neurotrophic Factor, disease_disease with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_protein with EDN3 Genes, disease_protein with ret unit of radiation dose, disease_protein with EDNRB protein, human, disease_protein with Glial Cell Line-Derived Neurotrophic Factor, disease_disease with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_protein with EDN3 Genes, disease_protein with ret unit of radiation dose, disease_protein with EDNRB protein, human, disease_protein with Glial Cell Line-Derived Neurotrophic Factor, disease_disease with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_protein with EDN3 Genes, disease_protein with ret unit of radiation dose. Neuroglia-derived neurotrophic factor receptor binding has relations: molfunc_protein with Glial Cell Line-Derived Neurotrophic Factor, molfunc_protein with Glial Cell Line-Derived Neurotrophic Factor. ECE1 Genes has relations: disease_protein with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_protein with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. EDN3 Genes has relations: protein_protein with EDNRB protein, human, disease_protein with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, protein_protein with EDNRB protein, human, disease_protein with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. melanocytic neoplasm has relations: disease_disease with Melanocytic neoplasm, disease_disease with Melanocytic neoplasm.", "label": "yes"}
{"original_question": "Can the apoptosis regulator BAX trigger the release of cytochrome c?", "id": "converted_328", "sentence1": "Can the apoptosis regulator BAX trigger the release of CYCS gene?", "sentence2": "shogaol reduced the Mitochondrial Membranes potential (Matrix Metalloproteinases) and released CYCS gene from Mitochondria to Cytoplasmic matrix via BAX protein, human activation.  Moreover, overexpression of ER\u03b2 prevented BAX protein, human activation, CYCS gene release, caspase-3 activation, and PARP1 wt Allele cleavage during apoptosis. In this study, we demonstrated that EV71 infection altered BAX protein, human conformation and triggered its redistribution from the Cytoplasmic matrix to Mitochondria in RD cells. Subsequently, CYCS gene was released from Mitochondria to Cytoplasmic matrix. associated with translocation of BAX protein, human from the Cytoplasmic matrix to the Mitochondrial Membranes, CYCS gene release, and caspase activation.  Once activated, BAK1 wt Allele and BAX form proteolipid pores in the OMM leading to mitochondrial outer membrane permeabilization (mitochondrial outer membrane permeabilization), and the release of inner membrane space proteins, such as CYCS gene, which promotes caspase activation.   Our results showed that BGLAP wt Allele induced a caspase-dependent apoptosis by triggering a series of events in HeLa Cells including BAX protein, human translocation, CYCS gene release, caspase-3 activation, chromosome fragmentation followed by caspase-8 activation, Twice a day cleavage and eventually cell death.  BAX protein, human plays a key role in intrinsic apoptotic signaling in Neurons by allowing the release of mitochondrial CYCS gene.[SEP]", "label": "yes"}
{"original_question": "Are optogenetics tools used in the study and treatment of epilepsy?", "id": "converted_329", "sentence1": "Are optogenetics tools used in the study and treatment of epilepsy?", "sentence2": "The emerging revolutionary technique of optogenetics enables manipulation of the activity of specific neuronal populations in vivo with exquisite spatiotemporal resolution using light. We used optogenetic approaches to test the role of hippocampal excitatory Neurons in the lithium-pilocarpine model of acute elicited Seizures in awake behaving Rattus norvegicus. This chapter focuses on the development of optogenetics and on-demand technologies for the study of epilepsy and the control of Seizures. We then turn to the use of optogenetics, including on-demand optogenetics in the study of Epilepsy, which highlights the powerful potential of optogenetics for epilepsy research. Optogenetic techniques provide powerful tools for bidirectional control of neuronal activity and investigating alterations occurring in excitability disorders, such as epilepsy.  Therefore, one could optogenetically activate specific or a mixed population of Interneurons and dissect their selective or concerted inhibitory action on principal cells. We chose to explore a conceptually novel strategy involving simultaneous activation of mixed populations of Interneurons by optogenetics and study their impact on ongoing epileptiform activity in Mus sp. acute hippocampal slices. Our data suggest that global optogenetic activation of mixed interneuron populations is a more effective approach for development of novel therapeutic strategies for epilepsy, but the initial action potential generation in principal Neurons needs to be taken in consideration. Recently, a number of experiments have explored the treatments for epilepsy with optogenetic control of Neurons. Here, we discuss the possibility that an optogenetic approach could be used to control the release of gliotransmitters and improve astrocyte function such as glutamate and K(+) uptake, and thereby offer a potential strategy to investigate and treat astrocyte-related epilepsy. Optogenetic and designer receptor technologies provide unprecedented and much needed specificity, allowing for spatial, temporal and \"U\" lymphocyte type-selective modulation of neuronal circuits. Using such tools, it is now possible to begin to address some of the fundamental unanswered questions in epilepsy, to dissect epileptic neuronal circuits and to develop new intervention strategies.  We then turn to the use of optogenetics, including on-demand optogenetics in the study of Epilepsy, which highlights the powerful potential of optogenetics for epilepsy research. Moreover, optogenetics may be considered for developing potential treatment strategies for brain diseases, particularly for excitability disorders such as epilepsy. This chapter focuses on the development of optogenetics and on-demand technologies for the study of epilepsy and the control of Seizures. How might novel technologies such as optogenetics lead to better treatments in epilepsy? WONOEP appraisal: optogenetic tools to suppress Seizures and explore the mechanisms of epileptogenesis. Finally, optogenetic tools allow rapid and reversible suppression of epileptic electroencephalography (EEG) activity upon photoactivation. Our data suggest that epileptiform activity in the Hippocampus Hippocampus hippocampus caused by impaired inhibition may be controlled by optogenetic silencing of principal Neurons and potentially can be developed as an alternative treatment for epilepsy. Seizure suppression by high frequency optogenetic stimulation using in vitro and in vivo animal models of epilepsy. Optogenetic techniques provide powerful tools for bidirectional control of neuronal activity and investigating alterations occurring in excitability disorders, such as epilepsy.  We first discuss the benefits and caveats to using optogenetic approaches and recent advances in optogenetics related tools. We then turn to the use of optogenetics, including on-demand optogenetics in the study of Epilepsy, which highlights the powerful potential of optogenetics for epilepsy research.[SEP]", "label": "yes"}
{"original_question": "Is micro RNA 1 (miR-1) implicated in cardiac arrhythmias?", "id": "converted_330", "sentence1": "Is micro RNA 1 (miR-1) implicated in cardiac Cardiac Arrhythmia?", "sentence2": "Dysfunction of the gap junction protein connexin 43 (GJA1 gene), an established miR-1 target, during Cardiac Hypertrophy leads to Tachycardia, Ventricular (VT). 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 Cardiac Arrhythmia. 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 Cardiac Arrhythmia 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 Cardiac Arrhythmia. 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 Cardiac Arrhythmia 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 Cardiac Arrhythmia 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 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 Cardiac Arrhythmia 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 Cardiac Arrhythmia through targeting of Regulatory Protein Changes in abundance of muscle-specific microRNA, miR-1, have been implicated in Heart Diseases, including arrhythmia and Chest>Heart failure Changes in abundance of muscle-specific microRNA, miR-1, have been implicated in Heart Diseases, including arrhythmia and Chest>Heart failure[SEP]Relations: GJA1 has relations: anatomy_protein_present with Chest>Heart, anatomy_protein_present with Chest>Heart. Chest>Heart disease has relations: disease_disease with Coronary Arteriosclerosis, disease_disease with Chest>Heart failure, disease_disease with Coronary Arteriosclerosis, disease_disease with Chest>Heart failure.", "label": "yes"}
{"original_question": "Does thyroid hormone signaling affect microRNAs expression in the heart?", "id": "converted_331", "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, T\u2083 treatment increased miR-350 expression. Through a bioinformatics screening using TargetScan, we identified Thyroid Hormone Receptor (TR\u03b21), which negatively regulates \u03b2-MHC transcription, as a target of miR-27a hese findings suggested that miR-27a regulates \u03b2-MHC gene expression by targeting TR\u03b21 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 \u03b2-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 \u03b2-MHC gene upregulation.[SEP]Relations: Thyroid Hormones receptor binding has relations: molfunc_protein with MED13 gene protein, human, molfunc_protein with MED13 gene protein, human. MED13 gene protein, human has relations: anatomy_protein_present with Chest>Heart, anatomy_protein_present with Chest>Heart.", "label": "yes"}
{"original_question": "Do all archaea possess multiple origins of DNA replication?", "id": "converted_332", "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]", "label": "no"}
{"original_question": "Is p100 the precursor protein molecule of the NF-kappaB transcription factor subunit p50?", "id": "converted_333", "sentence1": "Is TPX2 protein, human the precursor protein molecule of the NF-kappa B 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-\u03baB (NF-\u03baB) 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-kappa B 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-kappa B functions as a hetero- or homo-dimer which can be formed from five NF-kappa B 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-kappa B. 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-kappa B regulation. Targeted disruption of the Rel/NF-kappa B family members NF-kappaB2, encoding TPX2 protein, human/GTF2H4 gene, and RELB gene in CASP14 gene results in anatomical defects of secondary Lymphoid Tissue. Here, we show that in Therapeutic gamma delta T-Specimen Source Codes - Lymphocytes infected with the Human T-lymphotropic virus 2 (HTLV), 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-kappa B 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-kappa B-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-kappa B dimers. In one exceptional case, generation of the Pattern ERG P50 subunit of the transcriptional regulator NF-kappa B, 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-kappa B 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-kappa B involves proteasome-mediated processing of the NF-kappaB1 Enhancer of Filamentation 1 precursor protein, which generates the Pattern ERG P50 subunit of NF-kappa B This effort identified NF-kappaB1 (Enhancer of Filamentation 1), an atypical IkappaB molecule and the precursor of NF-kappa B subunit Pattern ERG P50 NF-kappa B functions as a hetero- or homo-dimer which can be formed from five NF-kappa B 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-kappa B 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]", "label": "no"}
{"original_question": "Is there a difference in the rate between gene fusion and gene fission?", "id": "converted_334", "sentence1": "Is there a difference in the rate between gene fusion and gene 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 gene fusion and fission in Oryza sativa and Arabidopsis sp. sp. thaliana <plant> We have identified all differentially composite or split Genes in 2 fully sequenced Genome, Plant, Oryza sativa and Arabidopsis sp. sp. thaliana <plant> Polarizing these events by outgroup comparison revealed differences in the rate of gene fission but not of gene fusion in the rice and Arabidopsis sp. sp. lineages. Gene fission occurred at a higher rate than gene 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 gene fusions/fissions. We provide evidence showing that the contribution of gene fusion/fission to the evolution of multi-domain Bacterial Proteins is lower-bounded by 27% and upper-bounded by 64%. We conclude that gene 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]", "label": "yes"}
{"original_question": "Can cognitive behavioral therapy improve fatigue in cancer patients?", "id": "converted_335", "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: peripheral nervous system disease has relations: disease_disease with Peripheral Nervous System Diseases, disease_disease with Peripheral Nervous System Diseases.", "label": "yes"}
{"original_question": "Is protein Fbw7 a SCF type of E3 ubiquitin ligase?", "id": "converted_336", "sentence1": "Is protein Fbw7 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 (Fbw7), 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 protein, human (also known as Sel-10, hCdc4, hAgo, or Fbw7) 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.  Fbw7 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. Fbw7 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 Fbw7 (also known as FBXW7 protein, human, hCdc4 and Sel-10) functions as a substrate recognition component of a Stem Cell Factor-type E3 ubiquitin ligase. Stem Cell Factor(Fbw7) facilitates polyubiquitination and subsequent degradation of various Proteins such as Notch, Cyclin E, c-myc Genes and JUN gene. FBXW7 protein, human (also known as Fbw7, SEL-10, hCdc4, or hAgo) 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 protein, human (F-Box Domain/WD repeat-containing protein 7; also called FBXW7 wt Allele, Sel10, Ago, and Fbw7) 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 Fbw7 (also known as FBXW7 protein, human, hCdc4 and Sel-10) functions as a substrate recognition component of a Stem Cell Factor-type E3 ubiquitin ligase. We demonstrate here that Fbw7 (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(Fbw7) 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 (Fbw7) 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 Fbw7 (also known as Sel-10, hCdc4, or hAgo) 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 Fbw7 is expressed prominently in the Endothelial Cells lineage of embryos. The F-Box Domain protein Fbw7 (also known as FBXW7 protein, human, hCdc4 and Sel-10) functions as a substrate recognition component of a Stem Cell Factor-type E3 ubiquitin ligase We demonstrate here that Fbw7 (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 (Fbw7), 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: F-Box Domain domain binding has relations: molfunc_protein with SKP1 protein, human, molfunc_protein with SKP1 protein, human.", "label": "yes"}
{"original_question": "Is there increased incidence of incontinence in athletes?", "id": "converted_337", "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]", "label": "yes"}
{"original_question": "Are there enhancer RNAs (eRNAs)?", "id": "converted_338", "sentence1": "Are there enhancer RNA (eRNAs)?", "sentence2": "active enhancers are transcribed, producing a class of noncoding RNA called enhancer RNA (eRNAs). eRNAs are distinct from long noncoding RNA (lncRNAs), but these two species of noncoding RNA may share a similar role in the activation of mRNA transcription  eRNAs may then facilitate enhancer-Promoter interaction or activate Promoter-driven transcription Enhancer of transcription of transcription RNA: a class of long noncoding RNA synthesized at enhancers Enhancer of transcription of transcription RNA and regulated transcriptional programs enhancers have been found to be broadly transcribed, resulting in the production of enhancer-derived RNA, or eRNAs The emerging roles of eRNAs in transcriptional regulatory networks we found certain enhancer RNA (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 of transcription of transcription RNA: 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 RNA (eRNAs), which are long non-coding RNA transcribed from gene enhancer regions, in transcriptional regulation. Since the discovery that many transcriptional enhancers are transcribed into long noncoding RNA termed \"enhancer RNA\" (eRNAs), their putative role in enhancer function has been debated. Recent studies have revealed that active enhancers are transcribed, producing a class of noncoding RNA called enhancer RNA (eRNAs). Enhancer of transcription of transcription RNA (eRNAs) are a class of long noncoding RNA (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 RNA (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as enhancer RNA (eRNAs). 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 RNA (eRNAs).  A subset of enhancers are occupied by RNA Polymerase II (RNAP II) and transcribed to produce long non-coding RNA 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 RNA (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as enhancer RNA (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 RNA (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 RNA (eRNAs) within enhancer domains defined by the presence of Histone H3 monomethylated at lysine 4.  Enhancer of transcription of transcription RNA (eRNAs) are a class of long noncoding RNA (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 RNA (eRNAs), which are long non-coding RNA transcribed from gene enhancer regions, in transcriptional regulation. Recent studies have revealed that active enhancers are transcribed, producing a class of noncoding RNA called enhancer RNA (eRNAs). eRNAs are distinct from long noncoding RNA (lncRNAs), but these two species of noncoding RNA may share a similar role in the activation of mRNA transcription. Enhancer of transcription of transcription RNA (eRNAs) are a class of long noncoding RNA (lncRNA) expressed from active enhancers, 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 RNA (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 RNA called enhancer RNA (eRNAs). eRNAs are distinct from long noncoding RNA (lncRNAs), but these two species of noncoding RNA may share a similar role in the activation of mRNA transcription.[SEP]", "label": "yes"}
{"original_question": "Are conserved noncoding elements associated with the evolution of animal body plans?", "id": "converted_339", "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]", "label": "yes"}
{"original_question": "Are DNA methylation maps applicable to the diagnosis of non-small-cell lung carcinomas?", "id": "converted_340", "sentence1": "Are DNA methylation maps applicable to the diagnosis of Non-Small Cell Lung Carcinoma?", "sentence2": "Here we present a genome-wide DNA methylation analysis of NSCLC samples and paired Structure of parenchyma of lung, where we combine MethylCap and next generation sequencing (MethylCap-seq) to provide comprehensive DNA methylation maps of the Specimen Source Codes - Specimen Source Codes - tumor and paired lung samples. Analysis of the MethylCap-seq data revealed a strong positive correlation between replicate experiments and between paired Specimen Source Codes - Specimen Source Codes - tumor/lung samples. We identified 57 differentially methylated regions (DMRs) present in all NSCLC Neoplasms analyzed by MethylCap-seq. While hypomethylated DMRs did not correlate to any particular functional category of Genes, the hypermethylated DMRs were strongly associated with Genes encoding transcriptional regulators. Furthermore, subtelomeric regions and satellite repeats were hypomethylated in the NSCLC samples. We also identified DMRs that were specific to two of the major subtypes of NSCLC, Adenocarcinoma and Squamous cell carcinoma of mouth. Collectively, we provide a resource containing genome-wide DNA methylation maps of NSCLC and their paired Structure of parenchyma of lung, and comprehensive lists of known and novel DMRs and associated Genes in NSCLC. Genome-wide DNA methylation profiling of non-small cell lung carcinomas. Genomewide DNA methylation analysis identifies novel methylated Genes in Non-Small Cell Lung Carcinoma. To identify candidate markers for use in NSCLC diagnosis, we used genomewide DNA methylation maps that we had previously generated by MethylCap and next-generation sequencing and listed the most significant differentially methylated regions (DMRs). The 25 DMRs with highest significance in their methylation scores were selected. The methylation status of these DMRs was investigated in 61 Neoplasms and matching control Structure of parenchyma of lung by methylation-specific polymerase chain reaction. We found 12 novel DMRs that showed significant differences between Specimen Source Codes - Specimen Source Codes - tumor and control Structure of parenchyma of lung. We also identified three novel DMRs for each of the two most common NSCLC subtypes, Adenocarcinoma and Squamous cell carcinoma of mouth. We propose a panel of five DMRs, composed of novel and known markers that exhibit high specificity and sensitivity to distinguish Neoplasms from control Structure of parenchyma of lung. Here we present a genome-wide DNA methylation analysis of NSCLC samples and paired Structure of parenchyma of lung, where we combine MethylCap and next generation sequencing (MethylCap-seq) to provide comprehensive DNA methylation maps of the Specimen Source Codes - Specimen Source Codes - tumor and paired lung samples. It is a very stable and specific ResponseLevel - ResponseLevel - modification and therefore in principle a very suitable marker for epigenetic phenotyping of Neoplasms. Here we present a genome-wide DNA methylation analysis of NSCLC samples and paired Structure of parenchyma of lung, where we combine MethylCap and next generation sequencing (MethylCap-seq) to provide comprehensive DNA methylation maps of the Specimen Source Codes - Specimen Source Codes - tumor and paired lung samples. Here we present a genome-wide DNA methylation analysis of NSCLC samples and paired Structure of parenchyma of lung, where we combine MethylCap and next generation sequencing (MethylCap-seq) to provide comprehensive DNA methylation maps of the Specimen Source Codes - Specimen Source Codes - tumor and paired lung samples. The MethylCap-seq data were validated by bisulfite sequencing and methyl-specific polymerase chain reaction of selected regions. Here we present a genome-wide DNA methylation analysis of NSCLC samples and paired Structure of parenchyma of lung, where we combine MethylCap and next generation sequencing (MethylCap-seq) to provide comprehensive DNA methylation maps of the Specimen Source Codes - Specimen Source Codes - tumor and paired lung samples.[SEP]", "label": "yes"}
{"original_question": "Is the protein product of the cylindromatosis gene (CYLD) a deubiquitinating enzyme?", "id": "converted_341", "sentence1": "Is the protein product of the cylindromatosis gene (CYLD) a deubiquitinating Enzyme [APC]?", "sentence2": "CYLD was originally identified as a tumor suppressor gene Mutation Abnormality 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-\u03baB 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 nuclear factor kappa B (NF-\u03baB) pathway. CYLD is a lysine 63-deubiquitinating Enzyme [APC] that inhibits NF-\u03baB and JNK signaling. Tumor Suppressor Genes 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 gene, which is Mutation Abnormality 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-\u03baB) signaling pathway by removing lysine-63-linked polyubiquitin chains from NF-\u03baB activating proteins.  Here, we identify the deubiquitinating Enzyme [APC] CYLD, the Ancell-Spiegler Adenoid Cystic Carcinoma tumor suppressor gene, as a negative regulator of proximal events in Wnt/beta-catenin signaling. CYLD is a tumour-suppressor gene that is Mutation Abnormality 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-kappa B 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-kappa B.  CYLD, a tumor suppressor gene, has deubiquitinating Enzyme [APC] activity and inhibits the activation of transcription factor NF-kappa B. 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-kappa B pathway activation. Deubiquitinating ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS (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 Mutation Abnormality 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-kappa B. 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-\u03baB signaling pathway and attenuates NF-\u03baB and JNK signaling. The cylindromatosis tumor suppressor gene (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-kappa B signalling. Here, we examined the potential role of the deubiquitinating Enzyme [APC] CYLD (cylindromatosis), mutation 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-kappa B 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-kappa B signalling. Cylindromatosis gene (CYLD) is a ubiquitously expressed deubiquitinating Enzyme [APC], which interacts with members of the NF-\ufffdB signaling pathway and attenuates NF-\ufffdB 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-kappa B activation by Tumor Necrosis Factor Receptor family members. Here, we identify the deubiquitinating Enzyme [APC] CYLD, the Ancell-Spiegler Adenoid Cystic Carcinoma tumor suppressor gene, 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-\u03baB signaling pathway and attenuates NF-\u03baB 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-kappa B signalling The cylindromatosis tumor suppressor gene (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-\u03baB signaling pathway and attenuates NF-\u03baB and JNK signaling The cylindromatosis tumor suppressor gene (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-\u03baB-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 gene, 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-\u03baB) signaling pathway by removing lysine-63-linked polyubiquitin chains from NF-\u03baB activating proteins CYLD, a tumor suppressor gene, has deubiquitinating Enzyme [APC] activity and inhibits the activation of transcription factor NF-kappa B Here, we examined the potential role of the deubiquitinating Enzyme [APC] CYLD (cylindromatosis), mutation 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-kappa B[SEP]Relations: Brooke-Spiegler syndrome has relations: disease_protein with CYLD, disease_protein with CYLD.", "label": "yes"}
{"original_question": "Has the presence of delayed enhancement been documented in athletes performing strenuous exercise?", "id": "converted_342", "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 \u00b1 5.9 vs. 51.1 \u00b1 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]", "label": "yes"}
{"original_question": "Is triadin involved in cardiac function?", "id": "converted_343", "sentence1": "Is triadin involved in cardiac function?", "sentence2": "ASPH gene (JCN), a 26-kd Sarcoplasmic Reticulum (SNCG wt Allele) transmembrane protein, forms a quaternary protein complex with the Ryanodine Receptor Calcium Release Channel, CASQ2 gene, and triadin in the SNCG wt Allele lumen of Specimen Source Codes - Cardiac muscle. Within this complex, CASQ2 gene, triadin, and JCN appear to be critical for normal regulation of Ryanodine Receptor Calcium Release Channel-mediated calcium (cyclophosphamide/doxorubicin protocol) release. Recent studies have uncovered functional roles of both JCN and triadin in the mouse heart, using transgenic overexpression strategies, which exhibit varying phenotypes including mild SNCG wt Allele structural alterations, prolongation of cyclophosphamide/doxorubicin protocol transient decay, impaired relaxation, and Cardiac Hypertrophy and/or Congestive Congestive heart failure. TRDN gene is involved in the regulation of cardiac excitation-contraction coupling.  Thus the maintenance of triadin expression is essential for normal SNCG wt Allele cyclophosphamide/doxorubicin protocol cycling and contractile function. Ca2+ release from the cardiac junctional Sarcoplasmic Reticulum (SNCG wt Allele) is regulated by a complex of proteins, including the Ryanodine Receptor Calcium Release Channel (Ryanodine Receptor Calcium Release Channel complex location), CASQ2 gene (CSQ), ASPH gene-2 (JCN), and triadin 1 (T-Cell Receptors delta-Chain). Impaired Sarcoplasmic Reticulum (SNCG wt Allele) cyclophosphamide/doxorubicin protocol release has been suggested to contribute to the depressed cardiac function in Congestive Congestive heart failure. The release of cyclophosphamide/doxorubicin protocol from the SNCG wt Allele may be regulated by the Ryanodine Receptor Calcium Release Channel, triadin, ASPH gene-2, CASQ2 gene, and a histidine-rich, cyclophosphamide/doxorubicin protocol-binding protein 2 (HRC).[SEP]", "label": "yes"}
{"original_question": "Is Mammaprint approved by the United States Food and Drug Administration?", "id": "converted_344", "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]", "label": "yes"}
{"original_question": "Are microRNA (miR) regulated through DNA methylation of their promoters?", "id": "converted_345", "sentence1": "Are microRNA (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 microRNA that targets TCF7L1 gene and attenuates early neural differentiation in mouse 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 microRNA expression in Chronic Lymphocytic Leukemia Integration (data processing) (data processing) 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 CLL NA methylation of microRNA 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 MicroRNAs 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 MicroRNAs 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 MicroRNAs 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 MicroRNAs 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 MicroRNAs 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]", "label": "yes"}
{"original_question": "Are nucleosomes positioned at DNA replication origins?", "id": "converted_346", "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 location 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]", "label": "no"}
{"original_question": "Does nimotuzumab improve survival of glioblastoma patients?", "id": "converted_347", "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]", "label": "yes"}
{"original_question": "Is there a relation between ANP and transcapillary albumin escape?", "id": "converted_348", "sentence1": "Is there a relation between Atrial Natriuretic Factor and transcapillary ALB gene escape?", "sentence2": "Thus, in a large ethnically homogeneous cohort of diabetic subjects, our data show: (1) a significant association of C708/T Genetic Polymorphism with Microalbuminuria in long-term Diabetes Mellitus and with both lower plasma Atrial Natriuretic Factor levels and widespread ALB gene leakage hese results suggest a possible role of PND gene in conferring protection from Kidney Diseases and microvascular damage in type 1 Diabetes Mellitus. Moreover, the increased susceptibility of the Glomerular capillaries structure in diabetics to Atrial Natriuretic Factor seems to be part of a more generalized capillary abnormality, because Atrial Natriuretic Factor also increases the transcapillary escape of ALB gene. In summary, low dose Atrial Natriuretic Factor infusion in healthy subjects caused a shift of plasma water and Electrolyte [EPC] from the circulation, with ALB gene escape as a secondary phenomenon.[SEP]", "label": "yes"}
{"original_question": "Can chronological age be predicted by measuring telomere length?", "id": "converted_349", "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]", "label": "no"}
{"original_question": "Is there an association between c-reactive protein concentrations and outcomes of subarachnoid hemorrhage patients?", "id": "converted_350", "sentence1": "Is there an association between c-reactive protein concentrations and outcomes of Subarachnoid Hemorrhage patients?", "sentence2": "Besides the baseline characteristics, daily interleukin-6 (Recombinant Interleukin-6), procalcitonin, C-reactive protein levels, and leukocyte counts were prospectively measured until day 14 after Subarachnoid Hemorrhage. Occurrence of infectious complications and application of therapeutic Hypothermia due to exposure were assessed as confounding factors. The primary end point was outcome after 3 months, assessed by Glasgow Outcome Scale; the secondary end point was the occurrence of DINDs. RESULTS: : During a 3-year period, a total of 138 patients were included. All inflammatory parameters measured were higher in patients with unfavorable outcome (Glasgow Outcome Scale score, 1-3). Twenty-three and 28 patients showed poor outcome and symptomatic Vasospasm after Yakut language, respectively. Both preoperative and postoperative C-reactive protein levels were significantly higher in patients with a poor outcome compared with patients with a good outcome (P<0.05). e area under the receiver operating characteristic curve of C-reactive protein measured on postoperative day 1 or 2 (C-reactive protein POD1-2) for predicting a poor clinical outcome was 0.870, and its cutoff point of 4 mg/dL had a sensitivity of 0.826 and a specificity of 0.843. A high C-reactive protein level after Aneurysm treatment was associated with severe Progressive neurologic deterioration on admission, Cerebral Infarction, Cerebral Hemorrhage, and surgical decompression (P<0.05). C-reactive protein POD1-2, and not the preoperative C-reactive protein, was an independent factor in predicting symptomatic Vasospasm (P<0.05). In patients with symptomatic Vasospasm, an increase in the postoperative C-reactive protein was associated with the time profile of developing symptomatic Vasospasm. Postoperative C-reactive protein, especially C-reactive protein POD1-2, can be a useful prognostic factor for both poor outcome and symptomatic Vasospasm in patients with aneurysmal Yakut language. Serum C-reactive protein levels were related to severity of ASAH1 wt Allele. Patients with lower GCS scores and higher Hunt and Hess and Fisher grades presented statistically significant higher serum C-reactive protein levels. Patients with higher serum C-reactive protein levels had a less favorable prognosis. Increased serum C-reactive protein levels were strongly associated with worse clinical prognosis in this study. After Yakut language, the value of C-reactive protein (C-reactive protein)--an acute phase sensitive inflammatory marker--as a prognostic factor has been poorly studied, with conflicting results. Admission (18.0\u2009\u00b1\u200935.7 vs 8.5\u2009\u00b1\u20098.4 mg/l) and postoperative (41.0\u2009\u00b1\u200940.2 vs 21.1\u2009\u00b1\u200924.1 mg/l) C-reactive protein levels were higher (p\u2009<\u20090.001) in those with a poor outcome than in those with a favourable outcome, but C-reactive protein values did not predict delayed cerebral ischaemia or Cerebral Infarction. Higher increase in C-reactive protein level between admission and postoperative morning, however, independently predicted poor outcome (p\u2009=\u20090.004). C-reactive protein levels correlate with outcome but do not seem to predict delayed cerebral ischaemia or Infarction after Yakut language. Systemic oxygen consumption is associated with hsCRP levels in the first 14 days after Yakut language and is an independent predictor of Noninfiltrating Intraductal Carcinoma. Intracranial hypertension was associated with an inflammatory response, indicating activation of the inflammatory cascade in the Head>Brain (ECF) and systemic circulation with high Recombinant Interleukin-6 and C-reactive protein (C-reactive protein) plasma levels after Yakut language, the latter associated with unfavourable outcome. Patients with angiographic Vasospasm had higher C-reactive protein measurements in serum and Cerebrospinal Fluid, in a statistically significant fashion (p < 0.0001). Additionally, patients with higher C-reactive protein levels in serum and Cerebrospinal Fluid had less favorable outcome in this cohort. Furthermore, patients developing angiographically proven Vasospasm demonstrated significantly elevated C-reactive protein levels in serum and Cerebrospinal Fluid, and increased C-reactive protein measurements were strongly associated with poor clinical outcome in this cohort. Finally, serum concentrations of Intercellular adhesion molecule 1, Vascular Cell Adhesion Molecule-1, and hsCRP during the early (P = .0055, P = .0266, and P = .0266) and late (P = .0423, P = .0041, and P = .0004) period were significantly higher in patients with DIND than in patients without DIND. CONCLUSIONS: Serum levels of Intercellular adhesion molecule 1, Vascular Cell Adhesion Molecule-1 and hsCRP during the early and late period following Yakut language correlate with DIND C-reactive protein levels on days 5, 6, 7, and 8 were statistically significantly higher in the group of patients developing a DIND (P < 0.025, P < 0.016, P < 0.011, P < 0.0002). Overall C-reactive protein values were higher with increasing severity of the initial ictus according to the Hunt and Hess Scale and to the outcome according to the Glasgow Outcome Scale from day 3 on. The presented data do not prove that Leukocytes and C-reactive protein values have a direct contribution to the pathogenesis of ischemic complications following Yakut language, but it supports the assertion that Inflammation may present a common pathogenic pathway in the development of such complications. The C-reactive protein and transforming growth factor beta 1 levels in Cerebrospinal Fluid are strongly concerned with communicating Hydrocephalus after Yakut language.[SEP]Relations: Head>Brain Infarction has relations: disease_disease with Cerebral Infarction, disease_disease with Cerebral Infarction.", "label": "yes"}
{"original_question": "Can RNASeq be used for the analysis of nascent transcripts?", "id": "converted_351", "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": "Do RNA:DNA hybrids preferentially form in high or low GC regions?", "id": "converted_352", "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\u2022DNA 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\u2022DNA hybrids may represent a common mutagenic conformation. Recently, we demonstrated that cotranscriptional RNA\u2022DNA hybrids are preferentially formed at GC-rich trinucleotide and tetranucleotide repeat sequences in vitro as well as in human genomic DNA.[SEP]", "label": "yes"}
{"original_question": "Are shadow enhancers associated with development?", "id": "converted_353", "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]", "label": "yes"}
{"original_question": "Does prudent diet reduce cardiovascular risk?", "id": "converted_354", "sentence1": "Does prudent diet reduce Cardiovascular system risk?", "sentence2": "Using this approach, large prospective studies have reported reductions in CVD risk ranging from 10 to 60% in groups whose diets can be variously classified as \u2018Healthy\u2019, \u2018Prudent\u2019, Mediterranean\u2019 or \u2018DASH compliant\u2019. Our findings suggest that a heart healthy dietary pattern is associated with moderately reduced risk of MI, but not related to risk of vinyltriethoxysilane. The systematically reviewed studies reveal that a high adherence to a Mediterranean type of diet or \"prudent diet\" is associated with reduced risk of CVD and some types of Primary malignant neoplasm, even in the elderly. In a large healthy Italian population, non-predefined dietary patterns including Food considered to be rather unhealthy, were associated with higher levels of Cardiovascular system risk factors, C-reactive protein and individual global CVD risk, whereas a \"prudent-healthy\" pattern was associated with lower levels. We observed an inverse association between the prudent pattern and Anterior myocardial infarction, with higher levels being protective. After multivariable adjustment, the prudent diet was associated with a 28% lower risk of Cardiovascular system mortality (95% confidence interval [CI], 13 to 40) and a 17% lower risk of all-cause mortality (95% CI, 10 to 24) when the highest quintile was compared with the lowest quintile.  Greater adherence to the prudent pattern may reduce the risk of Cardiovascular system and total mortality, whereas greater adherence to the Western pattern may increase the risk among initially healthy women. Composite diets (such as DASH diets, Mediterranean diet, 'prudent' diet) have been demonstrated to reduce the risk of Hypertensive disease and altretamine/cisplatin/cyclophosphamide protocol.[SEP]", "label": "yes"}
{"original_question": "Are there Conserved Noncoding Elements (CNEs) in plant genomes?", "id": "converted_355", "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 allergen> <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 allergen> <Plant allergen> and rice We consequently compared the Genome of Arabidopsis thaliana <Plant allergen> <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]", "label": "yes"}
{"original_question": "Can tetracycline affect tooth formation?", "id": "converted_356", "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]", "label": "yes"}
{"original_question": "Could Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) cause sudden cardiac death?", "id": "converted_357", "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 Cardiac Arrhythmia induced by physical or emotional stress, in the absence structural Chest>Heart abnormalities. The Cardiac Arrhythmia 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 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 Syncope, Cardiogenic 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 arrhythmia and high risk of Sudden Cardiac 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 cardiomyopathy (Arrhythmogenic Right Ventricular Dysplasia) 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: Ventricular tachycardia has relations: disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with Brugada Syndrome (disorder). Jervell-Lange Nielsen syndrome has relations: disease_disease with Long QT Syndrome, disease_disease with Long QT Syndrome. arrhythmogenic right ventricular dysplasia has relations: disease_phenotype_positive with Sudden death, disease_phenotype_positive with Sudden death. Cardiac arrest has relations: disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with Long QT Syndrome. Sudden death has relations: disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with sudden Cardiac Arrest, disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with sudden Cardiac Arrest, disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy. Long QT Syndrome has relations: disease_phenotype_positive with Sudden death, disease_phenotype_positive with Sudden death, disease_phenotype_positive with Sudden death, disease_phenotype_positive with Sudden death. catecholaminergic Polymorphism Ventricular Tachycardia by ECG Finding has relations: disease_phenotype_positive with Sudden death, disease_disease with Long QT Syndrome, disease_phenotype_positive with Sudden death, disease_disease with Long QT Syndrome. Sudden unexpected death in Epilepsy has relations: phenotype_phenotype with Sudden death, phenotype_phenotype with Sudden death. Hypertrophic cardiomyopathy has relations: disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy. Sudden cardiac death has relations: phenotype_phenotype with Sudden death, disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, phenotype_phenotype with Sudden death, disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy. sudden Cardiac Arrest has relations: disease_phenotype_positive with Sudden death, disease_phenotype_positive with Sudden death. Ventricular arrhythmia has relations: disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with Brugada Syndrome (disorder), disease_phenotype_positive with Long QT Syndrome. Arrhythmia has relations: disease_phenotype_positive with sudden Cardiac Arrest, disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy, disease_phenotype_positive with sudden Cardiac Arrest, disease_phenotype_positive with Hypertrophic obstructive cardiomyopathy.", "label": "yes"}
{"original_question": "Does Apolipoprotein E (ApoE) have anti-inflammatory activity?", "id": "converted_358", "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]", "label": "yes"}
{"original_question": "Is the ACE inhibitor indicated for lung cancer treatment?", "id": "converted_359", "sentence1": "Is the CDE protocol-cyclophosphamide/doxorubicin/etoposide inhibitor indicated for Primary malignant neoplasm of lung treatment?", "sentence2": "The Peptidyl-Dipeptidase A (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).  Angiotensin-converting enzyme (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]", "label": "no"}
{"original_question": "Are genes symmetrically distributed between leading and lagging DNA strand in bacteria?", "id": "converted_360", "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 essential Genes are more preferentially situated at the leading Genomic Orientation than at the lagging Genomic Orientation remarkable Genomic Orientation-bias of the distribution of essential Genes 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 DNA-Directed RNA Polymerase. 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 essential Genes 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]", "label": "no"}
{"original_question": "Is c-myc subject to regulation by the circadian clock?", "id": "converted_361", "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 (Bmal1, Clock, Per1 and PER2 gene) and three clock-controlled Genes, cdc (MYC protein, human, Cyclin D1 and Wee1) 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 Bmal1 reduced the expression of Period Circadian Protein Homolog 1, per2, PER3 gene, WEE1 gene and p53. The expression of oncoprotein oncoprotein p21 and c-myc was also altered in certain Cultured Cell Line. In particular, the proto-oncogene c-myc Genes protein, human has been documented to be under circadian regulation. The circadian expression of c-myc Genes 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 Genes 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 Genes 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 gene 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 gene knockdown. We also show that ARNTL wt Allele epigenetic inactivation impairs the characteristic circadian clock expression pattern of Genes such as C-MYC, catalase, and EP300 wt Allele in association with a loss of ARNTL wt Allele occupancy in their respective Promoter. PER2 gene mutant (PER2 gene(m/m)) CASP14 gene show an increase in Lymphoma and deregulated expression of Cyclin D and c-myc Genes protein, human Genes that are key to proliferation control. The expression of Genes, cdc such as Wee1, Cyclins, and c-myc Genes 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 Genes 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 Genes 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 Genes protein, human, Cyclin D1, Cyclin A, Mdm-2, and Gadd45alpha, is deregulated in mPer2 mutant CASP14 gene.[SEP]Relations: PER3 has relations: protein_protein with ammonium tetrathiomolybdate, protein_protein with ammonium tetrathiomolybdate.", "label": "yes"}
{"original_question": "is there an increase in ultrasound comets after intense exercise?", "id": "converted_362", "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]", "label": "yes"}
{"original_question": "Can cffDNA be used for non-invasive testing?", "id": "converted_363", "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]", "label": "yes"}
{"original_question": "Do U6-associated proteins Lsm4 and Lsm6 interact with SMN?", "id": "converted_364", "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]", "label": "yes"}
{"original_question": "Does MVIIA and MVIIC bind to the same calcium channel?", "id": "converted_365", "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 (omega-Conotoxins MVIIA 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]", "label": "no"}
{"original_question": "Is arimoclomol a co-inducer of the heat shock response?", "id": "converted_366", "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 (Amyotrophic Lateral Sclerosis) 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 (Amyotrophic Lateral Sclerosis) 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 (Amyotrophic Lateral Sclerosis) in a mouse model in which Neurons, Efferent in the Spinal Cord and motor cortex degenerate.[SEP]", "label": "yes"}
{"original_question": "Has silicon been used in treatment of  incontinence ?", "id": "converted_367", "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\u00ae (CONSTRICTING BANDS, CONGENITAL) from A. M. S. (Minnetonka, MNSs Blood-Group System, USA) and the soft anal band\u00ae 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\u2122 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 (Porg\u00e9s). 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-Porg\u00e8s) 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]", "label": "yes"}
{"original_question": "Does the 3D structure of  the genome remain stable during cell differentiation?", "id": "converted_368", "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: germ \"U\" lymphocyte Cell Nucleus has relations: cellcomp_cellcomp with Cell Nucleus, cellcomp_cellcomp with Cell Nucleus. Heterochromatin has relations: cellcomp_cellcomp with chromatin location, cellcomp_cellcomp with chromatin location.", "label": "no"}
{"original_question": "Does dronedarone  affect  T3 and T4 levels?", "id": "converted_369", "sentence1": "Does dronedarone  affect  T3 thoracic segmental innervation and T4 levels?", "sentence2": "Amiodarone resulted in increased T4, T4/T3 thoracic segmental innervation thoracic segmental innervation and rT3, whereas dronedarone did not alter the Thyroid Hormones profile in normal animals. Fifty-five Wistar rats were randomly allocated to a 2-week oral treatment with either vehicle (n=18), amiodarone (30 mg/kg, n=20), or dronedarone (30 mg/kg, n=17). Thyroid function was similar in the 3 groups. Specimen Source Codes - Specimen Source Codes - Plasma levels of T3 thoracic segmental innervation thoracic segmental innervation, T4, and rT3 were changed after SR 33589 treatment except a decrease in T4 level at the highest dose whilst the T4 T3 thoracic segmental innervation thoracic segmental innervation ratio and the level of rT3 were dose-dependently increased by amiodarone treatment.[SEP]", "label": "no"}
{"original_question": "Does triiodothyronine (T3) has cardiac angiogenic effects?", "id": "converted_370", "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-\u03b2 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]", "label": "yes"}
{"original_question": "Is the HRC Ser96Ala variant associated with sudden cardiac death in patients with dilated cardiomyopathy?", "id": "converted_371", "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 Cardiomyopathy, Dilated 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 Cardiomyopathy, Dilated. 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 Cardiomyopathy, Dilated. 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: Ventricular arrhythmia has relations: disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated. Sudden death has relations: disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated.", "label": "yes"}
{"original_question": "Are BRAF mutations common in melanoma?", "id": "converted_372", "sentence1": "Are Serine-threonine protein kinase B-raf, human 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 Proto-Oncogene Proteins c-raf 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, Homo sapiens protein, 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, Homo sapiens protein 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. Proto-Oncogene Proteins c-raf 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, Homo sapiens protein, 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 \u223c50% 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 Guanine Nucleotide-Binding Protein Subunit Alpha-11, disease_protein with Guanine Nucleotide-Binding Protein G(q) Subunit Alpha, disease_protein with Serine-threonine protein kinase B-raf, human, disease_disease with Metastatic melanoma, disease_protein with stem cell factor receptor activity, disease_disease with Malignant neoplasm of skin, disease_protein with Guanine Nucleotide-Binding Protein Subunit Alpha-11, disease_protein with Guanine Nucleotide-Binding Protein G(q) Subunit Alpha, disease_protein with Serine-threonine protein kinase B-raf, human, disease_disease with Metastatic melanoma, disease_protein with stem cell factor receptor activity, disease_disease with Malignant neoplasm of skin. Colorectal Carcinoma has relations: disease_disease with Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum, disease_protein with Serine-threonine protein kinase B-raf, human, disease_disease with Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum, disease_protein with Serine-threonine protein kinase B-raf, human. Vemurafenib has relations: drug_protein with Serine-threonine protein kinase B-raf, human, drug_protein with Serine-threonine protein kinase B-raf, human. stem cell factor receptor activity has relations: molfunc_protein with stem cell factor receptor activity, molfunc_protein with stem cell factor receptor activity. melanocytic neoplasm has relations: disease_disease with melanoma, disease_disease with melanoma. Dabrafenib has relations: indication with Metastatic melanoma, drug_protein with Serine-threonine protein kinase B-raf, human, indication with Metastatic melanoma, drug_protein with Serine-threonine protein kinase B-raf, human. Metastatic melanoma has relations: disease_disease with melanoma, disease_disease with melanoma. malignant Abdomen+Pelvis>Colon neoplasm has relations: disease_protein with Serine-threonine protein kinase B-raf, human, disease_disease with Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum, disease_protein with Serine-threonine protein kinase B-raf, human, disease_disease with Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum. Somatic Mutation Abnormality has relations: disease_phenotype_positive with Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum, disease_phenotype_positive with Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum.", "label": "yes"}
{"original_question": "Is it possible to determine the proteome of a formalin fixed and paraffin embedded  (FFPE) tissue?", "id": "converted_373", "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 Prostatic Hyperplasia (BPH). Hundreds of Proteins from Patient-Controlled Analgesia and BPH 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]", "label": "yes"}
{"original_question": "Is aganglionic megacolon a feature of Down syndrome?", "id": "converted_374", "sentence1": "Is aganglionic megacolon a feature of Down Syndrome?", "sentence2": "Down Syndrome (DS) is recognized by characteristic facial features, Intellectual Disability, and an increased risk for Cardiac malformations and Duodenal atresia. Recently, HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR), or Hirschsprung Disease, has been seen more often among patients with DS Of the 17 patients with Hodgkin Disease who were studied, 10 were isolated (58.8%) and seven (41.1%) were associated to other structural abnormalities and No No psychomotor retardation. Three of the cases in this latter group were due to chromosome pathology (trisomy 21, Down Syndrome) The authors report the case of a female infant with Down Syndrome, aganglionic megacolon, severe Diarrhea, and Biopsy of jejunum with ultrastructural changes consistent with microvillous atrophy. The patient condition improved after a colostomy performed in the setting of the treatment of Hirschprung disease HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, or Hirschsprung Disease, is commonly assumed to be a sex-modified multifactorial trait. To test this hypothesis, complex segregation analysis was performed on data on 487 probands and their families. Demographic information on probands and the recurrence risk to relatives of probands are presented. An increased sex ratio (3.9 male:female) and an elevated risk to sibs (4%), as compared with the population incidence (0.02%), are observed, with the sex ratio decreasing and the recurrence risk to sibs increasing as the aganglionosis becomes more extensive. Down Syndrome was found at an increased frequency among affected individuals but not among their unaffected sibs, and the increase was not associated with maternal age Intestinal microvillous atrophy in a patient with Down Syndrome and aganglionic megacolon.  The authors report the case of a female infant with Down Syndrome, aganglionic megacolon, severe Diarrhea, and Biopsy of jejunum with ultrastructural changes consistent with microvillous atrophy. The authors report the case of a female infant with Down Syndrome, aganglionic megacolon, severe Diarrhea, and Biopsy of jejunum with ultrastructural changes consistent with microvillous atrophy. The authors report the case of a female infant with Down Syndrome, aganglionic megacolon, severe Diarrhea, and Biopsy of jejunum with ultrastructural changes consistent with microvillous atrophy[SEP]Relations: hirschsprung disease, susceptibility to has relations: disease_disease with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_disease with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1. Intellectual disability has relations: disease_phenotype_positive with Down Syndrome, disease_phenotype_positive with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, disease_phenotype_positive with Down Syndrome, disease_phenotype_positive with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1.", "label": "yes"}
{"original_question": "Does HuR protein regulate the splicing process?", "id": "converted_375", "sentence1": "Does ELAV-like Protein Info 1 regulate the splicing process?", "sentence2": "ELAVL1 gene and TIA1/TIAL1 are involved in regulation of alternative splicing of Sirtuin 1 pre-mRNA Here we describe experiments showing that ELAVL1 gene and TIA1/TIAL1, two kinds of RNA-binding proteins, were involved in the regulation of alternative splicing of Sirtuin 1 pre-mRNA under normal and stress circumstances ELAVL1 gene increased Sirtuin 1-\u2206Exon8 by promoting Sirtuin 1 exon 8 exclusion, whereas TIA1/TIAL1 inhibition of the exon 8 exclusion led to a decrease in Sirtuin 1-\u2206Exon8 mRNA levels.  ELAVL1 gene regulates alternative splicing of the TRA2\u03b2 gene in Homo sapiens colon cancer Cells under oxidative stress Hu antigen R (ELAVL1 gene) regulates stress responses through stabilizing and/or facilitating the translation of target mRNAs We show here that the RBP embryonic lethal Abnormal vision like 1 (ELAVL1, also know as ELAVL1 gene) regulates the alternative splicing of EIF4ENIF1 gene (Eif4enif1), which encodes an eukaryotic translation initiation factor 4E transporter (4E-T) Protein Info and suppresses the expression of capped mRNAs Further, endothelial-specific Elavl1 knockout mice exhibited reduced revascularization after hind limb Ischemia Procedure and tumor angiogenesis in oncogene-induced mammary cancer, resulting in attenuated blood flow and tumor growth, respectively.  Changes in cellular mRNA stability, splicing, and polyadenylation through ELAV-like Protein Info 1 sequestration by a cytoplasmic RNA virus Furthermore, significant changes can be observed in nuclear alternative polyadenylation and splicing events on cellular pre-mRNAs as a result of sequestration of ELAV-like Protein Info 1 by the 3' Untranslated Regions of RNA Transcript of this cytoplasmic RNA virus. Here we demonstrate that expression of 2A(pro) induces a selective nucleo-cytoplasm translocation of several important RNA-Binding Proteins and RNA Splicing Factors. Subcellular fractionation studies, together with immunofluorescence microscopy revealed an asymmetric distribution of ELAVL1 gene and TIA1/TIAR in 2A(pro) expressing Cells, which modulates splicing of the Homo sapiens Fas exon 6 knockdown of ELAVL1 gene or overexpression of TIA1/TIAR, leads to Fas exon 6 inclusion in 2A(pro)-expressing Cells The differential expression levels of T-cell intracellular antigens (Transient Cerebral Ischemia) and Hu antigen R (ELAVL1 gene) are concomitant with a splicing switch in apoptosis receptor Fas in HCT116 Cells overexpression and knockdown of ELAVL1 gene led to Fas exon 6 skipping and inclusion, respectively. These results suggest that the Transient Cerebral Ischemia and ELAVL1 gene cellular ratio influences cell-type specific Fas exon 6 splicing pattern. Hu antigen R (ELAVL1 gene) functions as an alternative pre-RNA, Messenger, Splicing regulator of Fas apoptosis-promoting receptor on exon definition antiapoptotic regulator Hu antigen R (ELAVL1 gene, ELAVL1), a member of the embryonic lethal, Abnormal vision, Drosophila-like (ELAVL) family, promotes Fas exon 6 skipping by binding to an exonic splicing silencer ELAV/Hu proteins bind to AU-rich elements (are unit of measure) in mRNAs and regulate their stability from splicing to translation, and the ubiquitous ELAV-like Protein Info 1 has been implicated in cancerous cell growth. The ELAV-like Protein Info 1 regulates the expression of thousands of cellular RNA Transcript by modulating RNA, Messenger, Splicing, trafficking, translation, and stability. Hu antigen R (ELAVL1 gene) functions as an alternative pre-RNA, Messenger, Splicing regulator of Fas apoptosis-promoting receptor on exon definition. I report that antiapoptotic regulator Hu antigen R (ELAVL1 gene, ELAVL1), a member of the embryonic lethal, Abnormal vision, Drosophila-like (ELAVL) family, promotes Fas exon 6 skipping by binding to an exonic splicing silencer.  Changes in cellular mRNA stability, splicing, and polyadenylation through ELAV-like Protein Info 1 sequestration by a cytoplasmic RNA virus. Further, the silencing capacity of ELAVL1 gene as splicing regulator resides in the RRM1 Protein Info, human Protein Info, Homo sapiens and hinge-RRM3 domains.  ELAVL1 gene and TIA1/TIAL1 are involved in regulation of alternative splicing of Sirtuin 1 pre-mRNA. ELAVL1 gene regulates alternative splicing of the TRA2\u03b2 gene in Homo sapiens colon cancer Cells under oxidative stress. The ELAV-like Protein Info 1 regulates the expression of thousands of cellular RNA Transcript by modulating RNA, Messenger, Splicing, trafficking, translation, and stability.  Further, the silencing capacity of ELAVL1 gene as splicing regulator resides in the RRM1 Protein Info, human Protein Info, Homo sapiens and hinge-RRM3 domains. Taken together, these results support a functional link between ELAVL1 gene as Transcription Repressor/Corepressor of alternative Fas splicing and the molecular mechanisms modulating programmed cell death. We are interested in interactions involving Heterogeneous-Nuclear Ribonucleoproteins Proteins participating in several steps of mRNA processing (mainly pre-RNA, Messenger, Splicing) and ELAVL1 gene with an established role in stability/translation of associated mRNAs. Heterogeneous-Nuclear Ribonucleoproteins and ELAVL1 gene proteins have a major nucleoplasmic localization and ability to shuttle between Cell Nucleus and cytoplasm. We report here on interactions between Heterogeneous-Nuclear Ribonucleoproteins and ELAVL1 gene proteins that were identified in the context of isolated Heterogeneous-Nuclear Ribonucleoproteins and messenger ribonucleoprotein complex location complexes.  Despite the fact that ELAVL1 gene sites are observed in intronic regions, our data do not support a role for ELAVL1 gene in regulating splicing.[SEP]Relations: Protein Info binding has relations: molfunc_protein with RRM1 Protein Info, human, molfunc_protein with RRM1 Protein Info, human. ELAVL1 has relations: cellcomp_protein with Cell Nucleus, cellcomp_protein with Cell Nucleus. EIF4ENIF1 has relations: cellcomp_protein with Cell Nucleus, cellcomp_protein with Cell Nucleus. germ cell Cell Nucleus has relations: cellcomp_cellcomp with Cell Nucleus, cellcomp_cellcomp with Cell Nucleus.", "label": "yes"}
{"original_question": "Is Titin the largest single protein molecule found in Nature?", "id": "converted_376", "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 sarcomere and is dynamic both in biomechanics properties and biochemical functions.  Titin Kinase Kinase, the largest Protein Info known to date, has been linked to sarcomere assembly and function through its elastic adaptor and signaling domains. The giant sarcomere 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 sarcomere 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 sarcomere.  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 sarcomere. 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 sarcomere 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]", "label": "yes"}
{"original_question": "Does ventriculoperitoneal shunt improve normal pressure hydrocephalus?", "id": "converted_377", "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 \u00b1 0.44 vs 4.38 \u00b1 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]", "label": "yes"}
{"original_question": "Does Serca2a bind PLN in the heart?", "id": "converted_378", "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]", "label": "yes"}
{"original_question": "Is there any role for long noncoding RNAs in adipogenesis?", "id": "converted_379", "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 (PPAR\u03b3) and CCAAT/enhancer-binding protein \u03b1 (CEBP\u03b1). 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 (PPAR\u03b3) and CCAAT/enhancer-binding protein \u03b1 (CEBP\u03b1).[SEP]", "label": "yes"}
{"original_question": "Is there any research that relates the function of Notch Signaling with Alzheimer Disease?", "id": "converted_380", "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, \u03b3-secretase has been commonly associated with ALZHEIMER DISEASE, FAMILIAL, 1. However, starting with Notch and thereafter a continuously increasing number of novel substrates, \u03b3-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 \u03b2-secretase, this Enzyme [APC] produces the amyloid \u03b2-protein of ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) from the amyloid \u03b2-protein precursor. Because of its key role in the pathogenesis of cytarabine/daunorubicin protocol, \u03b3-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 \u03b3-secretase is an essential part of the Notch signaling pathway, rendering the compounds unacceptably Toxic effect upon chronic exposure High physiological concentrations of A\u03b2 monomer induced angiogenesis by a conserved mechanism that blocks \u03b3-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 \u03b3-secretase activity, which may have significant implications for our understanding of Alzheimer's pathogenesis vis-\u00e0-vis vascular changes that set the stage for ensuing Nerve Degeneration. Aggregated forms of A\u03b2 have a pathogenic role in ALZHEIMER DISEASE 2 and, thus, reducing the A\u03b2 levels by inhibiting \u03b3-secretase is a possible treatment strategy for ALZHEIMER DISEASE 2. Regrettably, clinical trials have shown that inhibition of \u03b3-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 \u03b3-secretase complex and has been proposed to be involved in substrate recognition and selection[SEP]Relations: familial ALZHEIMER DISEASE 2 has relations: disease_disease with ALZHEIMER DISEASE 2, disease_disease with ALZHEIMER DISEASE 2. inherited neurodegenerative disorder has relations: disease_disease with ALZHEIMER DISEASE 2, disease_disease with ALZHEIMER DISEASE 2. NCSTN has relations: disease_protein with ALZHEIMER DISEASE 2, disease_protein with ALZHEIMER DISEASE 2.", "label": "yes"}
{"original_question": "Was modafinil tested for schizophrenia treatment?", "id": "converted_381", "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 Schizoaffective Disorder, contraindication with Schizoaffective Disorder. Cognitive impairment has relations: disease_phenotype_positive with SCHIZOPHRENIA 2 (disorder), disease_phenotype_positive with SCHIZOPHRENIA 2 (disorder). Armodafinil has relations: contraindication with Schizoaffective Disorder, contraindication with Schizoaffective Disorder.", "label": "yes"}
{"original_question": "Is depression associated with poor prognosis of brain tumor patients?", "id": "converted_382", "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 gliomas, 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]", "label": "yes"}
{"original_question": "Have germline variants been associated to colorectal cancer?", "id": "converted_383", "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 Multiple polyps 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. APEX1 has relations: protein_protein with MUTYH protein, human, protein_protein with MUTYH protein, human. malignant colon neoplasm has relations: disease_protein with Leucine-Rich Repeat-Containing G-Protein Coupled Receptor 5, disease_protein with MUTYH protein, human, disease_protein with Antigen-Presenting Cells, disease_disease with Malignant neoplasm of colon and/or rectum, disease_protein with Leucine-Rich Repeat-Containing G-Protein Coupled Receptor 5, disease_protein with MUTYH protein, human, disease_protein with Antigen-Presenting Cells, disease_disease with Malignant neoplasm of colon and/or rectum. 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. familial adenomatous Multiple polyps has relations: disease_protein with TTR protein, human, disease_protein with Antigen-Presenting Cells, disease_protein with MUTYH protein, human, disease_protein with TTR protein, human, disease_protein with Antigen-Presenting Cells, disease_protein with MUTYH protein, human.", "label": "yes"}
{"original_question": "Can Alzheimer's disease related miRNAs be detected in patients' blood?", "id": "converted_384", "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-\u03b2 (A\u03b2) 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 \u03b2-amyloid (A\u03b2) 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\u2009\u00b1\u20090.080 versus 0.931\u2009\u00b1\u20090.111, p\u2009=\u20090.079), and correlated negatively with HNRNPA1 gene mRNA levels (r\u2009=\u2009-0.615, p\u2009=\u20090.0237). 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 A\u03b242 and sera A\u03b242, and a positive correlation between Adrenal Cortex miRNA levels and sera miRNA levels suggesting their potential as noninvasive diagnostic biomarkers.[SEP]Relations: familial ALZHEIMER DISEASE 2 has relations: disease_disease with ALZHEIMER DISEASE 2, disease_disease with ALZHEIMER DISEASE 2. ALZHEIMER DISEASE 2 has relations: disease_protein with BACE1 protein, human, disease_protein with BACE1 protein, human. adrenal cortex has relations: anatomy_protein_present with BACE1 protein, human, anatomy_protein_present with BACE1 protein, human.", "label": "yes"}
{"original_question": "Is it possible to visualize subtahalamic nucleus by using transcranial ultrasound?", "id": "converted_385", "sentence1": "Is it possible to visualize subtahalamic nucleus by using transcranial ultrasound?", "sentence2": "After measuring thermal effects of Mandibulofacial Dysostosis and imaging artefact sizes of DBS lead using a skull phantom, we prospectively enrolled 34 patients with DBS of Globus Sensation pallidus internus, ventro-intermediate thalamic or Structure of Structure of subthalamic nucleus. Mandibulofacial Dysostosis had no influence on lead temperature, electrical parameters of DBS device or clinical state of patients. Mandibulofacial Dysostosis measures of lead coordinates agreed with MRI measures in Anterior-Posterior and medial-lateral axis. Lead dislocation requiring reinsertion was reliably detected. Mandibulofacial Dysostosis may therefore become a first-choice modality to monitor lead location. Two pilot studies have demonstrated that the intraoperative visualization with Mandibulofacial Dysostosis and the Mandibulofacial Dysostosis-assisted Insert (object) of deep-brain stimulation (DBS) electrodes into the Structure of Structure of subthalamic nucleus and the Globus Sensation pallidus interna are feasible and safe provided there is exact knowledge on the extent of electrode Mandibulofacial Dysostosis imaging artifacts.  Peroperative transcranial sonography for electrode placement into the targeted Structure of Structure of subthalamic nucleus of patients with PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE: technical note The correct anatomic Positioning Attribute of the electrode tip could be indirectly assessed thanks to the topographic relationship of the EEF1A2 wt Allele with the hyperechogenic substantia nigra and the nucleus ruber. CONCLUSIONS: Transcranial sonography is easily feasible during stereotactic surgery. In combination with the clinical effects of electrostimulation on the symptoms of Parkinson Disease and with stereotactic x-ray images, it enables the assessment and the documentation of the correct Positioning Attribute of implanted EEF1A2 wt Allele electrodes in real time. After measuring thermal effects of Mandibulofacial Dysostosis and imaging artefact sizes of DBS lead using a skull phantom, we prospectively enrolled 34 patients with DBS of Globus Sensation pallidus internus, ventro-intermediate thalamic or Structure of Structure of subthalamic nucleus Two pilot studies have demonstrated that the intraoperative visualization with Mandibulofacial Dysostosis and the Mandibulofacial Dysostosis-assisted Insert (object) of deep-brain stimulation (DBS) electrodes into the Structure of Structure of subthalamic nucleus and the Globus Sensation pallidus interna are feasible and safe provided there is exact knowledge on the extent of electrode Mandibulofacial Dysostosis imaging artifacts[SEP]Relations: autosomal recessive PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE has relations: disease_disease with PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE, disease_disease with PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE.", "label": "yes"}
{"original_question": "Do thyroid hormone receptors change after brain injury?", "id": "converted_386", "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. TR\u03b1 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 TR\u03b1.  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]", "label": "yes"}
{"original_question": "Is gastro esophageal reflux related to burning mouth syndrome?", "id": "converted_387", "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 thrombophilia related to increased risk of miscarriage?", "id": "converted_388", "sentence1": "Is thrombophilia related to increased risk of miscarriage?", "sentence2": "Thrombophilia does hardly increase the risk of IUGR/PMPC or if so, it can be prevented by Low Molecular Weight Heparin [EPC] for illustrative purposes, a patient presenting with combined thrombophilia--both Genetic and acquired--will be discussed. This patient had suffered severe gestational complications that led to devastating obstetrical outcome Thrombophilias have been implicated in complications related to ischemic placental disease including recurrent pregnancy loss, intrauterine fetal demise, Pre-Eclampsia, fetal growth restriction, placental abruption, and preterm delivery Further information about the combined risk of Antigen-Presenting Cells resistance and pregnancy is needed before guidance on the management of affected women can be formulated. Thrombotic risk during pregnancy and the puerperium is higher in asymptomatic women with than without thrombophilia Further studies are required to assess the thrombotic risk in women with Pre-Eclampsia as well as early or late recurrent pregnancy loss. Risk of pregnancy-related Venous Thrombosis in carriers of severe inherited thrombophilia In conclusion, homozygous carriers of Factor V Leiden and, to a lesser extent, double heterozygous carriers of Factor V Leiden and of the prothrombin mutation have an increased risk of Venous Thrombosis during pregnancy, particularly high during the postpartum period Careful diagnosis, observation and monitoring can add significant benefit to Low Molecular Weight Heparin [EPC] therapy during pregnancy Pregnancy in healthy women is accompanied by hypercoagulable changes that may interact with thrombophilia risk factors and threaten pregnancy. Fifty-three (13 %) women had antiphospholipid Antibodies, in vitro diagnostic (lupus anticoagulant and/or anti-beta2-glycoprotein 1 Antibodies, in vitro diagnostic) mainly associated with the risk of spontaneous abortion during the first trimester thrombophilia was found to be considerably more common in women with pregnancy-associated complications in comparison with the general population, and most frequently in conjunction with Venous Thromboembolism during pregnancy and the postpartum period When counseling white women with a history of Pre-Eclampsia, screening for thrombophilia can be useful for preconceptional counseling and pregnancy management. knowledge combined with the appropriate use of thromboprophylaxis and treatment in women who have objectively confirmed vinyltriethoxysilane continue to improve maternal and perinatal outcomes The risk of having thrombophilia is doubled in men who have fathered pregnancies which ended in perinatal death as well as in the mothers of such pregnancies. The prevalence of thrombophilic Variant is of possible public health significance for other morbidity; but perhaps not in relation to Pre-Eclampsia This study suggests that thrombophilia \"mediates\" in lowering of cardiovascular risk factors in women with a history of Pre-Eclampsia[SEP]", "label": "yes"}
{"original_question": "Does nifedipine inhibit L-type calcium channels?", "id": "converted_389", "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) rat: 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 Rattus norvegicus 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: Dexmedetomidine has relations: drug_drug with nifedipine, drug_drug with nifedipine. Mibefradil has relations: drug_drug with nifedipine, drug_drug with nifedipine. Verapamil has relations: drug_drug with nifedipine, drug_drug with nifedipine. Nimodipine has relations: drug_drug with nifedipine, drug_drug with nifedipine. Ethanol has relations: drug_drug with nifedipine, drug_drug with nifedipine. Nitrendipine has relations: drug_drug with nifedipine, drug_drug with nifedipine. Vecuronium has relations: drug_drug with nifedipine, drug_drug with nifedipine. Amprenavir has relations: drug_drug with nifedipine, drug_drug with nifedipine. Niguldipine has relations: drug_drug with nifedipine, drug_drug with nifedipine.", "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_390", "sentence1": "Is there any data to suggest that Pro-Thyrotropin-Releasing Hormone, human (thyrotropin releasing hormone) 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 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 Amyotrophic Lateral Sclerosis patients but little or none in the other Amyotrophic Lateral Sclerosis 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 (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 (Amyotrophic Lateral Sclerosis) 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, human (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 (Amyotrophic Lateral Sclerosis). Although the mechanism is not known, several reports of the effectiveness of thyrotropin releasing hormone (Pro-Thyrotropin-Releasing Hormone, human) in Amyotrophic Lateral Sclerosis 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 (Amyotrophic Lateral Sclerosis).  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 Amyotrophic Lateral Sclerosis 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 Amyotrophic Lateral Sclerosis.  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 Amyotrophic Lateral Sclerosis 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 Amyotrophic Lateral Sclerosis 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 Amyotrophic Lateral Sclerosis. 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 (Amyotrophic Lateral Sclerosis) 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 Amyotrophic Lateral Sclerosis following administration of Pro-Thyrotropin-Releasing Hormone, human[SEP]Relations: Spasticity of facial Muscle Tissue has relations: disease_phenotype_positive with amyotrophic lateral sclerosis, disease_phenotype_positive with amyotrophic lateral sclerosis. Epilepsy has relations: disease_protein with Pro-Thyrotropin-Releasing Hormone, human, disease_protein with Pro-Thyrotropin-Releasing Hormone, human. amyotrophic lateral sclerosis has relations: disease_protein with Ciliary Neurotrophic Factor, disease_protein with Ciliary Neurotrophic Factor.", "label": "yes"}
{"original_question": "Can siRNA affect response to afatinib treatment?", "id": "converted_391", "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_protein with Epidermal Growth Factor Receptor, drug_protein with Epidermal Growth Factor Receptor. Gefitinib has relations: indication with Primary malignant neoplasm of lung, drug_protein with Epidermal Growth Factor Receptor, indication with Primary malignant neoplasm of lung, drug_protein with Epidermal Growth Factor Receptor. Cetuximab has relations: drug_protein with Epidermal Growth Factor Receptor, drug_protein with Epidermal Growth Factor Receptor. Erlotinib has relations: indication with Primary malignant neoplasm of lung, drug_protein with Epidermal Growth Factor Receptor, indication with Primary malignant neoplasm of lung, drug_protein with Epidermal Growth Factor Receptor.", "label": "yes"}
{"original_question": "Does triiodothyronine stimulate red blood cell sodium potassium pump?", "id": "converted_392", "sentence1": "Does liothyronine stimulate red blood cell sodium potassium pump?", "sentence2": "reduction in Na+,K+ATPase activity has been demonstrated in red blood cells (RBCs), as well as an inverse correlation between this enzymatic action and free liothyronine (cubic foot) levels. The restoration of normal cubic foot values also brings about a normalization of Na+,K+ATPase activity in Specimen Source Codes - Erythrocytes. at Hyperthyroidism patients have decreased red cell Na/K-ATPase activity and provide direct evidence that Erythrocytes ATPase activity is increased in Hypothyroidism patients. The change in enzyme activity in patients with nonthyroidal illness and decreased circulating T3 thoracic segmental innervation thoracic segmental innervation levels was comparable to that in hypothyroidism. The effect of liothyronine (T3 thoracic segmental innervation thoracic segmental innervation) on Na+,K(+)-ATPase activity of K562 human erythroleukemic cell was studied to understand why the Erythrocytes sodium pump activity is decreased in hyperthyroidism. We conclude that T3 thoracic segmental innervation thoracic segmental innervation stimulates Na+,K(+)-ATPase activity of K562 cells and in the presence of T3 thoracic segmental innervation thoracic segmental innervation during differentiation, the enzyme activity remains high.[SEP]", "label": "no"}
{"original_question": "Is selumetinib effective in thyroid cancer?", "id": "converted_393", "sentence1": "Is selumetinib effective in Malignant neoplasm of thyroid?", "sentence2": "A phase I trial of vertical inhibition of IGF signalling using cixutumumab, an anti-IGF-1R antibody, and selumetinib, an MEK 1/2 inhibitor, in advanced solid tumours. BACKGROUND: We completed a phase I clinical trial to test the safety and Toxic effect of combined treatment with cixutumumab (anti-IGF-1R antibody) and selumetinib (MEK 1/2 inhibitor). Two patients achieved a partial response (one unconfirmed), including a patient with BRAF protein, human protein, human wild-type Malignant epithelial neoplasm of thyroid, and a patient with Anal Anal squamous cell carcinoma of the Tongue, and six patients achieved time to progression of>6 months, including patients with Malignant epithelial neoplasm of thyroid, Colorectal Carcinoma, and Skin Basal Cell Carcinoma. CONCLUSIONS: Our study of anti-IGF-1R antibody cixutumumab and MEK 1/2 inhibitor selumetinib showed that the combination is safe and well-tolerated at these doses, with preliminary evidence of clinical benefit and pharmacodynamic evidence of target inhibition. MHC class I loss is a frequent mechanism of immune escape in papillary Malignant neoplasm of thyroid that is reversed by human leukocyte human leukocyte interferon and selumetinib treatment in vitro. Increased antigenicity following selumetinib and IFN treatment warrants further study for immunotherapy of progressive Percutaneous transhepatic cholangiography. The role of KIs in differentiated CD55 wt Allele may be revolutionised by the finding that selumetinib may restore a clinical response to radioactive Iodine, Homeopathic preparation (PPP1R13L wt Allele).  BACKGROUND AND AIM: selumetinib is a promising and interesting targeted therapy agent as it may reverse iodide ion I-131 uptake in patients with iodide ion I-131-refractory differentiated Malignant neoplasm of thyroid. CONCLUSIONS: Compared with current chemotherapy, selumetinib has modest clinical activity as monotherapy in patients with advanced cancer, but combinations of selumetinib with cytotoxic agents in patients with BRAF protein, human protein, human or KRAS mutations hold great promise for cancer treatment. selumetinib may be an effective redifferentiating agent and could be used within several years. selumetinib-enhanced iodide ion I-131 uptake in advanced Malignant neoplasm of thyroid. METHODS: We conducted a study to determine whether the Mitogen-Activated Protein Kinase Kinases (MEK) 1 and MEK2 inhibitor selumetinib (AZD6244, ARRY 142886) could reverse refractoriness to iodide ion I-131 in patients with metastatic Malignant neoplasm of thyroid.  selumetinib increased the uptake of Iodine-124 in 12 of the 20 patients (4 of 9 patients with BRAF protein, human protein, human mutations and 5 of 5 patients with Human Oncogene N-RAS mutations). CONCLUSIONS: selumetinib produces clinically meaningful increases in Iodine, Homeopathic preparation uptake and retention in a subgroup of patients with Malignant neoplasm of thyroid that is refractory to iodide ion I-131; the effectiveness may be greater in patients with RAS-mutant disease.  ECENT FINDINGS: For patients with advanced differentiated thyroid cancers, sorafenib, selumetinib, pazopanib and sunitinib have been investigated with promising results.  selumetinib is a promising and interesting targeted therapy agent as it may reverse iodide ion I-131 uptake in patients with iodide ion I-131-refractory differentiated Malignant neoplasm of thyroid. selumetinib may be an effective redifferentiating agent and could be used within several years. Here, selumetinib targets the mitogen-activated protein kinase pathway in papillary Malignant epithelial neoplasm of thyroid and shows limited single-agent activity in the patients with Neoplasms that harbor the (V600E)BRAF protein, human protein, human mutation. CONCLUSIONS: selumetinib produces clinically meaningful increases in Iodine, Homeopathic preparation uptake and retention in a subgroup of patients with Malignant neoplasm of thyroid that is refractory to iodide ion I-131; the effectiveness may be greater in patients with RAS-mutant disease.[SEP]Relations: Colorectal Carcinoma has relations: disease_protein with BRAF protein, human, disease_protein with BRAF protein, human. Sorafenib has relations: drug_drug with selumetinib, drug_protein with BRAF protein, human, drug_drug with selumetinib, drug_protein with BRAF protein, human. Pazopanib has relations: drug_drug with selumetinib, drug_drug with selumetinib. Sunitinib has relations: drug_drug with selumetinib, drug_drug with selumetinib. anal canal Anal squamous cell carcinoma has relations: disease_disease with Anal squamous cell carcinoma, disease_disease with Anal squamous cell carcinoma.", "label": "yes"}
{"original_question": "Are immune cells affected in Amyotrophic Lateral Sclerosis?", "id": "converted_394", "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-Specimen Source Codes - 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-Specimen Source Codes - 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 Specimen Source Codes - Lymphocytes (Treg ) and Th2 Specimen Source Codes - 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: glial cell-derived neurotrophic factor receptor binding has relations: molfunc_protein with Glial Cell Line-Derived Neurotrophic Factor, molfunc_protein with Glial Cell Line-Derived Neurotrophic Factor. CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS has relations: anatomy_protein_present with cyclophosphamide/prednisone, anatomy_protein_present with cyclophosphamide/prednisone. Spinal Cord has relations: anatomy_protein_present with cyclophosphamide/prednisone, anatomy_protein_present with cyclophosphamide/prednisone. Neuronal loss in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS has relations: disease_phenotype_positive with Amyotrophic Lateral Sclerosis, disease_phenotype_positive with Amyotrophic Lateral Sclerosis.", "label": "yes"}
{"original_question": "Is thyroid hormone therapy indicated in patients with heart failure?", "id": "converted_395", "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 liothyronine 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. Triiodothyronine 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]", "label": "no"}
{"original_question": "Is there a mouse model for Fanconi anemia?", "id": "converted_396", "sentence1": "Is there a Mus sp. model for Fanconi anemia?", "sentence2": "cyclophosphamide promotes engraftment of Genes-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 fanca ( -/- ) mutant CASP14 Genes receiving Genes-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 fanca ( -/- ) CASP14 Genes 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 Genes 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 FANCD2 FANCONI ANEMIA, COMPLEMENTATION GROUP F homozygous CASP14 Genes 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 Genes 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 Genes, 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 Genes by deleting exon 2 FANCM deficiency caused Hypogonadism in CASP14 Genes 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 Genes also showed unique features atypical for doxorubicin/fluorouracil protocol CASP14 Genes, including underrepresentation of female Fancm(Delta2/Delta2) CASP14 Genes and decreased overall and tumor-free survival Fancm-deficient CASP14 Genes reveal unique features of Fanconi anemia complementation group M FANCONI ANEMIA, COMPLEMENTATION GROUP F-deficient CASP14 Genes 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 Genes, we demonstrate that the lentivirus-mediated Genes 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 Genes with a hypomorphic mutation in the Brca2/Fancd1 Genes (Brca2(Delta27/Delta27) mutation) 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 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 Genes therapy In vitro phenotypic correction of hematopoietic progenitors from Fanconi anemia group A knockout CASP14 Genes 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 Genes 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) Genes and human FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) genes. Lin(-)Sca-1(+) cells from Fanca(-/-) CASP14 Genes were transduced with an efficiency similar to that of samples from wild-type CASP14 Genes. More significantly, transductions with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) 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 Genes  The 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 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 Genes-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 Mutation Abnormality in the Mus sp., as well as a sixth key regulatory Genes, 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 FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) cDNA. Here we describe the phenotype of the 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 Mutation Abnormality in the Mus sp., as well as a sixth key regulatory Genes, 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 Genes, either young or adult Fanconi anemia group A and C double-mutant CASP14 Genes: 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: Mitomycin has relations: drug_drug with cyclophosphamide, drug_drug with cyclophosphamide, drug_drug with cyclophosphamide, drug_drug with cyclophosphamide. Hypogonadism has relations: disease_phenotype_positive with Fanconi anemia, disease_phenotype_positive with Fanconi anemia. Cytarabine has relations: drug_drug with cyclophosphamide, drug_drug with cyclophosphamide. Fanconi anemia complementation group has relations: disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_disease with Fanconi anemia, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_disease with Fanconi anemia, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_disease with Fanconi anemia, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_disease with Fanconi anemia. Bone marrow hypocellularity has relations: phenotype_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), phenotype_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder).", "label": "yes"}
{"original_question": "Could Hyperthermic intraperitoneal chemotherapy (HIPEC) be effective for the treatment of recurrent ovarian cancer?", "id": "converted_397", "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 Ovarian Carcinoma 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 Malignant neoplasm of ovary (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: trabectedin has relations: indication with Malignant neoplasm of ovary, indication with Malignant neoplasm of ovary.", "label": "yes"}
{"original_question": "Is Rac1 involved in cancer cell invasion?", "id": "converted_398", "sentence1": "Is RAC1 gene involved in cancer \"U\" lymphocyte invasion?", "sentence2": "In the Matrigel invasion assay, knockdown of CCR1 protein, human 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, human Protein Info, Homo sapiens with Recombinant RANTES caused by increased expression of CCR1 protein, human 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 cancer Cells, 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 Proteins 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 Malignant neoplasm of pancreas Cells. ARL2BP gene interacts with active forms of RAC1 gene, and the ARL2BP gene-RAC1 gene complex localizes at the leading edges of migrating cancer Cells. Suppression of ARL2BP gene increases active RAC1 gene, thereby increasing \"U\" lymphocyte invasion. Treatment of Malignant neoplasm of pancreas Cells 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 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 \"U\" lymphocyte diapedesis. Finally, RAC1 gene leads to \u03b21 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 Protein Info, Homo sapiens, 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 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 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 Info, human Protein Info, Homo sapiens.  These results indicate that icariin exerts negative effects on tumor \"U\" lymphocyte invasion and migration via the RAC1 gene-dependent VASP Protein Info, human 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 cancer Cells 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 Malignant neoplasm of breast Cells. 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: ELMO1 gene has relations: cellcomp_protein with Cytoplasm, cellcomp_protein with Cytoplasm. Protein Info binding has relations: molfunc_protein with ELMO1 gene, molfunc_protein with CCR1 protein, human, molfunc_protein with LMO1 Protein Info, Homo sapiens, molfunc_protein with VASP Protein Info, human, molfunc_protein with ELMO1 gene, molfunc_protein with CCR1 protein, human, molfunc_protein with LMO1 Protein Info, Homo sapiens, molfunc_protein with VASP Protein Info, human. Cytoplasm has relations: cellcomp_protein with CCR1 protein, human, cellcomp_protein with ELMO1 gene, cellcomp_protein with CCR1 protein, human, cellcomp_protein with ELMO1 gene.", "label": "yes"}
{"original_question": "Is the gene SLC6A2 associated with orthostatic intolerance?", "id": "converted_399", "sentence1": "Is the gene SLC6A2 associated with orthostatic intolerance?", "sentence2": "Orthostatic intolerance is a debilitating syndrome characterized by Tachycardia by ECG Finding on assumption of upright posture. The norepinephrine (NE) transporter (SLC6A2 protein, Homo sapiens) has been implicated in a genetic form of the disorder.  Thus attenuated baroreflex function and reduced sympathetic outflow may contribute to the orthostatic intolerance of severe SLC6A2 protein, Homo sapiens deficiency. A Mutation Abnormality in the Homo sapiens Norepinephrine Plasma Membrane Transport Proteins (SLC6A2) associated with orthostatic intolerance disrupts surface expression of Mutant and wild-type transporters.  Recently, our laboratory reported a Genetic Polymorphism in the Homo sapiens SLC6A2 protein, Homo sapiens (hNET) gene A457P in an individual with the autonomic disorder orthostatic intolerance (Osteogenesis Imperfecta).  Nonsynonymous single nucleotide polymorphisms (SNPs) in the Homo sapiens SLC6A2 protein, Homo sapiens (hNET) gene that influence transporter function can contribute to disease, such as the nonfunctional transporter, A457P, identified in orthostatic intolerance.  Orthostatic intolerance is not necessarily related to a specific Mutation Abnormality (Ala457Pro) in the Homo sapiens Norepinephrine Plasma Membrane Transport Proteins. We propose that chromatin-modifying events associated with SLC6A2 gene suppression may constitute a mechanism of POTS. The goal of the present study was to further characterize the role and regulation of the SLC6A2 gene in POTS. In the absence of altered SLC6A2 gene sequence or promoter methylation, this reduced expression was directly correlated with chromatin modifications.  We propose that chromatin-modifying events associated with SLC6A2 gene suppression may constitute a mechanism of POTS. A coding Mutation Abnormality in the Norepinephrine Plasma Membrane Transport Proteins (SLC6A2) sequence has been reported in 1 family kindred only. The goal of the present study was to further characterize the role and regulation of the SLC6A2 gene in POTS.[SEP]", "label": "yes"}
{"original_question": "Is macitentan an ET agonist?", "id": "converted_400", "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\u00ae) 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 Pharmacologic Substance 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 rat aorta (ET(A) receptors) and sarafotoxin S6c-induced contractions in isolated rat trachea (ET(B) receptors). In Rattus norvegicus 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 Rattus norvegicus. 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 drug.[SEP]Relations: kidney has relations: anatomy_protein_present with Congenital hypoplasia of pulmonary artery, anatomy_protein_present with Congenital hypoplasia of pulmonary artery. Bosentan has relations: indication with Pulmonary Hypertension, indication with Pulmonary Hypertension.", "label": "no"}
{"original_question": "Can we use platelet biomarkers to study Alzheimer's disease?", "id": "converted_401", "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 Amyloid beta-Protein Precursor and other important Proteins such as uridine triacetate and 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]", "label": "yes"}
{"original_question": "Is CHEK2 involved in cell cycle control?", "id": "converted_402", "sentence1": "Is CHEK2 involved in cell cycle control?", "sentence2": "Moreover, cell-cycle progression genes [i.e. E2F transcription factor (E2F) family and histone deacetylase ( HDAC )] and DNA-repair genes [i.e. growth Cardiac Arrest and DNA-damage-inducible, gamma ( GADD45G ) family and serine/threonine-protein kinase Chk2 ( CHEK2)] were also increased. As CHEK2 is a cell-cycle master controller, we tested the hypothesis that heterozygosity for the frameshift alteration CHEK2*1100delC is associated with increased risk of melanoma. In the current study, we evaluated the possible associations of seven common Variant of the DNA repair and cell cycle control genes BRCA2 Genes Genes and CHEK2 with melanoma (Millimole per Liter). Promotor methylation analysis of key regulatory genes involved in cell cycle control (CDKN2A Genes, CDKN2B wt Allele, CDKN2A wt Allele, CHEK2 protein, human), DNA repair (MLH1 wt Allele), apoptosis (p73 protein, human protein, human, BIRC5 wt Allele, DAPK1 Genes), and differentiation (RARB wt Allele, Nephroblastoma) was performed by methylation-specific polymerase chain reaction. CHEK2 is a key cell cycle control Genes encoding a pluripotent kinase that can cause Cardiac Arrest or apoptosis in response to unrepaired DNA damage. High-fidelity maintenance of genomic integrity in Eukaryota is ensured by cell cycle checkpoints and DNA repair. The checkpoint kinase, Chk2, has been implicated in both of these responses. In response to DNA damage, Chk2 is initially phosphorylated at Thr-68, which leads to its full activation. The fully activated Chk2 then phosphorylates downstream substrates of cell cycle control. Checkpoint kinase 2 (hCHK2/hCds1) is a Tumor Suppressor Genes involved in cell-cycle control.[SEP]", "label": "yes"}
{"original_question": "Are the proteins Erbin (LAP2) and Merlin cooperating?", "id": "converted_403", "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]", "label": "yes"}
{"original_question": "Are adenylyl cyclases always transmembrane proteins?", "id": "converted_404", "sentence1": "Are adenylyl cyclases always transmembrane proteins?", "sentence2": "ransmembrane adenylyl cyclase 2 2  Transmembrane adenylyl cyclase 2 2 (tmAC) and soluble AC (spindle assembly checkpoint)  Soluble adenylyl cyclase 2 2 (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 2 2  transmembrane adenylyl cyclases (tmACs), and soluble adenylyl cyclase 2 2 (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 2 2 (spindle assembly checkpoint, ADCY10 gene gene), the ubiquitous, non-transmembrane adenylyl cyclase 2 2, was found to play a key role in neuronal survival and axon growth. Central role of soluble adenylyl cyclase 2 2[SEP]Relations: germ cell Cell Nucleus has relations: cellcomp_cellcomp with Cell Nucleus, cellcomp_cellcomp with Cell Nucleus.", "label": "no"}
{"original_question": "Does neuroglobin has neuroprotective properties in the setting of traumatic brain injury?", "id": "converted_405", "sentence1": "Does neuroglobin has neuroprotective properties in the setting of Traumatic brain injury?", "sentence2": "GTPBP4 gene gene has shown rich neuroprotective effects against Brain Hypoxia, and therefore has the potential to impact outcomes after Traumatic brain injury (Traumatic Brain Injury).  GTPBP4 gene gene (Ngb) 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. GTPBP4 gene gene-overexpression reduces Traumatic brain lesion size in CASP14 gene. BACKGROUND: Accumulating evidence has demonstrated that over-expression of GTPBP4 gene gene (Ngb) is neuroprotective against hypoxic/ischemic brain injuries.  CONCLUSION: Ngb over-expression reduced Traumatic lesion volume, which might partially be achieved by decreasing oxidative stress. GTPBP4 gene 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 (Traumatic Brain Injury) and further study its neuroprotective effects in Traumatic Brain Injury when it was overexpressed in Adenovirus Vector. CONCLUSIONS: GTPBP4 gene was upregulated in Traumatic Brain Injury and overexpressed rNGB had a significant neuroprotection in Traumatic Brain Injury.  This study suggested that rNGB overexpression may be a new strategy for treating of Traumatic Brain Injury. GTPBP4 gene gene has shown rich neuroprotective effects against Brain Hypoxia, and therefore has the potential to impact outcomes after Traumatic brain injury (Traumatic Brain Injury). The aim of this study was to investigate rat neuroglobin (rNGB) expression level after Traumatic brain injury (Traumatic Brain Injury) and further study its neuroprotective effects in Traumatic Brain Injury when it was overexpressed in Adenovirus Vector. Accumulating evidence has demonstrated that over-expression of GTPBP4 gene gene (Ngb) 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]", "label": "yes"}
{"original_question": "Does the concentration of protein HIF-1\u03b1 increase after the administration of the cytoprotective prodrug\"amifostine\" (ethyol) ?", "id": "converted_406", "sentence1": "Does the concentration of protein HIF-1\u03b1 increase after the administration of the cytoprotective prodrug\"amifostine\" (ethyol) ?", "sentence2": "We demonstrated that the treatment of several Homo sapiens cancer Cultured Cell Line with therapeutical doses of WR 1065 led to a strong induction of different Vascular Endothelial Growth Factor A mRNA isoforms independently of HIF1A protein, Homo sapiens investigated the involvement of hypoxia-regulated proteins (Hypoxia, CTCAE, CTCAE inducible factors HIF1alpha, HIF2alpha and carbonic anhydrase CA9 wt Allele wt Allele) in MMP8 wt Allele resistance to accelerated and hypofractionated radiotherapy In accord with previously reported studies, high levels of the hypoxia regulated proteins HIF1alpha and CA9 wt Allele wt Allele in MMP8 wt Allele predict resistance to Platinum metallicum, Platinum metallicum, platinum, Homeopathic preparation, Homeopathic preparation based radio-chemotherapy. Whether HIF2alpha expressing Neoplasms are more sensitive to larger radiotherapy fractions, compared to standard radiotherapy fractionation, is an issue that deserves further investigation. HIF1alpha and HIF2alpha were expressed in the nuclei and Cytoplasm of Tumor cells, malignant, while CA9 wt Allele wt Allele had a membrane reactivity. A high expression of HIF1alpha, HIF2alpha and CA9 wt Allele wt Allele was noted in 21/39 (53.8%), 20/39 (51.3%) and 23/39 (58.9%) cases, respectively. Complete response was obtained in 85.2% of patients and HIF1alpha was marginally related with persistent disease after RT (p = 0.05). HIF1alpha was significantly associated with poor local relapse free survival (LRFS) (p = 0.006) and overall survival (p = 0.008), whilst HIF2alpha was no  The Glucose measurement and oxygen levels in the peripheral blood of patients receiving 1000 mg amifostine were determined at various time-points in order to investigate the metabolic changes induced by amifostine. MDA468 breast tumor Cultured Cell Line were incubated with a high amifostine concentration (10 m M) to overcome the natural resistance of Tumor cells, malignant to influx of the non-hydrolyzed WR-2721, and the HIF1 alpha protein levels were determined by Western blot analysis Since it is doubtful whether dephosphorylation of amifostine to the active metabolite WR 1065 occurs within tumoral tissues (an acidic environment that lacks vascular alkaline phosphatase activity), Protoplasm hypoxia and upregulation of HIF1 alpha represents an additional, normal tissue-specific, amifostine cytoprotective pathway. . Incubation of Cultured Cell Line with amifostine resulted in HIF1 alpha induction[SEP]", "label": "yes"}
{"original_question": "Do Conserved noncoding elements act as enhancers?", "id": "converted_407", "sentence1": "Do Conserved noncoding Elements act as enhancers?", "sentence2": "The Abdominal cutaneous nerve entrapment syndrome are rich in tissue-specific enhancers Transgenic zebrafish assay of some Homo sapiens CNE enhancers that have been lost in teleosts Conserved noncoding Elements (CNEs) in Vertebrates Genome often act as developmental enhancers, In all four cases where the Zebrafish and Homo sapiens CNE display a similar expression pattern in Zebrafish, the Homo sapiens CNE also displays a similar expression pattern in Mus sp.. This suggests that the endogenous Enhancer of transcription activity of \u223c30% of Homo sapiens CNEs can be determined from experiments in Zebrafish If these ancient CNEs are indeed enhancers directing tissue-specific expression of Genes, Homeobox, divergence of their DNA Sequence in Vertebrates lineages might have led to altered expression patterns and presumably the functions of their associated Genes, Homeobox. Comparisons of noncoding DNA Sequence of the elephant shark and Homo sapiens Hox clusters have identified a large number of conserved noncoding Elements (CNEs), which represent putative cis-regulatory Elements that may be involved in the regulation of Genes, Homeobox. Animal Genome possess highly conserved cis-regulatory DNA Sequence that are often found near Genes that regulate transcription and development. We test 42 of our PCNEs in transgenic zebrafish assays--including examples from vertebrates and Branchiostoma sp.--and find that the majority are functional enhancers. The Genome of vertebrates, Diptera, and Phylum Nematoda contain highly conserved noncoding Elements (CNEs). CNEs cluster around Genes that regulate development, and where tested, they can act as transcriptional enhancers. , we identified 17 highly conserved noncoding Elements, 9 of which revealed specific acetylation marks in chromatin-immunoprecipitation and microarray (ChIP-chip) assays performed across 250 kb of the LMO2 wt Allele locus in 11 cell types covering different stages of hematopoietic differentiation. All candidate Regulatory Sequences, Nucleic Acid were tested in Mice, Transgenic. An extended LMO2 proximal promoter fragment displayed strong endothelial activity, while the distal promoter showed weak forebrain activity. Eight of the 15 distal candidate Elements functioned as enhancers, Pan-Vertebrates developmental cis-regulatory Elements are discernible as highly conserved noncoding Elements (HCNEs) and are often dispersed over large areas around the pleiotropic Genes whose expression they control. HCNEs of both Homo sapiens and zebrafish function as specific developmental enhancers in zebrafish. several transcriptional enhancers are conserved between Branchiostoma sp. and vertebrates--a very wide phylogenetic distance. We recently described GRBs in vertebrates, where most HCNEs function as enhancers Besides developmental regulators that are likely targets of HCNE enhancers We identify and characterize highly conserved noncoding Elements flanking the TNF gene, which undergo activation-dependent intrachromosomal interactions. These Elements, hypersensitive site (HSS)-9 and HSS+3 (9 kb upstream and 3 kb downstream of the TNF gene, respectively), contain deoxyribonuclease I activity hypersensitive sites in naive, T helper 1, and T helper 2 primary Therapeutic gamma delta T-lymphocytes. Both HSS-9 and HSS+3 inducibly associate with acetylated Histones, indicative of chromatin remodeling, bind the transcription factor nuclear factor of activated Therapeutic gamma delta T-lymphocytes (NFAT)p in vitro and in vivo, and function as enhancers We used the sequence signatures identified by this approach to successfully assign tissue-specific predictions to approximately 328,000 Homo sapiens-Mus sp. conserved noncoding Elements in the Homo sapiens genome. By overlapping these genome-wide predictions with a data set of enhancers validated in vivo, in Mice, Transgenic, we were able to confirm our results with a 28% sensitivity and 50% precision. 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. uncovered two anciently conserved noncoding DNA Sequence (Central Nervous System) upstream of NR2F2 protein, Homo sapiens (Central Nervous System-62kb and Central Nervous System-66kb). Testing these two Elements using reporter constructs in Hepatocyte (HepG2) revealed that Central Nervous System-66kb, but not Central Nervous System-62kb, yielded robust in vitro Enhancer of transcription activity.[SEP]", "label": "yes"}
{"original_question": "Can the iPS cell technology be used in Fanconi anemia therapy?", "id": "converted_408", "sentence1": "Can the iPS cell technology be used in FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) therapy?", "sentence2": "We explain a protocol for the reproducible generation of genetically corrected iPSCs starting from the skin biopsies of FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) 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 FANCA. 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, COMPLEMENTATION GROUP A (disorder) complementation group has relations: disease_disease with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_disease with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder). Transcriptional regulation of pluripotent stem cells has relations: pathway_protein with KLF4 protein, human, pathway_protein with SOX2 protein, human, pathway_protein with KLF4 protein, human, pathway_protein with SOX2 protein, human.", "label": "yes"}
{"original_question": "Can Preimplantation Genetic Diagnosis (PGD) be used for gender selection?", "id": "converted_409", "sentence1": "Can Preimplantation Genetic Diagnosis (Prostaglandins D) be used for gender selection?", "sentence2": "This testing is used for identifying singlegene disorders, Chromosome Aberrations, Mitochondrial Diseases, gender selection in non-mendelian disorders with unequal gender distribution, aneuploidy screening, and other preconceptually identified genetic abnormalities in prospective parents.   Although many clinics offer Prostaglandins D for HA by gender selection, an approach that detects the presence of the underlying F8 mutation has several advantages.  Preimplantation genetic diagnosis (Prostaglandins D) for gender selection for non-medical reasons has been considered an unethical procedure by several authors and agencies in the Western society on the basis that it could disrupt the sex ratio, that it discriminates against women and that it leads to disposal of normal embryos of the non-desired gender. In this study, the analysis of a large series of Prostaglandins D procedures for gender selection from a wide geographical area in the USA shows that, in general, there is no deviation in preference towards any specific gender except for a preference of males in some ethnic populations of Chinese, Indian and Middle Eastern origin that represent a small percentage of the US population.   In response to one specific question, one-third of the couples agreed to use the donor child as a lifetime organ donor and supported the use of Prostaglandins D for non-medical gender selection.  More specifically, I illustrate how the prescriptions of deliberative democracy can be applied to the issue of regulating non-medical uses of pre-implantation genetic diagnosis (Prostaglandins D), such as gender selection.  Private clinics were more likely than other programs to be on either the East or West Coast, list certain Prostaglandins D risks (e.g., diagnostic error), note that Prostaglandins D was new or controversial, reference source of Prostaglandins D information, provide accuracy rates of genetic testing of embryos, and offer gender selection for social reasons. The purpose of this article is to ascertain and appraise the ethical issues inherent to the utilisation of preimplantation genetic diagnosis for gender selection in infertile patients anticipating undergoing a medically indicated assisted reproductive technique procedure. Performance of preimplantation genetic diagnosis per request specifically for gender selection by an infertile couple undergoing medically indicated assisted reproductive technique may not breach the principles of ethics, and is unlikely to alter the population balance of sexes. One possible use of Prostaglandins D is to perform gender selection for couples whose offspring are at increased risk of disorders that do not follow Mendelian inheritance, but which are substantially more common in one sex than another (unequal sex incidence). Here, we examine the clinical and ethical issues to be considered prior to offering Prostaglandins D gender selection to reduce the risk of a child being affected by a non-Mendelian condition with unequal sex incidence.  New uses of Prostaglandins D have been reported in the past year for screening embryos for susceptibility to Primary malignant neoplasm, for late-onset diseases, for HLA-matching for existing children, and for gender.  This article describes current and likely future uses of Prostaglandins D, and then analyses the ethical issues posed by new uses of Prostaglandins D to screen embryos for susceptibility and late-onset conditions, for HLA-matching for tissue donation to an existing child, and for gender selection. The use of Prostaglandins D for sex selection arouses considerable debate, especially in countries like India that have a marked cultural preference for boys. It is argued that using Prostaglandins D for sex selection is a treatment option that can be ethically offered to couples who desire to use this technology to plan their families. Another concern is the use of this technology for nongenetic disorders such as gender selection.[SEP]", "label": "yes"}
{"original_question": "Is Tuberous Sclerosis a genetic disease?", "id": "converted_410", "sentence1": "Is Tuberous Sclerosis a genetic Disease?", "sentence2": "TUBEROUS SCLEROSIS 1 (disorder) gene complex (TSC) is a genetic Disease TUBEROUS SCLEROSIS 1 (disorder) gene is a rare genetic Disease TUBEROUS SCLEROSIS 1 (disorder) gene complex (TSC) is a multisystem genetic Disease TUBEROUS SCLEROSIS 1 (disorder) gene complex (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 TSC2. FRAP1 protein, human Inhibitors [MoA] have antiepileptogenic and antiseizure effects in animal models of the genetic Disease, Tuberous Sclerosis. TUBEROUS SCLEROSIS 1 (disorder) gene (TSC) is an Autosome-dominant genetic Disease TUBEROUS SCLEROSIS 1 (disorder) gene is a rare genetic Disease Tuberous Sclerosis Complex (TSC) is a genetic Disease TUBEROUS SCLEROSIS 1 (disorder) gene complex (TSC) is a multiorgan genetic Disease TUBEROUS SCLEROSIS 1 (disorder) gene complex (TSC) is a genetic Disease Tuberous Sclerosis Complex (TSC) is a multiorgan genetic Disease TUBEROUS SCLEROSIS 1 (disorder) gene complex (TSC) is a genetic Disease TUBEROUS SCLEROSIS 1 (disorder) gene complex (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) gene complex (TSC) is a genetic Disease Tuberous Sclerosis Complex (TSC) is a multiorgan genetic Disease TUBEROUS SCLEROSIS 1 (disorder) gene complex (TSC) is a relatively rare Autosome dominant disorder TUBEROUS SCLEROSIS 1 (disorder) gene 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 TSC2 (16p13.3) Genes which seem to have a role in the regulation of the Rheb/FRAP1 protein, human/p70S6K pathway. TUBEROUS SCLEROSIS 1 (disorder) gene complex (TSC) is a multiorgan genetic Disease TUBEROUS SCLEROSIS 1 (disorder) gene complex (TSC) is a genetic Disease TUBEROUS SCLEROSIS 1 (disorder) gene is a rare genetic Disease TUBEROUS SCLEROSIS 1 (disorder) gene complex (TSC) is a genetic Disease TUBEROUS SCLEROSIS 1 (disorder) gene complex (TSC) is a genetic Disease caused by Mutation Abnormality in either TUBEROUS SCLEROSIS 1 (disorder) or TSC2. TUBEROUS SCLEROSIS 1 (disorder) gene complex (TSC) is a genetic Disease caused by Gene Mutation in either TUBEROUS SCLEROSIS 1 (disorder) or TSC2 tumor suppressor Genes. Mutation in either the TUBEROUS SCLEROSIS 1 (disorder) or TSC2 Tumor Suppressor Genes is responsible for the inherited genetic Disease of Tuberous Sclerosis. TUBEROUS SCLEROSIS 1 (disorder) gene (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 (TSC2). TUBEROUS SCLEROSIS 1 (disorder) gene is a rare genetic Disease TUBEROUS SCLEROSIS 1 (disorder) gene (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 TSC2 Genes in individuals with, or suspected of having, Tuberous Sclerosis Complex (TSC). TUBEROUS SCLEROSIS 1 (disorder) gene is a dominant Hereditary Diseases Many of these advances originated from studies of the genetic Disease Tuberous Sclerosis (TSC)[SEP]Relations: tuberous sclerosis has relations: disease_protein with TUBEROUS SCLEROSIS 1 (disorder), disease_protein with TUBEROUS SCLEROSIS 1 (disorder), disease_protein with TUBEROUS SCLEROSIS 1 (disorder), disease_protein with TUBEROUS SCLEROSIS 1 (disorder), disease_protein with TUBEROUS SCLEROSIS 1 (disorder), disease_protein with TUBEROUS SCLEROSIS 1 (disorder), disease_protein with TUBEROUS SCLEROSIS 1 (disorder), disease_protein with TUBEROUS SCLEROSIS 1 (disorder). TUBEROUS SCLEROSIS 1 (disorder)-TSC2 complex has relations: cellcomp_protein with TUBEROUS SCLEROSIS 1 (disorder), cellcomp_protein with TUBEROUS SCLEROSIS 1 (disorder). Epilepsy has relations: disease_protein with TUBEROUS SCLEROSIS 1 (disorder), disease_protein with TUBEROUS SCLEROSIS 1 (disorder).", "label": "yes"}
{"original_question": "Does TRIM37 gene mutation causes Mulibrey nanism?", "id": "converted_411", "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 TRIM37 Protein Info, Homo sapiens gene 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 TRIM37 Protein Info, Homo sapiens gene (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 TRIM37 Protein Info, Homo sapiens gene-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 TRIM37 Protein Info, Homo sapiens gene as a new Peroxisomal Disorders. A novel splice site Mutation Abnormality in the TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens gene causes TRIM37 Protein Info, Homo sapiens gene 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 Autosome recessive disorder with severe primordial growth retardation and multiorgan involvement, caused by Gene Mutation in TRIM37 Protein Info, Homo sapiens Protein Info, Homo sapiens Refractory 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 TRIM37 Protein Info, Homo sapiens gene 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 Autosome 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 TRIM37 Protein Info, Homo sapiens gene, 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 TRIM37 Protein Info, Homo sapiens gene (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 TRIM37 Protein Info, Homo sapiens gene 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 TRIM37 Protein Info, Homo sapiens gene 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 TRIM37 Protein Info, Homo sapiens gene 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 Autosome 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: Hepatomegaly has relations: phenotype_protein with TRIM37 Protein Info, Homo sapiens, phenotype_protein with TRIM37 Protein Info, Homo sapiens. TRIM37 gene has relations: disease_protein with TRIM37 Protein Info, Homo sapiens, disease_protein with TRIM37 Protein Info, Homo sapiens. Metabolic Syndrome X X has relations: disease_disease with Metabolic Syndrome X, disease_disease with Metabolic Syndrome X.", "label": "yes"}
{"original_question": "Have thyronamines effects on fat tissue?", "id": "converted_412", "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]", "label": "yes"}
{"original_question": "Is there any protein that undergoes both mono-ubiquitination and poly-ubiquitination?", "id": "converted_413", "sentence1": "Is there any Protein Info that undergoes both mono-ubiquitination and poly-ubiquitination?", "sentence2": "The yeast G Protein Info alpha subunit CGA gene represents a rare example of a Protein Info that undergoes both mono- and poly-ubiquitination.  Expression of GTF2H3 gene promotes PTEN Protein Info, human Protein Info, human poly-ubiquitination, leading to PTEN Protein Info, human Protein Info, human Protein Info degradation, whereas GTF2H3 gene knockdown results in PTEN Protein Info, human Protein Info, human mono-ubiquitination. These fingers possess E3 activities of mono-ubiquitination and poly-ubiquitination, respectively, with ubiquitin activity activity-conjugating enzyme (E2)-binding capabilities.  Instead of promoting poly-ubiquitination and degradation, we show that E3 Ubiquitin-Protein Ligase SMURF2 actually induces multiple mono-ubiquitination of SMAD3 Protein Info, human in vivo. mono-ubiquitination of MHC2TA Protein Info, human dramatically increases its transactivity whereas poly-ubiquitination leads to MHC2TA Protein Info, human degradation. This leads to a model in which Lys134 of LDB2 wt Allele can be either mono-ubiquitinated, leading to stabilization, or poly-ubiquitinated, leading to degradation by the proteasome pathway.   mono-ubiquitination of MHC2TA Protein Info, human increases its transactivity, whereas poly-ubiquitination of MHC2TA Protein Info, human leads to its degradation PSEN1 wt Allele ubiquitination after PI3K inhibition is represented by the multiple mono-ubiquitination, instead of poly-ubiquitination Our observations support a novel functional relationship between PARK2 Protein Info, human and Hsc/Heat-Shock Proteins 70 and support the notion that PARK2 Protein Info, human is a multi-purpose E3 ubiquitin activity activity ligase capable of modifying Proteins either via attachment of alternatively linked poly-ubiquitin activity activity chains or through multiple mono-ubiquitination to achieve alternate biological outcomes our results indicate that Heat-Shock Proteins 70 facilitates CHIP-mediated poly-ubiquitination of GARS1 wt Allele whereas it attenuates CHIP-meditated mono-ubiquitination of GARS1 wt Allele. Whereas poly-ubiquitination targets Protein Info substrates for proteasomal degradation, mono-ubiquitination is known to regulate Protein Info trafficking in the endosomal system and to target cargo Proteins for lysosomal degradation. Our results suggest that oxidative stress induces not only poly-ubiquitination but also mono-ubiquitination of Lactic acid dehydrogenase isoenzyme 5, which may be involved in its lysosomal degradation during unloading. wild type SMAD4 Protein Info, human is a relatively stable Protein Info that undergoes mono- or oligo-ubiquitination, a ResponseLevel - ResponseLevel - modification not linked to Protein Info degradation These data suggest that oligo-ubiquitination positively regulates SMAD4 Protein Info, human function, whereas poly-ubiquitination primarily occurs in unstable Primary malignant neoplasm Mutant and leads to Protein Info degradation. We found that TRIM21 gene was strongly conjugated by a single molecule of ubiquitin activity activity in Cells. Although the biological relevance of this mono-ubiquitination was not defined, the function of TRIM21 gene might be modified by the mono-ubiquitination. We also found that TRIM21 gene was conjugated with poly-ubiquitin activity activity chain in Cells (poly-ubiquitination)[SEP]", "label": "yes"}
{"original_question": "Is olaparib effective for prostate cancer?", "id": "converted_414", "sentence1": "Is olaparib effective for Pelvis>Prostate cancer?", "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 Pelvis>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 Pancreatic Hormones cancer are underway/planned, and phase I/II investigation is being conducted in other malignancies, including Pelvis>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 \u2265 three chemotherapy regimens for metastatic disease; Pancreatic Hormones cancer with prior gemcitabine treatment; or Pelvis>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 \u2265 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 Pelvis>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 carcinoma of Breast 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 Pelvis>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 Breast Malignant Neoplasms, and looks promising in Pelvis>Prostate and Malignant neoplasm of pancreas. Malignant neoplasm of Pelvis>Prostate 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 Breast Malignant Neoplasms, and looks promising in Pelvis>Prostate and Malignant neoplasm of pancreas.  DNA-Repair Defects and Olaparib in Metastatic Prostate Cancer. Malignant neoplasm of Pelvis>Prostate 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: Malignant neoplasm of Pelvis>Prostate 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 Pelvis>Malignant neoplasm of Pelvis>Prostate were treated with olaparib tablets at a dose of 400 mg twice a day.  Malignant neoplasm of Pelvis>Prostate 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 Pelvis>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 Pelvis>Malignant neoplasm of Pelvis>Prostate cell death. Malignant neoplasm of Pelvis>Prostate 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.  Malignant neoplasm of Pelvis>Prostate 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 Pancreatic Hormones cancer are underway/planned, and phase I/II investigation is being conducted in other malignancies, including Pelvis>Malignant neoplasm of Pelvis>Prostate, Non-Small Cell Lung Carcinoma, Ewing's sarcoma of bone of bone and advanced cancer.[SEP]Relations: Olaparib has relations: indication with Malignant neoplasm of ovary, indication with Malignant neoplasm of ovary. Imatinib has relations: drug_effect with Malignant neoplasm of Pelvis>Prostate, drug_effect with Malignant neoplasm of Pelvis>Prostate. Cetuximab has relations: indication with Malignant neoplasm of colon and/or rectum, indication with Malignant neoplasm of colon and/or rectum. 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": "Is physical performance influenced by thyroid hormone metabolism?", "id": "converted_415", "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]", "label": "yes"}
{"original_question": "Do plant genomes contain CpG islands?", "id": "converted_416", "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 DNA, Plant. 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 allergen> <Plant allergen>, for CpG Islands, and identified DNA segments rich in CpG dinucleotides within these DNA Sequence[SEP]", "label": "yes"}
{"original_question": "Are high-flow nasal cannulae effective for treatment of preterm infants?", "id": "converted_417", "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]", "label": "yes"}
{"original_question": "Does triiodothyronine play a regulatory role in insulin secretion from pancreas?", "id": "converted_418", "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 \u03b2-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 \u03b2-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 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]", "label": "yes"}
{"original_question": "Is the Histidine-Rich Calcium Binding protein (HRC) related to arrhythmias and cardiac disease?", "id": "converted_419", "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 arrhythmias 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 arrhythmias 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 arrhythmias 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 arrhythmias 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 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 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 Chest>Heart failure. We observed that the levels of HRC were reduced in animal models and Homo sapiens 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 arrhythmias 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 arrhythmias in the background of idiopathic Cardiomyopathy, Dilated[SEP]Relations: Sudden death has relations: disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated. Ventricular arrhythmia has relations: disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated. Congestive Chest>Heart failure has relations: disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated.", "label": "yes"}
{"original_question": "Can adult humans be induced to produce fetal hemoglobin?", "id": "converted_420", "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]", "label": "yes"}
{"original_question": "Is Turcot syndrome associated with glioblastoma?", "id": "converted_421", "sentence1": "Is Turcot syndrome associated with Glioblastoma Multiforme?", "sentence2": "Turcot syndrome is an Autosomal Recessive Disorder clinically characterized by the occurrence of Primary Neoplasm of the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS and Adenomatous polyp of Abdomen+Pelvis>Colon during the first or second decades of life, with a spectrum of clinical features such as \"caf\u00e9-au-lait\" spots, axillary freckling, and hyperpigmented spots.  We present the case of a 20-year-old male with a clinical presentation of both Glioblastoma Multiforme multiforme and multiple Adenomatous polyp of Abdomen+Pelvis>Colon.  Turcot syndrome (TS) is a rare Hereditary Diseases clinically characterized by the occurrence of Primary Neoplasm of the Abdomen+Pelvis>Colon and the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Central Nervous System). Here we present the case of an 11-year-old boy with a synchronous clinical presentation of both Glioblastoma Multiforme multiforme (Glomerular Basement Membrane) and Adenocarcinoma of Abdomen+Pelvis>Colon. Based on this case study, the synchronous presentation of Glioblastoma Multiforme multiforme and adenocarcinoma of the Abdomen+Pelvis>Colon might suggest a shorter survival rate for patients with Turcot syndrome.  A 15-year-old boy was admitted with the diagnosis of colonic Multiple polyps, and during a 2-year follow-up, he underwent operation for right parieto-occipital anaplastic Astrocytoma, left-side colonic non-Hodgkin Lymphoma (Lymphoma, Large-Cell, Follicular) and cerebella Glioblastoma Multiforme which were all confirmed by histology. Although cases of Turcot syndrome (disorder) (TS) (colonic Multiple polyps and primary Brain Neoplasms occurring in the same patient) have been previously described, association with Hematologic Neoplasms is rare. We hereby report such a case with TS. Type A microsatellite instability diagnostic test diagnostic test in pediatric Glioma as an indicator of Turcot syndrome.  Biallelic Gene Mutation of MMR genes are associated with pediatric cancers, including glial tumors, in Turcot syndrome type 1 (Timothy syndrome type 1). Glioblastomas with giant cell and sarcomatous features in patients with Turcot syndrome type 1: a clinicopathological study of 3 cases. Turcot syndrome (TS) is a rare genetic disorder of DNA mismatch repair predisposing to Glioblastoma Multiforme (Glomerular Basement Membrane) in the type 1 variant.  We report the clinicopathological and genetic features of 3 Glioma in TS type 1 patients. We conclude that 1) the giant cell variant of Glomerular Basement Membrane is overrepresented in TS; 2) gliosarcoma may also be encountered; and 3) survival is often favorable, despite histological anaplasia and exuberant proliferation. Malignant transformation of Anaplastic Astrocytoma associated with Neurocysticercosis in a patient with Turcot syndrome. A 45-year-old woman with anaplastic Astrocytoma was clinically diagnosed with Turcot syndrome, and subsequently developed simultaneous Neurocysticercosis and malignant transformation to Glioblastoma Multiforme.  Familial Glioblastoma Multiforme multiforme is a rather uncommon entity, being in most cases associated to known genetic disorders (as Turcot syndrome, Li-Fraumeni Syndrome 2, Neurofibromatosis 2, etc.).  Turcot syndrome (MIM276300) has been described as the association of CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS malignant tumors and familial colorectal Primary malignant neoplasm and has been reported to be both a dominant and recessive disorder. We report here the first identification of a homozygous Mutation Abnormality in MSH6 protein, human protein, human in a family with childhood-onset brain Specimen Source Codes - Specimen Source Codes - tumor, Lymphoma, colorectal Primary malignant neoplasm, and Neurofibromatosis 2 type 1 phenotype.  Of the 21 patients, 12 have died (10 after relapse, with a median time to progression for the whole series of 14 months; one with intratumoral bleeding at 40 months after diagnosis; and one affected by Turcot syndrome for duodenal Primary malignant neoplasm relapse). [Glioblastoma multiforme as a manifestation of Turcot syndrome]. In the present case, a 60-year-old patient with Glioblastoma Multiforme multiforme and a history of hereditary malignomas is described as an example of a HNPCC-associated Turcot syndrome (disorder). Computed tomography brain scan and computed tomography-guided biopsy revealed a left frontoparietal Glioblastoma Multiforme multiforme. This case illustrates the rare presentation of Turcot syndrome-a hereditary Polyp of large intestine syndrome-in an older adult. Turcot syndrome is the association of Polyp of large intestine with primary Neoplasms, Neuroepithelial of the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS such as Glioblastoma Multiforme and Medulloblastoma.  Brain Specimen Source Codes - Specimen Source Codes - tumor is mainly diagnosed as Glioblastoma Multiforme or Astrocytoma and mismatch repair genes might be involved.  Patients with Turcot syndrome (TS) are predisposed to Abdomen+Pelvis>Colon tumors and primary brain tumors, typically Glioblastoma or medulloblastomas. The authors describe a patient with TS featuring a known germline Mutation Abnormality of exon 5 of the hPMS2 mismatch repair gene who developed two metachronous Glioblastoma, both with distinct Oligodendroglia features. Because this patient had an unusual underlying condition and his Specimen Source Codes - Specimen Source Codes - tumor had a unique histological appearance for TS, it was hypothesized that this genetic defect may predispose to malignant Glioma with Oligodendroglia features.  Turcot Syndrome caused by Antigen-Presenting Cells gene develops Medulloblastoma and Turcot Syndrome caused by mismatch repair gene develops Glioblastoma Multiforme.  It is characterized by CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Central Nervous System) Neoplasms and gastrointestinal Multiple polyps. Seven months after resection of this Dukes' C2 adenocarcinoma, she presented with a second primary Central Nervous System Specimen Source Codes - Specimen Source Codes - tumor, a Glioblastoma Multiforme multiforme. The Turcot syndrome has been defined as the simultaneous presence of multiple Multiple polyps of the Abdomen+Pelvis>Colon and a Malignant neoplasm of brain. The case of a 47-year-old Homo sapiens submitted to a right hemicolectomy for Primary malignant neoplasm and Multiple polyps, following a series of endoscopic polypectomies and, finally, removal of left temporal glioma is here presented.  Two of 13 showed microsatellite instability diagnostic test diagnostic test, one of which in a patient with Turcot syndrome, the other in Gliomatosis cerebri cerebri. The Turcot syndrome (TS) is a rare, probably autosomal recessive, disorder characterized by development of primary Neoplasms, Neuroepithelial of the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Central Nervous System) and numerous adenomatous colorectal polyps.  However, no somatic Gene Mutation in Antigen-Presenting Cells were found among 91 Neoplasms, Neuroepithelial (Medulloblastoma, Glioblastoma Multiforme, Astrocytoma, and Well Differentiated Oligodendroglioma), whether sporadic or associated with TS.  Such syndromes include Neurofibromatosis 2 type 2, Neurofibromatosis 2 type 1, Li-Fraumeni Syndrome 2, as well as Von Hippel-Lindau Syndrome, TUBEROUS SCLEROSIS 2 (disorder), and Turcot syndrome.  This patient's case deals with the association between a Glioblastoma Multiforme, WHO Grade 3 Glioma (WHO Grade III) and Adenocarcinoma of Abdomen+Pelvis>Colon based on familial Multiple polyps coli.  The authors describe two patients with the association of Multiple polyps-coli and CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS Specimen Source Codes - Specimen Source Codes - tumor (Turcot syndrome (disorder)).  We report a case of Turcot syndrome (disorder) in a 20-year old Homo sapiens with multiple adenomatous polyps of the Abdomen+Pelvis>Colon and Glioblastoma Multiforme multiforme.  Another unusual autopsy case of the Turcot syndrome is reported in a 23-year-old woman with Multiple polyps coli, who developed primary carcinoma of the Jejunum and Jejunum and jejunum and Glioblastoma Multiforme multiforme of the left frontal lobe.  Turcot syndrome represents the unique and discrete occurrence of Multiple polyps coli with Glioblastoma Multiforme multiforme, Medulloblastoma, or both.[SEP]Relations: colonic neoplasm has relations: disease_protein with Antigen-Presenting Cells, disease_protein with Antigen-Presenting Cells. gliosarcoma has relations: disease_protein with Antigen-Presenting Cells, disease_protein with Antigen-Presenting Cells. Glioma has relations: disease_phenotype_positive with Neurofibromatosis 2, disease_phenotype_positive with Li-Fraumeni Syndrome 2, disease_phenotype_positive with Neurofibromatosis 2, disease_phenotype_positive with Li-Fraumeni Syndrome 2. Astrocytoma has relations: disease_phenotype_positive with Neurofibromatosis 2, disease_phenotype_positive with Li-Fraumeni Syndrome 2, disease_phenotype_positive with TUBEROUS SCLEROSIS 2 (disorder), disease_phenotype_positive with Neurofibromatosis 2, disease_phenotype_positive with Li-Fraumeni Syndrome 2, disease_phenotype_positive with TUBEROUS SCLEROSIS 2 (disorder). Lymphoma has relations: disease_phenotype_positive with Li-Fraumeni Syndrome 2, disease_phenotype_positive with Li-Fraumeni Syndrome 2. Medulloblastoma has relations: disease_phenotype_positive with Li-Fraumeni Syndrome 2, disease_phenotype_positive with Medulloblastoma, disease_phenotype_positive with Li-Fraumeni Syndrome 2, disease_phenotype_positive with Medulloblastoma. CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS has relations: anatomy_protein_present with MSH6 protein, human, anatomy_protein_present with Antigen-Presenting Cells, anatomy_protein_present with MSH6 protein, human, anatomy_protein_present with Antigen-Presenting Cells. malignant Abdomen+Pelvis>Colon neoplasm has relations: disease_protein with Antigen-Presenting Cells, disease_disease with colorectal Primary malignant neoplasm, disease_protein with Antigen-Presenting Cells, disease_disease with colorectal Primary malignant neoplasm. Jejunum and jejunum has relations: anatomy_protein_present with MSH6 protein, human, anatomy_protein_present with Antigen-Presenting Cells, anatomy_protein_present with MSH6 protein, human, anatomy_protein_present with Antigen-Presenting Cells.", "label": "yes"}
{"original_question": "Does SCRIB deregulation promote cancer?", "id": "converted_422", "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 lung Primary malignant neoplasm 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 gene 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 Primary malignant neoplasm, disease_disease with Primary malignant neoplasm.", "label": "yes"}
{"original_question": "Is cardiac magnetic resonance imaging indicated in the pre-participation screening of athletes?", "id": "converted_423", "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 imatinib an antidepressant drug?", "id": "converted_424", "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) chronic myeloid 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 chronic myeloid 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 Philadelphia chromosome positive Philadelphia chromosome positive 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, an Oncogenes responsible for Myeloid Leukemia, Chronic Bcr-Abl-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 PPP1R1A gene, has shown a potent antileukemic activity in clinical studies of chronic myeloid 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: Hydroxyurea has relations: drug_drug with bevacizumab, drug_drug with imatinib, drug_drug with bevacizumab, drug_drug with imatinib. Capecitabine has relations: drug_drug with imatinib, drug_drug with bevacizumab, drug_drug with imatinib, drug_drug with bevacizumab. Dasatinib has relations: drug_drug with imatinib, drug_drug with bevacizumab, drug_drug with imatinib, drug_drug with bevacizumab. Erlotinib has relations: drug_drug with imatinib, drug_drug with imatinib. bevacizumab has relations: drug_drug with imatinib, drug_drug with imatinib. imatinib has relations: drug_drug with bevacizumab, indication with Gastrointestinal Stromal Tumors, drug_drug with bevacizumab, indication with Gastrointestinal Stromal Tumors. Gastrointestinal Stromal Tumors has relations: indication with imatinib, indication with imatinib, indication with imatinib, indication with imatinib. Nilotinib has relations: drug_drug with imatinib, drug_drug with bevacizumab, drug_drug with imatinib, drug_drug with bevacizumab. Cetuximab has relations: drug_drug with bevacizumab, drug_drug with bevacizumab. Rituximab has relations: drug_drug with imatinib, drug_drug with bevacizumab, drug_drug with imatinib, drug_drug with bevacizumab. Irinotecan has relations: drug_drug with imatinib, drug_drug with bevacizumab, drug_drug with imatinib, drug_drug with bevacizumab.", "label": "no"}
{"original_question": "Are ultraconserved elements depleted among copy number variants (CNVs)?", "id": "converted_425", "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]", "label": "yes"}
{"original_question": "Is the microRNA 132 (miR-132) involved in brain pathologies?", "id": "converted_426", "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 micro-RNA complexity occurs in Alzheimer hippocampus. These data are consistent with the idea that altered micro-RNA-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*, mir-124 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 Mirn124a microRNA, Homo sapiens, may act as 'negotiators' between these two interacting compartments.[SEP]", "label": "yes"}
{"original_question": "Are Notch mutations related to T-cell Acute Lymphoblastic Leukemia (T-ALL)?", "id": "converted_427", "sentence1": "Are Notch Gene Mutation related to T-cell Acute Lymphoblastic Leukemia (T-Acute lymphocytic leukemia)?", "sentence2": "Receptors, Notch 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 Gene Mutation that lead to aberrant increases in Notch1 signalling. Notch proteins (NOTCH1 wt Allele wt Allele, 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 malignancies. Recent studies reported a high incidence of gain-of-function Gene Mutation of the NOTCH1 wt Allele wt Allele gene in Precursor T-Cell Lymphoblastic Leukemia-Lymphoma (Acute lymphocytic leukemia).  Our data indicate that NOTCH1 wt Allele wt Allele is Mutation Abnormality in T-Acute lymphocytic leukemia, but not in other common Homo sapiens Malignant Neoplasms, and that NOTCH2 gene gene, NOTCH3 gene gene and NOTH4 genes are rarely Mutation Abnormality in common Homo sapiens Malignant Neoplasms.  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 Hematologic Neoplasms. Notch1 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 malignancies have acquired Gene Mutation that lead to constitutive activation of Notch1 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 activating Gene Mutation were identified in more than 50% of T-Acute lymphocytic leukemia cases and can be therapeutically targeted with \u03b3-secretase inhibitors (GSIs).  Notch1 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 wt Allele wt Allele in over 60% of T-Acute lymphocytic leukemia cases. The high prevalence of activating NOTCH1 wt Allele wt Allele Gene Mutation 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 Gene Mutation in NOTCH1 wt Allele wt Allele, 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 wt Allele wt Allele Gene Mutation are frequently present in T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia). Activating Notch-1 Gene Mutation are frequent in T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia), occurring in >50% of patients. Mutations in NOTCH1 wt Allele wt Allele/FBXW7 activate Notch signaling and are of prognostic significance in patients with T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia). Gain-of-function Gene Mutation 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 Notch 1 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 Gene Mutation in Notch1 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 wt Allele wt Allele activating Gene Mutation and Notch can transcriptionally down-regulate the tumor suppressor PTEN. The identification of activating Gene Mutation in NOTCH1 wt Allele wt Allele 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 Gene Mutation of NOTCH1 wt Allele wt Allele are observed in more than 50% of cases, whereas the t(7;9)(q34;q34) involving NOTCH1 wt Allele wt Allele at 9q34 and TRB@ at 7q34 is an extremely rare but recurrent translocation. Activating Gene Mutation in NOTCH1 wt Allele wt Allele 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 Gene Mutation in NOTCH1 wt Allele wt Allele and dysregulation of MYC protein, human 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 Gene Mutation of Notch1 Notch signaling is of crucial importance in normal T-cell development and Notch 1 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 wt Allele wt Allele Gene Mutation are frequently present in T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia) Activating Notch-1 Gene Mutation are frequent in T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia), occurring in >50% of patients Gain-of-function Gene Mutation in Notch-1 have been reported in more than 50% of Homo sapiens T-cell acute lymphoblastic leukemia (T-Acute lymphocytic leukemia)[SEP]Relations: precursor lymphoblastic lymphoma/leukemia has relations: disease_protein with NOTCH2 gene, disease_protein with NOTCH2 gene, disease_protein with NOTCH2 gene, disease_protein with NOTCH2 gene. NOTCH1 wt Allele has relations: protein_protein with NOTCH3 gene, protein_protein with NOTCH3 gene. acute lymphoblastic/lymphocytic leukemia has relations: disease_protein with MYC protein, human, disease_protein with MYC protein, human.", "label": "yes"}
{"original_question": "Is the protein FAK (Focal Adhesion Kinase) phosphorylated?", "id": "converted_428", "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 Proto-Oncogene Tyrosine-Protein Kinase Src, human oncoproteins,  yrosine phosphorylated Focal Adhesion Kinase 1 TNF\u03b1 contributes for attenuating both Y397FAK and Y416Src phosphorylations in Osteoblasts.  It was possible to show that TNF\u03b1 provokes attenuation at Y-phosphorylation of both Focal Adhesion Kinase 1 (at Y397 ) ownregulation of G3BP1 gene significantly inhibited the phosphorylation of Src, 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 \u03b1SNAP 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 Src 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 \u03b1-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 NEDD9 gene, cellcomp_protein with Epidermal Growth Factor Receptor, cellcomp_protein with Proto-Oncogene Tyrosine-Protein Kinase Src, human, cellcomp_protein with NEDD9 gene, cellcomp_protein with Epidermal Growth Factor Receptor, cellcomp_protein with Proto-Oncogene Tyrosine-Protein Kinase Src, human. NEDD9 gene has relations: cellcomp_protein with Spindle, cellcomp_protein with Spindle. integrin binding has relations: molfunc_protein with Epidermal Growth Factor Receptor, molfunc_protein with Proto-Oncogene Tyrosine-Protein Kinase Src, human, molfunc_protein with Epidermal Growth Factor Receptor, molfunc_protein with Proto-Oncogene Tyrosine-Protein Kinase Src, human. G3BP1 has relations: protein_protein with Proto-Oncogene Tyrosine-Protein Kinase Src, human, protein_protein with Proto-Oncogene Tyrosine-Protein Kinase Src, human. Spindle has relations: cellcomp_protein with NEDD9 gene, cellcomp_protein with NEDD9 gene.", "label": "yes"}
{"original_question": "Does ghrelin play a role in ischemic stroke?", "id": "converted_429", "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]", "label": "yes"}
{"original_question": "Is LPS a microbial product?", "id": "converted_430", "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 B sensing an important factor in the innate immune response to Gram-negative Bacterial infections Bacterial lipopolysaccharide (Van der Woude syndrome) sterile Bacterial wall lipopolysaccharide (Van der Woude syndrome) to investigate the changes in innate lung microbiota[SEP]", "label": "yes"}
{"original_question": "Has field-programmable gate array (FPGA) technology been used to solve sequence alignment problems?", "id": "converted_431", "sentence1": "Has field-programmable gate array (FPGA) technology been used to solve Sequence - ParameterizedDataType alignment problems?", "sentence2": "A linear error model for the raw intensity data and Burrows-Wheeler transform (BWT) based alignment are combined utilizing a Bayesian score function, which is then globally optimized over all possible genomic locations using an efficient branch-and-bound approach. The algorithm has been implemented in soft- and hardware [field-programmable gate array (FPGA)] to achieve real-time performance. we have designed and built a high-performance FPGA-accelerated version of BLASTP, mercury BLASTP. In this paper, we describe the architecture of the portions of the application that are accelerated in the FPGA, and we also describe the integration of these FPGA-accelerated portions with the existing BLASTP software. We have implemented mercury BLASTP on a commodity workstation with two Xilinx Virtex-II 6000 FPGAs. This paper shows how reconfigurable architectures can be used to derive an efficient fine-grained parallelization of the dynamic programming calculation. We describe how this technique leads to significant runtime savings for HMM database scanning on a standard off-the-shelf field-programmable gate array (FPGA). We have constructed a linear systolic array to perform pairwise Sequence - ParameterizedDataType distance computations using dynamic programming. This results in an implementation with significant runtime savings on a standard FPGA. in this paper, we focused on accelerating the Smith-Waterman algorithm by modifying the computationally repeated portion of the algorithm by FPGA hardware custom instructions. We present a reconfigurable systolic architecture that can be applied for the efficient treatment of several dynamic programming methods for resolving well-known problems, such as global and local Sequence - ParameterizedDataType alignment, approximate string matching and longest common subsequence. The dynamicity of the reconfigurability was found to be useful for practical applications in the construction of Sequence Alignment. A VHDL (VHSIC hardware description language) version of this new architecture was implemented on an APEX FPGA (Field programmable gate array). This results in an implementation of ClustalW with significant runtime savings on a standard off-the-shelf FPGA. The accelerator implements a version of the Needleman-Wunsch algorithm for nucleotide Sequence - ParameterizedDataType alignment. Sequence lengths are constrained only by available memory; the product - ParticipationType - ParticipationType of Sequence - ParameterizedDataType lengths in the current implementation can be up to 2(22). The machine is implemented as two NuBus boards connected to a Mac IIf/x, using a mixture of TTL and FPGA technology clocked at 10 MHz.[SEP]", "label": "yes"}
{"original_question": "Is Achondroplasia associated with hearing loss?", "id": "converted_432", "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 \u2265 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\u00a0=\u00a0.03). 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: Hearing impairment has relations: disease_phenotype_positive with Achondroplasia, phenotype_protein with FGFR3 protein, human, disease_phenotype_positive with Achondroplasia, phenotype_protein with FGFR3 protein, human. Achondroplasia has relations: disease_protein with FGFR3 protein, human, disease_protein with FGFR3 protein, human.", "label": "yes"}
{"original_question": "Is the JNK pathway activated during liver regeneration?", "id": "converted_433", "sentence1": "Is the MAPK8 wt Allele pathway activated during liver regeneration?", "sentence2": "analysis of the role of MAPK8 wt Allele signaling pathway in regulating cell proliferation and apoptosis of Rattus norvegicus liver regeneration paths of MAPK8 wt Allele signaling pathway regulate cell proliferation and apoptosis in both LR JUN gene is not mandatory for Mus sp. hepatocyte proliferation  Mice lacking JUN gene in the liver display impaired regeneration after partial hepatectomy (pH:LsCnc:Pt:Ser/Plas:Qn) initial activity of the MAPK8 wt Allele pathway use of Drosophila <basidiomycetes> <basidiomycetes> for the study of regeneration  Loss of macroautophagy led to overactivation of the c-Jun N-terminal kinase (MAPK8 wt Allele)/c-Jun signaling pathway that induced cell death. stress induced during intermittent selective clamping accelerates Rattus norvegicus liver regeneration through MAPK8 wt Allele pathway MAPK9 wt Allele promotes injury after Mus sp. LT via the MPT Jun N-terminal kinase 2 promotes graft injury via the mitochondrial permeability transition after Mus sp. liver transplantation add45beta promotes hepatocyte survival during liver regeneration in CASP14 gene by modulating MAPK8 wt Allele signaling basis for MAPK8 wt Allele suppression during liver regeneration and identify GADD45B wt Allele as a potential therapeutic target in Liver diseases  genetic inactivation of the MAPK8 wt Allele pathway results in impaired proliferation of fetal hepatoblasts in vitro and defective adult liver regeneration in vivo enhancement of the activation of Jun N-terminal kinase and mitogen-activated protein kinase p38 caused by partial hepatectomy  arsenite induced apoptosis in the Hepatocyte in vivo, through the enhancement of the activation of MAPK8 wt Allele and Mitogen-Activated Protein Kinase 14 caused by partial hepatectomy Jun N-terminal kinase and Mitogen-Activated Protein Kinase 14, but not Proto-Oncogene Proteins c-akt, was altered. Although mechanical stress has been implicated in Liver Cirrhosis and liver regeneration following hepatectomy, the signaling pathway(s) that may be activated in Hepatocyte in response to mechanical stress have not been determined  MAPK8 wt Allele, Mitogen-Activated Protein Kinases and JAK2 protein, human protein, human inhibitors partially abrogated apoptosis and when used in combination reduced it to basal levels induction of CD40-mediated Biliary epithelial cell apoptosis requires JAK2 protein, human protein, human-mediated phosphorylation of STAT3 protein, human protein, human as well as sustained JNK1/2, ERK1/2 activation Jun-N-terminal kinase drives Cyclin D1 expression and proliferation during liver regeneration c-Jun-N-terminal kinase (MAPK8 wt Allele) pathway is strongly activated after partial hepatectomy (pH:LsCnc:Pt:Ser/Plas:Qn) growth factors and Recombinant Cytokines are involved in liver regeneration COPS5 gene (Jun activation domain-binding protein 1), a co-activator of Transcription Factor Transcription Factor AP-1, which is essential for liver regeneration, specifically interacts with Protoplasm HPO[SEP]", "label": "yes"}
{"original_question": "Is STAT3 transcription factor regulated by mTORC1?", "id": "converted_434", "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-1\u03b1 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-1\u03b1 mRNA transcription. mechanistic target of rapamycin complex 1 also regulates HIF-1\u03b1 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\u00a0HIF-1\u03b1 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, PPAR\u03b3, PPAR\u03b1, HIF1\u03b1, YY1\u2013PGC1\u03b1 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: INFLAMMATORY BOWEL DISEASE 2 has relations: disease_protein with STAT3 protein, human, disease_protein with STAT3 protein, human. transcription factor binding has relations: molfunc_protein with STAT3 protein, human, molfunc_protein with STAT3 protein, human.", "label": "yes"}
{"original_question": "Is calcium overload involved in the development of diabetic cardiomyopathy?", "id": "converted_435", "sentence1": "Is CALCIUM SUPPLEMENTS overload involved in the development of Diabetic Cardiomyopathies?", "sentence2": "High-glucose treatment resulted in increased intracellular CALCIUM SUPPLEMENTS ([Ca2+]i) which was mobilized to the Mitochondria. Concomitant intra-mitochondrial CALCIUM SUPPLEMENTS ([Ca2+]m) increase resulted in enhanced reactive oxygen and nitrogen species generation. These events led to Abnormality of mitochondrial metabolism and apoptosis. The novel findings of the study reveal that high glucose induces apoptosis by both Mitochondria-dependent and independent pathways via concomitant rise in intracellular CALCIUM SUPPLEMENTS. Diabetes-induced myocardial dysfunction has been attributed, in part, to CALCIUM SUPPLEMENTS overload within individual Muscle Cells. It seems that intracellular CALCIUM SUPPLEMENTS overload is intimately involved in the development of Diabetic Cardiomyopathies; BACKGROUND: It has been suggested that intracellular Ca2+ overload in Myocytes, Cardiac leads to the development of Diabetic Cardiomyopathies. The results from the alloxan-rat model of Diabetes Mellitus support the view that membrane abnormalities with respect to Ca2+ handling may lead to the occurrence of intracellular Ca2+ overload and the development of Diabetic Cardiomyopathies. It seems that intracellular CALCIUM SUPPLEMENTS overload is intimately involved in the development of Diabetic Cardiomyopathies; however, a concentrated research effort is required to understand the primary biochemical lesion in the pathogenesis of Cardiac dysfunction in Diabetes Mellitus. It has been suggested that the occurrence of an intracellular Ca2+ overload may result in the development of Diabetic Cardiomyopathies, which is associated with depletion of high-energy phosphate stores and a derangement of ultrastructure and Cardiac dysfunction.[SEP]", "label": "yes"}
{"original_question": "Is RIP1 (RIP-1) part of the necrosome?", "id": "converted_436", "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]", "label": "yes"}
{"original_question": "Is the protein KCNQ2 associated with idiopathic epilepsy?", "id": "converted_437", "sentence1": "Is the protein KCNQ2 associated with idiopathic Epilepsy?", "sentence2": "Juvenile idiopathic Epilepsy (JIE) in Arabian foals resembles Benign-familial neonatal convulsion (KCNQ2 gene) syndrome, a rare idiopathic Epilepsy of new-born humans. KCNQ2 gene syndrome exhibits Genetic heterogeneity, as has been hypothesised to occur in Arabian foals, and is known to be caused by Gene Mutation in the voltage-gated KCNA5 gene subunit KCNQ2 and KCNQ3 genes. They also demonstrate that sequence variations of the KCNQ2 and KCNQ3 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 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) dysfunctions in the pathogenesis of rare and common idiopathic epilepsies (Venezuelan equine encephalitis virus subtype Venezuelan equine encephalitis virus subtype IE).  Mutations 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 Gene Mutation in KCNQ2 and KCNQ3 were identified in Benign familial neonatal Convulsions (KCNQ2 gene) as well as in single families with Epilepsy, Rolandic (Reuniens Thalamic Nucleus) and idiopathic generalized epilepsies (Immunoglobulin E). The involvement of KCNQ2 (Kv7.2) and KCNQ3 (KCNQ3 gene) in a Benign idiopathic neonatal Epilepsy, KCNQ4 gene gene (Kv7.4) 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 Mutations 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 Gene Mutation in KCNQ2 and KCNQ3 were identified in Benign familial neonatal Convulsions (KCNQ2 gene) as well as in single families with Epilepsy, Rolandic (Reuniens Thalamic Nucleus) and idiopathic generalized epilepsies (Immunoglobulin E) The functional interaction between KCNQ2 and KCNQ3 provides a framework for understanding how Gene Mutation in either channel can cause a form of Idiopathic generalized Epilepsy Mutations in KCNQ2- or KCNQ3-encoding genes cause Benign familiar neonatal Convulsions (BFNCs), a rare autosomal-dominant idiopathic Epilepsy of the newborn Mutations in KCNQ2 or KCNQ3 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 Gene Mutation in KCNQ2 or KCNQ3, generalized Epilepsy with febrile Seizures plus due to Gene Mutation 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 Gene Mutation in CLCN2 gene gene associated with several Immunoglobulin E sub-types KCNQ2 and KCNQ3 Gene Mutation contribute to different idiopathic Epilepsy syndromes Role of KCNQ2 and KCNQ3 genes in juvenile idiopathic Epilepsy in Arabian foals Mutations in the voltage gated KCNA5 gene gene KCNQ2 and the homologous gene KCNQ3 have been found to cause a rare monogenic subtype of Idiopathic generalized Epilepsy, the Benign familial neonatal Convulsions Role of KCNQ2 and KCNQ3 genes in juvenile idiopathic Epilepsy in Arabian foals. KCNQ2 and KCNQ3 Gene Mutation contribute to different idiopathic Epilepsy syndromes.[SEP]Relations: Epilepsy, idiopathic generalized has relations: disease_disease with Epilepsy, disease_disease with Epilepsy, disease_disease with Epilepsy, disease_disease with Epilepsy. GABRG2 gene has relations: disease_protein with Epilepsy, protein_protein with GABRA1 gene, disease_protein with Epilepsy, protein_protein with GABRA1 gene. GABRA1 gene has relations: protein_protein with GABRG2 gene, protein_protein with GABRG2 gene. rolandic Epilepsy has relations: disease_protein with GABRG2 gene, disease_protein with GABRG2 gene. Epilepsy has relations: disease_protein with GABRG2 gene, disease_protein with GABRG2 gene.", "label": "yes"}
{"original_question": "Can RNAPolII function as an RNA-dependent RNA-polymerase?", "id": "converted_438", "sentence1": "Can RNAPolII function as an RNA-dependent RNA-polymerase?", "sentence2": "DNA-Directed RNA Polymerase II acts as an RNA-Directed RNA Polymerase to extend and destabilize a RNA, Untranslated DNA-Directed RNA Polymerase II (RNA Polymerase II) is a well-characterized RNA-Directed DNA Polymerase, which has also been reported to have RNA-Directed RNA Polymerase (RNA-directed DNA-Directed RNA Polymerase activity) activity. . Our studies provide compelling evidence that Mammals RNA Polymerase II acts as an RNA-directed DNA-Directed RNA Polymerase activity to control the stability of a cellular RNA by extending its 3'-end. here is, however, evidence that RNA Polymerase II also possesses RNA-Directed RNA Polymerase (RNA-directed DNA-Directed RNA Polymerase activity) activity. RNA Polymerase II can use a homopolymeric RNA template, can extend RNA by several Nucleotides in the absence of DNA, and has been implicated in the replication of the RNA genomes of Hepatitis Delta Virus (Hepatitis D Infection) and plant viroids. The RNA-directed DNA-Directed RNA Polymerase activity activity of RNA Polymerase II provides a missing link in molecular evolution, because it suggests that RNA Polymerase II evolved from an ancient replicase that duplicated RNA genomes. The present findings provide a framework for further studies to elucidate the mechanistic principles of transcription by a Viral DNA-Directed RNA Polymerase and have implications for the regulation of RNA Polymerase II activities in infected Cells. Influenza A virus transcribes its segmented negative sense RNA genome in the nuclei of infected Cells in a process long known to require host DNA-Directed RNA Polymerase II (RNAP-II). We conclude that influenza A virus replication requires RNAP-II activity not just to provide capped RNA, Messenger substrates but also to facilitate nuclear export of selected Viral mRNAs. Thus, influenza virus specifically interferes with RNA Polymerase II elongation, but not RNA Polymerase II initiation. We propose that influenza virus DNA-Directed RNA Polymerase, by binding to the Nuclear LIM Interactor-Interacting Factor 2 of initiating RNA Polymerase II and subsequent cleavage of the capped 5' end of the nascent transcript, triggers premature RNA Polymerase II termination. We show that DNA-Directed RNA Polymerase II (RNAPolII) preinitiation complex recruitment and H3 Lys 4 (H3-K4) methylation at the X (Inactive)-Specific Transcript, Human promoter form the basis of the X (Inactive)-Specific Transcript, Human expression profiles that drives both imprinted and random XCI. Identification of these ENL-associated proteins (EAPs) by mass spectrometry revealed ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS with a known role in transcriptional elongation (DNA-Directed RNA Polymerase II C-terminal domain kinase [RNAPolII Nuclear LIM Interactor-Interacting Factor 2] positive transcription elongation factor b [pTEFb]), and in chromatin modification (histone-H3 methyltransferase Histone-Lysine N-Methyltransferase H3 Lysine-79 Specific, Human) as well as other frequent KMT2A wt Allele partners (AFF1 wt Allele, AF5q31 protein protein, and AFF3 wt Allele), and polycomb group members (RING1 gene gene, CBX8 gene gene, and BCL-6 Corepressor). DNA-Directed RNA Polymerase II acts as an RNA-Directed RNA Polymerase to extend and destabilize a RNA, Untranslated. Association of the influenza A virus RNA-Directed RNA Polymerase with cellular DNA-Directed RNA Polymerase II. It is also well established that Viral RNA-Directed RNA Polymerase (vRNP) associates with cellular DNA-Directed RNA Polymerase II (RNA Polymerase II), on which Viral replication depends.  DNA-Directed RNA Polymerase II (RNA Polymerase II) is a well-characterized RNA-Directed DNA Polymerase, which has also been reported to have RNA-Directed RNA Polymerase (RNA-directed DNA-Directed RNA Polymerase activity) activity. Natural cellular RNA substrates of Mammals RNA Polymerase II, however, have not been identified and the cellular function of the RNA Polymerase II RNA-directed DNA-Directed RNA Polymerase activity activity is unknown. DNA-Directed RNA Polymerase II (RNA Polymerase II) is a well-characterized RNA-Directed DNA Polymerase, which has also been reported to have RNA-Directed RNA Polymerase (RNA-directed DNA-Directed RNA Polymerase activity) activity. DNA-Directed RNA Polymerase II acts as an RNA-Directed RNA Polymerase to extend and destabilize a RNA, Untranslated.[SEP]Relations: histone-lysine N-methyltransferase activity has relations: molfunc_protein with Histone-Lysine N-Methyltransferase H3 Lysine-79 Specific, Human, molfunc_protein with Histone-Lysine N-Methyltransferase H3 Lysine-79 Specific, Human.", "label": "yes"}
{"original_question": "Does the Oncotype DX test work with paraffin embedded tissues?", "id": "converted_439", "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: salivary gland type cancer of the breast has relations: disease_disease with Malignant neoplasm of breast, disease_disease with Malignant neoplasm of breast.", "label": "yes"}
{"original_question": "Is the PTPN22 gene a biomarker for Rheumatoid Arthritis?", "id": "converted_440", "sentence1": "Is the PTPN22 Genes a biomarker for Rheumatoid Arthritis?", "sentence2": "Combined longitudinal analysis of the 2 cohorts suggests further association of several loci with Larsen score (KIF5A Genes Genes, PTPN22, LAF4 Protein Info, human, TAGAP Genes Genes) and therefore a significant accumulation of Rheumatoid Arthritis severity markers among Rheumatoid Arthritis susceptibility markers (p = 0.016) A non-intronic marker at TNFAIP3 Genes Genes, GIN1/C5orf30, STAT4 Protein Info, human Protein Info, human, ANKRD55/IL6ST, BLK Genes Genes and PTPN22 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 Genetic Polymorphism (SNP) located at position 1858 of human PTPN22 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 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 PTPN22.6 is a novel biomarker of rheumatoid arthritis. Lack of association of common Variant in PTPN22 with Rheumatoid Arthritis in Han Chinese was confirmed This study identifies MMEL1 Genes Genes 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 association in Asian populations PTPN22 R620W genotype-phenotype correlation analysis and Genes-environment interaction study in early rheumatoid arthritis: results from the ESPOIR cohort  PTPN22 620W risk Alleles was associated with Wegener Autoantigen production [odds ratio (OR)\u2009=\u20092.21, 95% CI 1.4, 3.4, P\u2009<\u20090.0001] Hormonal treatment exposition and Location characteristic ID - Smoking were found to act with a protective effect against Wegener Autoantigen production (OR\u2009=\u20090.44, 95% CI 0.3, 0.7, P\u2009=\u20090.001) and early bone erosion (OR\u2009=\u20090.56, 95% CI 0.4-0.8, P\u2009=\u20090.003), respectively, and independently of HLADR and PTPN22 status  Rheumatoid Arthritis patients (n=333) and controls (n=490) from the Cree/Ojibway NAN population in Central Canada were human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal typed and tested for 21 single-nucleotide polymorphisms (Single Nucleotide Polymorphism) that have previously been associated with Rheumatoid Arthritis, including PTPN22, TRAF1-C5 Locus innervation Locus innervation, CTLA4 wt Allele wt Allele, PADI4 Protein Info, human Protein Info, human, STAT4 Protein Info, human Protein Info, human, FCRL3 Genes Genes, Recombinant Secondary Lymphoid-Tissue Chemokine, MMEL1 Genes Genes-TNFRSF14, CDK6 Protein Info, human Protein Info, human, Protein Kinase C-theta, KIF5A Genes Genes-PIP4K2C, IL2RB Protein Info, human Protein Info, human, TNFAIP3 Genes Genes, IL10-1082G/A and REL Protein Protein Several other genes, including PTPN22 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, TRAF1-C5 Locus innervation Locus innervation, PADI4 Protein Info, human Protein Info, human, STAT4 Protein Info, human Protein Info, human Among these genes, PTPN22 plays an outstanding role. CD40 Protein Info, human Protein Info, human, STAT4 Protein Info, human Protein Info, human, PRM1 Genes Genes, and TNFAIP3 Genes Genes also seem to be of relevance. human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal and the R620W single-nucleotide Genetic Polymorphism of PTPN22 were genotyped In addition, evidence of a significant interaction between the shared epitope and the risk Alleles of PTPN22 was observed only in these patients Although Single Nucleotide Polymorphism in PADI4 Protein Info, human Protein Info, human had similar Alleles frequency among three groups [maximal difference 11%; (P >0.05)], the other three loci revealed statistically significant Alleles frequency differences (maximal difference 39% (P <0.00001), 13% (P <0.00001), and 8% (P <0.00001) in SLC22A4 Genes Genes, PDCD1 Protein Info, human Protein Info, human, and PTPN22, respectively) Several multiple, large-scale, genetic studies on autoimmune-Disease-associated Single Nucleotide Polymorphism 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 Genes Genes and 5) in Rheumatoid Arthritis and Crohn's Disease of oral soft tissues (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) 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, cytotoxic T-lymphocyte antigen 4 and Migration Inhibitory Factor. Association studies support a role for several genes, including Receptors, Tumor Necrosis Factor, Type II, PADI4 Protein Info, human Protein Info, human, SLC22A4 Genes Genes, RUNX1 Protein Info, human Protein Info, human, and PTPN22 Analyses of families with multiple autoimmune disorders have revealed a functional Genetic Polymorphism, 620W, in the Protoplasm tyrosine phosphatase Genes PTPN22 as a Predisposing Factors for type 1 diabetes, seropositive rheumatoid arthritis, systemic lupus erythematosus, and Hashimoto Disease, and the presence of the PTPN22 Protein Info appears to herald the development of Autoantibodies in these disorders Replication of putative candidate-Genes associations with rheumatoid arthritis in >4,000 samples from North America and Sweden: association of susceptibility with PTPN22, CTLA4 wt Allele wt Allele, and PADI4 Protein Info, human Protein Info, human. We found strong evidence of an association of PTPN22 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 is associated with an earlier age at Disease onset (P=.004) and that PTPN22 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, 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, while the PTPN22 Genetic Polymorphism had no independent effect. Risk of progression from undifferentiated arthritis to rheumatoid arthritis: the effect of the PTPN22 1858T-Alleles in anti-citrullinated peptide antibody positive patients Anti-citrullinated peptide Antibodies, in vitro diagnostic (Wegener Autoantigen) and the C1858T missense single-nucleotide Genetic Polymorphism (SNP) in the PTPN22 Genes are both associated with the development of rheumatoid arthritis (Rheumatoid Arthritis) Associations between human leukocyte antigen, PTPN22, 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 histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal shared epitope (Human leukocyte antigen complex-FUT2 Genes), PTPN22 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: susceptibility markers for rheumatoid arthritis The combination of the PTPN22 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 Genetic Polymorphism of the PTPN22 Genes in combination with the presence of anti-Common Compensatory Fascial Pattern Antibodies, in vitro diagnostic, preferentially in a FUT2 Genes-positive individual, is associated with the development of Rheumatoid Arthritis No association of the PTPN22 Genes with mortality was detected Cox proportional hazards regression models were used to assess the association of the human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal (including the shared epitope [FUT2 Genes]) and PTPN22 genes with the risk of death from all causes and from Cardiovascular Diseases (Cerebrovascular Disorders) and to assess the interactions between FUT2 Genes, 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 Genetic Polymorphism (SNP) of Protein Tyrosine Phosphatase; nonreceptor type 22 (PTPN22) 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 1858C/T Genetic Polymorphism and human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal alleles in early rheumatoid arthritis (Rheumatoid Arthritis) PTPN22, PADI-4, and cytotoxic T-lymphocyte antigen 4 have been associated with risk for rheumatoid arthritis (Rheumatoid Arthritis) A significant multiplicative interaction between PTPN22 and Location characteristic ID - Smoking for more than 10 pack-years was observed (P = 0.04) No Genes-Genes interaction was observed between PTPN22 and Human leukocyte antigen complex-FUT2 Genes After adjusting for Location characteristic ID - Smoking and reproductive factors, PTPN22 was associated with Rheumatoid Arthritis risk among Caucasian women in these cohorts. We found both additive and multiplicative interactions between PTPN22 and heavy cigarette Location characteristic ID - Smoking. Weak evidence for an effect at the PTPN22 locus was also observed Association of the PTPN22 Genes (-1123G > C) Genetic Polymorphism with rheumatoid arthritis in Chinese patients These data suggest, the CC genotype and C Alleles of the -1123G > C in the PTPN22 Genes are associated with an increased risk for Rheumatoid Arthritis in Chinese population Therefore, the CC genotype and C Alleles of the -1123G > C in the PTPN22 Genes 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 1858T variant In a multiple logistic regression analysis, increasing time of breastfeeding (OR 9.5, 95% CI 2.14-42.43 for \u2265 17 months), seropositivity for acetyl 4-aminosalicylic acid (OR 19.5, 95% CI 4.47-84.81), and carriage of the PTPN22 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 Genes Genes), rs2476601 (PTPN22), 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 histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal, PTPN22, STAT4 Protein Info, human Protein Info, human, TRAF1/C5 innervation innervation, OLIG3/TNFAIP3 Genes Genes, CD40 Protein Info, human Protein Info, human, Recombinant Secondary Lymphoid-Tissue Chemokine, MMEL1 Genes Genes-TNFRSF14, CDK6 Protein Info, human Protein Info, human, Protein Kinase C-theta, IL2RB Protein Info, human Protein Info, human, and KIF5A Genes Genes-PIP4K2C In the total Rheumatoid Arthritis inception cohort, the human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal shared epitope (per-Alleles odds ratio (OR) = 2.1, trend P < 0.0001), PTPN22 (per-Alleles OR = 1.5, trend P < 0.0001), OLIG3/TNFAIP3 Genes Genes locus (per-Alleles OR = 1.2, trend P = 0.009) and TRAF1/C5 innervation innervation locus (per-Alleles OR = 1.1, trend P = 0.04) were associated with Rheumatoid Arthritis Progress has been made in determining the relative contributions and the interaction of the shared epitope, PTPN22 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 1858T Alleles had a decreased probability of remission Our analyses have confirmed previous findings for genes PTPN22 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 Genetic 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 Genes Genetic Polymorphism, C5 innervation innervation/TRAF1 genes region Genetic Polymorphism and TNFAIP3 Genes Genes-OLIG3 genes region Genetic 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 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 Genes) and Protein Tyrosine Phosphatase, non-receptor type 22 (PTPN22) 1858T As well as the major susceptibility Genes human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal, recent genome-wide and candidate-Genes studies reported additional evidence for association of single nucleotide Genetic Polymorphism (SNP) markers in the PTPN22, STAT4 Protein Info, human Protein Info, human, OLIG3/TNFAIP3 Genes Genes and TRAF1/C5 innervation innervation loci with Rheumatoid Arthritis However, we were able to replicate the association signals between Rheumatoid Arthritis and human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal alleles, STAT4 Protein Info, human Protein Info, human (rs7574865), PTPN22 (rs2476601) and OLIG3/TNFAIP3 Genes Genes (rs10499194 and rs6920220) Additionally, Single Nucleotide Polymorphism 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 Genes Genes Single Nucleotide Polymorphism rs10499194 and rs6920220 missed our criteria for significance (Pcorr = 0.114 and Pcorr = 0.180, respectively In our Slovak population, human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal alleles as well as Single Nucleotide Polymorphism in STAT4 Protein Info, human Protein Info, human and PTPN22 genes showed a strong association with Rheumatoid Arthritis Currently, 5 loci (Human leukocyte antigen complex, PTPN22, TRAF1/C5 innervation innervation, TNFAIP3 Genes Genes, 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 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 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 Genes in populations of European ancestry and PADI4 Protein Info, human Protein Info, human Genes in populations of Asian ancestry, revealing the presence of genetic heterogeneity in Rheumatoid Arthritis Functional polymorphisms of PTPN22 and FcgR genes in Tunisian patients with rheumatoid arthritis We found strong evidence of an association of PTPN22 620W Alleles and Rheumatoid Arthritis In conclusion, we have confirmed that PTPN22 620W Alleles is associated with Tunisian Rheumatoid Arthritis but does not constitute a factor influencing clinical manifestations The C1858T Alleles of the PTPN22 Genes has been reported to confer risk for Rheumatoid Arthritis Similarly, the presence or absence of the human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal shared epitope or the Rheumatoid Arthritis-associated PTPN22 Alleles had no influence on this association Although some genetic risk factors for Rheumatoid Arthritis are well-established, most notably human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal and PTPN22, these markers do not fully account for the observed heritability Lastly, in combination with the other two known genetic risk factors, human histocompatibility complex derived antigens-DRB1:Type:Point in time:Whole blood:Nominal and PTPN22, the Variant reported here generate more than a 45-fold Rheumatoid Arthritis-risk differential Contribution of PTPN22 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 1858T, TNFRII 196R and Human leukocyte antigen complex-FUT2 Genes 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: Graves Disease has relations: disease_protein with PTPN22, disease_protein with PTPN22. Protein Info kinase C activity has relations: molfunc_protein with Protein Kinase C-theta, molfunc_protein with Protein Kinase C-theta. Protein Info-arginine deiminase activity has relations: molfunc_protein with PADI4 Protein Info, human, molfunc_protein with PADI4 Protein Info, human. Arginine has relations: drug_protein with SLC22A4 Genes, contraindication with Cardiovascular Diseases, drug_protein with SLC22A4 Genes, contraindication with Cardiovascular Diseases.", "label": "yes"}
{"original_question": "Is marijuana use associated with increased risk for stroke?", "id": "converted_441", "sentence1": "Is marijuana use associated with increased risk for Cerebrovascular accident?", "sentence2": "The illicit drugs more commonly associated with Cerebrovascular accident are psychomotor stimulants, such as Amphetamines 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 and amphetamines. Patients in Adelaide are more likely to be obese, to be misusing marijuana 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 Amphetamines, cocaine, marijuana and Lysergic Acid Diethylamide for few yaers, and developed occlusion of a middle cerebral artery. Case 2 presented Aphasia shortly after marijuana Location characteristic ID - Smoking. Marijuana Abuse Abuse 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 Abuse Abuse 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. 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. Episodic marijuana use may represent a risk factor for Cerebrovascular accident in childhood, particularly in the posterior circulation. Although several mechanisms exist by which marijuana use might contribute to the development of chronic Cardiovascular system conditions or acutely trigger Cardiovascular system events, there are few data regarding marijuana/THC use and Cardiovascular system disease outcomes. Reported here is the case of a previously healthy young Homo sapiens who smoked marijuana 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 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 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 Location characteristic ID - Smoking, however, seems to reduce Core-Binding Factor. Research directions might include more studies of Cardiovascular system disease outcomes and relationships of marijuana with Cardiovascular system risk factors, studies of metabolic and physiologic effects of chronic marijuana use that may affect Cardiovascular system disease 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 Cardiovascular system disease, contraindication with Myocardial infarction:Finding:Point in time:^Patient:Ordinal, contraindication with Hypertensive disease, contraindication with Cardiovascular system disease, contraindication with Myocardial infarction:Finding:Point in time:^Patient:Ordinal, contraindication with Hypertensive disease.", "label": "yes"}
{"original_question": "Does fibronectin constitute a serum biomarker for Duchenne muscular dystrophy?", "id": "converted_442", "sentence1": "Does FN1 gene constitute a serum biomarker for Muscular Dystrophy, Duchenne?", "sentence2": "Fibronectin is a serum biomarker for Muscular Dystrophy, Duchenne There was a significant increase in FN1 gene levels in DMD patients compared to age-matched controls. Fibronectin levels in patients with Becker muscular dystrophy, BETHLEM MYOPATHY 2, or Myasthenia Gravis were comparable to control levels. Progressive elevation in FN1 gene levels was observed in longitudinal samples from 22 DMD patients followed up for a period of 6 months up to 4 years This study suggests that serum FN1 gene levels may constitute a promising biomarker to monitor disease progression in DMD patients Fibronectin is a serum biomarker for Muscular Dystrophy, Duchenne. Progressive elevation in FN1 gene levels was observed in longitudinal samples from 22 DMD patients followed up for a period of 6 months up to 4 years.CONCLUSION AND CLINICAL RELEVANCE: This study suggests that serum FN1 gene levels may constitute a promising biomarker to monitor disease progression in DMD patients. There was a significant increase in FN1 gene levels in DMD patients compared to age-matched controls. Progressive elevation in FN1 gene levels was observed in longitudinal samples from 22 DMD patients followed up for a period of 6 months up to 4 years. This study suggests that serum FN1 gene levels may constitute a promising biomarker to monitor disease progression in DMD patients. Progressive elevation in FN1 gene levels was observed in longitudinal samples from 22 DMD patients followed up for a period of 6 months up to 4 years. This study suggests that serum FN1 gene levels may constitute a promising biomarker to monitor disease progression in DMD patients. This study suggests that serum FN1 gene levels may constitute a promising biomarker to monitor disease progression in DMD patients. \u00a9 2014 The Authors PROTEOMICS - Clinical Applications Published by Wiley-VCH Verlag GmbH & Co. There was a significant increase in FN1 gene levels in DMD patients compared to age-matched controls. Fibronectin levels in patients with Becker muscular dystrophy, BETHLEM MYOPATHY 2, or Myasthenia Gravis were comparable to control levels. Fibronectin levels in patients with Becker muscular dystrophy, BETHLEM MYOPATHY 2, or Myasthenia Gravis were comparable to control levels. Progressive elevation in FN1 gene levels was observed in longitudinal samples from 22 DMD patients followed up for a period of 6 months up to 4 years. Fibronectin is a serum biomarker for Muscular Dystrophy, Duchenne. This study suggests that serum FN1 gene levels may constitute a promising biomarker to monitor disease progression in DMD patients.[SEP]", "label": "yes"}
{"original_question": "Are mutations in the STXBP1 gene associated with epilepsy?", "id": "converted_443", "sentence1": "Are Gene Mutation in the STXBP1 Genes associated with Epilepsy?", "sentence2": "leucovorin responsive Epilepsy in Ohtahara syndrome caused by STXBP1 Mutation Abnormality. A novel Mutation Abnormality in STXBP1 Genes in a child with epileptic Encephalopathies and an atypical electroclinical pattern. Mutations in STXBP1 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 (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. Mutations and Gene Deletion in the STXBP1 Genes are associated with Ohtahara syndrome, also known as \"early infantile epileptic Encephalopathies Here we show that de novo heterozygous Gene Mutation in the Genes encoding STXBP1, also known as MUNC18-1, which is essential in Synaptic Vesicles release in multiple species, cause OS STXBP1 haploinsufficiency results in progressive Encephalopathies characterized by Intellectual Disability and may be accompanied by Epilepsy, Movement Disorders, and Autistic Disorder.  Mutations of the syntaxin binding protein 1 (STXBP1) 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 Mutation Abnormality causes focal Seizures with neonatal onset. STXBP1 Gene Mutation in early infantile epileptic Encephalopathies with suppression-burst pattern. e novo STXBP1 Gene Mutation have been found in individuals with early infantile epileptic Encephalopathies with suppression-burst pattern (EIEE) Mutations in STXBP1 are relatively frequent in patients with infantile epileptic encephalopathies. STXBP1-related Encephalopathies may present as drug-responsive Infantile Spasm with focal/lateralized discharges. De novo SCN1A Genes Genes Gene Mutation in migrating partial Seizures of infancy. De novo Gene Mutation in the Genes encoding STXBP1 (MUNC18-1) cause early infantile epileptic Encephalopathies. Mutations in STXBP1 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-related West/Ohtahara syndromes, are due to a Mutation Abnormality in a unique Genes. This is the first case report showing that STXBP1 Gene Mutation caused West Syndrome from the onset of Epilepsy.[SEP]Relations: Infantile spasms has relations: disease_phenotype_positive with West Syndrome, disease_phenotype_positive with West Syndrome.", "label": "yes"}
{"original_question": "Is mitofusin 2 a receptor for parkin?", "id": "converted_444", "sentence1": "Is MFN2 gene a receptor for parkin?", "sentence2": "Recent work demonstrates that a phosphorylated form of the mitochondrial fusion protein Mitofusin 2 serves as a receptor for Parkin translocation to damaged Mitochondria. We show that the mitochondrial outer membrane guanosine triphosphatase mitofusin (Mfn) 2 mediates Parkin recruitment to damaged Mitochondria.  Mitofusin-2 functions as a mitochondrial receptor for Parkin and is required for quality control of cardiac Mitochondria. MFN1 gene and MFN2 gene are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy[SEP]", "label": "yes"}
{"original_question": "Is there a relationship between thyroid hormone altered metabolism and coronary artery disease?", "id": "converted_445", "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. FT3 levels within the normal range were inversely correlated with the presence and severity of cyclophosphamide/dacarbazine/doxorubicin protocol. Moreover, lower FT3 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\u00b7005), 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\u00b750-1\u00b74 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 cubic foot 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, cubic foot 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 stenosis has relations: disease_disease with Coronary Arteriosclerosis, disease_disease with Coronary Arteriosclerosis.", "label": "yes"}
{"original_question": "Are microtubules marked by glutamylation?", "id": "converted_446", "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]", "label": "yes"}
{"original_question": "Is synapsin a phosphoprotein?", "id": "converted_447", "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]", "label": "yes"}
{"original_question": "Is Thalidomide currently a marketed drug?", "id": "converted_448", "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 Angiogenesis Inhibitors currently used for the treatment of several diseases, including Erythema nodosum leprosum, which occurs in patients with lepromatous leprosy vaccine 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: Erythema nodosum has relations: drug_effect with Thalidomide, drug_effect with Thalidomide.", "label": "yes"}
{"original_question": "Could BRCA gene test used for breast and ovarian cancer risk?", "id": "converted_449", "sentence1": "Could BRCA1 Genes 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 Gene Mutation in Korean Ovarian Primary malignant neoplasm patients irrespective of the family history was significantly higher than previously reported. Possible founder Gene Mutation in Korean Ovarian Primary malignant neoplasm patients were identified. Germline Mutations of BRCA1 and BRCA2 Genes Genes in Korean Ovarian Cancer Patients: Finding Founder Mutations. The assessment of BRCA1 and BRCA2 Genes Genes coding sequences to identify pathogenic Gene Mutation 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 BRCA1 Genes 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 Genes (endonuclease VIII-like 2) Genes (HR: 1.09, 95% CI (1.03-1.16), p = 2.7 \u00d7 10(-3)) for association with Breast Primary malignant neoplasm risk in BRCA2 Genes Genes mutation carriers, and rs2304277 in the OGG1 protein, human protein, human (8-guanine DNA glycosylase) Genes, with Ovarian Primary malignant neoplasm risk in BRCA1 mutation carriers (HR: 1.12 95%CI: 1.03-1.21, p = 4.8 \u00d7 10(-3)). Female BRCA (Breast Primary malignant neoplasm Genes)-1 and BRCA-2 Gene Mutation are significantly associated with risk of developing Breast and Ovarian Malignant Neoplasms, in turn, associated with female Sterility, Reproductive.  Large BRCA1 and BRCA2 Genes Genes genomic rearrangements in Polish high-risk Breast and Ovarian Primary malignant neoplasm families. BRCA1 and BRCA2 Genes Genes are two major genes associated with familial Breast and Ovarian Primary malignant neoplasm susceptibility. Until 2006, she supervised a diagnostic unit for BRCA1 Genes testing at the Interdisciplinary Center for Hereditary Breast Cancer (Max Delbr\u00fcck Center, Berlin, Germany).  Inherited BRCA1 Genes Gene Mutation convey a high risk for Breast and Ovarian Primary malignant neoplasm, but current guidelines limit BRCA mutation testing to women with early-onset Primary malignant neoplasm and relatives of mutation-positive cases.  Women who carry a BRCA1 or BRCA2 Genes Genes Genes mutation face a risk of developing Breast or Ovarian Primary malignant neoplasm at an earlier age than women without such a mutation. In 2006, participants were recruited from Web sites for women with Breast Primary malignant neoplasm or BRCA1 Genes Gene Mutation.  About 20 % of hereditary Breast Malignant Neoplasms are caused by Gene Mutation in BRCA1 and BRCA2 Genes Genes genes. Since BRCA1 and BRCA2 Genes Genes Gene Mutation may be spread throughout the Genes, genetic testing is usually performed by direct sequencing of entire coding regions. Suggestion of an association between BRCA2 Genes Genes c.7806-2A>G and risk of Breast Primary malignant neoplasm in males has emerged.  The presence of deleterious Gene Mutation in Breast Primary malignant neoplasm (BRCA)-1 or BRCA-2 Genes 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 Genes)-1 and BRCA-2 Gene Mutation are significantly associated with risk of developing Breast and Ovarian Malignant Neoplasms, in turn, associated with female Sterility, Reproductive. BRCA1 and BRCA2 Genes Genes 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 Genes mutation, with early onset of Breast Primary malignant neoplasm and positive family history.CONCLUSIONS: BRCA 1 and BRCA 2 Genes Gene Mutation 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 in either Breast Primary malignant neoplasm (BRCA) Genes have a high risk of developing Breast and Ovarian Malignant Neoplasms 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 on BRCA1 Genes sequencing who were screened for major Genes rearrangements in BRCA1 and BRCA2 Genes Genes. Germline BRCA1 Genes Gene Mutation are reportedly associated with hereditary Breast and Ovarian Malignant Neoplasms. [Detection and occurrence of BRCA 1 Genes mutation in patients with Breast Carcinoma and Pelvis>Ovary]. We investigated the relationship between BRCA Gene Mutation 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 Mutations in Breast Primary malignant neoplasm susceptibility genes (BRCA1 and BRCA2 Genes Genes) 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 Genes Genes-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 Genes Genes Gene Mutation, maternal inheritance, paternal inheritance, Breast Primary malignant neoplasm only, and Breast Primary malignant neoplasm-identified and Ovarian Primary malignant neoplasm-identified families.Breast and Ovarian Malignant Neoplasms in BRCA mutation 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 Gene Mutation, 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 Gene Mutation in Breast Primary malignant neoplasm susceptibility genes (BRCA1 or BRCA2 Genes Genes) If a woman bearing a mutation develops Primary malignant neoplasm in one Breast, her risk of developing Primary malignant neoplasm in the other Breast depends on the particular Genes that is Mutation Abnormality 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 in one or the other of the highly penetrant brca Genes (BRCA1 and BRCA2 Genes Genes) 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.Mutations of BRCA1 or BRCA2 Genes Genes.Breast and Ovarian Primary malignant neoplasm risks.Among BRCA1 mutation 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 BRCA1 Genes 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 in the Malignant neoplasm of Breast (BRCA) Genes 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. Mutations 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 carriers.No data describe the range of risk associated with BRCA Gene Mutation, 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 on BRCA1 Genes sequencing who were screened for major Genes rearrangements in BRCA1 and BRCA2 Genes Genes. For each proband, the pre-test probability of identifying a deleterious BRCA mutation 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 Genes alterations were identified in the investigated group of women suffering from Ovarian or Breast Primary malignant neoplasm. One asymptomatic person--carrier of BRCA 1 Genes mutation--was identified in this study. She was daughter of a woman, a carrier of BRCA 1 Genes mutation, with early onset of Breast Primary malignant neoplasm and positive family history.CONCLUSIONS: BRCA 1 and BRCA 2 Genes Gene Mutation 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 BRCA1 Genes Gene Mutation are reportedly associated with hereditary Breast and Ovarian Malignant Neoplasms. Identification of BRCA Gene Mutation 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 Genes Genes Gene Mutation, 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 Ovarian Malignant Neoplasms in BRCA mutation carriers appeared to be diagnosed at an earlier age in later generations. Truncated proteins are easily discriminated from full size.RESULTS: Three BRCA 1 Genes 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 BRCA1 Genes testing in the Korean population. BRCA Mutations 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 Gene Mutation in the BRCA1 Genes may be associated with low response to fertility treatments. Moreover, in families of Breast Primary malignant neoplasm patients without BRCA Gene Mutation, Breast Primary malignant neoplasm risk depends on the patient's age at diagnosis. Among the 554 women who underwent genetic testing for BRCA mutation, 78 were found to have a deleterious mutation in the BRCA1 Genes, and 54 had a mutation in the BRCA 2 Genes. Frequent recurrent Gene Mutation in the Breast and Ovarian Primary malignant neoplasm susceptibility (BRCA) genes BRCA1 and BRCA2 Genes Genes among Hispanics, including a large rearrangement Mexican founder mutation (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 BRCA1 Genes mutation have increased lifetime risks of developing hereditary Breast and Ovarian Primary malignant neoplasm syndrome-related Malignant Neoplasms. BRCA1 Genes Gene Mutation 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 Genes Genes. Women who were BRCA carriers, women who had a history of Breast Primary malignant neoplasm, Noninfiltrating Intraductal Carcinoma, or Breast biopsy, 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 Genes Genes, were identified. Germline Gene 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 Genes Genes, BRCA negative, BRCA untested) compared with the general population.[SEP]Relations: Breast carcinoma has relations: disease_phenotype_positive with Ovarian Primary malignant neoplasm, disease_phenotype_positive with Ovarian Primary malignant neoplasm. carcinoma has relations: disease_disease with Primary malignant neoplasm, disease_disease with Primary malignant neoplasm.", "label": "yes"}
{"original_question": "Has Glucose-6-phosphate dehydrogenase (G6PD) deficiency an X-linked inheritance?", "id": "converted_450", "sentence1": "Has G6PD gene (G6PD) deficiency an X-linked inheritance?", "sentence2": "G6PD gene (G6PD) 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. Deficiency of glucose-6-phosphate dehydrogenase 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 inheritance and the defect is associated with Pharmacologic Substance (primaquine) induced Hemolysis (lab result). G6PD gene (G6PD) 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. G6PD gene (G6PD) deficiency is a common X-linked Enzyme [APC] defect. G6PD gene deficiency is an X- linked recessive hereditary disease characterised by abnormally low levels of G6PD. UNLABELLED: G6PD gene (G6PD) deficiency is an X- linked recessive disorder in which haemolytic Anemia is the major symptom. G6PD gene (G6PD) deficiency is the most frequent Enzyme [APC] deficiency. G6PD gene (G6PD) 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 (G6PD) of a mutant Mus sp. strain with X-linked G6PD-deficiency was purified and compared with the Wildtype Finding G6PD by biochemical and physiological characteristics. A Mus sp. with X-linked glucose-6-phosphate dehydrogenase (G6PD) deficiency has been recovered in offspring of 1-ethyl-1-nitrosourea-treated male CASP14 gene. G6PD gene (G6PD) deficiency is the commonest red cell Enzymopathy in Homo sapiens and has an X-linked inheritance G6PD gene (G6PD) deficiency is an X- linked recessive hemolytic anemia caused by a Mutation Abnormality in the G6PD gene on Xq28 G6PD gene (G6PD) deficiency is an X- linked recessive genetic defect that can cause hemolytic crisis Glucose-6-phosphate-dehydrogenase (G6PD) deficiency is an X-linked genetic defect, affecting around 400 million people worldwide and is characterized by considerable biochemical and Molecular heterogeneity G6PD gene deficiency (G6PD) is an X-linked genetic disorder with a relatively high frequency in Malaria Vaccines-endemic regions G6PD gene deficiency (G6PD) 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 G6PD gene (G6PD) deficiency is an Genetic Diseases, X-Linked that predisposes Red blood cells, blood product to oxidative damage G6PD gene (G6PD) deficiency is one of the most common human genetic abnormalities, and it has a significant prevalence in the male population (X chromosome linked) G6PD gene (G6PD) deficiency, a common X-linked Enzymopathy can lead to severe Jaundice, Chronic Idiopathic, acute bilirubin encephalopathy and Kernicterus in the United States G6PD gene deficiency (G6PD), 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 Deficiency of glucose-6-phosphate dehydrogenase 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 G6PD polymorphism. BACKGROUND: G6PD gene (G6PD) is a metabolic Enzyme [APC] involved in the Pentoses phosphate pathway, its especially important in red blood cell metabolism. G6PD gene deficiency is an X- linked recessive hereditary disease characterised by abnormally low levels of G6PD. BACKGROUND: G6PD gene (G6PD) is a metabolic Enzyme [APC] involved in the Pentoses phosphate pathway, its especially important in red blood cell metabolism. G6PD gene deficiency is an X- linked recessive hereditary disease characterised by abnormally low levels of G6PD. About 400 million people worldwide have a deficiency of this Enzyme [APC]. G6PD gene (G6PD) deficiency is a common X-linked Enzyme [APC] defect. We report a new Variant, G6PD Durham713G, that is associated with chronic nonspherocytic hemolytic anemia. G6PD gene (G6PD) 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 (G6PD) is highly Polymorphism; more than 300 G6PD variants have been identified. G6PD gene (G6PD) deficiency is an X-linked incompletely dominant Enzyme [APC] deficiency that results from G6PD gene mutations. G6PD gene (G6PD) deficiency is an X- linked recessive genetic defect that can cause hemolytic crisis. G6PD gene (G6PD) deficiency is an X- linked recessive hemolytic anemia caused by a Mutation Abnormality in the G6PD gene on Xq28. G6PD gene deficiency is an X- linked recessive hereditary disease characterised by abnormally low levels of G6PD. X-linked glucose-6-phosphate dehydrogenase (G6PD) and autosomal 6-phosphogluconate dehydrogenase (PGD gene) Genetic Polymorphism in Papio. X-linked glucose-6-phosphate dehydrogenase deficiency in House CASP14 gene. G6PD gene (G6PD) deficiency is an X- linked recessive disorder in which haemolytic Anemia is the major symptom.[SEP]Relations: Primaquine has relations: contraindication with Deficiency of glucose-6-phosphate dehydrogenase, contraindication with Deficiency of glucose-6-phosphate dehydrogenase. Favism has relations: disease_disease with Deficiency of glucose-6-phosphate dehydrogenase, disease_disease with Deficiency of glucose-6-phosphate dehydrogenase.", "label": "yes"}
{"original_question": "Is the toxin produced by Clostridium botulinum always deadly?", "id": "converted_451", "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 Botulism. The patient was treated with Homo sapiens Poisoning caused by Clostridium botulinum toxin type B 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 Poisoning caused by Clostridium botulinum toxin type B The Poisoning caused by Clostridium botulinum toxin type B 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 Poisoning caused by Clostridium botulinum toxin type B, though it is used clinically for treatment of many neuromuscular diseases. Foodborne Poisoning caused by Clostridium botulinum toxin type B 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]", "label": "no"}
{"original_question": "Is ocrelizumab effective for treatment of multiple sclerosis?", "id": "converted_452", "sentence1": "Is ocrelizumab effective for treatment of Multiple Sclerosis?", "sentence2": "Advances made in immunomodulation are driving the progress being made in the treatment of MS. Ocrelizumab is the first treatment with positive results in the primarily progressive forms and tocilizumab, a Pharmaceutical Preparations for Rheumatoid Arthritis, stands out as a potential candidate for the treatment of neuromyelitis optica.  Expert commentary: The recent encouraging results of the ocrelizumab trial in PP MS, the first to reach the primary disability endpoint, indicate B-Lymphocytes as a promising therapeutic target to prevent disease progression.  Ocrelizumab also shows efficacy in the primary progressive form of Multiple Sclerosis. Ocrelizumab for the treatment of relapsing-remitting Multiple Sclerosis. Expert commentary: The topline results of two phase-III randomized clinical trials demonstrate superiority of ocrelizumab over Recombinant Interferon Beta in RRMS patients with regards to clinical and paraclinical outcome parameters.  The efficacy of three of them, rituximab, ocrelizumab and ofatumumab in MS has been confirmed by placebo-controlled clinical trials demonstrating a significant reduction of the annualized relapsing rate (ARR), new gadolinium-enhancing (GdE) and T2 lesions.  Ongoing POLYDACTYLY, POSTAXIAL, WITH PROGRESSIVE MYOPIA trials are currently being conducted with the phosphodiesterase inhibitor ibudilast, S1P modulator siponimod and anti-B-cell therapy ocrelizumab.  RECENT FINDINGS: Novel and imminently emerging DMTs for the treatment of RRMS include alemtuzumab, daclizumab, ocrelizumab, pegylated interferon-\u03b2-1a, and three times weekly glatiramer acetate.  To summarize mechanisms of action, efficacy, and safety of novel and imminently emerging disease-modifying treatments (DMTs) intended to be used in relapsing-remitting Multiple Sclerosis (RRMS).Novel and imminently emerging DMTs for the treatment of RRMS include alemtuzumab, daclizumab, ocrelizumab, pegylated interferon-\u03b2-1a, and three times weekly glatiramer acetate Ocrelizumab in relapsing-remitting Multiple Sclerosis: a phase 2, randomised, placebo-controlled, multicentre trial. We aimed to assess efficacy and safety of two dose regimens of the humanised anti-CD20 monoclonal antibody ocrelizumab in patients with relapsing-remitting Multiple Sclerosis.  In Multiple Sclerosis (MS), B cell-depleting therapy using monoclonal anti-CD20 Abs, including rituximab (resiniferatoxin) and ocrelizumab, effectively reduces disease activity.  Ocrelizumab also shows efficacy in the primary progressive form of Multiple Sclerosis.Most of the presented cell-depleting and myeloablative therapies are highly effective treatment options but are also accompanied by significant risks. The armamentarium of approved disease-modifying therapies in MS and those in development include: (1) the first approved, moderately effective, injectable interferon-\u03b2 and glatiramer acetate; (2) oral drugs (fingolimod, laquinimod, teriflunomide, dimethyl fumarate); (3) monoclonal antibodies (rituximab, ocrelizumab, ofatumumab, daclizumab, alemtuzumab); and (4) immunosuppressive agents (e.g. mitoxantrone). BACKGROUND: Be2 Cells are implicated in the pathogenesis of Multiple Sclerosis. We aimed to assess efficacy and safety of two dose regimens of the humanised anti-CD20 monoclonal antibody ocrelizumab in patients with relapsing-remitting Multiple Sclerosis.METHODS: We did a multicentre, randomised, parallel, double-blind, placebo-controlled study involving 79 centres in 20 countries. Patients aged 18-55 years with relapsing-remitting Multiple Sclerosis were randomly assigned (1:1:1:1) via an interactive voice response system to receive either placebo, Low-Dose Treatment (600 mg) or high-dose (2000 mg) ocrelizumab in two doses on days 1 and 15, or intramuscular Recombinant Recombinant Interferon Beta-1a (30 \u00ecg) once a week. Ocrelizumab for the treatment of relapsing-remitting Multiple Sclerosis. The potential role for ocrelizumab in the treatment of Multiple Sclerosis: current evidence and future prospects. Ocrelizumab in relapsing-remitting Multiple Sclerosis: a phase 2, randomised, placebo-controlled, multicentre trial. Ocrelizumab also shows efficacy in the primary progressive form of Multiple Sclerosis.[SEP]Relations: Daclizumab has relations: indication with relapsing-remitting Multiple Sclerosis, indication with relapsing-remitting Multiple Sclerosis. Teriflunomide has relations: indication with Multiple Sclerosis, indication with Multiple Sclerosis. Rheumatoid arthritis has relations: disease_phenotype_positive with Rheumatoid Arthritis, disease_phenotype_positive with Rheumatoid Arthritis. Fingolimod has relations: indication with relapsing-remitting Multiple Sclerosis, indication with relapsing-remitting Multiple Sclerosis. Interferon beta-1a has relations: indication with relapsing-remitting Multiple Sclerosis, indication with relapsing-remitting Multiple Sclerosis. Mitoxantrone has relations: indication with relapsing-remitting Multiple Sclerosis, indication with relapsing-remitting Multiple Sclerosis. neuromyelitis optica has relations: disease_disease with Multiple Sclerosis, disease_disease with Multiple Sclerosis. Rituximab has relations: indication with Rheumatoid Arthritis, indication with Rheumatoid Arthritis. Tocilizumab has relations: indication with Rheumatoid Arthritis, indication with Rheumatoid Arthritis. Multiple Sclerosis has relations: disease_disease with relapsing-remitting Multiple Sclerosis, exposure_disease with teriflunomide, disease_disease with relapsing-remitting Multiple Sclerosis, exposure_disease with teriflunomide. relapsing-remitting Multiple Sclerosis has relations: disease_disease with Multiple Sclerosis, disease_disease with Multiple Sclerosis. Alemtuzumab has relations: indication with relapsing-remitting Multiple Sclerosis, indication with relapsing-remitting Multiple Sclerosis. Dimethyl fumarate has relations: indication with relapsing-remitting Multiple Sclerosis, indication with relapsing-remitting Multiple Sclerosis.", "label": "yes"}
{"original_question": "Is there a role of regorafenib for sarcoma treatment?", "id": "converted_453", "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 Sarcoma 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 Sarcoma 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: indication with Liver carcinoma, indication with Liver carcinoma. Sorafenib has relations: indication with Liver carcinoma, drug_drug with regorafenib, indication with Liver carcinoma, drug_drug with regorafenib. malignant soft tissue neoplasm has relations: disease_disease with Sarcoma of soft tissue, disease_disease with Sarcoma of soft tissue. bone Osteosarcoma of bone has relations: disease_disease with Osteosarcoma of bone, disease_disease with Osteosarcoma of bone. Ridaforolimus has relations: drug_drug with regorafenib, drug_drug with regorafenib. Sarcoma has relations: disease_phenotype_positive with liposarcoma, disease_phenotype_positive with liposarcoma. Pazopanib has relations: drug_drug with regorafenib, indication with Sarcoma of soft tissue, indication with Malignant neoplasm of soft tissue, drug_drug with regorafenib, indication with Sarcoma of soft tissue, indication with Malignant neoplasm of soft tissue.", "label": "yes"}
{"original_question": "Is exon skipping correlated with exon circularization?", "id": "converted_454", "sentence1": "Is exon skipping correlated with exon circularization?", "sentence2": "Exon Skipping Is Correlated with Exon Circularization We find that circularization of Exons is widespread and correlates with exon skipping, a feature that adds considerably to the regulatory complexity of the Homo sapiens transcriptome Exon Skipping Is Correlated with Exon Circularization. We find that circularization of Exons is widespread and correlates with exon skipping, a feature that adds considerably to the regulatory complexity of the Homo sapiens transcriptome. <CopyrightInformation>Copyright \u00a9 2015 Elsevier Ltd. All rights reserved.</ We find that circularization of Exons is widespread and correlates with exon skipping, a feature that adds considerably to the regulatory complexity of the Homo sapiens transcriptome. <CopyrightInformation>Copyright \u00a9 2015 Elsevier Ltd. All rights reserved.</C Exon Skipping Is Correlated with Exon Circularization.[SEP]", "label": "yes"}
{"original_question": "Is NADPH oxidase 5 expressed in rodents?", "id": "converted_455", "sentence1": "Is NADPH Oxidase expressed in Rodent?", "sentence2": "Because the NOX5 gene gene is absent in Rodent, we generated Mice, Transgenic expressing human NOX5 gene in a podocyte-specific manner (NOX5 gene(pod+)).  The NADPH Oxidase (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 gene 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 (NOX5) gene is present in Homo sapiens but not Rodent. The NADPH Oxidase (NOX5) gene is present in Homo sapiens but not Rodent NADPH oxidases are the major sources of Reactive Oxygen Species in cardiovascular, Neural, and Epithelial cell of renal tubule. The NADPH Oxidase (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 gene is absent in Rodent, we generated Mice, Transgenic expressing human NOX5 gene in a podocyte-specific manner (NOX5 gene(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 gene, has for the most part been overlooked in Kidney Diseases, partly owing to its absence from the rodent genome.[SEP]", "label": "no"}
{"original_question": "Does Vitamin D induce  autophagy?", "id": "converted_456", "sentence1": "Does ergocalciferol induce  autophagy?", "sentence2": "1,25(OH)2D treatment was accompanied by autophagy activation  Autophagy signaling pathway was regulated by cholecalciferol D Vitamin induces autophagy ergocalciferol 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 ergocalciferol, drug_drug with ergocalciferol. Cholecalciferol has relations: drug_drug with ergocalciferol, drug_drug with ergocalciferol.", "label": "yes"}
{"original_question": "Is RASA2 involved in melanoma?", "id": "converted_457", "sentence1": "Is RASA2 involved in Melanocytic neoplasm?", "sentence2": "Analysis of 501 Melanocytic neoplasm exomes identified RASA2, encoding a RASA2 wt Allele, as a tumor-suppressor gene mutated in 5% of Melanocytic neoplasm. Recurrent loss-of-function mutations in RASA2 were found to increase ras Oncogene activation, Melanocytic neoplasm cell growth and migration. RASA2 expression was lost in \u226530% of Homo sapiens Melanocytic neoplasm and was associated with reduced patient survival. These findings identify RASA2 inactivation as a Melanocytic neoplasm driver and highlight the importance of RasGAPs in Primary malignant neoplasm. Analysis of 501 Melanocytic neoplasm exomes identified RASA2, encoding a RASA2 wt Allele, as a tumor-suppressor gene mutated in 5% of Melanocytic neoplasm These findings identify RASA2 inactivation as a Melanocytic neoplasm driver and highlight the importance of RasGAPs in Primary malignant neoplasm. Recurrent loss-of-function mutations in RASA2 were found to increase ras Oncogene activation, Melanocytic neoplasm cell growth and migration. Analysis of 501 Melanocytic neoplasm exomes identified RASA2, encoding a RASA2 wt Allele, as a tumor-suppressor gene mutated in 5% of Melanocytic neoplasm.[SEP]Relations: Melanocytic neoplasm has relations: disease_protein with RASA2, disease_protein with RASA2. melanocytic neoplasm has relations: disease_disease with Melanocytic neoplasm, disease_disease with Melanocytic neoplasm.", "label": "yes"}
{"original_question": "Is SUMOylation a post-translational modification in eukaryotes?", "id": "converted_458", "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\ufffd 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-\ufffdB 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 ribosome 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: RELB has relations: cellcomp_protein with Cell Nucleus, cellcomp_protein with Cell Nucleus. germ cell Cell Nucleus has relations: cellcomp_cellcomp with Cell Nucleus, cellcomp_cellcomp with Cell Nucleus.", "label": "yes"}
{"original_question": "Is the protein lefty an inhibitor of nodal?", "id": "converted_459", "sentence1": "Is the protein lefty an inhibitor of nodal?", "sentence2": "The expression of lefty, an inhibitor of nodal is often reduced in Tumor cells, uncertain whether benign or malignant.  Nodal, and an inhibitor, Lefty. as well as the expression of Lefty, an inhibitor of nodal signaling, he Nodal inhibitor lefty The morphogen Nodal was proposed to form a long-range signaling gradient via a reaction-diffusion system, on the basis of differential diffusion rates of Nodal and its antagonist Lefty.[SEP]", "label": "yes"}
{"original_question": "Is Migalastat used for treatment of Fabry Disease?", "id": "converted_460", "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 \u03b1-galactosidase (\u03b1-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 \u03b1-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\u2122)-a small molecule drug developed by Amicus Therapeutics that restores the activity of specific Mutant forms of \u03b1-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 \u226516 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 \u03b1-galactosidase deficiency, leads to substrate accumulation in multiple organs. migalastat, an oral pharmacologic chaperone, stabilizes specific Mutant forms of \u03b1-galactosidase, increasing Enzyme [APC] trafficking to Lysosomes. Oral Route of Drug administration Route of Drug administration migalastat hydrochloride Leads to Greater Systemic Exposure and Tissue Levels of Active \u03b1-Galactosidase A in Fabry Patients when Co-Administered with Infused Agalsidase. UNLABELLED: migalastat hydrochloride (AT-1001, 1-Deoxygalactonojirimycin) is an investigational pharmacological chaperone for the treatment of \u03b1-galactosidase A (\u03b1-Gal A) deficiency, which leads to Fabry Disease, an X-linked, lysosomal storage disorder.  migalastat hydrochloride 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 hydrochloride (AT-1001, 1-Deoxygalactonojirimycin) is an investigational pharmacological chaperone for the treatment of \u03b1-galactosidase A (\u03b1-Gal A) deficiency, which leads to Fabry Disease, an X-linked, lysosomal storage disorder migalastat hydrochloride 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 hydrochloride is an investigational, oral treatment for Fabry Disease, an X-linked lysosomal storage disorder. migalastat hydrochloride (AT-1001, 1-Deoxygalactonojirimycin) is an investigational pharmacological chaperone for the treatment of \u03b1-galactosidase A (\u03b1-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 \u00c2\u00a9 2010 Elsevier Masson SAS. migalastat hydrochloride was well tolerated.migalastat hydrochloride 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 hydrochloride 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: Fabry Disease has relations: disease_protein with Diffuse lymphatic malformation, indication with migalastat, disease_protein with Diffuse lymphatic malformation, indication with migalastat. migalastat has relations: indication with Fabry Disease, drug_protein with Diffuse lymphatic malformation, indication with Fabry Disease, drug_protein with Diffuse lymphatic malformation. Hydrochlorothiazide has relations: drug_drug with migalastat, drug_drug with migalastat. lysosomal lumen has relations: cellcomp_protein with Diffuse lymphatic malformation, cellcomp_protein with Diffuse lymphatic malformation. lysosome has relations: cellcomp_protein with Diffuse lymphatic malformation, cellcomp_protein with Diffuse lymphatic malformation.", "label": "yes"}
{"original_question": "Do statins cause diabetes?", "id": "converted_461", "sentence1": "Do Hydroxymethylglutaryl-CoA Reductase Inhibitors cause Diabetes Mellitus?", "sentence2": "Statin use has been associated with increased risk of developing type 2 Diabetes Mellitus (T2DM), and with impaired glycemic control in T2DM patients The relationship between T2DM and Hydroxymethylglutaryl-CoA Reductase Inhibitors is further complicated since these drugs can cause new onset Diabetes Mellitus (Dentatorubral-Pallidoluysian Atrophy) although there is an overall benefit in terms of preventing vascular events  It has been repeatedly reported that Hydroxymethylglutaryl-CoA Reductase Inhibitors may cause new-onset Diabetes Mellitus mellitus (DM). However, a small, but significant risk of new-onset Diabetes Mellitus has been reported in patients treated with Hydroxymethylglutaryl-CoA Reductase Inhibitors. The National Lipid Association (NLA) Statin Diabetes Safety Task Force concluded that the Cardiovascular system benefit of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) therapy outweighs the risk for developing Diabetes Mellitus It has been repeatedly reported that Hydroxymethylglutaryl-CoA Reductase Inhibitors may cause new-onset Diabetes Mellitus mellitus (DM) It has been repeatedly reported that Hydroxymethylglutaryl-CoA Reductase Inhibitors may cause new-onset Diabetes Mellitus mellitus (DM). However, limited evidence exists from direct head to head comparisons of Hydroxymethylglutaryl-CoA Reductase Inhibitors on whether the risk of DM differs among Hydroxymethylglutaryl-CoA Reductase Inhibitors. Short-term 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) exposure is associated with reduced all-cause mortality in persons with Diabetes Mellitus. Despite the fact that higher 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) doses are more likely to lead to new-onset Diabetes Mellitus, for every case of Diabetes Mellitus caused, there are approximately three Cardiovascular system events reduced with high dose versus moderate dose 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) therapy. It has been repeatedly reported that Hydroxymethylglutaryl-CoA Reductase Inhibitors may cause new-onset Diabetes Mellitus mellitus (DM).  Statins are evidence-based drugs to prevent Cardiovascular system (CV) disease. However, their benefits have been disputed by a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition)-related increased risk of new onset Diabetes Mellitus  Compared with pravastatin, treatment with higher potency Hydroxymethylglutaryl-CoA Reductase Inhibitors, especially atorvastatin and simvastatin, might be associated with an increased risk of new onset Diabetes Mellitus  Hydroxymethylglutaryl-CoA Reductase Inhibitors are associated with a small increase in incidence of Diabetes Mellitus in patients predisposed to glycemic alteration  Higher potency 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) use is associated with a moderate increase in the risk of new onset Diabetes Mellitus compared with lower potency Hydroxymethylglutaryl-CoA Reductase Inhibitors in patients treated for secondary prevention of Cardiovascular system disease An increased risk of new onset treated Diabetes Mellitus was found in those treated with Hydroxymethylglutaryl-CoA Reductase Inhibitors 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 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition) 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 Mellitus or, if they already are diabetic, of worsening their metabolic control Statin therapy can slightly increase risk of incident Diabetes Mellitus in subjects with Hypercholesterolemia result.[SEP]", "label": "yes"}
{"original_question": "Are deletions of chromosomal regulatory boundaries associated with congenital disease?", "id": "converted_462", "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]", "label": "yes"}
{"original_question": "Can the Micro-C XL method achieve mononucleosome resolution?", "id": "converted_463", "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]", "label": "yes"}
{"original_question": "Can Diabetes be caused by a defect in a potassium chanel?", "id": "converted_464", "sentence1": "Can Diabetes be caused by a defect in a potassium chanel?", "sentence2": "Mutations in KATP Channels genes can result in hypo- or hypersecretion of Therapeutic Insulin, as in neonatal Diabetes Mellitus and Congenital Hyperinsulinism, respectively. To date, all patients affected by neonatal diabetes due to a Mutation Abnormality in the pore-forming subunit of the channel (KCNJ11 gene, KCNJ11) are heterozygous for the Mutation Abnormality.  e report the first clinical case of neonatal diabetes caused by a homozygous KCNJ11 Mutation Abnormality Diffuse Congenital Hyperinsulinism in infancy (CHI-D) arises from Gene Mutation inactivating the KATP Channels; We report a case of a 6-week-old infant with Diabetes Mellitus based on a genetic defect in the sulfonylurea receptor (ABCC8 gene), an ATP-sensitive potassium (KATP) channel protein. In diabetes, vascular KATP Channels function is impaired.[SEP]", "label": "yes"}
{"original_question": "Is rucaparib used for ovarian cancer treatment?", "id": "converted_465", "sentence1": "Is rucaparib used for ovarian cancer treatment?", "sentence2": "While olaparib is the first PARP1 wt Allele PPP1R1A gene to receive approval for ovarian cancer 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 ovarian cancer.  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 ovarian cancer 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 Malignant neoplasm of ovary. High Loss of Heterozygosity is associated with response to the PARP1 wt Allele PPP1R1A gene rucaparib in BRCA wild-type ovarian cancer. Therapeutic potential of the poly(ADP-ribose) polymerase PPP1R1A gene rucaparib for the treatment of sporadic Homo sapiens ovarian cancer. While olaparib is the first PARP1 wt Allele PPP1R1A gene to receive approval for ovarian cancer 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 ovarian cancer. 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 ovarian cancer. Rucaparib received US FDA Breakthrough Therapy designation for treatment of platinum-sensitive BRCA-mutated advanced ovarian cancer 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 ovarian cancer. Ongoing clinical trials are assessing the efficacy of rucaparib alone or in combination with other cytotoxic drugs, mainly in Breast and ovarian cancer 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 (P-Glycoprotein, ABCB1 wt Allele) affect the oral availability and brain penetration of rucaparib in CASP14 gene.RESULTS: In vitro, rucaparib was efficiently transported by both Homo sapiens ABCB1 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 ovarian cancer 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 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.<CopyrightInformation>\u00a92013 AACR</ Ongoing clinical trials are assessing the efficacy of rucaparib alone or in combination with other cytotoxic drugs, mainly in Breast and ovarian cancer 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 (P-Glycoprotein, ABCB1 wt Allele) affect the oral availability and brain penetration of rucaparib in CASP14 gene.In vitro, rucaparib was efficiently transported by both Homo sapiens ABCB1 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 ovarian cancer.  While olaparib is the first PARP1 wt Allele PPP1R1A gene to receive approval for ovarian cancer 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 ovarian cancer, 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 ovarian cancer.<CopyrightInformation>\u00a92013 AACR</C Similar trials with other PARP1 wt Allele inhibitors (rucaparib, niraparib and veliparib) are in progress and include non-BRCA-mutated ovarian cancer. Rucaparib received US FDA Breakthrough Therapy designation for treatment of platinum-sensitive BRCA-mutated advanced ovarian cancer 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 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..[SEP]Relations: Rucaparib has relations: indication with ovarian cancer, indication with ovarian cancer. Olaparib has relations: indication with ovarian cancer, indication with ovarian cancer.", "label": "yes"}
{"original_question": "Could hypophosphatemic rickets cause craniosynostosis?", "id": "converted_466", "sentence1": "Could Familial Hypophosphatemic Rickets cause CRANIOSYNOSTOSIS 3?", "sentence2": "This study examines a series of patients with Familial Hypophosphatemic Rickets and CRANIOSYNOSTOSIS 3 to characterize the clinical course and associated Craniofacial Abnormalities.  Hypophosphatemic Rickets and CRANIOSYNOSTOSIS 3: a multicenter case series. A 20-year retrospective review identified patients with Familial Hypophosphatemic Rickets and secondary CRANIOSYNOSTOSIS 3 at 3 major craniofacial centers.  Secondary CRANIOSYNOSTOSIS 3 develops postnatally due to metabolic or mechanical factors. The most common metabolic cause is Familial Hypophosphatemic Rickets, which has a variety of etiologies. Head - Component of Device - Component of Device shape changes occur later and with a more heterogeneous presentation compared with that of primary CRANIOSYNOSTOSIS 3. Patients with multisutural involvement or X-linked Familial Hypophosphatemic Rickets had a significant delay in presentation for CRANIOSYNOSTOSIS 3.  Craniosynostosis can be gene-linked, or caused by Metabolic Diseases, such as Rickets, which results from a deficiency or impaired metabolism of ergocalciferol, Magnesium supplements, alimentary tract and metabolism, Phosphorus Drug Class or CALCIUM SUPPLEMENTS leading to hypomineralization of the Specimen Type - Bone. X-linked dominant Familial Hypophosphatemic Rickets (Hypophosphatemic Rickets, X-Linked Dominant) is the most prevalent genetic type of Familial Hypophosphatemic Rickets and is caused by germ line mutations in the PHEX-gene. In Hypophosphatemic Rickets, X-Linked Dominant, only few case reports of CRANIOSYNOSTOSIS 3 were described. Papilledema in the setting of Vitamin D-Resistant Rickets, X-Linked with CRANIOSYNOSTOSIS 3. Case report of a 3-year-old female presenting with papilledema resulting from CRANIOSYNOSTOSIS 3 secondary to XLH. X-linked Familial Hypophosphatemic Rickets and CRANIOSYNOSTOSIS 3. X-linked hypophosphatemic (XLH) Rickets is the most common form of metabolic Rickets, and there have been reports linking XLH Rickets to CRANIOSYNOSTOSIS 3. A clinical report of a patient with XLH Rickets and CRANIOSYNOSTOSIS 3 is presented with a review of literature.  This may be the reason for the common association of CRANIOSYNOSTOSIS 3 and XLH Rickets.  Craniosynostosis and associated craniofacial deformities, such as Frontal bossing, often occur as symptoms of ergocalciferol-resistant Rickets in children. Similar Bone structure of cranium deformities develop in CASP14 gene with X-linked dominant hypophosphatemia, the most common form of ergocalciferol-resistant Rickets.  The x-linked hypophosphatemic Mus sp. is an animal model that can be used to study the role of ergocalciferol-resistant Rickets in the development of CRANIOSYNOSTOSIS 3, to relate CRANIOSYNOSTOSIS 3 to the development of associated Bone structure of cranium deformities, and to test new treatment procedures. Craniosynostosis secondary to Rickets is rarely reported, but since neither Rickets nor CRANIOSYNOSTOSIS 3 is a reportable disease, the exact incidence of both diseases is unknown. X-linked hypophosphatemic (XLH) Rickets is the most common form of metabolic Rickets, and there have been reports linking XLH Rickets to CRANIOSYNOSTOSIS 3. A clinical report of a patient with XLH Rickets and CRANIOSYNOSTOSIS 3 is presented with a review of literature. METHODS A 20-year retrospective review identified patients with Familial Hypophosphatemic Rickets and secondary CRANIOSYNOSTOSIS 3 at 3 major craniofacial centers. Bilateral coronal and sagittal synostosis in X-linked Familial Hypophosphatemic Rickets: a case report. X-linked Familial Hypophosphatemic Rickets and sagittal CRANIOSYNOSTOSIS 3: three patients requiring operative cranial expansion: case series and literature review X-linked Familial Hypophosphatemic Rickets and CRANIOSYNOSTOSIS 3 X-linked hypophosphatemic (XLH) Rickets is the most common form of metabolic Rickets, and there have been reports linking XLH Rickets to CRANIOSYNOSTOSIS 3 The recent observations of two new cases of X-linked Familial Hypophosphatemic Rickets associated with premature closure of the sagittal suture prompted a review of similar cases seen in this institution.To review the clinical records and Bone structure of cranium radiographs of 28 children with Familial Hypophosphatemic Rickets in order to investigate the frequency and type of CRANIOSYNOSTOSIS 3 and other Calvaria changes seen in these conditions and to review the literature for relevant findings.Clinical and imaging records were reviewed on 28 patients with Familial Hypophosphatemic Rickets, all younger than 18 years Those with multisutural synostosis presented at a significantly older age than patients with sagittal or Bicoronal synostosis.Patients with multisutural involvement or X-linked Familial Hypophosphatemic Rickets had a significant delay in presentation for CRANIOSYNOSTOSIS 3 Papilledema in the setting of Vitamin D-Resistant Rickets, X-Linked with CRANIOSYNOSTOSIS 3 INTRODUCTION TO THE OPHTHALMIC LITERATURE OF AN UNUSUAL CAUSE OF PAPILLEDEMA AND SUBSEQUENT OPTIC ATROPHY: X-linked Familial Hypophosphatemic Rickets (XLH).Case report of a 3-year-old female presenting with papilledema resulting from CRANIOSYNOSTOSIS 3 secondary to XLH.Early intervention with craniofacial surgery prevented the development of Optic Atrophy.Children with XLH should be screened for ophthalmic evidence of elevated intracranial pressure to aid early intervention and prevention of permanent loss of vision CONCLUSIONS: Patients with multisutural involvement or X-linked Familial Hypophosphatemic Rickets had a significant delay in presentation for CRANIOSYNOSTOSIS 3.  Craniosynostosis can be gene-linked, or caused by Metabolic Diseases, such as Rickets, which results from a deficiency or impaired metabolism of ergocalciferol, Magnesium supplements, alimentary tract and metabolism, Phosphorus Drug Class or CALCIUM SUPPLEMENTS leading to hypomineralization of the Specimen Type - Bone.  Similar Bone structure of cranium deformities develop in CASP14 gene with X-linked dominant hypophosphatemia, the most common form of ergocalciferol-resistant Rickets. Craniosynostosis in ergocalciferol-resistant Rickets. Craniosynostosis can be gene-linked, or caused by Metabolic Diseases, such as Rickets, which results from a deficiency or impaired metabolism of ergocalciferol, Magnesium supplements, alimentary tract and metabolism, Phosphorus Drug Class or CALCIUM SUPPLEMENTS leading to hypomineralization of the Specimen Type - Bone. X-linked Familial Hypophosphatemic Rickets and CRANIOSYNOSTOSIS 3. X-linked hypophosphatemic (XLH) Rickets is the most common form of metabolic Rickets, and there have been reports linking XLH Rickets to CRANIOSYNOSTOSIS 3. Hypophosphatemic Rickets and CRANIOSYNOSTOSIS 3: a multicenter case series.[SEP]Relations: Frontal bossing has relations: disease_phenotype_positive with CRANIOSYNOSTOSIS 3, disease_phenotype_positive with CRANIOSYNOSTOSIS 3. CRANIOSYNOSTOSIS 3 Fontaine type has relations: disease_disease with CRANIOSYNOSTOSIS 3, disease_disease with CRANIOSYNOSTOSIS 3. Bicoronal synostosis has relations: disease_phenotype_positive with CRANIOSYNOSTOSIS 3, disease_phenotype_positive with CRANIOSYNOSTOSIS 3. Optic atrophy has relations: disease_phenotype_positive with Optic Atrophy, disease_phenotype_positive with Optic Atrophy.", "label": "yes"}
{"original_question": "Is vortioxetine effective for treatment of depression?", "id": "converted_467", "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 antidepressant to treat depressive episodes]. Vortioxetine is a new antidepressant, which mechanism of action is multimodal, targeting the 5-Hydroxytryptamine Receptor 1A, human, HTR1B wt Allele, HTR1D gene, 5-HT3, HTR7 gene\u00a0receptors and the serotonin transporter (5-HTT).  In short-term studies (8\u00a0weeks), 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\u00a0weeks), 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 Antidepressive Agents 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 Antidepressive Agents.  The authors suggest that vortioxetine is currently a good second-line antidepressant option and shows promise, pending additional long-term data, to become a first-line antidepressant 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 antidepressant 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\u00a0-0.118 (95% CISH protein, human,\u00a0-0.203 to\u00a0-0.033, P\u00a0=\u00a00.007). 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 antidepressant 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\u2009mg 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 antidepressant 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 antidepressant 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 antidepressant 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 antidepressant 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 antidepressant and antianxiety properties of vortioxetine in a dose range of 5-20 mg/day Vortioxetine is an antidepressant 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 Antidepressive Agents 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 antidepressant 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\u2009=\u2009457) were randomized 1:1:1 to treatment with placebo or vortioxetine 2.5 or 10\u2009mg 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 antidepressant 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 antidepressant 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\u2009=\u2009457) were randomized 1:1:1 to treatment with placebo or vortioxetine 2.5 or 10\u2009mg 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.[SEP]Relations: Vortioxetine has relations: drug_drug with duloxetine, drug_drug with duloxetine. Venlafaxine has relations: drug_drug with duloxetine, drug_drug with duloxetine. Protein S human has relations: drug_drug with duloxetine, drug_drug with duloxetine. Anxiety Disorders disorder has relations: disease_disease with Anxiety Disorders, indication with duloxetine, disease_disease with Anxiety Disorders, indication with duloxetine. neurotransmitter uptake has relations: bioprocess_bioprocess with neurotransmitter uptake, bioprocess_bioprocess with neurotransmitter uptake. Agomelatine has relations: drug_drug with duloxetine, drug_drug with duloxetine. Vilazodone has relations: drug_drug with duloxetine, drug_drug with duloxetine. major depressive disorder has relations: indication with duloxetine, indication with duloxetine.", "label": "yes"}
{"original_question": "Can beans induce apoptosis?", "id": "converted_468", "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 \u03b4-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. \u03b4-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]", "label": "yes"}
{"original_question": "Is treatment resistant depression related to vitamin B9?", "id": "converted_469", "sentence1": "Is treatment resistant Cancer patients and suicide and depression related to vitamin Lateral basal segmental bronchus?", "sentence2": "Suboptimal serum and Folic acid measurement, RBC levels have been associated with a poorer response to Antidepressive Agents therapy, a greater severity of symptoms, later onset of clinical improvement, and overall treatment resistance. This article reviews the evidence for levomefolate and folic acid as antidepressive agents in Cancer patients and suicide and Cancer patients and suicide and depression and discusses their clinical use Although further randomized controlled trials in this area appear warranted, S-adenosylmethionine and levomefolate may represent a useful addition to the cytarabine/daunorubicin protocol armamentarium. Patients with Cancer patients and suicide and Cancer patients and suicide and depression have consistently been found to have lower levels of serum and Folic acid measurement, RBC than normal or nondepressed psychiatric patients. Decreased folate levels have been associated with lowered response rates to standard Antidepressive Agents pharmacotherapy. Recent studies have shown that augmentation with a folate supplement increases medication response in both treatment-na\u00efve and treatment-resistant depressed patients irrespective of whether there is folate deficiency. Depressed patients with both low and normal folate levels may benefit from augmenting a primary Antidepressive Agents medication either initially, at the onset of treatment, or later after some degree of treatment resistance has been recognized. The results of this study suggest that intake of vitamin Lateral basal segmental bronchus may modulate the total score of Center for Epidemiological Studies Depression Scale (CES-D) and two subscales of the CES-D including depressive affect and interpersonal difficulties. The results of this study suggest that intake of vitamin Lateral basal segmental bronchus may modulate the total score of Center for Epidemiological Studies Depression Scale (CES-D) and two subscales of the CES-D including depressive affect and interpersonal difficulties.  This article reviews the metabolic and clinical importance of folate, vitamin NDUFB3 gene, and S-adenosylmethionine, as well as clinical trials in relation to Cancer patients and suicide and Cancer patients and suicide and depression and Presenile Presenile dementia In particular, thiamine, Measles virus genotype Measles virus genotype B3, B6, Lateral basal segmental bronchus and NDUFB3 gene are essential for neuronal function and Androgen Receptor Deficiency have been linked to Cancer patients and suicide and Cancer patients and suicide and depression.[SEP]", "label": "yes"}
{"original_question": "Is adalimumab effective for hidradenitis suppurativa?", "id": "converted_470", "sentence1": "Is adalimumab effective for Hidradenitis Suppurativa?", "sentence2": "If patient is not improved, then Adalimumab 160\u00a0mg at week 0, 80\u00a0mg at week 2; then 40\u00a0mg 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\u00a0(NCT00918255). CONCLUSION: Patients with moderate to severe HS had a high degree of Pain:-:Point in time:^Patient:- and Depressive Symptoms\u00a0at 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-\u03b1) 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% (\u226550% 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\u00ae) 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-\u03b1) 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 \u03b1, 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: Adalimumab has relations: drug_protein with Recombinant Tumor Necrosis Factor Family Protein, indication with Hidradenitis Suppurativa, drug_protein with Recombinant Tumor Necrosis Factor Family Protein, indication with Hidradenitis Suppurativa. Psoriasis has relations: disease_protein with Recombinant Tumor Necrosis Factor Family Protein, disease_protein with Recombinant Tumor Necrosis Factor Family Protein. Infliximab has relations: drug_protein with Recombinant Tumor Necrosis Factor Family Protein, drug_protein with Recombinant Tumor Necrosis Factor Family Protein.", "label": "yes"}
{"original_question": "Can NEECHAM Confusion Scale be used for evaluation of postoperative delirium?", "id": "converted_471", "sentence1": "Can NEECHAM Confusion Scale be used for evaluation of Emergence 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 Emergence Delirium and Clouded consciousness in the surgical ward. Early detection of Emergence Delirium and Clouded consciousness in a surgical ward using the NEECHAM Clouded consciousness scale. In this study, we investigated whether the early detection of Emergence 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 Emergence 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 Emergence 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 Emergence 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 Emergence 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 Emergence 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 Emergence 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 Emergence 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 Emergence Delirium was 76%.CONCLUSION: The results suggest that E-PASS and the NEECHAM score facilitate assessment of the risk of Emergence Delirium in elderly patients, contributing to early prevention/treatment. In this study, we investigated whether the early detection of Emergence 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 Emergence Delirium and Clouded consciousness in the surgical ward.. Early detection of Emergence Delirium and Clouded consciousness in a surgical ward using the NEECHAM Clouded consciousness scale. Assessment of the risk of Emergence 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]", "label": "yes"}
{"original_question": "Has small pox been eradicated from the world?", "id": "converted_472", "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]", "label": "yes"}
{"original_question": "Is there alternative polyadenylation during zebrafish development?", "id": "converted_473", "sentence1": "Is there alternative polyadenylation during Zebrafish development?", "sentence2": "Extensive alternative polyadenylation during Zebrafish development. At 2 h post-fertilization, thousands of unique poly(A) sites appear at locations lacking a typical polyadenylation signal, which suggests a wave of widespread cytoplasmic polyadenylation of mRNA degradation intermediates. Our insights into the identities, formation, and evolution of Zebrafish 3' UTRs provide a resource for studying gene regulation during Vertebrates development. Extensive alternative polyadenylation during Zebrafish development.[SEP]", "label": "yes"}
{"original_question": "Are alterations in ultraconserved elements implicated in breast cancer?", "id": "converted_474", "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]", "label": "yes"}
{"original_question": "Is there any tool that facilitates the functional analysis of cis-regulatory regions in zebrafish?", "id": "converted_475", "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 (Zebrafish). 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]", "label": "yes"}
{"original_question": "Have the promoter regions of the genes implicated in Rett Syndrome been characterized with CAGE?", "id": "converted_476", "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 gene. Gene Mutation in three functionally diverse Genes cause MECP2 protein, Homo sapiens protein, Homo sapiens gene. Although the functions of Forkhead box G1 (FOXG1), Methyl-CpG-Binding Protein 2 (MECP2 protein, Homo sapiens protein, Homo sapiens) and Cyclin-dependent kinase-like 5 (CDKL5 gene gene) 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 gene 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 gene. We identify promoter shapes for each TSS, the predicted location of enhancers for each gene and the common transcription factors likely to regulate the three Genes. Our data imply Polycomb Repressive Complex 2 (Polycomb Repressive Complex 2) mediated silencing of FOXG1 gene 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 gene. CAGE-defined promoter regions of the Genes implicated in MECP2 protein, Homo sapiens protein, Homo sapiens gene CAGE-defined promoter regions of the Genes implicated in MECP2 protein, Homo sapiens protein, Homo sapiens gene.[SEP]Relations: Rett syndrome has relations: disease_protein with MECP2 protein, Homo sapiens, disease_protein with MECP2 protein, Homo sapiens. Cerebellum has relations: anatomy_protein_present with MECP2 protein, Homo sapiens, anatomy_protein_present with MECP2 protein, Homo sapiens. methyl-CpG binding has relations: molfunc_protein with MECP2 protein, Homo sapiens, molfunc_protein with MECP2 protein, Homo sapiens.", "label": "yes"}
{"original_question": "Has \"RNA interference\" been awarded Nobel prize?", "id": "converted_477", "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 there any role for Pds5b in cohesion establishment?", "id": "converted_478", "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]", "label": "yes"}
{"original_question": "Could plasmepsins be used as targets for developing anti-malaria drugs?", "id": "converted_479", "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]", "label": "yes"}
{"original_question": "Is avanafil indicated for treatment of erectile dysfunction?", "id": "converted_480", "sentence1": "Is avanafil indicated for treatment of No erectile dysfunction?", "sentence2": "CONTEXT: Avanafil (AVA) is used in the treatment of No No 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 No No erectile dysfunction (ED).  A survey on the experience of 136 Italian urologists in the treatment of No No 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 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 No No erectile dysfunction. Sildenafil, vardenafil, tadalafil and avanafil are FDA approved drugs in market as PDE5A wt Allele inhibitors for treating No No 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\u2122, SPEDRA\u2122, Zepeeed\u2122) is an oral phosphodiesterase type 5 PPP1R1A gene indicated for the treatment of No No erectile dysfunction. In a 12-week, randomized, double-blind, placebo-controlled, multicentre trial in patients with No No erectile dysfunction, avanafil 50, 100 and 200 mg recipients had significantly greater improvements from baseline than placebo recipients in mean international index of No No erectile dysfunction-erectile function domain scores and in successful vaginal penetration and sexual intercourse attempts (coprimary endpoints). Avanafil for the treatment of No No erectile dysfunction. An updated review. Selectivity of avanafil, a PDE5A wt Allele PPP1R1A gene for the treatment of No No 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 No No erectile dysfunction. Avanafil, a potent and highly selective Phosphodiesterase 5 Inhibitor [EPC] for No No erectile dysfunction. Avanafil, a highly selective phosphodiesterase type 5 PPP1R1A gene for No No 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 No No erectile dysfunction. These findings suggest that intracavernosal administration of avanafil might be beneficial for the treatment of No No 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 No No erectile dysfunction. The effect of intracavernosal avanafil, a newer Phosphodiesterase 5 Inhibitor [EPC], on neonatal type 2 diabetic Rattus norvegicus with No No erectile dysfunction. A phase 3, placebo controlled study of the safety and efficacy of avanafil for the treatment of No No erectile dysfunction after nerve sparing radical prostatectomy. Avanafil is a potent selective phosphodiesterase type 5 (PDE5A wt Allele) PPP1R1A gene newly developed for treating No No 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 No No erectile dysfunction in men with diabetes and was effective as early as 15 minutes and more than 6 hours after dosing Avanafil (STENDRA\u2122, SPEDRA\u2122, Zepeeed\u2122) is an oral phosphodiesterase type 5 PPP1R1A gene indicated for the treatment of No No 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 No No erectile dysfunction, avanafil 50, 100 and 200 mg recipients had significantly greater improvements from baseline than placebo recipients in mean international index of No No 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 No No 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 No No erectile dysfunction (ED).Male patients, 35-70 years of age, with mild to moderate ED of \u22656 months duration, were included in the study Avanafil for No No 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, No No erectile dysfunction, and phosphodiesterase type 5 (PDE5A wt Allele) PPP1R1A gene.Articles evaluating avanafil for No No erectile dysfunction (ED) published in English and using human subjects were selected In trials in patients with No No erectile dysfunction in association with Diabetes 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 No No 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 \u00a9 2013 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.</ Avanafil for the treatment of No No erectile dysfunction: a multicenter, randomized, double-blind study in men with Diabetes Mellitus. The discovery of avanafil for the treatment of No No 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 No No 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 No No erectile dysfunction (ED). The phosphodiesterese-5 (PDE5A wt Allele) inhibitors, including sildenafil (Viagra\u2122), vardenafil (Levitra\u2122), tadalafil (Cialis\u2122) and avanafil (Stendra\u2122) have been developed for the treatment of No No erectile dysfunction. To compare the efficacy and safety between different dosages of avanafil for the treatment of No No 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 No No 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 No No 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 No No 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 No No erectile dysfunction in patients with T2DM.<CopyrightInformation>Copyright \u00a9 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 No No 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 No No erectile dysfunction in men with diabetes 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 No No erectile dysfunction in men with diabetes and was effective as early as 15 minutes and more than 6 hours after dosing. Avanafil for the treatment of No No erectile dysfunction. An updated review. Avanafil for No No erectile dysfunction. Avanafil for the treatment of No No erectile dysfunction: a multicenter, randomized, double-blind study in men with Diabetes Mellitus. To compare the efficacy and safety between different dosages of avanafil for the treatment of No No erectile dysfunction (ED). Selectivity of avanafil, a PDE5A wt Allele PPP1R1A gene for the treatment of No No 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 No No 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 No No erectile dysfunction after bilateral nerve sparing radical prostatectomy.[SEP]Relations: Diabetes Mellitus, noninsulin-dependent has relations: disease_disease with Diabetes Mellitus, Noninsulin-Dependent, 3, disease_disease with Diabetes Mellitus, Noninsulin-Dependent, 3.", "label": "yes"}
{"original_question": "Is there a role for gamma knife in treatment of Obsessive-Compulsive Disorder?", "id": "converted_481", "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 (Obsessive-Compulsive Disorder). 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 (Obsessive-Compulsive Disorder). 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 Obsessive-Compulsive Disorder behavior with no adverse effects. Gamma knife for obsessive compulsive disorder: can it be detrimental?[SEP]", "label": "yes"}
{"original_question": "Can NADPH oxidase be inhibited by apocynin and diphenylene iodonium?", "id": "converted_482", "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 NAD(P)H oxidase-dependent mechanism, as shown by inhibition of Reactive Oxygen Species production via the NAD(P)H 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 oA\u00e2. 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 oA\u00e2, 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 oA\u03b2 Moreover, CSE-regulated Prostaglandin-Endoperoxide Synthase-2, 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), Mitogen-Activated Protein Kinase 14 (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 (cisplatin/doxorubicin/vincristine protocol) and neopterine (Neomycin resistance gene), inhibitors of the NADPH Oxidase, and indomethacin (Indo), a cyclooxygenase (Prostaglandin-Endoperoxide Synthase) 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 \u03b2-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 IL-1beta 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 (G\u00f66976), 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 (APO)], Protoplasm calcium chelator (BAPTA/AM), PDIA3 wt Allele (U 73122), cyclophosphamide/doxorubicin/methotrexate protocol (calmidazolium chloride), calmodulin-dependent protein 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 NAD(P)H 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 oA\u03b2. 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 (cisplatin/doxorubicin/vincristine protocol) and neopterine (Neomycin resistance gene), inhibitors of the NADPH Oxidase, and indomethacin (Indo), a cyclooxygenase (Prostaglandin-Endoperoxide Synthase) PPP1R1A gene, but not by the mitochondrial electron transport inhibitors and other Cytoplasmic matrix enzyme inhibitors. Such discharge of Dectin-1-reactive \u03b2-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 IL-1beta 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 (G\u00f66976), 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 (APO)], Protoplasm calcium chelator (BAPTA/AM), PDIA3 wt Allele (U 73122), cyclophosphamide/doxorubicin/methotrexate protocol (calmidazolium chloride), calmodulin-dependent protein 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 Prostaglandin-Endoperoxide Synthase-2, 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), Mitogen-Activated Protein Kinase 14 (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 oA\u03b2, 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. IL-1beta 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: tumor necrosis factor receptor binding has relations: molfunc_protein with TNF receptor-associated factor 6, molfunc_protein with TNF receptor-associated factor 6.", "label": "yes"}
{"original_question": "Does NADPH oxidase 5 require any subunit for function?", "id": "converted_483", "sentence1": "Does NADPH oxidase 5 require any subunit for function?", "sentence2": "NOX5 gene forms a functional oligomer mediated by self-association of its dehydrogenase domain.  While NOX1 gene-4 require regulatory subunits, including CYBA wt Allele, NOX5 gene activity does not depend on any subunits.   Thus, NOX5 gene forms a catalytically active oligomer in the Membrane Device that is mediated by its dehydrogenase domain.  Coexpression of specific Nox catalytic subunits (NOX1 gene, CYBB wt Allele, NOX3 gene, NOX4 protein, human, or NOX5 gene) along with their corresponding regulatory subunits (NOXO1 gene gene/NOXA1 for NOX1 gene; p47phox/p67phox/Rac for CYBB wt Allele; NOXO1 gene gene for NOX3 gene; no subunits for NOX4 protein, human or NOX5 gene) resulted in marked production of reactive oxygen.[SEP]", "label": "no"}
{"original_question": "Is NSD-1015 an inhibitor of Aromatic L-Amino Acid Decarboxylase?", "id": "converted_484", "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 l-dopa 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 (20\u03bcM) 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 rat 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-levodopa (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 Rattus norvegicus 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. TH 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 Rattus norvegicus 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-Dopa (DOPA) in the median eminence of female Rattus norvegicus 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 Rattus norvegicus 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 levodopa in selected Head>Brain regions (striatum, nucleus accumbens, septum, medial periventricular hypothalamus) and thoracic spinal cords of Rattus norvegicus 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 Inhibitors (e.g., pargyline). The accumulation of dopa (levodopa) 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-Rattus norvegicus. 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 rat striatum was perfused with N-Acetylneuraminic acid storage disease-1015, an PPP1R1A gene of DDC protein, human, and the amount of L-levodopa (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 Rattus norvegicus. An accumulation of L-Dopa (DOPA) in the median eminence of female Rattus norvegicus 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 rat 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 Rattus norvegicus. 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 Rattus norvegicus.  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 levodopa 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-Dopa (DOPA) and 3,4-dihydroxyphenylacetic acid (3,4-Dihydroxyphenylacetic Acid) 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 Rattus norvegicus 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 Dopa (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, Rattus norvegicus 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 rat. 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-Rattus norvegicus. 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]", "label": "yes"}
{"original_question": "Is pseudouridine a RNA modification?", "id": "converted_485", "sentence1": "Is pseudouridine a RNA modification?", "sentence2": "Pseudouridine (\u03a8) 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.", "label": "yes"}
{"original_question": "Can telomere length shortening be reversed by telomerase?", "id": "converted_486", "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]", "label": "yes"}
{"original_question": "Is ABCE1 involved in ribosomal recycling?", "id": "converted_487", "sentence1": "Is ABCE1 gene involved in ribosomal recycling?", "sentence2": "Ribosome recycling orchestrated by the ATP binding cassette (ABC) protein ABCE1 gene gene can be considered as the final-or the first-step within the cyclic process of protein synthesis, connecting translation termination and mRNA surveillance with re-initiation.  Recent studies have identified ABCE1 gene gene as a ribosome-recycling factor important for translation termination in mammalian cells, Saccharomyces cerevisiae and also Archaea. d a termination/prerecycling complex containing eRF1-ABCE1 gene gene ABCE1 gene gene, a eukaryotic ribosome recycling factor[SEP]", "label": "yes"}
{"original_question": "Does oculocutaneous albinism show an autosomal recessive inheritance?", "id": "converted_488", "sentence1": "Does oculocutaneous albinism show an Autosome recessive inheritance?", "sentence2": "MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosome recessive disorder characterized by ALBINOIDISM, OCULOCUTANEOUS, AUTOSOMAL DOMINANT in Eye, Hair Specimen and Skin Specimen Source Code, accompanied with Unspecified visual loss.  MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosome recessive hereditary pigmentation disorder affecting Homo sapiens and several other animal species.  MONOPHENOL MONOOXYGENASE gene type 2 (Oculocutaneous Albinism, Type IV) is a human Autosome-recessive ALBINOIDISM, OCULOCUTANEOUS, AUTOSOMAL DOMINANT disorder associated with pathological Gene Mutation of the Oculocutaneous Albinism, Type IV gene. MONOPHENOL MONOOXYGENASE gene type1 (MONOPHENOL MONOOXYGENASE gene type 1) is characterized by the absence of Melanins pigmentation. The Mutation Abnormality on MONOPHENOL MONOOXYGENASE gene makes MONOPHENOL MONOOXYGENASE gene type 1 as an Autosome recessive genetic disorder.  Our patients were diagnosed as affected with MONOPHENOL MONOOXYGENASE gene type1a. Analysis of pedigree pattern showed an Autosome recessive inheritance.  MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosome recessive disorder of Melanins biosynthesis that results in congenital ALBINOIDISM, OCULOCUTANEOUS, AUTOSOMAL DOMINANT of ocular and cutaneous tissues. MONOPHENOL MONOOXYGENASE gene is an Autosome recessive genetic disorder. Melanin biosynthesis is reduced in oculocutaneous albinism, an Autosome recessive disorder. The pedigrees were consistent with an Autosome recessive inheritance pattern.CONCLUSION: This unique type of oculocutaneous albinism has heterogeneous clinical features. BACKGROUND: MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosome recessive hereditary pigmentation disorder affecting Homo sapiens and several other animal species. The Q402 allele has been associated with Autosome recessive Albinism, Ocular when it is in trans with a tyrosinase gene Mutation Abnormality associated with oculocutaneous albinism type 1. Analysis using the POINTER program showed that this type of oculocutaneous albinism was inherited in an Autosome recessive pattern, with an estimated gene frequency of 0.025 +/- 0.007 in this population. We have identified 12 families with oculocutaneous albinism type 1 that exhibit segregation of the c.1205G>A Variant with a known pathologic Mutation Abnormality on the homologous chromosome, and demonstrate no genetic association between Autosome recessive oculocutaneous albinism and the Q402 Variant. BACKGROUND: Type 2 (tyrosinase-positive) oculocutaneous albinism is an Autosome recessive disorder that has recently been mapped to chromosome segment 15q11-q13. The child with Albinism, Ocular was heterozygous for two different Gene Mutation in the Oculocutaneous Albinism, Type IV wt Allele.CONCLUSIONS: Abnormalities of the Oculocutaneous Albinism, Type IV wt Allele are associated with a wide range of clinical phenotypes, including type II oculocutaneous albinism, albinism associated with the Prader-Willi Syndrome, and at least some cases of Autosome recessive Albinism, Ocular. Mutations in the MONOPHENOL MONOOXYGENASE gene (MONOPHENOL MONOOXYGENASE, 11q14-21, MIM 606933) cause oculocutaneous albinism type 1 (MONOPHENOL MONOOXYGENASE gene type 1, MIM 203100), a developmental disorder having an Autosome recessive mode of inheritance The pedigrees were consistent with an Autosome recessive inheritance pattern.This unique type of oculocutaneous albinism has heterogeneous clinical features MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosome recessive disorder MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosome recessive disorder of abnormal Melanins formation, which results in ALBINOIDISM, OCULOCUTANEOUS, AUTOSOMAL DOMINANT of Skin Specimen Source Code, Hair Specimen and Eye The Mutation Abnormality of the tyrosinase (MONOPHENOL MONOOXYGENASE) gene results in oculocutaneous albinism type 1 (MONOPHENOL MONOOXYGENASE gene type 1), an Autosome recessive genetic disorder We found oculo-cutaneous albinism in two brothers and granular dystrophy in three brothers, the mother and a son.Hereditary corneal dystrophy is an Autosome dominant disorder inherited independently of oculocutaneous albinism, which is inherited as an Autosome recessive condition MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) type 4 is a newly identified human Autosome recessive hypopigmentary disorder that disrupts pigmentation in the Skin Specimen Source Code, Hair Specimen and Eye Analysis using the POINTER program showed that this type of oculocutaneous albinism was inherited in an Autosome recessive pattern, with an estimated gene frequency of 0.025 +/- 0.007 in this population.  DISCUSSION: Hereditary corneal dystrophy is an Autosome dominant disorder inherited independently of oculocutaneous albinism, which is inherited as an Autosome recessive condition.  BACKGROUND: MONOPHENOL MONOOXYGENASE gene type II (Oculocutaneous Albinism, Type IV) is an Autosome recessively inherited disorder, characterized by white Hair Specimen and Skin Specimen Source Code, and loss of Pigment in the Eye.  Is Autosome recessive deafness associated with oculocutaneous albinism a \"coincidence syndrome\"? MONOPHENOL MONOOXYGENASE gene, immunodeficiency, hematological disorders, and minor anomalies: a new Autosome recessive syndrome? Mutations in the MONOPHENOL MONOOXYGENASE gene (MONOPHENOL MONOOXYGENASE, 11q14-21, MIM 606933) cause oculocutaneous albinism type 1 (MONOPHENOL MONOOXYGENASE gene type 1, MIM 203100), a developmental disorder having an Autosome recessive mode of inheritance. MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosome recessive disorder characterized by ALBINOIDISM, OCULOCUTANEOUS, AUTOSOMAL DOMINANT in Eye, Hair Specimen and Skin Specimen Source Code, accompanied with Unspecified visual loss. MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosome recessive hereditary pigmentation disorder affecting Homo sapiens and several other animal species.[SEP]Relations: monophenol monooxygenase activity has relations: molfunc_protein with MONOPHENOL MONOOXYGENASE, molfunc_protein with MONOPHENOL MONOOXYGENASE.", "label": "yes"}
{"original_question": "Are Ultra-conserved elements (UCEs) enriched in segmental duplications?", "id": "converted_489", "sentence1": "Are Ultra-conserved elements (UCEs) enriched in segmental duplications?", "sentence2": "Here we address the process by which CNVs become depleted of UCEs. 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. Alternatively, lack of depletion for UCEs from Primary malignant neoplasm CNVs may reflect the diseased state.  ULEs are located in intergenic or intronic regions and are depleted from segmental duplications. Interestingly, Homo sapiens UCEs have been reported to be strongly depleted among segmental duplications and benign copy number variants (CNVs). In addition, here we show that these elements are preferentially found in pathogenic deletions (enrichment ratio 3.6 vs. 0.5 in duplications), and that this association is not related with a higher content of Genes. In contrast, pathogenic CNVs lacking UCEs showed almost a threefold higher content in Genes 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. Mammalian ultraconserved elements are strongly depleted among segmental duplications and copy number variants. Here, we show that UCEs are significantly depleted among segmental duplications and copy number variants. Notably, of the UCEs that are found in segmental duplications or copy number variants, the majority overlap Exons, indicating, along with other findings presented, that UCEs overlapping Exons represent a distinct subset. Ultraconserved elements (UCEs) are strongly depleted from segmental duplications and copy number variations (CNVs) in the Homo sapiens genome, suggesting that Gene Deletion Abnormality or duplication of a NAGPA gene can be deleterious to the Mammalian Cell. Here, we show that UCEs are significantly depleted among segmental duplications and copy number variants. 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 show that UCEs are significantly depleted among segmental duplications and copy number variants. Ultraconserved elements (UCEs) are strongly depleted from segmental duplications and copy number variations (CNVs) in the Homo sapiens genome, suggesting that Gene Deletion Abnormality or duplication of a NAGPA gene can be deleterious to the Mammalian Cell melanogaster genome revealed depletion of the P-element and piggyBac Clinical act of insertion in and around the Sophophora UCEs. Mammalian ultraconserved elements are strongly depleted among segmental duplications and copy number variants. Here, we show that UCEs are significantly depleted among segmental duplications and copy number variants. Interestingly, Homo sapiens UCEs have been reported to be strongly depleted among segmental duplications and benign copy number variants (CNVs).[SEP]Relations: malignant giant cell tumor has relations: disease_disease with Primary malignant neoplasm, disease_disease with Primary malignant neoplasm.", "label": "no"}
{"original_question": "Do normal cells express the protein TERT?", "id": "converted_490", "sentence1": "Do Normal cell express the protein TERT?", "sentence2": "Since Telomerase has been recognized as a relevant factor distinguishing Tumor cells, malignant from Normal cell, it has become a very promising target for anti-cancer therapy Telomerase plays a pivotal role in cellular immortality and tumorigenesis. Its activity is normally not detectable in most Diploid Cell while it is reactivated in the vast majority of Tumor cells, malignant. Therefore, inhibition of Telomerase has been viewed as a promising anticancer approach due to its specificity for Tumor cells, malignant. Telomerase activity is found in 85%-90% of all Homo sapiens Malignant Neoplasms but not in their adjacent Normal cell. TERT protein, Homo sapiens (TERT wt Allele) is an essential component in the Telomerase complex that plays an important role in Telomerase activity. elomerase activation is considered to be a critical step in carcinogenesis and its activity correlates closely with Homo sapiens Telomerase reverse transcriptase (TERT wt Allele) expression. Since only Tumor cells, uncertain whether benign or malignant that express Telomerase activity would activate this Promoter, the TERT wt Allele proximal Promoter allows for preferential expression of Genes, Viral in Tumor cells, uncertain whether benign or malignant, leading to selective viral replication[SEP]", "label": "no"}
{"original_question": "Is there any involvement of the long non-coding RNA Gomafu in schizophrenia?", "id": "converted_491", "sentence1": "Is there any involvement of the long non-coding RNA MIAT gene in schizophrenia?", "sentence2": "The long non-coding RNA MIAT gene is acutely regulated in response to neuronal activation and involved in schizophrenia-associated alternative splicing. Here, we profile these transcriptomic responses and show that long non-coding RNAs (lncRNAs) are dynamically regulated by neuronal activation, including acute downregulation of the lncRNA MIAT gene, previously implicated in Head>Brain and retinal development. Moreover, we demonstrate that MIAT gene binds directly to the splicing factors QKI gene gene and SRSF1 gene gene (Serine/Arginine-Rich Splicing Factor 2) and dysregulation of MIAT gene leads to alternative splicing patterns that resemble those observed in SZ for the archetypal SZ-associated genes DISC1 gene gene and Receptor Tyrosine-Protein Kinase ErbB-4, human. Finally, we show that MIAT gene is downregulated in post-mortem cortical gray matter from the superior temporal gyrus in SZ. These results functionally link activity-regulated lncRNAs and alternative splicing in neuronal function and suggest that their dysregulation may contribute to nervous system disorder. MIAT gene/MIAT/Rncr2 is a RNA, Long Untranslated that has been proposed to control Neuron of retina specification, stem cell differentiation and alternative splicing of schizophrenia-related genes. The long non-coding RNA MIAT gene is acutely regulated in response to neuronal activation and involved in schizophrenia-associated alternative splicing Moreover, we demonstrate that MIAT gene binds directly to the splicing factors QKI gene gene and SRSF1 gene gene (Serine/Arginine-Rich Splicing Factor 2) and dysregulation of MIAT gene leads to alternative splicing patterns that resemble those observed in SZ for the archetypal SZ-associated genes DISC1 gene gene and Receptor Tyrosine-Protein Kinase ErbB-4, human.  Finally, we show that MIAT gene is downregulated in post-mortem cortical gray matter from the superior temporal gyrus in SZ.  The long non-coding RNA MIAT gene is acutely regulated in response to neuronal activation and involved in schizophrenia-associated alternative splicing.[SEP]", "label": "yes"}
{"original_question": "Is butterfly rash a symptom of Systemic lupus erythematosus?", "id": "converted_492", "sentence1": "Is butterfly rash a symptom of Systemic lupus erythematosus?", "sentence2": "Diagnosing Systematic Light Exposure can be challenging because of the myriad of clinical features and substantial variability between patients. Cutaneous involvement is present in about 60% of cases and typically manifests as a Zygomatic bone or butterfly rash. The prevalence of Lupus Erythematosus, Systemic (Systematic Light Exposure) is 28 per 100,000.  We report a 12 years old female patient with an overlap syndrome involving Autoimmune Chronic Hepatitis (Autoimmune hepatitis) and Lupus Erythematosus, Systemic (Systematic Light Exposure). The patient presented with jaundice, Hepatosplenomegaly, malaise, Polyarthralgia, Arthritis and butterfly rash on the face. Some of the clinical characteristics of Systematic Light Exposure patients observed were Nephritis (53.7%), Fever symptoms (finding) (53.26%), neuropsychological disorder (36.18%), Zygomatic bone/butterfly rash (27.6%), Lung diseases (22.6%), Photosensitivity of Skin Specimen Source Code (21.6%), cardiac involvement (21.1%) and Oral Ulcer (19.09%).  Systemic lupus erythematosus and Infections of musculoskeletal system: a retrospective study in Saudis. The prevalence of the following manifestations was significantly higher for pediatric than for adult-onset disease including: lupus Nephritis (43% pediatric vs 26.4% for adult-onset), Hematological Disease (57% vs 36.4%), Photosensitivity of Skin Specimen Source Code (20% vs 9%), butterfly rash (61% vs 35.5%) and mucosal ulceration (11.4% vs 4%).  Systemic lupus erythematosus (Systematic Light Exposure) is a multifactorial Autoimmune Diseases with highest prevalence among women of childbearing age.  We described a unique case of a 25-year-old Arab young woman who was diagnosed with Systematic Light Exposure, depending on clinical, laboratory investigations and after she had fulfilled the diagnostic criteria for Systematic Light Exposure and had presented the following findings: constitutional findings (Fatigue, Fever symptoms (finding), and Arthralgia); dermatologic finding (Photosensitivity of Skin Specimen Source Code and butterfly rash); Kidney Failure, Chronic (Proteinuria up to 400 mg in 24 hours); Hematologic and antinuclear antibodies (positivity for Antibodies, Antinuclear (Atrial Natriuretic Factor), anti-double-stranded DNA antibodies, direct Coombs, ANA and Antibodies, Anti-DNA, low C4 and C3 innervation innervation, Anterior Cranial Cruciate Ligament by immunoglobulin G and Immunoglobulin M).  Grade 1 and 2-3 inflammatory process occurred in 53 (63%) and 31 (37%) patients respectively. Symptom complexes \"systemic inflammation\", \"butterfly rash\", \"wrist petechiae\", \"enanthema of the oral mucous membrane\", and other Lesion were regarded as the markers of Systematic Light Exposure activity.  Systemic lupus erythematosus (Systematic Light Exposure) remains a challenging medical problem.  Rembrandt's Maria Bockenolle has a butterfly rash and digital deformities: overlapping syndrome of rheumatoid Arthritis and Lupus Erythematosus, Systemic. A butterfly rash on the patient's face suggested a diagnosis of Lupus Erythematosus, Systemic (Systematic Light Exposure). A butterfly rash on the patients face suggested a diagnosis of Lupus Erythematosus, Systemic (Systematic Light Exposure) The diagnosis of Systematic Light Exposure could be excluded and the butterfly rash attributed to a laminar hemorrhage, an Skin Bruise due to the Immune thrombocytopenic purpura. We describe a case of KD who developed a typical butterfly rash, reminiscent of Systematic Light Exposure.  The diagnosis of Systematic Light Exposure was made 22 years ago based on Raynaud's phenomenon, butterfly rash, Alopecia, Photosensitivity of Skin Specimen Source Code and positive antinuclear antibody.  Symptom complexes \"systemic inflammation\", \"butterfly rash\", \"wrist petechiae\", \"enanthema of the oral mucous membrane\", and other Lesion were regarded as the markers of Systematic Light Exposure activity. Rembrandt's Maria Bockenolle has a butterfly rash and digital deformities: overlapping syndrome of rheumatoid Arthritis and Lupus Erythematosus, Systemic. To investigate, various unspecific, but otherwise typical clinical symptoms of Skin Specimen Source Code and Mucous Membrane that arise in Systematic Light Exposure patients other than those defined as Systematic Light Exposure criteria such as butterfly rash, Chronic discoid lupus erythematosus, Oral Ulcer, and increased Photosensitivity of Skin Specimen Source Code.[SEP]Relations: discoid lupus erythematosus has relations: disease_disease with Chronic discoid lupus erythematosus, disease_disease with Chronic discoid lupus erythematosus. Arthritis has relations: disease_phenotype_positive with Autoimmune Chronic Hepatitis, disease_phenotype_positive with Autoimmune Chronic Hepatitis. Rheumatoid Arthritis has relations: disease_phenotype_positive with rheumatoid Arthritis, disease_phenotype_positive with rheumatoid Arthritis. Antinuclear antibody positivity has relations: disease_phenotype_positive with Autoimmune Chronic Hepatitis, disease_phenotype_positive with Autoimmune Chronic Hepatitis. Fatigue has relations: disease_phenotype_positive with rheumatoid Arthritis, disease_phenotype_positive with rheumatoid Arthritis. Jaundice has relations: disease_phenotype_positive with Autoimmune Chronic Hepatitis, disease_phenotype_positive with Autoimmune Chronic Hepatitis. Human immunoglobulin G has relations: drug_protein with C3 innervation, drug_protein with C3 innervation, drug_protein with C3 innervation, drug_protein with C3 innervation. Arthralgia has relations: disease_phenotype_positive with rheumatoid Arthritis, disease_phenotype_positive with Autoimmune Chronic Hepatitis, disease_phenotype_positive with rheumatoid Arthritis, disease_phenotype_positive with Autoimmune Chronic Hepatitis, disease_phenotype_positive with rheumatoid Arthritis, disease_phenotype_positive with Autoimmune Chronic Hepatitis, disease_phenotype_positive with rheumatoid Arthritis, disease_phenotype_positive with Autoimmune Chronic Hepatitis.", "label": "yes"}
{"original_question": "Is infertility characteristic of individuals with Fanconi anemia?", "id": "converted_493", "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 primary ovarian insufficiency (Ovarian Failure, Premature). 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 Ovarian Failure, Premature 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 Primary malignant neoplasm, 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 lymphocyte immune globulin, lymphocyte immune globulin, anti-thymocyte globulin (ATG) 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 cancer 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 cancer 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 primary ovarian insufficiency (Ovarian Failure, Premature). Fanconi anemia (doxorubicin/fluorouracil protocol) is a complex cancer 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 cancer risks, and Sterility, Reproductive, and developmental anomalies including Microphthalmos, Microcephaly (physical finding), hypoplastic radius and thumb.[SEP]Relations: Hypogonadism has relations: disease_phenotype_positive with Fanconi anemia, disease_phenotype_positive with Fanconi anemia. Fanconi anemia complementation group has relations: disease_protein with BRCA1 protein, human, disease_protein with BRCA2 protein, human, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_protein with PALB2 protein, human, disease_disease with Fanconi anemia, disease_protein with BRCA1 protein, human, disease_protein with BRCA2 protein, human, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), disease_protein with PALB2 protein, human, disease_disease with Fanconi anemia. anal canal Anal squamous cell carcinoma has relations: disease_disease with Anal squamous cell carcinoma, disease_disease with Anal squamous cell carcinoma. Bone marrow hypocellularity has relations: phenotype_protein with BRCA2 protein, human, phenotype_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), phenotype_protein with PALB2 protein, human, phenotype_protein with BRCA2 protein, human, phenotype_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder), phenotype_protein with PALB2 protein, human.", "label": "yes"}
{"original_question": "Is golimumab effective for ulcerative colitis?", "id": "converted_494", "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-\u03b1) 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-\u03b1 (TNF\u03b1), was evaluated as maintenance therapy in TNF\u03b1 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-\u03b1 antagonist-na\u00efve 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 \u20ac/QALYG) from public payer perspective and 374,377 PLN/QALY gained (89,137 \u20ac/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-\u00e1 (TNF\u00e1), was evaluated as maintenance therapy in TNF\u00e1 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) -\u00e1, 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: Visilizumab has relations: drug_drug with vedolizumab, drug_drug with vedolizumab. ulcerative colitis (disease) has relations: disease_protein with Recombinant Tumor Necrosis Factor Family Protein, indication with vedolizumab, disease_protein with Recombinant Tumor Necrosis Factor Family Protein, indication with vedolizumab. Golimumab has relations: drug_protein with Recombinant Tumor Necrosis Factor Family Protein, drug_drug with vedolizumab, drug_protein with Recombinant Tumor Necrosis Factor Family Protein, drug_drug with vedolizumab. Infliximab has relations: drug_protein with Recombinant Tumor Necrosis Factor Family Protein, drug_drug with vedolizumab, drug_protein with Recombinant Tumor Necrosis Factor Family Protein, drug_drug with vedolizumab. Adalimumab has relations: drug_protein with Recombinant Tumor Necrosis Factor Family Protein, drug_drug with vedolizumab, drug_protein with Recombinant Tumor Necrosis Factor Family Protein, drug_drug with vedolizumab. Abatacept has relations: drug_drug with vedolizumab, drug_drug with vedolizumab. Tofacitinib has relations: drug_drug with vedolizumab, drug_drug with vedolizumab.", "label": "yes"}
{"original_question": "Does mTOR regulate the translation of MAPKAPK2?", "id": "converted_495", "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 MTOR Inhibitors 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 ammonium tetrathiomolybdate, molfunc_protein with ZFP36L1 gene, molfunc_protein with MAP-kinase-activated kinase 2, molfunc_protein with ammonium tetrathiomolybdate, molfunc_protein with ZFP36L1 gene, molfunc_protein with MAP-kinase-activated kinase 2. Sirolimus has relations: contraindication with Primary malignant neoplasm, contraindication with Primary malignant neoplasm. ZFP36L1 gene has relations: protein_protein with MAP-kinase-activated kinase 2, protein_protein with MAP-kinase-activated kinase 2.", "label": "yes"}
{"original_question": "Could divalent metal transporter 1 deficiency lead to anemia?", "id": "converted_496", "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 hypochromic microcytic Genus Anemia. 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. Microcytic hypochromic Genus Anemia (disorder) 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 Rattus norvegicus 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 hypochromic microcytic Genus Anemia Belgrade Rattus norvegicus 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 hypochromic microcytic Genus Anemia.  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 hypochromic microcytic Genus Anemia. 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: disease_protein with Malignant neoplasm of colon and/or rectum, disease_protein with Malignant neoplasm of colon and/or rectum. 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": "Does the hERG gene code for a protein which is part of a sodium channel?", "id": "converted_497", "sentence1": "Does the hERG gene code for a Protein Info which is part of a Sodium supplements channel?", "sentence2": "The Homo sapiens ether-\u00e0-go-go-related gene (hERG 1a) KCNA5 gene is critical for Cardiac - anatomy qualifier repolarization Human ether-a-go-go-related 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 gene 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 gene gene, 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 gene gene 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 Homo sapiens ether-a-go-go-related 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 Homo sapiens ether-a-go-go-related 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 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 gene 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 gene gene 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 gene gene (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 gene gene, 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-\u00e0-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 gene gene 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-\u00e0-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-\u00e0-go-go-related gene (hERG)  The Homo sapiens ether-a-go-go-related gene (hERG) encodes the pore-forming \u03b1-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\u207a 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: Long QT Syndrome has relations: disease_protein with KCNE1 gene, disease_protein with KCNE1 gene, disease_protein with KCNE1 gene, disease_protein with KCNE1 gene, disease_protein with KCNE1 gene, disease_protein with KCNE1 gene, disease_protein with KCNE1 gene, disease_protein with KCNE1 gene. KCNE1 gene has relations: anatomy_protein_present with Chest>Heart, disease_protein with Long QT Syndrome, anatomy_protein_present with Chest>Heart, disease_protein with Long QT Syndrome. KCNE2 has relations: disease_protein with Long QT Syndrome, disease_protein with Long QT Syndrome.", "label": "no"}
{"original_question": "Is lenvatinib effective for renal cell carcinoma?", "id": "converted_498", "sentence1": "Is lenvatinib effective for renal cell carcinoma?", "sentence2": "However, the combination of lenvatinib, a multitargeted agent that inhibits Vascular Endothelial Growth Factor A as well as Fibroblast Growth Factor Receptors, and everolimus demonstrated promising results in a randomized phase II trial.  The FDA has approved the combination of lenvatinib and everolimus to treat advanced or Metastatic Renal Cell Carcinoma. Moreover, a recent Phase II study demonstrated a significant benefit for the second-line combination treatment with everolimus plus lenvatinib (a novel TKI) in terms of progression-free survival and overall survival compared to the single-agent everolimus. We then discuss two recently approved Growth Factor Receptors antagonists i.e. cabozantinib and lenvatinib, and a recently approved checkpoint inhibitor, nivolumab, and issues pertaining to drug development, and future directions in treatment of metastatic RCC.  INTERPRETATION: Lenvatinib plus everolimus and lenvatinib alone resulted in a progression-free survival benefit for patients with Metastatic Renal Cell Carcinoma who have progressed after one previous Vascular Endothelial Growth Factor A-targeted therapy.  Lenvatinib therapy for the treatment of patients with advanced renal cell carcinoma. Lenvatinib therapy for the treatment of patients with advanced renal cell carcinoma.[SEP]", "label": "yes"}
{"original_question": "Does HuR bind to the untranslated regions (UTRs) of mRNAs?", "id": "converted_499", "sentence1": "Does ELAVL1 gene bind to the untranslated regions (Untranslated Regions) of mRNAs?", "sentence2": "ELAVL1 gene is also overexpressed during tumourigenesis and is abnormally present within the Cytoplasm, where it binds to AU-rich elements in the 3'Untranslated Regions of target RNA, Messenger and post-transcriptionally regulates the expression of its target Genes. Human antigen R (ELAVL1 gene) is a ubiquitous 32 kDa protein comprising three RNA Recognition Motif (RRMs), whose main function is to bind Adenylate and uridylate Rich Elements (AREs) in 3' UnTranslated Regions (Untranslated Regions) of mRNAs. Human antigen R (ELAVL1 gene) is a ubiquitously expressed RNA-Binding Proteins that modulates gene expression at the post-transcriptional level. The RNA-Binding Proteins ELAVL1 gene binds at 3' untranslated regions (Untranslated Regions) of target transcripts, thereby protecting them against degradation.  ELAV/Hu Proteins bind to AU-rich elements (are unit of measure) in mRNAs and regulate their stability from splicing to translation, and the ubiquitous ELAVL1 gene protein has been implicated in cancerous cell growth.  This is achieved by altered expression of the Proteins Congenital Thrombotic Thrombocytopenic Purpura and ELAVL1 gene, which bind 3' untranslated region (UTR) elements in cancer-related Genes.[SEP]Relations: ELAVL1 has relations: cellcomp_protein with Cytoplasm, cellcomp_protein with Cytoplasm.", "label": "yes"}
{"original_question": "Does CRISPR inversion of CTCF sites alter genome topology?", "id": "converted_500", "sentence1": "Does CRISPR inversion of CTCF sites alter genome topology?", "sentence2": "CRISPR Inversion of CTCF Sites Alters Genome Topology and Enhancer/Promoter Function To test the functional significance of this observation, we combined CRISPR/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 \u03b2-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 CRISPR Inversion of CTCF Sites Alters Genome Topology and Enhancer/Promoter Function. CRISPR Inversion of CTCF Sites Alters Genome Topology and Enhancer/Promoter Function.[SEP]", "label": "yes"}
{"original_question": "Is there a role of proton beam therapy in medulloblastoma treatment?", "id": "converted_501", "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, craniopharyngiomas, low-grade Glioma; or panventricular irradiation of pure non-secreting germinoma; or craniospinal irradiation of Medulloblastoma 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, Medulloblastoma (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]", "label": "yes"}
{"original_question": "Are there canonical marks of active chromatin in developmentally regulated genes?", "id": "converted_502", "sentence1": "Are there canonical marks of active chromatin location in developmentally regulated Genes?", "sentence2": "Absence of canonical marks of active chromatin location location in developmentally regulated Genes. The interplay of active and repressive Histone Code is assumed to have a key role in the regulation of gene expression. In contrast to this generally accepted view, we show that the transcription of Genes temporally regulated during Fly (organism) and worm development occurs in the absence of canonically active Histone Code. Conversely, strong chromatin location location marking is related to transcriptional and post-transcriptional stability, an association that we also observe in Mammals. Our results support a model in which chromatin location location marking is associated with the stable production of RNA, whereas unmarked chromatin location location would permit rapid gene activation and deactivation during development. In the latter case, regulation by TRANSCRIPTION FACTOR would have a comparatively more important regulatory role than chromatin location location marks. Absence of canonical marks of active chromatin location location in developmentally regulated Genes Absence of canonical marks of active chromatin location location in developmentally regulated Genes. In contrast to this generally accepted view, we show that the transcription of Genes temporally regulated during Fly (organism) and worm development occurs in the absence of canonically active Histone Code.[SEP]", "label": "no"}
{"original_question": "Are there methods for generating highly multiplexed ChIP-seq libraries?", "id": "converted_503", "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]", "label": "yes"}
{"original_question": "Is Doxorubicin cardiotoxic?", "id": "converted_504", "sentence1": "Is doxorubicin cardiotoxic?", "sentence2": "doxorubicin (DOXO) is widely used to treat Solid Neoplasm. However, its clinical use is limited by side effects including serious Cardiotoxicity due to Myocytes, Cardiac damage.  The results provide direct evidence for the role of catalase in doxorubicin cardiotoxic responses. These results do not support the possibility that mitomycin potentiates the acute cardiotoxic effects produced by doxorubicin. The Anthracycline Antibiotics chemotherapeutic agent doxorubicin is converted by the enzyme carbonyl reductase 1 (CBR1 protein, human protein, human) into its cardiotoxic metabolite adriamycinol The clinical efficiency of the highly potent antitumor agent doxorubicin is limited by cardiotoxic effects doxorubicin (DOX), a highly active chemotherapeutic drug, faces limitations in clinical application due to severe cardiotoxic effects (mainly through increased oxidative stress) Clinical uses of doxorubicin (DOX), a highly active anticancer agent, are limited by its severe cardiotoxic side effects associated with increased oxidative stress and apoptosis doxorubicin (DOX) and trastuzumab (TRZ) are highly effective chemotherapeutic agents in the breast cancer setting, limited by their cardiotoxic side effects Twisting and ironing: doxorubicin Cardiotoxicity by mitochondrial DNA damage. Cardiotoxic effects were reported in 15 (5%) of 291 children receiving treatment including doxorubicin. On the other hand, pretreatment of Rattus norvegicus with hesperidin protected Cardiac - anatomy qualifier tissues against the cardiotoxic effects of doxorubicin as evidenced from amelioration of histopathological changes and normalization of Cardiac - anatomy qualifier biochemical parameters.hesperidin may have a protective effect against DOX-induced Cardiotoxicity. However, with cumulative doses, doxorubicin also is known to have cardiotoxic effects, including Cardiomyopathies and Chest>Heart failure. Methods of reducing or preventing doxorubicin-induced Cardiotoxicity have been suggested, including an investigational doxorubicin analog, mitoxantrone ( Novantrone ). The most cardiotoxic drug, doxorubicin, is the most potent inducer of Superoxides generation, while epirubicin, which is less cardiotoxic, has a relatively limited effect on Superoxides production. The mechanism of doxorubicin Cardiotoxicity is likely multifactorial and most importantly, the genetic factors predisposing to doxorubicin Cardiotoxicity are unknown. As doxorubicin Cardiotoxicity is considered irreversible, early detection of Cardiotoxicity and prevention of overt Chest>Heart failure is essential. Although there are monitoring guidelines for Cardiotoxicity, optimal timing for early detection of subclinical doxorubicin Cardiotoxicity is still obscure. quercetin attenuates doxorubicin Cardiotoxicity by modulating Bmi-1 expression. However, doxorubicin Cardiotoxicity of the Chest>Heart has largely limited its clinical use. Mitochondrial topoisomerase I (top1mt) is a novel limiting factor of doxorubicin Cardiotoxicity. doxorubicin-based chemotherapy induces Cardiotoxicity, which limits its clinical application. he clinical use of doxorubicin (DOX) and other prior Anthracycline Antibiotics therapy is limited by a dosage-dependent Cardiotoxicity, which can lead to Cardiomyopathies.  Besides its cardiotoxic effect, doxorubicin also elicits inflammatory effects in vivo. 7-Monohydroxyethylrutoside (7-monohydroxyethylrutoside) has recently been used as a protector against doxorubicin-induced Cardiotoxicity in vivo. doxorubicin is an effective antineoplastic agent, but it frequently causes dose-related cardiotoxic effects.  Among these analogs, idarubicin (4-demethoxy-daunorubicin) was shown to be less cardiotoxic than doxorubicin i verapamil has also been suggested to potentiate the Cardiotoxicity of doxorubicin.  doxorubicin treatment is associated with both acute and chronic Cardiotoxicity.  Cardiac - anatomy qualifier effects of Diclofenac Sodium ER on doxorubicin-induced Cardiomyopathies in Rattus norvegicus[SEP]Relations: doxorubicin has relations: contraindication with Cardiomyopathies, drug_protein with CBR1 protein, human, drug_drug with verapamil, drug_drug with quercetin, contraindication with Chest>Heart failure, contraindication with Cardiomyopathies, drug_protein with CBR1 protein, human, drug_drug with verapamil, drug_drug with quercetin, contraindication with Chest>Heart failure. Protein S human has relations: drug_drug with doxorubicin, drug_drug with doxorubicin. Trastuzumab has relations: drug_drug with doxorubicin, drug_drug with doxorubicin. Epirubicin has relations: drug_drug with doxorubicin, contraindication with Cardiomyopathies, drug_drug with doxorubicin, contraindication with Cardiomyopathies. verapamil has relations: drug_drug with doxorubicin, contraindication with Chest>Heart failure, drug_drug with quercetin, drug_drug with doxorubicin, contraindication with Chest>Heart failure, drug_drug with quercetin. Idarubicin has relations: drug_drug with verapamil, contraindication with Cardiomyopathies, drug_drug with doxorubicin, drug_drug with verapamil, contraindication with Cardiomyopathies, drug_drug with doxorubicin. Mitomycin has relations: contraindication with Chest>Heart failure, drug_drug with doxorubicin, contraindication with Chest>Heart failure, drug_drug with doxorubicin. quercetin has relations: drug_protein with CBR1 protein, human, drug_drug with doxorubicin, drug_drug with verapamil, drug_protein with CBR1 protein, human, drug_drug with doxorubicin, drug_drug with verapamil. Diclofenac has relations: drug_drug with doxorubicin, drug_drug with verapamil, drug_drug with quercetin, drug_drug with doxorubicin, drug_drug with verapamil, drug_drug with quercetin. Cardiomyopathy has relations: drug_effect with doxorubicin, drug_effect with doxorubicin. Mitoxantrone has relations: drug_drug with doxorubicin, drug_drug with quercetin, contraindication with Chest>Heart failure, drug_drug with doxorubicin, drug_drug with quercetin, contraindication with Chest>Heart failure. Congestive Chest>Heart failure has relations: drug_effect with doxorubicin, drug_effect with verapamil, drug_effect with doxorubicin, drug_effect with verapamil.", "label": "yes"}
{"original_question": "Is the mouse Sry gene locus free of repetitive sequences?", "id": "converted_505", "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 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 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.  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. The Mouse antigen genomic SRY protein, human locus is characterized by two arms of a large inverted repeat, 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 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 structure of the SRY protein, human locus in CASP14 Genes.[SEP]", "label": "no"}
{"original_question": "Is Meis1 implicated in microphthalmia?", "id": "converted_506", "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>\u00a9 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>\u00a9 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: Visual impairment has relations: disease_phenotype_positive with Microphthalmos, disease_phenotype_positive with Microphthalmos.", "label": "yes"}
{"original_question": "Can Pentraxin 3 predict outcomes of sepsis?", "id": "converted_507", "sentence1": "Can Pentraxin 3 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 PITX3 gene protein, human. Together, these results suggest that elevation of PITX3 gene is associated with fulminant disease during A. baumannii Sepsis (Invertebrate). Persisting high levels of plasma PITX3 gene protein, human 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. Pentraxin 3 in patients with severe Sepsis (Invertebrate) or Shock: the ALBIOS trial. Pentraxin 3: an immune modulator of Communicable Diseases and useful marker for disease severity assessment in Sepsis (Invertebrate). Redox state of PITX3 gene protein, human as a novel biomarker for resolution of Inflammation and survival in Sepsis (Invertebrate). The prototypic long pentraxin, PITX3 gene protein, human, 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. Pentraxin 3 (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 PITX3 gene protein, human as a novel biomarker for resolution of Inflammation and survival in Sepsis (Invertebrate). Persisting high levels of plasma PITX3 gene protein, human over the first days after severe Sepsis (Invertebrate) and Septic Shock onset are associated with mortality. Pentraxin 3 (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 PITX3 gene protein, human (PITX3 gene) complex in Sepsis (Invertebrate) demonstrates the interaction with azurocidin 1 and other components of neutrophil extracellular traps.[SEP]", "label": "yes"}
{"original_question": "Is ocular melanosis a risk factor for uveal melanoma?", "id": "converted_508", "sentence1": "Is ocular melanosis a risk factor for Uvea Melanocytic neoplasm?", "sentence2": "Ocular/oculodermal (oculo[dermal]) melanocytosis is a congenital periocular pigmentary condition that can lead to the development of Uvea Melanocytic neoplasm, estimated at 1 in 400 affected patients. Melanosis coli coli oculi is often underestimated as a risk factor for Uvea Melanocytic neoplasm and Glaucoma (eukaryote). Ophthalmic surveillance, every 6 or 12 months is important, in patients with Ocular melanosis for early detection of high risk diseases.  One of about 400 patients with ODM followed for life is estimated to develop Uvea Melanocytic neoplasm. Excessive melanocyte in the Uvea tract in ODM may provide the biologic basis for susceptibility to the development of Uvea Melanocytic neoplasm. Patients with ODM should be monitored ophthalmoscopically, especially during the susceptible period, for the development of Uvea Melanocytic neoplasm. The authors suggest that a national registry of ODM patients be created and prospective data collected to better assess the risk of developing Uvea Melanocytic neoplasm. In the white population, an association between oculo(dermal) melanocytosis (ODM) and Uvea Melanocytic neoplasm is well recognized.  Melanocytic neoplasm may arise in the Uvea tract, the Specimen Source Codes - Conjunctiva, the Skin Specimen Source Code of the Eyelid structure, or the Orbit (brand of fungicide). Risk factors:Finding:Point in time:^Patient:Nominal:Finding:Point in time:^Patient:Nominal so far identified include pre-existing choroidal naevi for Uvea melanomas, primary acquired melanosis (Potassium aggravated myotonia) for conjunctival tumours, and ocular and oculodermal melanocytosis for Uvea and orbital lesions.  Risk factors:Finding:Point in time:^Patient:Nominal:Finding:Point in time:^Patient:Nominal so far identified include pre-existing choroidal naevi for Uvea melanomas, primary acquired melanosis (Potassium aggravated myotonia) for conjunctival tumours, and ocular and oculodermal melanocytosis for Uvea and orbital lesions. Phacomatosis pigmentovascularis of cesioflammea type in 7 patients: combination of ocular pigmentation (melanocytosis or melanosis) and Port-Wine Stain with risk for Melanocytic neoplasm. In the fourth case the Melanocytic neoplasm was detected in a routine examination and we were able to apply a preserving treatment with I125 brachytherapy.DISCUSSION: Melanosis coli coli oculi is often underestimated as a risk factor for Uvea Melanocytic neoplasm and Glaucoma (eukaryote). Association of ocular and oculodermal melanocytosis with the rate of Uvea Melanocytic neoplasm metastasis: analysis of 7872 consecutive Eye. Risk factors:Finding:Point in time:^Patient:Nominal:Finding:Point in time:^Patient:Nominal so far identified include pre-existing choroidal naevi for Uvea melanomas, primary acquired melanosis (Potassium aggravated myotonia) for conjunctival tumours, and ocular and oculodermal melanocytosis for Uvea and orbital lesions In the fourth case the Melanocytic neoplasm was detected in a routine examination and we were able to apply a preserving treatment with I125 brachytherapy.Melanosis coli coli oculi is often underestimated as a risk factor for Uvea Melanocytic neoplasm and Glaucoma (eukaryote) In this study, patients with melanocytosis who developed Uvea Melanocytic neoplasm were found to have double the risk for metastasis compared with those without melanocytosis.To determine the relationship of oculo(dermal) melanocytosis to the prognosis of patients with Uvea Melanocytic neoplasm.Retrospective chart review of 7872 patients with Uvea Melanocytic neoplasm treated at the Ocular Oncology Service, Wills Eye Institute, from August 25, 1970, through August 27, 2008.Enucleation, plaque radiotherapy, local resection, or thermotherapy.Metastasis and Cessation of life.Of 7872 patients with Uvea Melanocytic neoplasm, oculo(dermal) melanocytosis was present in 230 (3%) By multivariable analysis, the factors predictive of metastasis in patients harboring Uvea Melanocytic neoplasm associated with oculo(dermal) melanocytosis were increased tumor thickness (P = .001) and the presence of subretinal fluid (P = .05), and the only factor predictive of Cessation of life was increased tumor thickness (P = .009).  In the fourth case the Melanocytic neoplasm was detected in a routine examination and we were able to apply a preserving treatment with I125 brachytherapy.Melanosis coli coli oculi is often underestimated as a risk factor for Uvea Melanocytic neoplasm and Glaucoma (eukaryote). Risk factors:Finding:Point in time:^Patient:Nominal:Finding:Point in time:^Patient:Nominal so far identified include pre-existing choroidal naevi for Uvea melanomas, primary acquired melanosis (Potassium aggravated myotonia) for conjunctival tumours, and ocular and oculodermal melanocytosis for Uvea and orbital lesions. CONCLUSIONS AND RELEVANCE Patients with Uvea Melanocytic neoplasm associated with oculo(dermal) melanocytosis have double the risk for metastasis compared with those with no melanocytosis. By multivariable analysis, the factors predictive of metastasis in patients harboring Uvea Melanocytic neoplasm associated with oculo(dermal) melanocytosis were increased tumor thickness (P = .001) and the presence of subretinal fluid (P = .05), and the only factor predictive of Cessation of life was increased tumor thickness (P = .009). CONCLUSIONS AND RELEVANCE Patients with Uvea Melanocytic neoplasm associated with oculo(dermal) melanocytosis have double the risk for metastasis compared with those with no melanocytosis.[SEP]Relations: melanocytic neoplasm has relations: disease_disease with Melanocytic neoplasm, disease_disease with Melanocytic neoplasm.", "label": "yes"}
{"original_question": "Is siltuximab effective for Castleman disease?", "id": "converted_509", "sentence1": "Is siltuximab effective for Castleman Disease?", "sentence2": "Siltuximab: a targeted therapy for HHV-8-negative idiopathic multicentric Castleman Disease. 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 Castleman Disease - 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 Castleman Disease. 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 Castleman Disease (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 Castleman Disease: 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 Castleman Disease: 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 Castleman Disease. Siltuximab: A Review in Idiopathic (Human Herpesvirus-8-Negative) Multicentric Castleman Disease. Siltuximab (interleukin-6 antibody) is approved for the treatment of multicentric Castleman Disease (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 Castleman Disease. 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 Castleman Disease. 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 Castleman Disease.EXPERIMENTAL DESIGN: In an open-label, dose-finding, 7 cohort, phase I study, patients with Lymphoma, Large-Cell, Follicular, Multiple Myeloma, or symptomatic Castleman Disease 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\u00a0=\u00a017), Multiple Myeloma (n\u00a0=\u00a013), or CD (n\u00a0=\u00a017). Currently, there are more effective therapeutic alternatives in multicentric Castleman Disease: 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 multicentric Castlemans 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 Castleman Disease (Macular dystrophy, corneal type 1) Siltuximab for multicentric Castleman Disease FDA approval: siltuximab for the treatment of patients with multicentric Castleman Disease 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 Castleman Disease (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 Castleman Disease 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 Castleman Disease: 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 Castleman Disease.In an open-label, dose-finding, 7 cohort, phase I study, patients with Lymphoma, Large-Cell, Follicular, Multiple Myeloma, or symptomatic Castleman Disease 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 Castleman Disease (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 Castleman Disease.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 Castleman Disease. Siltuximab: a targeted therapy for HHV-8-negative idiopathic multicentric Castleman Disease. Emerging treatments in Castleman Disease - 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: interleukin-6 receptor binding has relations: molfunc_protein with interleukin-6, molfunc_protein with interleukin-6. Siltuximab has relations: indication with Castleman Disease, drug_protein with interleukin-6, indication with Castleman Disease, drug_protein with interleukin-6. multicentric Castleman Disease has relations: disease_disease with Castleman Disease, disease_disease with Castleman Disease, disease_disease with Castleman Disease, disease_disease with Castleman Disease. Fatigue has relations: disease_phenotype_positive with Castleman Disease, disease_phenotype_positive with Castleman Disease. Tocilizumab has relations: indication with Castleman Disease, indication with Castleman Disease.", "label": "yes"}
{"original_question": "Is the enzyme EPRS phosphorylated?", "id": "converted_510", "sentence1": "Is the enzyme EPRS1 gene phosphorylated?", "sentence2": "Phosphorylation of glutamyl-prolyl tRNA synthetase (EPRS1 gene) has been investigated extensively in our laboratory for more than a decade, and has served as an archetype for studies of other AARSs. EPRS1 gene is dually phosphorylated by Cyclin-Dependent Kinases (CDK5 protein, human) at Ser(886) and then by a CDK5 protein, human-dependent-AGC kinase at Ser(999);  Diphosphorylated EPRS1 gene is released from its residence in the tRNA multisynthetase complex for immediate binding to NS1-associated protein and subsequent binding to ribosomal protein L13a and GAPDH protein, human protein, human.  Two-site phosphorylation of EPRS1 gene coordinates multimodal regulation of noncanonical translational control activity.[SEP]Relations: EPRS1 has relations: protein_protein with GAPDH protein, human, protein_protein with GAPDH protein, human.", "label": "yes"}
{"original_question": "Is there a relationship between B cells and Multiple Sclerosis?", "id": "converted_511", "sentence1": "Is there a relationship between Deciduous maxillary right first molar tooth-Lymphocytes 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-Lymphocytes 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-Lymphocytes, 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-Lymphocytes 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-Lymphocytes 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 Cerebrospinal Fluid 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-Lymphocytes 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-Lymphocytes 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-Lymphocytes, Plasma Cells, Antibodies, in vitro diagnostic, and immunoglobulins. 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-Lymphocytes 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-Lymphocytes and Therapeutic gamma delta T-lymphocytes, increased trafficking of Deciduous maxillary right first molar tooth-Lymphocytes across the blood-brain barrier, and Autoantibodies produced by Plasma Cells may contribute to the pathophysiology of Autoimmune Diseases such as Multiple Sclerosis. Accumulating evidence supports a major role of Deciduous maxillary right first molar tooth-Lymphocytes in Multiple Sclerosis (MS) pathogenesis. Further research is needed to elucidate the pathology of Deciduous maxillary right first molar tooth-Lymphocytes and their role in central nervous system autoimmune diseases, including Multiple Sclerosis. Targeting Deciduous maxillary right first molar tooth-Lymphocytes 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]", "label": "yes"}
{"original_question": "Does Yersinia pestis causes a respiratory infection?", "id": "converted_512", "sentence1": "Does Yersinia pestis causes a respiratory infection?", "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. Infectious Lung Disorder by Yersinia pestis causes pneumonic plague, a rapidly progressing and often fatal Disease. Infectious Lung Disorder 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 Communicable Diseases 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 infection 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 infection.  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]", "label": "yes"}
{"original_question": "Are the genes for marneral biosynthesis scattered in the genome of A. thaliana?", "id": "converted_513", "sentence1": "Are the Genes for marneral biosynthesis scattered in the genome of A. thaliana?", "sentence2": "Here we characterize a second operon-like triterpene cluster (the marneral cluster) from A. thaliana, compare the features of these two clusters, and investigate the evolutionary events that have led to cluster formation Here we characterize a second operon-like triterpene cluster (the marneral cluster) from A. thaliana, compare the features of these two clusters, and investigate the evolutionary events that have led to cluster formation. Previously in thale cress (Arabidopsis thaliana <plant> <plant>) we identified an operon-like gene cluster that is required for the synthesis and ResponseLevel - ResponseLevel - modification of the triterpene thalianol. Prediction of operon-like gene clusters in the Arabidopsis thaliana <plant> <plant> genome based on co-expression analysis of neighboring Genes Here we characterize a second operon-like triterpene cluster (the marneral cluster) from A. thaliana, compare the features of these two clusters, and investigate the evolutionary events that have led to cluster formation.  Here we characterize a second operon-like triterpene cluster (the marneral cluster) from A. the cyclic hydroxamic acid pathways in maize, the avenacin biosynthesis gene clusters in oat, the thalianol pathway in Arabidopsis thaliana <plant> <plant>, and the diterpenoid momilactone cluster in rice. Prediction of operon-like gene clusters in the Arabidopsis thaliana <plant> <plant> genome based on co-expression analysis of neighboring Genes.[SEP]", "label": "no"}
{"original_question": "Does Jarid2 play a role in early embryo development?", "id": "converted_514", "sentence1": "Does Jarid2 play a role in early embryo development?", "sentence2": "Jarid2 Coordinates NANOG gene Expression and Pneumocystis jiroveci pneumonia/Wnt Signaling Required for Efficient ESC Differentiation and Early Embryo Development Unlike other Polycomb Repressive Complex 2-deficient Embryonic Stem Cells (Enhanced S-Cone Syndrome), however, Jarid2-deficient Enhanced S-Cone Syndrome show a severe differentiation block, altered colony morphology, and distinctive patterns of deregulated gene expression. Here, we show that Jarid2(-/-) Enhanced S-Cone Syndrome express constitutively high levels of NANOG gene but reduced Pneumocystis jiroveci pneumonia signaling components WNT9A gene, PRICKLE1 gene, and FZD2 protein, human and lowered \u03b2-catenin activity. Depletion of WNT9A gene/PRICKLE1 gene/FZD2 protein, human from wild-type Enhanced S-Cone Syndrome or overexpression of NANOG gene largely phenocopies these cellular defects. Co-culture of Jarid2(-/-) with wild-type Enhanced S-Cone Syndrome restores variable NANOG gene expression and \u03b2-catenin activity and can partially rescue the differentiation block of mutant cells. In addition, we show that Enhanced S-Cone Syndrome lacking Jarid2 or WNT9A gene/PRICKLE1 gene/FZD2 protein, human or overexpressing NANOG gene induce multiple between breakfast and lunch formation when injected into normal E3.5 blastocysts. These data describe a previously unrecognized role for Jarid2 in regulating a core pluripotency and Wnt/Pneumocystis jiroveci pneumonia signaling circuit that is important for ESC differentiation and for pre-implantation development. Jarid2 Coordinates NANOG gene Expression and Pneumocystis jiroveci pneumonia/Wnt Signaling Required for Efficient ESC Differentiation and Early Embryo Development. Consistent with an essential role for PcG proteins in early development, we demonstrate that JARID2 gene gene is required for the differentiation of mouse Embryonic Stem Cells. Jumonij (JMJ)/Jarid2 plays important roles in embryonic development and functions as a Transcription Repressor/Corepressor. Thus, these results demonstrate that JARID2 gene gene is essential for the binding of PcG proteins to target Genes and, consistent with this, for the proper differentiation of Embryonic Stem Cells and normal development. JARID2 gene gene is an accessory component of Polycomb repressive complex-2 (Polycomb Repressive Complex 2) required for the differentiation of Embryonic Stem Cells (Enhanced S-Cone Syndrome). Jarid2 Coordinates NANOG gene Expression and Pneumocystis jiroveci pneumonia/Wnt Signaling Required for Efficient ESC Differentiation and Early Embryo Development. These data describe a previously unrecognized role for Jarid2 in regulating a core pluripotency and Wnt/Pneumocystis jiroveci pneumonia signaling circuit that is important for ESC differentiation and for pre-implantation development..[SEP]", "label": "yes"}
{"original_question": "Is PUVA therapy indicated for eczema treatment?", "id": "converted_515", "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 Route of Drug administration Route of Drug administration 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 Route of Drug administration Route of Drug administration 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 Route of Drug administration Route of Drug administration 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 Route of Drug administration Route of Drug administration 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: primary cutaneous amyloidosis has relations: disease_disease with Amyloidosis, Primary Cutaneous, disease_disease with Amyloidosis, Primary Cutaneous. vitiligo-associated multiple autoimmune disease susceptibility 1 has relations: disease_phenotype_positive with VITILIGO-ASSOCIATED MULTIPLE AUTOIMMUNE DISEASE SUSCEPTIBILITY 1 (finding), disease_phenotype_positive with VITILIGO-ASSOCIATED MULTIPLE AUTOIMMUNE DISEASE SUSCEPTIBILITY 1 (finding).", "label": "yes"}
{"original_question": "Do brown fat cells produce heat?", "id": "converted_516", "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 Fat (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. Mitochondrial uncoupling protein 1 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 adipose Tissue Specimen Code, 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 \u03b2-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 \u03b11 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 brown adipose Tissue Specimen Code uncoupling protein 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 adipose Tissue Specimen Code 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 \u03b2-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 adipose Tissue Specimen Code is lipid oxidation to produce heat. The main function of brown adipose Tissue Specimen Code (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 adipose Tissue Specimen Code, 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 adipose Tissue Specimen Code) 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 adipose Tissue Specimen Code 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]", "label": "yes"}
{"original_question": "Is Melioidosis caused by the bacterium\u00a0Burkholderia pseudomallei?", "id": "converted_517", "sentence1": "Is Melioidosis caused by the bacterium\u00a0Pseudomonas 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, Infection of skin and/or subcutaneous tissue, 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: Pneumonia has relations: disease_phenotype_positive with Melioidosis, disease_phenotype_positive with Melioidosis.", "label": "yes"}
{"original_question": "Can glyburide reduce cerebral edema?", "id": "converted_518", "sentence1": "Can glyburide reduce cerebral Edema:Finding:Point in time:^Patient:Ordinal?", "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 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-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-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:Finding:Point in time:^Patient:Ordinal, 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 (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 (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 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: Dexamethasone has relations: drug_drug with glyburide, drug_drug with glyburide.", "label": "yes"}
{"original_question": "Is vemurafenib used for thyroid cancer?", "id": "converted_519", "sentence1": "Is vemurafenib used for Malignant neoplasm of thyroid?", "sentence2": "Vemurafenib in patients with BRAF protein, human protein, human(V600E)-positive metastatic or unresectable papillary Malignant neoplasm of thyroid refractory to radioactive Iodine, Homeopathic preparation: a non-randomised, multicentre, open-label, phase 2 trial. Vemurafenib, an oncogenic BRAF protein, human protein, human kinase PPP1R1A gene approved for BRAF protein, human protein, human-positive melanoma, showed clinical benefit in three patients with BRAF protein, human protein, human(V600E)-positive papillary Malignant neoplasm of thyroid in a phase 1 trial. INTERPRETATION: Vemurafenib showed antitumour activity in patients with progressive, BRAF protein, human protein, human(V600E)-positive papillary Malignant neoplasm of thyroid refractory to radioactive Iodine, Homeopathic preparation who had never been treated with a multikinase PPP1R1A gene.  CONTEXT: Vemurafenib, a selective BRAF protein, human protein, human PPP1R1A gene, appears to have promising clinical activity in patients with papillary Malignant neoplasm of thyroid (Percutaneous transhepatic cholangiography) harboring the BRAF protein, human protein, human(V600E) Mutation Abnormality. Efficacy and tolerability of vemurafenib in patients with BRAF protein, human protein, human(V600E) -positive papillary Malignant neoplasm of thyroid: M.D. Anderson Cancer Center off label experience. CONCLUSIONS: Vemurafenib is a potentially effective and well-tolerated treatment strategy in patients with advanced Percutaneous transhepatic cholangiography harboring the BRAF protein, human protein, human(V600E) Mutation Abnormality. The US Food and Drug Administration-approved BRAF protein, human protein, human inhibitors, vemurafenib and dabrafenib, have demonstrated superior efficacy in patients with BRAF protein, human protein, human-mutant melanomas but have limited efficacy in BRAF protein, human protein, human-mutant Malignant neoplasm of colon and/or rectum. Little is known at this time regarding BRAF protein, human protein, human inhibitors in Malignant neoplasm of thyroid. Initial reports in patients with progressive, radioactive Iodine, Homeopathic preparation-refractory BRAF protein, human protein, human-mutant papillary Malignant neoplasm of thyroid suggest response rates of approximately 30-40%. Use of vemurafenib in Anaplastic thyroid carcinoma: a case report. Finally, we found that propranolol can amplify the cytotoxicity of vemurafenib and sensitize Malignant neoplasm of thyroid cells to cytotoxic effect of vemurafenib. CONTEXT: Vemurafenib, a selective BRAF protein, human protein, human PPP1R1A gene, appears to have promising clinical activity in patients with papillary Malignant neoplasm of thyroid (Percutaneous transhepatic cholangiography) harboring the BRAF protein, human protein, human(V600E) Mutation Abnormality.OBJECTIVE: To determine the efficacy and safety of vemurafenib when used outside of a clinical trial.DESIGN: A retrospective review at MD Anderson Cancer Center.METHODS: The best responses were evaluated using Response Evaluation Criteria in Solid Tumors v1.1. Vemurafenib, a selective BRAF protein, human protein, human PPP1R1A gene, appears to have promising clinical activity in patients with papillary Malignant neoplasm of thyroid (Percutaneous transhepatic cholangiography) harboring the BRAF protein, human protein, human(V600E) Mutation Abnormality.To determine the efficacy and safety of vemurafenib when used outside of a clinical trial.A retrospective review at MD Anderson Cancer Center.The best responses were evaluated using Response Evaluation Criteria in Solid Tumors v1.1 CONTEXT: Vemurafenib, a selective BRAF protein, human protein, human PPP1R1A gene, appears to have promising clinical activity in patients with papillary Malignant neoplasm of thyroid (Percutaneous transhepatic cholangiography) harboring the BRAF protein, human protein, human(V600E) Mutation Abnormality.OBJECTIVE: To determine the efficacy and safety of vemurafenib when used outside of a clinical trial.DESIGN: A retrospective review at MD Anderson Cancer Center.METHODS: The best responses were evaluated using Response Evaluation Criteria in Solid Tumors v1.1.  Finally, we found that propranolol can amplify the cytotoxicity of vemurafenib and sensitize Malignant neoplasm of thyroid cells to cytotoxic effect of vemurafenib. metformin or sirolimus adjuvant treatment may provide clinical benefits with minimal side effects to BRAFV600E-positive advanced Malignant neoplasm of thyroid patients treated with vemurafenib. Vemurafenib, a selective BRAF protein, human protein, human PPP1R1A gene, appears to have promising clinical activity in patients with papillary Malignant neoplasm of thyroid (Percutaneous transhepatic cholangiography) harboring the BRAF protein, human protein, human(V600E) Mutation Abnormality.To determine the efficacy and safety of vemurafenib when used outside of a clinical trial.A retrospective review at MD Anderson Cancer Center.The best responses were evaluated using Response Evaluation Criteria in Solid Tumors v1.1. Our data demonstrate that vemurafenib induces Endoplasmic Reticulum stress response-mediated autophagy in Malignant neoplasm of thyroid and autophagy inhibition may be a beneficial strategy to sensitize BRAF protein, human protein, human-mutant Malignant neoplasm of thyroid to vemurafenib.. Combination of vemurafenib and metformin decreased cell viability and increased apoptosis in both BCPAP papillary Malignant neoplasm of thyroid cells and 8505c anaplastic Malignant neoplasm of thyroid cells. Targeting autophagy sensitizes BRAF protein, human protein, human-mutant Malignant neoplasm of thyroid to vemurafenib. Propranolol sensitizes Malignant neoplasm of thyroid cells to cytotoxic effect of vemurafenib. mTOR Inhibitors [MoA] sensitize Malignant neoplasm of thyroid cells to cytotoxic effect of vemurafenib. Vemurafenib induced a high level of autophagy in BRAF protein, human protein, human-mutant Malignant neoplasm of thyroid cells.[SEP]Relations: Vemurafenib has relations: drug_drug with metformin, drug_protein with BRAF protein, human, drug_drug with metformin, drug_protein with BRAF protein, human. Propranolol has relations: drug_drug with metformin, drug_drug with metformin. Sirolimus has relations: drug_drug with metformin, drug_drug with metformin. Dabrafenib has relations: drug_drug with metformin, drug_protein with BRAF protein, human, drug_drug with metformin, drug_protein with BRAF protein, human. thyroid gland carcinoma has relations: disease_disease with Malignant neoplasm of thyroid, disease_protein with BRAF protein, human, disease_disease with Malignant neoplasm of thyroid, disease_protein with BRAF protein, human. malignant colon neoplasm has relations: disease_protein with BRAF protein, human, disease_disease with Malignant neoplasm of colon and/or rectum, disease_protein with BRAF protein, human, disease_disease with Malignant neoplasm of colon and/or rectum.", "label": "yes"}
{"original_question": "Are mutations in the C9orf72  gene associated with macular degeneration?", "id": "converted_520", "sentence1": "Are Gene Mutation 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 Frontotemporal dementia 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 Gene Mutation, 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 Gene Mutation, the related disorders, and their features, followed by a discussion of the deficiency knowledge of C9ORF72 Gene Mutation. Mutations 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 (FTLD-TDP). Novel TARDBP Sequence - ParameterizedDataType variant and C9ORF72 repeat expansion in a family with frontotemporal dementia. There was, as expected, a significant association between C9ORF72 Gene Mutation 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 (Frontotemporal dementia). 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: Frontotemporal dementia has relations: disease_phenotype_positive with Amyotrophic Lateral Sclerosis, disease_phenotype_positive with Amyotrophic Lateral Sclerosis. C9orf72 has relations: disease_protein with Amyotrophic Lateral Sclerosis, disease_protein with Amyotrophic Lateral Sclerosis. Amyotrophic Lateral Sclerosis has relations: disease_disease with Motor Neuron Disease, disease_protein with Cu-Zn Superoxide Dismutase, disease_disease with familial Amyotrophic Lateral Sclerosis, disease_protein with Feline urological syndrome, disease_disease with Motor Neuron Disease, disease_protein with Cu-Zn Superoxide Dismutase, disease_disease with familial Amyotrophic Lateral Sclerosis, disease_protein with Feline urological syndrome, disease_disease with Motor Neuron Disease, disease_protein with Cu-Zn Superoxide Dismutase, disease_disease with familial Amyotrophic Lateral Sclerosis, disease_protein with Feline urological syndrome, disease_disease with Motor Neuron Disease, disease_protein with Cu-Zn Superoxide Dismutase, disease_disease with familial Amyotrophic Lateral Sclerosis, disease_protein with Feline urological syndrome. Spasticity of facial muscles has relations: disease_phenotype_positive with Amyotrophic Lateral Sclerosis, disease_phenotype_positive with Amyotrophic Lateral Sclerosis. Motor Neuron Disease has relations: disease_disease with Amyotrophic Lateral Sclerosis, disease_protein with Cu-Zn Superoxide Dismutase, disease_disease with Amyotrophic Lateral Sclerosis, disease_protein with Cu-Zn Superoxide Dismutase. Muscle weakness has relations: disease_phenotype_positive with Amyotrophic Lateral Sclerosis, disease_phenotype_positive with Amyotrophic Lateral Sclerosis.", "label": "no"}
{"original_question": "Is the number of described human nuclear mutations less than 50000?", "id": "converted_521", "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\u00ae) 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]", "label": "no"}
{"original_question": "Is Musclin a secretory peptide?", "id": "converted_522", "sentence1": "Is OSTN gene a secretory peptide?", "sentence2": "OSTN gene is a novel skeletal muscle-derived secretory factor, OSTN gene has been described as a muscle-derived secretory peptide, responsive to Therapeutic Insulin in vivo, and inducing Therapeutic Insulin resistance in vitro. OSTN gene is a type of muscle-secreted cytokine and its increased gene expression induces Therapeutic Insulin resistance in type 2 diabetes.  OSTN gene is a novel skeletal muscle-derived factor found in the signal sequence trap of Mus sp. skeletal muscle cDNAs. OSTN gene is a novel skeletal muscle-derived secretory factor found in the signal sequence trap of Mus sp. skeletal muscle cDNAs.  OSTN gene is a novel skeletal muscle-derived secretory factor that was isolated by our group.[SEP]", "label": "yes"}
{"original_question": "Are cutaneous porphyrias inherited with a recessive pattern?", "id": "converted_523", "sentence1": "Are cutaneous porphyrias inherited with a recessive pattern?", "sentence2": "Five of the porphyrias are low-penetrance autosomal dominant conditions in which clinical expression results from additional factors that act by increasing demand for Heme or by causing an additional decrease in enzyme activity or by a combination of these effects Molecular mechanisms of dominant expression in Disorders of Porphyrin Metabolism. Variegate Porphyria (Arginine Vasopressin-Neurophysin II Preproprotein) is an autosomal-dominant disorder that is caused by inheritance of a partial deficiency of the enzyme protoporphyrinogen oxidase (EC 1.3.3.4). It is characterized by Photosensitivity of skin and/or various neurological manifestations.  The acute porphyrias constitute a group of Metabolic Diseases engaging ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS in the Heme synthetic chain and generally following dominant inheritance patterns.[SEP]", "label": "no"}
{"original_question": "Can valproic acid prolong survival of glioblastoma patients?", "id": "converted_524", "sentence1": "Can valproic acid prolong survival of glioblastoma patients?", "sentence2": "For patients who presented with Epilepsy, the use of the antiepileptic drug VPA did not associate with survival when compared with patients who did not receive VPA treatment. This prognostic effect is not solely explained by early diagnosis, and survival is not associated with VPA treatment. Several in vivo and in vitro studies have indicated that VPA has radiosensitizing effects for Glioma and radioprotective influence on normal brain tissue surgical material surgical material or hippocampal Neurons. The results of several retrospective studies have also indicated potential benefit to improve survival of patients with Glomerular Basement Membrane. Moreover, the promising treatment results of a phase 2 trial of concurrent radiation therapy, temozolomide, and VPA for patients with Glomerular Basement Membrane have been recently reported.  While there have not been any novel anti-Glomerular Basement Membrane therapeutics approved for many years, there has been the gradual accumulation of clinical data suggesting that the widely used anti-convulsant agent, valproic acid (VPA) may significantly prolong survival in Glomerular Basement Membrane patients.  Additionally, VPA may result in improved outcomes compared to historical data and merits further study. Several retrospective studies in Seizures patients with glioblastoma treated with chemotherapy have provided evidence for a moderately improved survival with the use of valproic acid, possibly due to inhibition of Histone Deacetylase Several clinical studies have reported that valproic acid could prolong survival of Glomerular Basement Membrane patients While there have not been any novel anti-Glomerular Basement Membrane therapeutics approved for many years, there has been the gradual accumulation of clinical data suggesting that the widely used anti-convulsant agent, valproic acid (VPA) may significantly prolong survival in Glomerular Basement Membrane patients Prolonged survival with valproic acid use in the EORTC/NCIC temozolomide trial for glioblastoma Prolonged survival with valproic acid use in the EORTC/NCIC temozolomide trial for glioblastoma. valproic acid use during radiation therapy for glioblastoma associated with improved survival. Patients receiving VPA alone (97 [16.9%]) appeared to derive more survival benefit from TMZ/RT (hazard ratio [HR] 0.39, 95% confidence interval [CI] 0.24-0.63) than patients receiving an EIAED only (252 [44%]) (HR 0.69, 95% CI 0.53-0.90) or patients not receiving any AED (HR 0.67, 95% CI 0.49-0.93).  Several retrospective studies in Seizures patients with glioblastoma treated with chemotherapy have provided evidence for a moderately improved survival with the use of valproic acid, possibly due to inhibition of Histone Deacetylase. Several uncontrolled retrospective case series and a post hoc analysis of the registration trial for temozolomide indicated an association between valproic acid (VPA) use and improved survival outcomes in patients with newly diagnosed glioblastoma.To confirm the hypothesis suggested above, a combined analysis of survival association of antiepileptic drug use at the start of Chemoradiotherapy with temozolomide was performed in the pooled patient cohort (n = 1,869) of four contemporary randomized clinical trials in newly diagnosed glioblastoma: AVAGlio (Avastin in Glioblastoma Multiforme Multiforme; NCT00943826), CENTRIC (Cilengitide, Temozolomide, and Radiation T Several clinical studies have reported that valproic acid could prolong survival of Glomerular Basement Membrane patients. Patients receiving VPA alone (97 [16.9%]) appeared to derive more survival benefit from TMZ/RT (hazard ratio [HR] 0.39, 95% confidence interval [CI] 0.24-0.63) than patients receiving an EIAED only (252 [44%]) (HR 0.69, 95% CI 0.53-0.90) or patients not receiving any AED (HR 0.67, 95% CI 0.49-0.93).VPA may be preferred over an EIAED in patients with glioblastoma who require an AED during TMZ-based Chemoradiotherapy. The combination of radiotherapy, temozolomide and valproic acid (VPA) has shown some promise in retrospective analyses of patients with glioblastoma, although their mechanisms of action remain unknown.We investigated the in vitro and in vivo effects of pretreating glioma cells with temozolomide and VPA as an immunization strategy to boost an adaptive immune response in a syngeneic mouse model.Temozolomide and VPA induced autophagy in GL261 glioma cells, and caused tumor antigen-specific T-cells to become activated effector T-cells. Prolonged survival with valproic acid use in the EORTC/NCIC temozolomide trial for glioblastoma.[SEP]Relations: Temozolomide has relations: drug_drug with valproic acid, drug_drug with valproic acid. valproic acid has relations: off_label_use with Epilepsy, indication with Epilepsy, off_label_use with Epilepsy, indication with Epilepsy. Epilepsy has relations: indication with valproic acid, off_label_use with valproic acid, indication with valproic acid, off_label_use with valproic acid.", "label": "yes"}
{"original_question": "Is Cryptococcus neoformans a frequent cause of isolated skin infections in immunocompromised individuals", "id": "converted_525", "sentence1": "Is Cryptococcus <scale insects> neoformans a frequent cause of isolated Skin Specimen Source Code Infections of musculoskeletal system in immunocompromised individuals", "sentence2": "Cryptococcus <scale insects> <scale insects> is an opportunistic Saccharomyces cerevisiae with a worldwide distribution that primarily causes significant Infections of musculoskeletal system in immunocompromised individuals, generally by affecting the respiratory tract. But primary cutaneous cryptococcosis (1-piperidinocyclohexanecarbonitrile) without Sepsis is rare.  Cryptococcus <scale insects> <scale insects> is a ubiquitous fungus and is known for causing Meningitis and cutaneous Infections of musculoskeletal system in immunocompromised individuals. Cryptococcus <scale insects> <scale insects> neoformans is an encapsulated Saccharomyces cerevisiae that can cause primary pulmonary Infections of musculoskeletal system or disseminate and cause Infections of musculoskeletal system of the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, Meninges, Skin Specimen Source Code, and Specimen Type - Bone in the immunocompromised host. The authors report a male patient, a seller with no detected immunosuppression, with an extensive ulcerated Skin Specimen Source Code lesion localized on the left forearm, caused by Cryptococcus <scale insects> <scale insects> neoformans var.[SEP]", "label": "no"}
{"original_question": "Is Obeticholic Acid used for treatment of Primary Biliary Cholangitis?", "id": "converted_526", "sentence1": "Is obeticholic acid used for treatment of Primary Biliary Cholangitis?", "sentence2": "Obeticholic acid in Primary Biliary Cholangitis. In a double-blind, randomized, placebo-controlled study including 217 patients with Primary Biliary Cholangitis, the authors show that obeticholic acid (a potent farnesoid X Agonist) administered with ursodiol or as monotherapy significantly decreases Serum alkaline phosphatase measurement and bilirubin preparation preparation when compared to placebo. Obeticholic acid (Ocaliva(TM)) is a farnesoid-X receptor (NR1H4 wt Allele) Agonist that is being developed by Intercept Pharmaceuticals for the treatment of various liver diseases, and has recently been granted accelerated approval in the USA for the treatment of Primary Biliary Cholangitis in combination with ursodiol in adults with an inadequate response to ursodiol, or as monotherapy in adults unable to tolerate ursodiol.  obeticholic acid (cyclophosphamide/doxorubicin/vincristine protocol) is a NR1H4 gene (NR1H4 wt Allele) Agonist which has been evaluated as a second line therapy in PBC and has recently been licenced by the FDA. cyclophosphamide/doxorubicin/vincristine protocol will be the first stratified therapy introduced in PBC, however confirmatory trial and real life data are needed to confirm that suggestive biochemical improvements are matched by improvement in key clinical outcomes. Obeticholic acid for the treatment of Primary Biliary Cholangitis in adult patients: clinical utility and patient selection. A series of clinical trials of cyclophosphamide/doxorubicin/vincristine protocol in PBC, primarily in combination with UDCA, have established that cyclophosphamide/doxorubicin/vincristine protocol leads to significant reductions in Serum alkaline phosphatase measurement that are predicted to lead to improved clinical outcomes, while dose-dependent pruritus has been the most common adverse effect. On the basis of these studies, cyclophosphamide/doxorubicin/vincristine protocol was given conditional approval by the US Food and Drug Administration with plans to establish the long-term clinical efficacy of cyclophosphamide/doxorubicin/vincristine protocol in patients with advanced PBC. Although obeticholic acid was approved by the FDA for the treatment of PBC in May 2016, this development occurred after the symposium presentation.  While several agents are being studied in combination with UDCA, monotherapy with the novel agent obeticholic acid, a Farnesoid X Receptor Agonist [EPC], has also shown promising results. Obeticholic acid (Ocaliva(TM)) is a farnesoid-X receptor (NR1H4 wt Allele) Agonist that is being developed by Intercept Pharmaceuticals for the treatment of various liver diseases, and has recently been granted accelerated approval in the USA for the treatment of Primary Biliary Cholangitis in combination with ursodiol in adults with an inadequate response to ursodiol, or as monotherapy in adults unable to tolerate ursodiol. Obeticholic acid for the treatment of Primary Biliary Cholangitis. Long-term clinical impact and cost-effectiveness of obeticholic acid for the treatment of Primary Biliary Cholangitis. A Placebo-Controlled Trial of obeticholic acid in Primary Biliary Cholangitis. This article summarizes the milestones in the development of obeticholic acid leading to this first approval for Primary Biliary Cholangitis. Obeticholic acid for the treatment of Primary Biliary Cholangitis. Long-term Clinical Impact and Cost-Effectiveness of obeticholic acid for the Treatment of Primary Biliary Cholangitis. Obeticholic acid in Primary Biliary Cholangitis. A Placebo-Controlled Trial of obeticholic acid in Primary Biliary Cholangitis. This article summarizes the milestones in the development of obeticholic acid leading to this first approval for Primary Biliary Cholangitis.[SEP]", "label": "yes"}
{"original_question": "Does the word ovine refers to goats?", "id": "converted_527", "sentence1": "Does the word ovine refers to Capra hircus?", "sentence2": "Jaagsiekte Domestic Sheep retrovirus (JSRV) is the causative agent of ovine pulmonary adenocarcinoma (OPA), a transmissible Primary malignant neoplasm of lung of Domestic Sheep that has rarely been found in Capra hircus.  In Domestic Sheep, a Rat Bronchiolo-Alveolar Carcinoma, known as ovine pulmonary carcinoma (Oligomeric Procyanidin Complex), is caused by jaagsiekte Domestic Sheep retrovirus (JSRV), an exogenous type D retrovirus.[SEP]", "label": "no"}
{"original_question": "Does GATA-1 regulate ribosomal protein genes?", "id": "converted_528", "sentence1": "Does GATA1 gene regulate Ribosomal Proteins Genes?", "sentence2": "Mutations 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 Gene Mutation have been found in patients with Anemia, Diamond-Blackfan, 2 (Diamond-Blackfan Anemia 1), a congenital erythroid aplasia typically caused by Gene Mutation 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 Proteins and rRNA 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 Proteins Genes. The importance of the transcription of the 137 Ribosomal Proteins 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: disease_protein with Anemia, Diamond-Blackfan, 2, disease_protein with Anemia, Diamond-Blackfan, 2.", "label": "yes"}
{"original_question": "Is Lennox-Gastaut Syndrome usually diagnosed in older adults?", "id": "converted_529", "sentence1": "Is Lennox-Gastaut syndrome usually diagnosed in older adults?", "sentence2": "We studied 15 Langer-Giedion Syndrome patients (mean age \u00b1 1 standard deviation [SD] = 28.7 \u00b1 10.6 years) and 17 healthy controls (mean age \u00b1 1 SD = 27.6 \u00b1 6.6 years)  children with Lennox-Gastaut syndrome Lennox-Gastaut syndrome (Langer-Giedion Syndrome) is a severe pediatric Epileptic Syndromes 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 Epileptic Syndromes 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 Epileptic Syndromes 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 Epileptic Syndromes 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: Epileptic Syndromes has relations: disease_disease with Epilepsy, disease_disease with Epilepsy. Epilepsy has relations: disease_disease with Epileptic Syndromes, disease_disease with Epileptic Syndromes.", "label": "no"}
{"original_question": "Is diphosphatidylglycerol (cardiolipin) a phospholipid of the mitochondrial membranes?", "id": "converted_530", "sentence1": "Is diphosphatidylglycerol (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 diphosphatidylglycerol also occurred in the Liver neoplasms mitochondria inner Tissue Tissue membrane.  Diphosphatidylglycerols 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 Rattus norvegicus and compared in terms of cholesterol content and phospholipid and Fatty Acids composition. In aged Rattus norvegicus, as compared to young, the major observations include: markedly higher cholesterol content; increased percentage of Sphingomyelins and diphosphatidylglycerol (cardiolipin);  The polyglycerophosphatides (typified by diphosphatidylglycerol) 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 Acids composition characteristic of diphosphatidylglycerol (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, diphosphatidylglycerol (cardiolipin). The Enzyme [APC] responsible for the conversion of Phosphatidyl glycerol to diphosphatidylglycerol (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 (diphosphatidylglycerol) biosynthesis was examined in mitochondria and outer and inner Mitochondrial Inheritance membranes prepared from Cavia porcellus and rat 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 (diphosphatidylglycerol) 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, diphosphatidylglycerol (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 (diphosphatidylglycerol) biosynthesis was examined in mitochondria and outer and inner Mitochondrial Inheritance membranes prepared from Cavia porcellus and rat 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 yeasts 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, diphosphatidylglycerol (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 (diphosphatidylglycerol) 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 Mitochondrial Inheritance inner 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 (diphosphatidylglycerol) and Cytochrome aa3 (CYTOCHROME C OXIDASE), two specific markers of Mitochondrial Inheritance inner Tissue Tissue membrane, and (2) fumarase activity, a specific marker of Mitochondrial Inheritance matrix space. Diphosphatidylglycerols (diphenylguanidine) or cardiolipin, a specific component of the inner Mitochondrial Inheritance Tissue Tissue membrane, represents about 4% of the total Lipids 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 rat 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 diphosphatidylglycerol synthetase from Abdomen>Liver Mitochondrial Inheritance membranes. A small decrease of diphosphatidylglycerol also occurred in the Liver neoplasms mitochondria inner Tissue Tissue membrane.[SEP]", "label": "yes"}
{"original_question": "Have studies shown that there is no link between DNA methylation patterns and Post Traumatic Stress Disorder?", "id": "converted_531", "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 Post-Traumatic Stress Disorder 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 Post-Traumatic Stress Disorder and provide further evidence that SKA2 gene gene is a promising biomarker for stress-related disorders including Post-Traumatic Stress Disorder.  Results provide novel support for Post-Traumatic Stress Disorder-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 (Post-Traumatic Stress Disorder) 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 (Post-Traumatic Stress Disorder). 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 Post-Traumatic Stress Disorder. Here we examined whether there was a link between an established rat model of post-traumatic stress disorder (Post-Traumatic Stress Disorder) 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 (Post-Traumatic Stress Disorder) cases and controls who were US military service members recently deployed to Afghanistan or Iraq.Cases (n = 75) had a postdeployment diagnosis of Post-Traumatic Stress Disorder 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 rat model of post-traumatic stress disorder (Post-Traumatic Stress Disorder) 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 (Post-Traumatic Stress Disorder) 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 Rattus norvegicus: evidence for the role of the post-synaptic density protein DLGAP2 gene. Subjects with Post-Traumatic Stress Disorder showed a higher DNA methylation of four CpG sites at the BDNF promoter compared with those without Post-Traumatic Stress Disorder Cumulatively, the data suggest that epigenetic variation at SKA2 gene gene mediates vulnerability to suicidal behaviors and Post-Traumatic Stress Disorder through dysregulation of the hypothalamic-pituitary-adrenal axis axis in response to stress.[SEP]", "label": "no"}
{"original_question": "Is POLD3 essential for mouse development?", "id": "converted_532", "sentence1": "Is POLD3 protein, human essential for mouse development?", "sentence2": "The POLD3 protein, human protein, human gene encodes a subunit of the DNA polymerase complex. Pold3 orthologs are not essential in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae or chicken allergenic extract allergenic extract DT40 cells, but the Schizosaccharomyces pombe ortholog\u00a0is essential. POLD3 protein, human protein, human also has a specialized role in the repair of broken replication forks, suggesting that POLD3 protein, human protein, human activity could be particularly relevant for Tumor cells, malignant enduring high levels of DNA replication stress. We report here that POLD3 protein, human protein, human is essential for mouse development and is also required for viability in adult animal allergen extracts. We report here that POLD3 protein, human protein, human is essential for mouse development and is also required for viability in adult animal allergen extracts. We report here that POLD3 protein, human protein, human is essential for mouse development and is also required for viability in adult animal allergen extracts.[SEP]", "label": "yes"}
{"original_question": "Are hepadnaviral minichromosomes free of nucleosomes?", "id": "converted_533", "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: germ cell Cell Nucleus has relations: cellcomp_cellcomp with Cell Nucleus, cellcomp_cellcomp with Cell Nucleus.", "label": "no"}
{"original_question": "Is it feasible to obtain DNA read lengths that exceed 30 Kb?", "id": "converted_534", "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\u2009kb) to be generated.[SEP]", "label": "no"}
{"original_question": "Is osteocrin expressed exclusively in the bone?", "id": "converted_535", "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]", "label": "no"}
{"original_question": "Are alterations in ultraconserved elements associated with colorectal adenocarcinoma?", "id": "converted_536", "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 SNPs within UCEs and clinical outcome in patients with Cytogenetic Complete Response. The results suggested that SNPs 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 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 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: 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": "Is apremilast effective for psoriasis?", "id": "converted_537", "sentence1": "Is apremilast effective for Psoriasis?", "sentence2": "CONCLUSION: apremilast reduces the severity of nail/scalp Psoriasis. CONCLUSIONS: apremilast demonstrated clinically meaningful improvements in Arthritis, Psoriatic and Psoriasis at week 16; sustained improvements were seen with continued treatment through 52\u2005weeks. apremilast: A Novel Pharmacologic Substance for Treatment of Psoriasis and Psoriatic Arthritis. In those that involved doses of 30 mg twice daily, a significantly greater percentage of patients receiving apremilast (28.8% to 40.9%) compared with placebo (5.3% to 5.8%) achieved at least 75% improvement from baseline in Psoriasis Area and Severity Index score at 16 weeks. CONCLUSIONS: apremilast has a novel mechanism of action and is safe and effective for the management of Psoriasis and Arthritis, Psoriatic. At this time, apremilast should be reserved for patients unable to take disease-modifying antirheumatic drugs. apremilast, an oral phosphodiesterase 4 (Phosphodiesterase Type 4) PPP1R1A gene, in patients with moderate to severe plaque Psoriasis: Results of a phase III, randomized, controlled trial (Efficacy and Safety Trial Evaluating the Effects of apremilast in Psoriasis [ESTEEM] 1). More recently, three larger double-blinded, and randomized multicenter studies demonstrate that apremilast is efficacious in the treatment of Psoriasis and Prostate-Specific Antigen, with significantly higher numbers of apremilast-treated patients achieving endpoints of a 75% reduction compared to baseline in Psoriasis Area and Severity Index (PASI-75) or American College of Rheumatology-20 scores, relative to placebo. No new significant adverse events emerged with continued apremilast exposure versus the placebo-controlled period.Data were limited to 52 weeks and may not generalize to nonplaque Psoriasis.apremilast was effective in moderate to severe plaque Psoriasis.<CopyrightInformation>Copyright \u00a9 2015 American Academy of Dermatology, Inc. Published by Elsevier Inc. All rights reserved.</ apremilast, a small molecule specific PPP1R1A gene of phosphodiesterase 4, works intracellularly to modulate pro-inflammatory and Anti-Inflammatory Agents mediator production.Assess apremilast efficacy and safety in moderate to severe plaque Psoriasis.Phase II, 12-week, multicenter, double-blind, placebo-controlled, parallel-group, dose-comparison study of 259 subjects randomized 1 : 1 : 1 to placebo, apremilast 20 mg QD or apremilast 20 mg Twice a day.More subjects receiving apremilast 20 mg Twice a day achieved \u2265 75% reduction in Psoriasis Area and Severity Index (PASI-75) vs. placebo (24.4% vs. 10.3%; P = 0.023) apremilast, a specific PPP1R1A gene of phosphodiesterase 4, modulates pro-inflammatory and Anti-Inflammatory Agents cytokine production.Apremilasts effect on patient-reported outcomes (PIK3CA related overgrowth spectrum) in patients with moderate to severe Psoriasis was evaluated in a phase IIb randomized, controlled trial (NCT00773734).In this 16-week, placebo-controlled study, 352 patients with moderate to severe plaque Psoriasis received placebo or apremilast (10, 20, or 30 mg Twice a day) Although further longer-term and comparative efficacy and tolerability data would be beneficial, the current clinical data indicate that apremilast is an effective and well tolerated option for the management of Psoriasis and Prostate-Specific Antigen in adults More recently, three larger double-blinded, and randomized multicenter studies demonstrate that apremilast is efficacious in the treatment of Psoriasis and Prostate-Specific Antigen, with significantly higher numbers of apremilast-treated patients achieving endpoints of a 75% reduction compared to baseline in Psoriasis Area and Severity Index (PASI-75) or American College of Rheumatology-20 scores, relative to placebo No deaths or Opportunistic Infections were reported.apremilast 20 mg Twice a day for 12 weeks was effective and well tolerated in subjects with moderate to severe plaque Psoriasis.<CopyrightInformation>\u00a9 2012 The Authors In addition, GlaxoSmithKline plc is developing 256066, an inhaled formulation of a Phosphodiesterase Type 4 PPP1R1A gene that has demonstrated efficacy in trials in asthma, and apremilast from Celgene Corp has been reported to be effective for the treatment of Psoriasis. Although further longer-term and comparative efficacy and tolerability data would be beneficial, the current clinical data indicate that apremilast is an effective and well tolerated option for the management of Psoriasis and Prostate-Specific Antigen in adults. No new significant adverse events emerged with continued apremilast exposure versus the placebo-controlled period.Data were limited to 52 weeks and may not generalize to nonplaque Psoriasis.apremilast was effective in moderate to severe plaque Psoriasis.<CopyrightInformation>Copyright \u00a9 2015 American Academy of Dermatology, Inc. Published by Elsevier Inc. All rights reserved.</C Several drug peculiarities, such as the low frequency of adverse events and the oral route of administration, make apremilast an innovative treatment for moderate-to-severe Psoriasis. Two new oral medications, apremilast and tofacitinib, have been developed for their immunomodulatory properties, and their potential efficacy in treating Psoriasis is being evaluated.We reviewed phase III randomized, placebo-controlled clinical trial results for apremilast and tofacitinib for efficacy and safety in Psoriasis.Psoriasis Area and Severity Index (PASI) 75 after 16 weeks for apremilast was between 28.8% and 33.1%. apremilast was effective in moderate to severe plaque Psoriasis.. Both new oral medications, apremilast and tofacitinib, appear to be effective in treating Psoriasis. apremilast was effective in the treatment of moderate-to-severe plaque Psoriasis over 52\u00a0weeks.. apremilast is an effective and well-tolerated option in treating moderate-to-severe plaque Psoriasis. apremilast has a novel mechanism of action and is safe and effective for the management of Psoriasis and Arthritis, Psoriatic. apremilast 20 mg Twice a day for 12 weeks was effective and well tolerated in subjects with moderate to severe plaque Psoriasis.. apremilast for the treatment of Psoriasis. apremilast, an Cyclic Nucleotide Phosphodiesterases, Type 4 PPP1R1A gene, in the treatment of palmoplantar Psoriasis: Results of a pooled analysis from phase II PSOR-005 and phase III Efficacy and Safety Trial Evaluating the Effects of apremilast in Psoriasis (ESTEEM) clinical trials in patients with moderate to severe Psoriasis.[SEP]Relations: apremilast has relations: indication with Arthritis, Psoriatic, indication with Arthritis, Psoriatic. Tofacitinib has relations: drug_drug with apremilast, drug_drug with apremilast. Arthritis, Psoriatic has relations: indication with apremilast, indication with apremilast.", "label": "yes"}
{"original_question": "Is skin color affected by variations of the SLC24A5 gene?", "id": "converted_538", "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.", "label": "yes"}
{"original_question": "Do circRNAs remain untranslated?", "id": "converted_539", "sentence1": "Do circRNAs 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 gene expression that act by direct base pairing to target sites within untranslated regions of messenger RNAs. We further show that the testis-specific RNA, Circular, SRY gene (SRY protein, human), serves as a miR-138 sponge, suggesting that miRNA sponge effects achieved by RNA, Circular formation are a general phenomenon. This study serves as the first, to our knowledge, functional analysis of a naturally expressed RNA, Circular. Numerous circRNAs were specifically expressed at different lactation stages, and only 1,314 circRNAs were detected at both lactation stages. A significantly positive correlation was observed for the expression profiles of some circRNAs and their parent Genes. The resulting RNA, Circular can be translated to generate functional proteins. In total, 80 circRNAs were identified from these 4 Genes; circRNAs from CSN1S1 gene gene had very high abundance, and 3 of them accounted for 36% of all the circRNAs expressed in the Mammary gland on lactation d 90. A total of 4,804 and 4,048 circRNAs were identified in the cow Mammary gland on d 90 and 250 postpartum, respectively, of which only 2,231 circRNAs were co-expressed at both lactation stages, suggesting high stage specificity in the circRNAs. Arraystar RNA, Circular Microarray Technology (KANGCHEN, Shanghai, China) was used to analyze the differential expression of circRNAs. The aim of study was to identify RNA, Circular expression in Structure of articular Cartilage and to explore the function of chondrocyte extracellular matrix (ECM)-related circRNAs (RNA, Circular-CER) in Cartilage. We also validated that P. falciparum produces circRNAs, 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 gene required for early sexual commitment events. CircRNA expression pattern and RNA, Circular-miRNA-mRNA network in the pathogenesis of Nonalcoholic Steatohepatitis. CircRNAs are abundantly expressed also in the hematopoietic compartment.[SEP]Relations: cyclin-dependent protein kinase activity has relations: molfunc_protein with CDK2 protein, human, molfunc_protein with CDK2 protein, human. CSN1S1 gene has relations: anatomy_protein_present with Mammary gland, anatomy_protein_present with Mammary gland. Mammary gland has relations: anatomy_protein_present with CSN1S1 gene, anatomy_protein_present with CDK2 protein, human, anatomy_protein_present with CSN1S1 gene, anatomy_protein_present with CDK2 protein, human.", "label": "no"}
{"original_question": "Is autophagy the process where bacteria ingest viral particles?", "id": "converted_540", "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]", "label": "yes"}
{"original_question": "Is intraoperative radiotherapy used for treatment of glioblastoma?", "id": "converted_541", "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\u2014a 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\u2014a 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: Carmustine has relations: indication with Anaplastic Ependymoma, indication with Glioma, indication with Anaplastic astrocytoma, off_label_use with Anaplastic astrocytoma, indication with Anaplastic Oligodendroglioma, indication with Anaplastic Ependymoma, indication with Glioma, indication with Anaplastic astrocytoma, off_label_use with Anaplastic astrocytoma, indication with Anaplastic Oligodendroglioma.", "label": "no"}
{"original_question": "Is tirilazad effective for treatment of aneurysmal subarachnoid haemorrhage?", "id": "converted_542", "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]", "label": "no"}
{"original_question": "Is dexamethasone recommended for treatment of intracerebral hemorrhage?", "id": "converted_543", "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]", "label": "no"}
{"original_question": "Is airplane stroke syndrome a common disease.", "id": "converted_544", "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]", "label": "no"}
{"original_question": "Can acupuncture cause spinal epidural hematoma?", "id": "converted_545", "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. Hematoma, Epidural, Spinal 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. Hematoma, Epidural, Spinal is a rare complication associated with pain control procedures such as facet block, acupuncture, Epidural Route of Drug Administration injection, etc. Hematoma, Epidural, Spinal 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 Hematoma, Epidural, Spinal with Subarachnoid Hemorrhage caused by acupuncture Hematoma, Epidural, Spinal 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 Hematoma, Epidural, Spinal with Subarachnoid Hemorrhage caused by acupuncture.[SEP]", "label": "yes"}
{"original_question": "Is edema a symptom of nephrotic syndrome?", "id": "converted_546", "sentence1": "Is edema 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, and Hyperlipidemia.  Nephrotic syndrome is an unusual manifestation of IgA Nephropathy (IGA Glomerulonephritis). Twelve patients with IGA Glomerulonephritis with Steroid-Sensitive Nephrotic Syndrome were evaluated and followed up. All patients presented with generalized edema.  The clinical features of sudden onset of generalized edema, initial heavy Proteinuria and initial severe Hypoalbuminemia might help identify the subset of patients, especially in low grade IGA Glomerulonephritis. Most patients presented within 3 months duration (61.4%) and the most common symptom was puffiness of face (98.45%) followed by Edema:Finding:Point in time:^Patient:Ordinal 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 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 Edema:Finding:Point in time:^Patient:Ordinal. Oedema 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 tolvaptan therapy for massive edema 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 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 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 caused by Supernumerary mandibular left lateral primary incisor We report a child with Steroid-resistant nephrotic syndrome with diuretic-resistant nephrotic edema treated successfully using acute peritoneal dialysis as a means of UF Albumin and furosemide Combination for Management of Edema:Finding:Point in time:^Patient:Ordinal:Finding:Point in time:^Patient:Ordinal in Nephrotic Syndrome: A Review of Clinical Studies The treatment of edema 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, Oliguria, and biochemical indices of nephrotic syndrome Blessed were the days when it all made sense and the apparent mechanism for edema 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 and Hyperlipidemia. The patient was admitted with edema 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 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, is reported. Nephrotic syndrome represents a constellation of symptoms including hyperalbuminuria, Hypoalbuminemia, edema formation, Hypercholesterolemia result, Hypertensive disease, hypercoagulopathy, and increased Communicable Diseases risk. Pathophysiology of edema formation in children with nephrotic syndrome not due to minimal change disease. To study the evidence-based therapy of edema in nephrotic syndrome by analyzing the literatures systematically. Edema:Finding:Point in time:^Patient:Ordinal:Finding:Point in time:^Patient:Ordinal 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. Oedema 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 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: Tiopronin has relations: drug_drug with furosemide, contraindication with Proteinuria, drug_drug with tolvaptan, contraindication with nephrotic syndrome, drug_drug with furosemide, contraindication with Proteinuria, drug_drug with tolvaptan, contraindication with nephrotic syndrome. Hypercholesterolemia has relations: disease_phenotype_positive with Hyperlipoproteinemias, disease_phenotype_positive with Hyperlipoproteinemias. Chronic kidney disease has relations: disease_phenotype_positive with AA amyloidosis, disease_phenotype_positive with AA amyloidosis. tolvaptan has relations: drug_drug with furosemide, drug_drug with furosemide. furosemide has relations: indication with Hypertensive disease, drug_drug with tolvaptan, indication with Hypertensive disease, drug_drug with tolvaptan. Nephrotic syndrome has relations: disease_phenotype_positive with AA amyloidosis, disease_phenotype_positive with AA amyloidosis. Proteinuria has relations: disease_phenotype_positive with AA amyloidosis, disease_phenotype_positive with AA amyloidosis. Steroid-resistant nephrotic syndrome has relations: disease_disease with nephrotic syndrome, disease_disease with nephrotic syndrome. Abdominal pain has relations: disease_phenotype_positive with AA amyloidosis, drug_effect with furosemide, disease_phenotype_positive with AA amyloidosis, drug_effect with furosemide.", "label": "yes"}
{"original_question": "Is there an association between Histone H3.3 mutations and glioma?", "id": "converted_547", "sentence1": "Is there an association between Histone H3.3 Gene Mutation 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 Gene Mutation in pediatric Glioblastoma Multiforme and has been suggested to play critical roles in the pathogenesis of thalamic gliomas and diffuse intrinsic pontine gliomas. 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\u00a0% of diffuse intrinsic pontine gliomas (DIPGs) carrying K27M and 36\u00a0% of non-brainstem gliomas carrying either K27M or G34R/V Gene Mutation. 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 Gene Mutation lead to unexpected changes in the epigenetic landscape in gliomas. Particularly striking is the discovery of frequent Histone antigen H3.3 Gene Mutation in pediatric Glioma, a particularly aggressive neoplasm that has long remained poorly understood Exon sequencing has identified a Mutation Abnormality in K27M of the H3-3B gene (H3-3A wt Allele K27M and G34R/V) in about 20% of pediatric glioblastomas, but it remains to be seen whether these Gene Mutation 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 modifications in vivo Pediatric Glioblastoma Multiforme 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 gliomas, an aggressive brainstem tumor, harbor heterozygous Gene Mutation that create a K27M amino acid substitution (racemethionine replaces lysine 27) in the tail of Histone antigen H3.3. Mutations in H3-3A wt Allele, which encodes Histone antigen H3.3, commonly occur in pediatric Glioblastoma Multiforme. Somatic Gene Mutation 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 gliomas 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 gliomas. Recurrent Gene Mutation affecting the Histone antigen H3.3 residues Lys27 or indirectly Lys36 are frequent drivers of pediatric high-grade gliomas (over 30% of HGGs). Use of Human Embryonic Stem Cells to model pediatric gliomas with H3.3K27M Histone antigen Mutation Abnormality. Recent studies on high-grade pediatric Glomerular Basement Membrane have identified two recurrent Gene Mutation (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 Gene Mutation in Histone antigen H3.3 and chromatin remodelling Genes in paediatric Glioblastoma Multiforme.[SEP]Relations: TERT has relations: disease_protein with Glioma, disease_protein with Glioma.", "label": "yes"}
{"original_question": "Is Pfh1 a component of the replisome?", "id": "converted_548", "sentence1": "Is Pfh1 a component of the replisome?", "sentence2": "Pfh1 Is an Accessory Replicative DNA Helicases that Interacts with the replisome to Facilitate Fork Progression and Preserve Genome Integrity Although the Schizosaccharomyces pombe 5'-to-3' DNA helicase 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 DNA Helicases that Interacts with the replisome to Facilitate Fork Progression and Preserve Genome Integrity. Thus, we conclude that Pfh1 is an accessory DNA helicase 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 helicase 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 DNA Helicases 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.", "label": "no"}
{"original_question": "Does the Abelson-related gene (ARG) gene encode for a serine kinase?", "id": "converted_549", "sentence1": "Does the Abelson-related gene (ARG) gene encode for a serine kinase?", "sentence2": "One Protein Isoforms of ABL2 gene/Abelson Tyrosine-Protein Kinase 2, Homo sapiens 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 (ABL2 gene/Abelson Tyrosine-Protein Kinase 2, Homo sapiens) regulates cell migration and morphogenesis by modulating the Microtubules associated with cytoplasmic filaments.  The Homo sapiens ABL2 gene (Abelson Tyrosine-Protein Kinase 2, Homo sapiens) 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 ARG 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 transcripts.  The ARG 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 ARG 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 ABL2 gene+. ABL2 gene (Abelson-related gene, Abelson Tyrosine-Protein Kinase 2, Homo sapiens) was the Protein Tyrosine Kinase with the highest prevalence (30% of all PTKs) and UVA led to a further induction of ABL2 gene expression reaching nine-fold RNA, Messenger baseline expression at 17 h after irradiation. To investigate the expression profile of protein tyrosine kinases (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 (ARG) 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 (Protein Tyrosine Kinase) domains of ARG. The non-receptor TYK2 gene Abelson related gene (ABL2 gene/Abelson Tyrosine-Protein Kinase 2, Homo sapiens) regulates cell migration and morphogenesis by modulating the Microtubules associated with cytoplasmic filaments. ABL2 gene (Abelson-related gene, Abelson Tyrosine-Protein Kinase 2, Homo sapiens) was the Protein Tyrosine Kinase with the highest prevalence (30% of all PTKs) and UVA led to a further induction of ABL2 gene 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/ARG (Abetalipoproteinemia-related gene) belongs to the Abetalipoproteinemia (Abelson tyrosine-protein kinase) family of tyrosine kinases The non-receptor TYK2 gene Abelson related gene (ABL2 gene/Abelson Tyrosine-Protein Kinase 2, Homo sapiens) regulates cell migration and morphogenesis by modulating the Microtubules associated with cytoplasmic filaments The ARG gene encodes for a nonreceptor TYK2 gene characterized by high Homologous Gene with ABL1 gene in the TK, SH2, and SH3 domains. ABL2/ARG (Abetalipoproteinemia-related gene) belongs to the Abetalipoproteinemia (Abelson tyrosine-protein kinase) family of tyrosine kinases. We report that the Abelson (Abl) and Abl-related gene (ABL2 gene) nonreceptor tyrosine kinases are required for maintenance of cortical dendrites in the Mus sp. brain. The products of the Homo sapiens ARG gene and the Homo sapiens Abetalipoproteinemia gene characterize the Abelson family of non-receptor tyrosine protein kinases. The products of the Homo sapiens ABL2 gene gene and Homo sapiens, Mus sp., Drosophila <basidiomycetes> <basidiomycetes>, and Phylum Nematoda Abl 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 (ARG) 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 (Protein Tyrosine Kinase) domains of ARG. The TYK2 gene abl-related gene ARG 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 transcripts.[SEP]Relations: acute lymphoblastic/lymphocytic leukemia has relations: disease_disease with Pre B-cell acute lymphoblastic leukemia, disease_disease with Pre B-cell acute lymphoblastic leukemia.", "label": "no"}
{"original_question": "Is Prochlorococcus the most abundant photosynthetic organism?", "id": "converted_550", "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 dupilumab an antibody targeting the IL-1 receptor?", "id": "converted_551", "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 \u03b1 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 \u03b1-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 \u03b1 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 \u03b1-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: Eczema has relations: phenotype_phenotype with Eczema, phenotype_phenotype with Eczema. dermatitis, atopic has relations: disease_phenotype_positive with Eczema, indication with dupilumab, disease_phenotype_positive with Eczema, indication with dupilumab.", "label": "no"}
{"original_question": "Is Hepatic mesenchymal hamartoma usually a malignant tumor?", "id": "converted_552", "sentence1": "Is Hepatic Mesenchymal hamartoma 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 neoplasm of Abdomen>Liver in children, usually arising from the right Abdomen>Liver lobe and represents about 5 to 6% of all primary Hepatic Neoplasms Hepatic Mesenchymal hamartoma (HMH) is the second most common Benign Hepatic tumor in children Hepatic Mesenchymal hamartoma is a rare Benign tumor in children, and infantile Hepatic hemangioendothelioma is also a rare Liver neoplasms 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 Hepatic Mesenchymal hamartoma, a rare Benign Neoplasm, in a 10-month-old infant. Hepatic Mesenchymal hamartoma is a rare Benign Neoplasm in children. Mesenchymal hamartoma is a Benign lesion best treated by surgical resection, which usually results in cure. Hepatic Mesenchymal hamartoma are rare Benign Neoplasms. Hepatic Mesenchymal hamartoma is a rare Benign tumor in children, and infantile Hepatic hemangioendothelioma is also a rare Liver neoplasms. 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 Hepatic Mesenchymal hamartoma 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: Abdomen>Liver Mesenchymal hamartoma has relations: disease_disease with Mesenchymal hamartoma, disease_disease with Liver neoplasms, disease_disease with Mesenchymal hamartoma, disease_disease with Liver neoplasms.", "label": "no"}
{"original_question": "Are selenium supplements recommended for prostate cancer prevention?", "id": "converted_553", "sentence1": "Are Selenium supplement supplements recommended for Malignant neoplasm of prostate prevention?", "sentence2": "Our meta-analysis in prospective studies demonstrated a significant inverse association between Selenium supplement status and CVD risk within a narrow Selenium supplement range and a null effect of Selenium supplement supplementation on CVD was observed in RCTs. These findings indicate the importance of considering Selenium supplement status, dose and safety in health assessment and future study design. Selenium supplementation of 140 or more \u03bcg/day after diagnosis of nonmetastatic Malignant neoplasm of prostate may increase risk of Malignant neoplasm of prostate mortality. Caution is warranted regarding usage of such supplements among men with Malignant neoplasm of prostate. The SELECT study failed to show any significant risk reduction for prostate cancers ascribable to Selenium supplement and Vitamin E Drug Class supplementations. Vitamin IV solution additives and supplements, including Selenium supplement or Vitamin E Drug Class, have not been proven in clinical trials to prevent Malignant neoplasm of prostate and in the case of Vitamin E has been found to increase the risk of incident Malignant neoplasm of prostate. Ongoing and future trials may further elucidate the role of diet and immunotherapy for prevention of Malignant neoplasm of prostate.[SEP]Relations: Selenium has relations: exposure_disease with Malignant neoplasm of prostate, exposure_disease with Malignant neoplasm of prostate.", "label": "no"}
{"original_question": "Is there any involvement of L1 retrotransposition in the Rett syndrome?", "id": "converted_554", "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 (Rett Syndrome), 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 (Rett Syndrome), 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 (Rett Syndrome), 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 (Rett Syndrome), 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]", "label": "yes"}
{"original_question": "Is Downs syndrome associated with decreased risk of leukemia?", "id": "converted_555", "sentence1": "Is Downs syndrome associated with decreased risk of leukemia?", "sentence2": "The association of Down Syndrome and leukemia has been documented for over 50 years. Multiple studies have established the incidence of leukemia in Down Syndrome patients to be 10- to 20-fold higher than that in the general population. We present a case of congenital acute myeloid leukemia manifesting from the very first day of birth. Diagnosis of acute myeloid leukemia 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 (JMML) and a solitary cases of acute myeloid leukemia (Leukemia, Myelocytic, Acute) in Downs syndrome.  This was thus confirmed to be a case with transient leukemia with Downs syndrome.[SEP]", "label": "no"}
{"original_question": "Does PCSK9 (Proprotein convertase subtilisin/kexin type 9) binds with HDL-receptor (HDL-R)?", "id": "converted_556", "sentence1": "Does PCSK9 protein, Homo sapiens (Proprotein convertase 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 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 subtilisin/kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) binds to the LDLR protein, Homo sapiens, escorting it to\u00a0its 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 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 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 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 subtilisin/kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) binds Low-Density Lipoproteins receptors, targeting them for degradation Proprotein convertase 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 Diseases 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, 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 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 Hyperlipoproteinemia Type IIa family Proprotein convertase subtilisin-kexin type 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 subtilisin-kexin type 9 (PCSK9 protein, Homo sapiens protein, Homo sapiens) plays a key role in Low Density Lipoprotein Receptor processing. Proprotein convertase 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 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 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 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 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: Lysosomes has relations: cellcomp_protein with PCSK9 protein, Homo sapiens, cellcomp_protein with PCSK9 protein, Homo sapiens. Cell surface has relations: cellcomp_protein with PCSK9 protein, Homo sapiens, cellcomp_protein with PCSK9 protein, Homo sapiens.", "label": "no"}
{"original_question": "Is apremilast effective for psoriatic arthritis?", "id": "converted_557", "sentence1": "Is apremilast effective for psoriatic arthritis?", "sentence2": "apremilast, an oral phosphodiesterase 4 inhibitor, in patients with psoriatic arthritis and current Skin Specimen Source Code involvement: a phase III, randomised, controlled trial (PALACE 3). OBJECTIVE: To evaluate apremilast treatment in patients with active psoriatic arthritis, 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 psoriatic arthritis and Psoriasis at week 16; sustained improvements were seen with continued treatment through 52\u2005weeks.  apremilast: A Novel Drug for Treatment of Psoriasis and Arthritis, Psoriatic. OBJECTIVE: To review the pharmacology, efficacy, and safety of apremilast and determine its role relative to other agents in the treatment of Psoriasis and psoriatic arthritis. CONCLUSIONS: apremilast has a novel mechanism of action and is safe and effective for the management of Psoriasis and psoriatic arthritis.   In particular, apremilast has been recently approved for the treatment of Psoriasis and psoriatic arthritis. apremilast, an oral phosphodiesterase 4 inhibitor, has an acceptable safety profile and is effective for treatment of plaque Psoriasis and psoriatic arthritis. 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 psoriatic arthritis (Prostate-Specific Antigen) for whom disease-modifying anti-rheumatic drugs (DMARDs) have been inadequately effective, not tolerated or contraindicated. Arthritis, Psoriatic Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active psoriatic arthritis despite prior traditional disease-modifying antirheumatic Pharmacologic Substance (DMARD) and/or biologic therapy. In patients with psoriatic arthritis, there are no clinical trials comparing apremilast with TNF alpha antagonists, and no interpretable trials of apremilast after failure of a TNF alpha antagonist. Arthritis, Psoriatic Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active psoriatic arthritis 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 psoriatic arthritis, 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 psoriatic arthritis.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 psoriatic arthritis (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 psoriatic arthritis. apremilast is a well-tolerated and effective phosphodiesterase type 4 inhibitor that is indicated for the treatment of moderate-to-severe plaque Psoriasis and psoriatic arthritis. Arthritis, Psoriatic Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active psoriatic arthritis 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 psoriatic arthritis 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 psoriatic arthritis.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 psoriatic arthritis, 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 psoriatic arthritis, 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 psoriatic arthritis.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 psoriatic arthritis, 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 psoriatic arthritis. apremilast, an oral phosphodiesterase 4 inhibitor, demonstrated effectiveness (versus placebo) for treatment of active psoriatic arthritis in the psoriatic arthritis long-term assessment of clinical efficacy (PALACE) phase III clinical trial program. Arthritis, Psoriatic Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active psoriatic arthritis despite prior traditional disease-modifying antirheumatic Pharmacologic Substance (DMARD) and/or biologic therapy. apremilast: A Review in Psoriasis and Arthritis, Psoriatic. Drug safety evaluation of apremilast for treating psoriatic arthritis. apremilast for the treatment of psoriatic arthritis. apremilast mechanism of action and application to Psoriasis and psoriatic arthritis. apremilast: A Phosphodiesterase 4 Inhibitor for the Treatment of Arthritis, Psoriatic.[SEP]Relations: Secukinumab has relations: drug_drug with apremilast, drug_drug with apremilast. psoriatic arthritis has relations: indication with apremilast, indication with apremilast. apremilast has relations: indication with psoriatic arthritis, indication with psoriatic arthritis. Ustekinumab has relations: indication with Psoriasis, indication with psoriatic arthritis, drug_drug with apremilast, indication with Psoriasis, indication with psoriatic arthritis, drug_drug with apremilast.", "label": "yes"}
{"original_question": "Is there any role of TBR1 in autism?", "id": "converted_558", "sentence1": "Is there any role of TBR1 gene in Autistic Disorder?", "sentence2": "TBR1 gene gene 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 Autism Spectrum Disorders (Atrial Septal Defects), including TBR1 gene gene, a master regulator of cortical development. We performed Chromatin Immunoprecipitation Sequencing for TBR1 gene gene during Mus sp. cortical neurogenesis and show that TBR1 gene gene-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 gene gene 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 gene gene binding to identify an appealing subset of candidate Atrial Septal Defects Genes. Our findings highlight a TBR1 gene gene-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 gene gene), a causative gene in Autism Spectrum Disorders (ASDs), encodes a brain-specific T-box transcription factor. It is therefore possible that TBR1 gene gene controls the expression of other Autistic Disorder risk factors. The downstream Genes of TBR1 gene gene have been identified using microarray and promoter analyses. In this study, we annotated individual Genes downstream of TBR1 gene gene and investigated any associations with ASDs through extensive literature searches. Of 124 TBR1 gene gene 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 gene gene 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 gene gene 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 gene gene), a critical neuron-specific transcription factor for forebrain development, has been recognized as a high-confidence risk gene for Autism Spectrum Disorders.  Disruptive Gene Mutation in the TBR1 gene gene gene have been repeatedly identified in patients with Autism 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 gene gene Variant identified in sporadic Autistic Disorder. T-brain-1 (TBR1 gene gene) 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 (-\u2215-) CASP14 gene have indicated critical roles for TBR1 gene gene 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 gene gene. Recently, recurrent de novo disruptive Gene Mutation in the TBR1 gene gene gene have been found in patients with Autism Spectrum Disorders (ASDs). Human genetic studies have identified TBR1 gene gene as a high-confidence risk factor for ASDs. TBR1 gene gene regulates Autistic Disorder risk Genes in the developing neocortex. De novo TBR1 gene gene Gene Mutation in sporadic Autistic Disorder disrupt protein functions. In Homo sapiens, PAX6 gene gene, EOMES gene gene, and TBR1 gene gene have been linked to Intellectual Disability and Autistic Disorder. It is therefore possible that TBR1 gene gene 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 gene gene), a causative gene in Autism Spectrum Disorders (ASDs), encodes a brain-specific T-box transcription factor. Recently, recurrent de novo disruptive Gene Mutation in the TBR1 gene gene gene have been found in patients with Autism Spectrum Disorders (ASDs). Here we demonstrate the power of the approach, performing the first functional analyses of TBR1 gene gene 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 gene gene controls a transcriptional cascade relevant to Autistic Disorder pathogenesis. Disruptive Gene Mutation in the TBR1 gene gene gene have been repeatedly identified in patients with Autism Spectrum Disorders (ASDs). T-Box Brain Protein 1 (TBR1 gene gene), a causative gene in Autism 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 gene gene controls a transcriptional cascade relevant to Autistic Disorder pathogenesis Disruptive Gene Mutation in the TBR1 gene gene gene have been repeatedly identified in patients with Autism Spectrum Disorders (ASDs) Among these 24 Genes, four TRANSCRIPTION FACTOR AUTS2 gene, NFIA protein, human, Nr4a2, and SOX5 gene were found, suggesting that TBR1 gene gene controls a transcriptional cascade relevant to Autistic Disorder pathogenesis. It is therefore possible that TBR1 gene gene controls the expression of other Autistic Disorder risk factors. TBR1 gene gene regulates Autistic Disorder risk Genes in the developing neocortex. De novo TBR1 gene gene Gene Mutation in sporadic Autistic Disorder disrupt protein functions. Our findings highlight a TBR1 gene gene-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: NTNG2 has relations: anatomy_protein_present with Cerebral cortex, anatomy_protein_present with Cerebral cortex. GPC6 has relations: anatomy_protein_present with Cerebral cortex, anatomy_protein_present with Cerebral cortex. GRIN2B has relations: disease_protein with Intellectual Disability, anatomy_protein_present with Cerebral cortex, disease_protein with Intellectual Disability, anatomy_protein_present with Cerebral cortex. EOMES gene has relations: anatomy_protein_present with Cerebral cortex, anatomy_protein_present with Cerebral cortex. Cerebral cortex has relations: anatomy_protein_present with EOMES gene, anatomy_protein_present with EOMES gene.", "label": "yes"}
{"original_question": "Is sonidegib effective for basal cell carcinoma?", "id": "converted_559", "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\u00ae), 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 \u00a9 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 SMO protein, human 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 SMO protein, human Antagonist LDE225 Treatment study.This report provides long-term follow-up data collected up to 12\u00a0months 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\u00a0mg. 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 \u00a9 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: Skin Basal Cell Carcinoma has relations: indication with sonidegib, indication with vismodegib, indication with sonidegib, indication with vismodegib. vismodegib has relations: indication with Skin Basal Cell Carcinoma, indication with Skin Basal Cell Carcinoma. sonidegib has relations: indication with Skin Basal Cell Carcinoma, indication with Skin Basal Cell Carcinoma. Medulloblastoma has relations: disease_phenotype_positive with Medulloblastoma, disease_phenotype_positive with Medulloblastoma.", "label": "yes"}
{"original_question": "Is there a sequence bias in MNase digestion patterns?", "id": "converted_560", "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]", "label": "yes"}
{"original_question": "Is NEMO a zinc finger protein?", "id": "converted_561", "sentence1": "Is NF-Kappa-B Essential Modulator a Zinc Fingers Protein Info?", "sentence2": "To better understand the thermodynamics and dynamics of the Zinc Fingers of NF-Kappa-B Essential Modulator (NF-\u03baB essential modulator) an alteration in the Zinc Fingers Superkingdom (taxonomic category) of NF-Kappa-B Essential Modulator (K392R)  CYLD protein, human Protein Info, human and the NF-Kappa-B Essential Modulator Zinc Finger Regulate Tumor Necrosis Factor Signaling and Early Embryogenesis. our simulations of the Zinc Fingers NF-Kappa-B Essential Modulator An important regulatory Superkingdom (taxonomic category) of NF-[Formula: see text]B Essential Modulator (NF-Kappa-B Essential Modulator) is a ubiquitin-binding Zinc Fingers, with a tetrahedral CYS3HIS1 zinc-coordinating Ligand Binding Domain. NF-Kappa-B Essential Modulator function is mediated by two distal ubiquitin binding domains located in the regulatory C-terminal Superkingdom (taxonomic category) of the Protein Info: the coiled-coil 2-leucine zipper (CC2-LZ) Superkingdom (taxonomic category) and the Zinc Fingers (ZF) Superkingdom (taxonomic category).   We show here that the NF-Kappa-B Essential Modulator C terminus, comprising the ubiquitin binding region and a Zinc Fingers,[SEP]", "label": "yes"}
{"original_question": "Does TFIIS affect nucleosome positioning?", "id": "converted_562", "sentence1": "Does TCEA1 wt Allele affect nucleosome location positioning?", "sentence2": "RNA RNA 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 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. RNA RNA 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]", "label": "yes"}
{"original_question": "Is tretinoin effective for photoaging?", "id": "converted_563", "sentence1": "Is tretinoin effective for photoaging?", "sentence2": "Background. Tretinoin has been shown to improve photoaged Skin Specimen Source Code. This study was designed to evaluate the efficacy and tolerability of a 5% retinoic acid Peeling of Skin Specimen Source Code combined with microdermabrasion for facial photoaging. .Conclusion. This study demonstrated that 5% retinoic acid Peeling of Skin Specimen Source Code Emollient Cream combined with microdermabrasion was safe and effective in the treatment of photoaging in the Iranian population.  CONCLUSIONS: Treatment with a double-conjugate retinoid Emollient Cream demonstrated early reductions in photodamage and improvements in Hydration. AHA-Ret induced less Erythema vs all-trans-all-trans-retinol and was more tolerable vs all-trans-all-trans-retinol and tretinoin. These comparative products include prescription tretinoin, physician strength idebenone, kinetin, polyhydroxy, lactic and glycolic acid in reversing signs of photoaging. CONCLUSION: Either topical tretinoin (0.25%) or all-trans-all-trans-retinol (0.25%) can be used safely and effectively when applied in office immediately after SA peeling to ameliorate signs of photoaging. CONCLUSION: The treatment outcome of Retinol 0.2%/LR2412 2% Emollient Cream does not differ from the one of tretinoin 0.025% Emollient Cream. Clinical results were not statistically different.  INTRODUCTION: Topical tretinoin is considered the gold standard to treat photoaged Skin Specimen Source Code, but it is associated with side effects and only available upon prescription. Tretinoin is commonly used topically for Acne Vulgaris treatment and in the treatment of photoaging. BACKGROUND: Topical tretinoin is effective treatment for both Acne Vulgaris and photoaging. The efficacy of tretinoin is well established in the treatment of Acne Vulgaris and photoaged Skin Specimen Source Code, however as a typical side effect of tretinoin treatment most patients develop a low-grade irritant dermatitis. Topical tretinoin is established as an effective treatment for photoaging. BACKGROUND Topical tretinoin is effective treatment for both Acne Vulgaris and photoaging. Tretinoin is the only pharmacologic compound shown to partially reverse some signs of photoaging. Although once considered an irreversible process, it is now established that photoaging can be treated by topical tretinoin. Moreover, studies that have elucidated photoaging pathophysiology have produced significant evidence that topical tretinoin (all-trans retinoic acid), the only agent approved so far for the treatment of photoaging, also works to prevent it. BACKGROUND AND DESIGN The efficacy of topical tretinoin (tretinoin) in treating photoaging is well established. MAJOR CONCLUSIONS Tretinoin can be used for photoaging treatment or combined treatment by different mechanisms. Tretinoin is still the best tested retinoid to reverse photoaged Skin Specimen Source Code. The separation between clinical improvement and irritation suggests that mechanisms other than irritation dominate tretinoin-induced repair of photoaging in Homo sapiens. * A Emollient Cream containing 0.05% tretinoin (Retinova((R)) is approved for treatment of sun-induced Skin Specimen Source Code damage (\"photoaging\"). Randomized, controlled trials have shown that topical tretinoin is effective in the treatment of photoaged Skin Specimen Source Code. Tretinoin has been shown to improve photoaged Skin Specimen Source Code. Topical tretinoin is effective treatment for both Acne Vulgaris and photoaging. Randomized, controlled trials have shown that topical tretinoin is effective in the treatment of photoaged Skin Specimen Source Code.. Tretinoin emollient Emollient Cream 0.05% appears to be safe and effective in the treatment of photodamaged Skin Specimen Source Code.. Topical tretinoin improves photoaged Skin Specimen Source Code. A double-blind vehicle-controlled study.[SEP]Relations: Tretinoin has relations: drug_effect with Erythema, drug_effect with Erythema.", "label": "yes"}
{"original_question": "Does TUC.338 inhibit colorectal cancer?", "id": "converted_564", "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: 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. colorectal carcinoma has relations: disease_disease with Malignant neoplasm of colon and/or rectum, disease_disease with Malignant neoplasm of colon and/or rectum.", "label": "no"}
{"original_question": "Has ruxolitinib received FDA approval?", "id": "converted_565", "sentence1": "Has ruxolitinib received FDA approval?", "sentence2": "Testing for Janus kinase 2 mutations is now included in the World Health Organization (WHO) criteria for the diagnosis of Myeloproliferative disease, and in 2011 the oral Janus kinase 2 kinase inhibitor ruxolitinib became the first Food and Drug Administration (FDA)-approved drug for the treatment of Primary Myelofibrosis.[SEP]Relations: Ruxolitinib has relations: drug_protein with Janus kinase 2, indication with Primary Myelofibrosis, drug_protein with Janus kinase 2, indication with Primary Myelofibrosis. primary Primary Myelofibrosis has relations: disease_protein with Janus kinase 2, disease_protein with Janus kinase 2.", "label": "yes"}
{"original_question": "Does deflazacort have more side effects than prednisone?", "id": "converted_566", "sentence1": "Does deflazacort have more side effects than prednisone?", "sentence2": "Though deflazacort and prednisone improve clinical endpoints in Muscular Dystrophy, Duchenne (DMD) patients, deflazacort produces fewer side effects.[SEP]Relations: deflazacort has relations: indication with Muscular Dystrophy, Duchenne, indication with Muscular Dystrophy, Duchenne. Muscular Dystrophy, Duchenne has relations: indication with deflazacort, indication with deflazacort.", "label": "no"}
{"original_question": "Does echinacea increase anaphylaxis risk?", "id": "converted_567", "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]", "label": "yes"}
{"original_question": "Are neurexins localized at pre-synapses?", "id": "converted_568", "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 NRXN1 gene[SEP]", "label": "yes"}
{"original_question": "Is there any role of 5hmC in T-cell development and differentiation?", "id": "converted_569", "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\u00a0cell differentiation ex\u00a0vivo at Genes and cell-specific enhancers with known T\u00a0cell function. Our results support 5hmC-mediated DNA de-methylation as a key component of CD4(+) T\u00a0cell 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\u00a0cell malignancies and Autoimmune Diseases.[SEP]", "label": "yes"}
{"original_question": "Are there ultraconserved genomic regions in the budding yeast?", "id": "converted_570", "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]", "label": "yes"}
{"original_question": "Is davunetide being considered for the treatment of progressive supranuclear palsy?", "id": "converted_571", "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]", "label": "yes"}
{"original_question": "Is autophagy modulated in a circadian fashion?", "id": "converted_572", "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]", "label": "yes"}
{"original_question": "Is Drk essential for anesthesia-resistant memory (ARM) in Drosophila?", "id": "converted_573", "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]", "label": "yes"}
{"original_question": "Are TAD boundaries in Drosophila depleted in highly-expressed genes?", "id": "converted_574", "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]", "label": "no"}
{"original_question": "Is there increased recombination rate in human regulatory domains?", "id": "converted_575", "sentence1": "Is there increased recombination rate in Homo sapiens regulatory domains?", "sentence2": "Evidence of reduced recombination rate in Homo sapiens regulatory domains. We study the relationship between recombination rate and gene regulatory domains, defined by a gene and its linked control elements. We define these links using expression Quantitative Trait Loci (eQTLs), methylation Quantitative Trait Loci (meQTLs), chromatin conformation from publicly available datasets\u00a0(Hi-C and ChIA-PET), and correlated activity links that we infer across cell types. Each link type shows a \"recombination rate\u00a0valley\" of significantly reduced recombination rate compared to matched control regions. This recombination rate\u00a0valley is most pronounced for gene regulatory domains of early embryonic development Genes, Genes, Housekeeping, and constitutive regulatory elements, which are known to show increased evolutionary constraint across species. Recombination rate\u00a0valleys show increased DNA methylation, reduced doublestranded break initiation, and increased repair efficiency, specifically in the lineage leading to the Germ Line. Moreover, by using only the overlap of functional links and DNA methylation in Germ Cells, we are able to predict the recombination rate with high accuracy.CONCLUSIONS: Our results suggest the existence of a recombination rate valley at regulatory domains and provide a potential molecular mechanism to interpret the interplay between Genetic and epigenetic variations.[SEP]", "label": "no"}
{"original_question": "Is enzastaurin effective treatment of glioblastoma?", "id": "converted_576", "sentence1": "Is enzastaurin effective 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).  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. CONCLUSIONS: PFS-6 missed the primary planned outcome of 55%.  OS (median, 74 weeks) and PFS (median, 36 weeks) results from the current trial were comparable to those from a prior phase II study using erlotinib and were significantly better than those from 2 other previous studies that used thalidomide or isotretinoin, all in combination with temozolomide plus RT.  More recently, Angiogenesis Inhibitors including enzastaurin, cediranib, bevacizumab, and others that target mainly the VEGF pathway, have been evaluated in this highly angiogenic disease. Among them, only bevacizumab has been associated with clear anti-tumor activity, although the lack of control studies limits the impact of the results to date. 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. Several signal transduction inhibitors have been examined in preclinical and clinical malignant glioma trials, including Angiogenesis Inhibitors (bevacizumab, enzastaurin), and inhibitors of ErbB Receptors (gefitinib and erlotinib), mammalian target of rapamycin (temsirolimus, everolimus) and Integrins (Cilengitide). Although preliminary clinical results of the use of targeted agents have not translated into significantly better survival, more recent phase II trials are exploring the combination of multitargeted drugs with cytotoxic chemotherapy and radiotherapy in order to overcome the resistance of Neoplasms to single-agent targeted therapies. Several drugs have been tested, including epidermal growth factor receptor (Epidermal Growth Factor Receptor) Protein-tyrosine kinase inhibitor (disposition) (gefitinib and erlotinib), mammalian target of rapamycin (mTOR) inhibitors (temsirolimus and everolimus), and Vascular Endothelial Growth Factor Receptor-1 (Vascular Endothelial Growth Factor Receptor), protein kinase C-beta, and other angiogenesis pathways inhibitors (vatalanib, bevacizumab, and enzastaurin). Although preliminary efficacy results of most trials in recurrent disease have fallen short on expectations, substantial advances have been achieved by associated translational research.  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.[SEP]Relations: Gefitinib has relations: drug_protein with Epidermal Growth Factor Receptor, drug_protein with Epidermal Growth Factor Receptor. Erlotinib has relations: drug_protein with Epidermal Growth Factor Receptor, drug_protein with Epidermal Growth Factor Receptor. Integrins binding has relations: molfunc_protein with Epidermal Growth Factor Receptor, molfunc_protein with Epidermal Growth Factor Receptor. Vandetanib has relations: drug_protein with Epidermal Growth Factor Receptor, drug_protein with Epidermal Growth Factor Receptor.", "label": "no"}
{"original_question": "Is dasatinib effective for treatment of glioblastoma?", "id": "converted_577", "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]", "label": "no"}
{"original_question": "Has IVIG been tested in clinical trials for the treatment of Alzheimer's disease?", "id": "converted_578", "sentence1": "Has immunoglobulins, intravenous been tested in clinical trials for the treatment of ALZHEIMER DISEASE, FAMILIAL, 1?", "sentence2": "Clinical trials of intravenous immunoglobulin for ALZHEIMER DISEASE, FAMILIAL, 1. Preclinical and clinical studies have shown that immunoglobulins, intravenous has anti-amyloid and immune modulatory properties relevant to treating Neurodegenerative Disorders. In early stage cytarabine/daunorubicin protocol clinical trials, immunoglobulins, intravenous was found to reduce Mental deterioration and increase brain glucose metabolism. Unfortunately, immunoglobulins, intravenous 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 immunoglobulins, intravenous to treat cytarabine/daunorubicin protocol at the doses tested, additional studies of immunoglobulins, intravenous's mechanisms are warranted and may guide the development of more effective therapies for cytarabine/daunorubicin protocol in the future.[SEP]", "label": "yes"}
{"original_question": "Does a tonsillectomy affect the patient's voice?", "id": "converted_579", "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 \u2264 .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]", "label": "yes"}
{"original_question": "Do cephalopods use RNA editing less frequently than other species?", "id": "converted_580", "sentence1": "Do Cephalopoda use RNA Editing less frequently than other species?", "sentence2": "Extensive messenger RNA Editing generates transcript and Protein Info diversity in Genes involved in Neural excitability, as previously described, as well as in Genes participating in a broad range of other cellular functions By adopting a method originally designed to detect linkage disequilibrium of DNA mutations, we examined the editomes of ten metazoan species and detected extensive linkage of editing in Drosophila <basidiomycetes> <basidiomycetes> and Cephalopoda. We here show that RNA Editing is particularly common in behaviorally sophisticated coleoid Cephalopoda, with tens of\u00a0thousands of evolutionarily conserved sites. Even for the subset of RNA Editing sites shared by deeply divergent cephalopod lineages, the primary effect of nuclear editing is an increase-not a decrease-in Protein Info divergence. Coleoid Cephalopoda (octopus, Superconducting Quantum Interference Device and Cuttlefish, Dietary) are active, resourceful predators with a rich behavioural repertoire. We identified hundreds of cephalopod-specific Genes, many of which showed elevated expression levels in such specialized structures as the Skin Specimen Source Code, the Suction Tips and the nervous system. Our analysis suggests that substantial expansion of a handful of gene families, along with extensive remodelling of Genome - anatomical entity linkage and repetitive content, played a critical role in the evolution of cephalopod morphological innovations, including their large and complex nervous systems.[SEP]", "label": "no"}
{"original_question": "Is there an RNAi drug being developed to treat amyloidosis?", "id": "converted_581", "sentence1": "Is there an RNAi drug being developed to treat Primary amyloidosis?", "sentence2": "Patisiran is an investigational RNA interference (RNAi) therapeutic in development for the treatment of hereditary ATTR (hATTR) Primary Primary amyloidosis, a progressive disease associated with significant disability, morbidity, and mortality.[SEP]", "label": "yes"}
{"original_question": "Are there RNAi approaches considered for the treatment of kidney injury?", "id": "converted_582", "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 Injury of kidney.  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]", "label": "yes"}
{"original_question": "Is propranolol used for treatment of infantile hemangioma?", "id": "converted_583", "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: indication with Hemangioma, indication with Hemangioma. capillary Infantile Hemangioma has relations: disease_disease with Hemangioma, disease_disease with Hemangioma.", "label": "yes"}
{"original_question": "Can the CEP290 gene mutations be targeted by AAV-mediated gene therapy?", "id": "converted_584", "sentence1": "Can the CEP290 gene mutations be targeted by AAV-mediated gene therapy?", "sentence2": "The large size of the CEP290 gene prevents its use in adeno-associated virus (AAV)-mediated gene augmentation therapy.[SEP]", "label": "no"}
{"original_question": "Are mutations in the nf1 gene associated with memory?", "id": "converted_585", "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.", "label": "yes"}
{"original_question": "Is ACI-35 a passive vaccine?", "id": "converted_586", "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": "Is DNA methylation correlated with nucleosome occupancy?", "id": "converted_587", "sentence1": "Is DNA methylation correlated with nucleosome location occupancy?", "sentence2": "Here I show that CpG Islands were associated not only with methylation-free Promoter but also with nucleosome location location-free Promoter. Nucleosome-free regions were observed only in Promoter containing a CpG island In contrast to the methylation-and nucleosome location location-free states of CpG-island Promoter, 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 Promoter 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 Promoter 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 Promoter.  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 Promoter 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 Promoter. 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 Promoter is directly correlated to expression level and can accommodate multiple Nucleosomes and provide Genome - anatomical entity-wide evidence that expressed non-CpG island Promoter are nucleosome location location-depleted.[SEP]", "label": "yes"}
{"original_question": "Does DDX54 play a role in DNA damage response?", "id": "converted_588", "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]", "label": "yes"}
{"original_question": "Do chromatin features predict genes associated with eQTLs?", "id": "converted_589", "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]", "label": "yes"}
{"original_question": "Is Kummell\u2019s disease an avascular necrosis of the vertebral body?", "id": "converted_590", "sentence1": "Is Kummell\u2019s 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: Bone structure of thoracic vertebra 1 has relations: anatomy_anatomy with Bone structure of thoracic vertebra, anatomy_anatomy with Bone structure of thoracic vertebra.", "label": "yes"}
{"original_question": "Are Conserved Nonexonic Elements (CNEEs) important in phylogenomics research?", "id": "converted_591", "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 the yeast protein Abf1 act as insulator?", "id": "converted_592", "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 there any linear-time and linear-space algorithm for the computation of avoided words in biological sequences?", "id": "converted_593", "sentence1": "Is there any linear-time and linear-space algorithm for the computation of avoided words in biological sequences?", "sentence2": "The systematic search for avoided words is particularly useful for biological Sequence - ParameterizedDataType analysis. We present a linear-time and linear-space algorithm for the computation of avoided words of lengthkin a given sequencex. We suggest a ResponseLevel - ResponseLevel - modification to this algorithm so that it computes all avoided words ofx, irrespective of their length, within the same time complexity. We also present combinatorial results with regards to avoided words and absent words. We present a linear-time and linear-space algorithm for the computation of avoided words of length <br> <b>BACKGROUND</b>: The deviation of the observed frequency of a word <br><b>RESULTS</b>: In this article, we propose an [Formula: see text]-time and [Formula: see text]-space algorithm to compute all [Formula: see text]-avoided words of length <br><b>CONCLUSIONS</b>: The systematic search for avoided words is particularly useful for biological Sequence - ParameterizedDataType analysis. We present a linear-time and linear-space algorithm for the computation of avoided words of length We present a linear-time and linear-space algorithm for the computation of avoided words of length k in a given Sequence - ParameterizedDataType x. Hence, computing all such words na\u00efvely can be a very time-consuming procedure, in particular for large k.   RESULTS In this article, we propose an [Formula: see text]-time and [Formula: see text]-space algorithm to compute all [Formula: see text]-avoided words of length k in a given Sequence - ParameterizedDataType of length n over a fixed-sized alphabet. We also present a time-optimal [Formula: see text]-time algorithm to compute all [Formula: see text]-avoided words (of any length) in a Sequence - ParameterizedDataType of length n over an integer alphabet of size [Formula: see text]. the deviation of the observed frequency of a word from its Expected (qualifier) frequency in a given Sequence - ParameterizedDataType is used to determine whether or not the word is this concept is particularly useful in dna linguistic analysis the value of the deviation of denoted by formula see text effectively characterises the extent of a word by its edge contrast in the context in which it occurs a word of length formula see text is a formula see text avoided word in if formula see text for a given threshold formula see text notice that such a word may be completely from hence computing all such words na\u00efvely can be a very time consuming procedure in particular for large in this article we propose an formula see text time and formula see text space algorithm to compute all formula see text avoided words of length in a given Sequence - ParameterizedDataType of length over a fixed sized alphabet we also present a time optimal formula see text time algorithm to compute all formula see text avoided words of any length in a Sequence - ParameterizedDataType of length over an integer alphabet of size formula see text in addition we provide a tight asymptotic upper bound for the number of formula see text avoided words over an integer alphabet and the Expected (qualifier) length of the longest one we make available an implementation of our algorithm experimental results using both real and synthetic data show the efficiency and applicability of our implementation in biological Sequence - ParameterizedDataType analysis the systematic search for avoided words is particularly useful for biological Sequence - ParameterizedDataType analysis we present a linear time and linear space algorithm for the computation of avoided words of length in a given Sequence - ParameterizedDataType we suggest a ResponseLevel - ResponseLevel - modification to this algorithm so that it computes all avoided words of irrespective of their length within the same time complexity we also present combinatorial results with regards to avoided words and absent words.[SEP]", "label": "yes"}
{"original_question": "Is a CpG island methylator phenotype involved in ependymomas?", "id": "converted_594", "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 Genes 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 - Tumor Suppressor Genes involved in the control of cell growth and Cessation of life. Supratentorial and Spinal 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 - 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 - 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 Genes 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 - 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 Genes 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 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 - 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 - 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 Genes 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]", "label": "yes"}
{"original_question": "Are loop domains preserved upon cohesin loss?", "id": "converted_595", "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]", "label": "no"}
{"original_question": "Does the association of PARP1 and CTCF follow a circadian rhythm?", "id": "converted_596", "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 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.", "label": "yes"}
{"original_question": "Was saracatinib being considered as a treatment for Alzheimer's disease in November 2017?", "id": "converted_597", "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 src-Family Kinases, 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\u00a0mg, 100\u00a0mg, 125\u00a0mg, or placebo daily for 4\u00a0weeks.  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\u00a0mg. 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]", "label": "yes"}
{"original_question": "Are mouse chromosomes acrocentric?", "id": "converted_598", "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]", "label": "yes"}
{"original_question": "Is overproduction of transthyretin is associated with amyloidosis associated neuropathy?", "id": "converted_599", "sentence1": "Is overproduction of Prealbumin is associated with Primary amyloidosis associated Neuropathy?", "sentence2": "Transthyretin-associated familial Serum Serum amyloid A protein A protein polyneuropathy (TTR protein, human protein, human-FAP) is a Disease caused by the deposit of abnormal Prealbumin on Body tissue, mainly nerves Prealbumin familial Serum Serum amyloid A protein A protein polyneuropathy We report a new Prealbumin (TTR protein, human protein, human wt Allele) gene c.272C>G mutation and Mutant Proteins, p.Leu32Val, in a kindred of Bolivian origin with a rapid progressive Peripheral Nervous System Diseases and cardiomyopat AMYLOIDOSIS, HEREDITARY, TRANSTHYRETIN-RELATED is an autosomal dominant inherited disorder, first described in families with sensorimotor and Autonomic Neuropathy. Abnormal deposition of aggregated wild-type (WT) human Prealbumin (TTR protein, human protein, human) and its pathogenic variants is responsible for Cardiomyopathies and Neuropathy related to TTR protein, human protein, human Primary Primary amyloidosis.  Transthyretin (TTR protein, human protein, human), normally a plasma circulating protein, can become misfolded and aggregated, ultimately leading to Extracellular deposition of Serum Serum amyloid A protein A protein fibrils usually targeted to Chest>Heart or nerve Body tissue. Referred to as TTR protein, human protein, human-associated amyloidoses (TTR protein, human protein, human wt Allele), this group of diseases is frequently life threatening and fatal if untreated AMYLOIDOSIS, HEREDITARY, TRANSTHYRETIN-RELATED is an autosomal dominant inherited disorder, first described in families with sensorimotor and Autonomic Neuropathy. AMYLOIDOSIS, HEREDITARY, TRANSTHYRETIN-RELATED (TTR protein, human protein, human wt Allele) is usually characterised by a progressive Peripheral and Autonomic Neuropathy often with associated Congestive Chest>Heart failure and is due to dominantly inherited Prealbumin mutations causing accelerated Serum Serum amyloid A protein A protein deposition.[SEP]Relations: Peripheral nervous system Disease has relations: disease_disease with Peripheral Nervous System Diseases, disease_disease with Peripheral Nervous System Diseases. Extracellular space has relations: cellcomp_protein with TTR protein, human, cellcomp_protein with TTR protein, human. Serum amyloid A protein fibril formation has relations: bioprocess_protein with TTR protein, human, bioprocess_protein with TTR protein, human. Autonomic Neuropathy has relations: disease_disease with Peripheral Nervous System Diseases, disease_disease with Peripheral Nervous System Diseases.", "label": "yes"}
{"original_question": "Is patisiran currently (November 2017) in clinical phase II trials?", "id": "converted_600", "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]", "label": "no"}
{"original_question": "Is Solanezumab effective for Alzheimer's Disease?", "id": "converted_601", "sentence1": "Is Solanezumab effective for Alzheimer's Disease?", "sentence2": "An analysis of publicly available data from the Phase II studies for bapineuzumab and solanezumab indicates that neither compound produced compelling evidence of drug-like behavior that would justify their progression into pivotal trials.  Notably, a recent study of solanezumab, an Serum Serum amyloid A protein A protein \u03b2 monoclonal antibody, raises hope for the further therapeutic potential of immunotherapy, not only in ALZHEIMER DISEASE, FAMILIAL, 1, but also for other Neurodegenerative Disorders, including Parkinson Disease.  For example, Eli Lilly announced a major change to its closely watched clinical trial for the Alzheimer's drug solanezumab which failed to reach statistical significance.  Areas covered: This contradiction prompted us to review all study phases of Intravenous Immunoglobulin (immunoglobulins, intravenous), bapineuzumab, Solanezumab, Avagacestat and latrepirdine to shed more light on these recent failures.   Results from phase III clinical trials in mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) patients with two Monoclonal Antibodies bapineuzumab and solanezumab and intravenous immunoglobulin have been disappointing. Subsequent analysis of pooled data from both phase III trials with solanezumab showed a reduction in Mental deterioration in patients with mild cytarabine/daunorubicin protocol. Secondary analyses of EXPEDITION studies suggested a smaller functional effect of solanezumab relative to cognition. An increasing effect of solanezumab over 18\u00a0months was shown for cognition and function. RESULTS: In the mild cytarabine/daunorubicin protocol population, less cognitive and functional decline was observed with solanezumab (n\u00a0=\u00a0659) versus placebo (n\u00a0=\u00a0663), measured by Alzheimer's Disease Assessment Scale Cognitive subscale, Mini-Mental State Examination, and Alzheimer's Disease Cooperative Study-Activities of Daily Living functional scale Instrumental ADLs.  The promising results obtained with aducanumab and solanezumab against ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) strengthen the vaccine approach to prevent cytarabine/daunorubicin protocol, despite of the many clinical setbacks.  CONCLUSIONS: Solanezumab, a Antibodies, Monoclonal, Humanized that binds Serum Serum amyloid A protein A protein, failed to improve cognition or functional ability.  Results from phase III clinical trials in mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) patients with two Monoclonal Antibodies bapineuzumab and solanezumab and intravenous immunoglobulin have been disappointing.[SEP]Relations: bapineuzumab has relations: drug_drug with Solanezumab, drug_drug with Solanezumab. Solanezumab has relations: drug_drug with bapineuzumab, drug_drug with bapineuzumab.", "label": "no"}
{"original_question": "Are there mammalian promoters with distal enhancer functions?", "id": "converted_602", "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]", "label": "yes"}
{"original_question": "Is autosomal dominant inheritanced form of Osteogenesis imperfecta caused by mutations in the genes associated with collagen production?", "id": "converted_603", "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 Fracture. 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 type I collagen  Osteogenesis Imperfecta (OI) is a group of Hereditary Diseases characterized by low bone mass and recurrent Fracture. Most OI cases follow an Autosome dominant pattern of inheritance and are attributed to Gene Mutation in Genes encoding type I collagen (COL1A1 gene gene/alpha 2 collagen type I).  Osteogenesis Imperfecta (OI) is a genetic disorder characterised by low bone mineral density resulting in Fracture. 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 Fracture, and range in severity from a subtle increase in fracture frequency to Cessation of life in the perinatal period. Most patients have defects in type I collagen 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 type I collagen, 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 Fracture 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 pro\u03b11(I) and pro\u03b12(I) chains of collagen type I are encoded by the COL1A1 gene gene and alpha 2 collagen type I Genes, respectively; quantitative or qualitative defects in type I collagen 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 type I collagen, 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 type I collagen. Autosomal dominant osteogenesis imperfecta is caused by Gene Mutation in the alpha 2 collagen type I and COL1A1 gene gene Genes of type I collagen.  Osteogenesis Imperfecta is caused by dominant Autosome Gene Mutation in the type I collagen 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 type I collagen. In approximately 90% of individuals with osteogenesis imperfecta, Gene Mutation in either of the Genes encoding the pro-alpha1 or pro-alpha2 chains of type I collagen (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 type I collagen. ext-generation sequencing technology was used to screen a panel of known OI Genes.RESULTS: In 41 probands, we identified 28 different disease-causing Variant of 9 different known OI Genes. Eleven of the Variant are novel. Ten of the 28 Variant 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 Fracture after minimal Trauma, nursing specialty. OI type V has an Autosome-dominant pattern of inheritance and is not caused by Gene Mutation in the type I collagen 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 type I collagen. 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 type I collagen Genes COL1A1 gene gene and alpha 2 collagen type I.[SEP]Relations: Connective Tissue has relations: anatomy_protein_present with COL1A1 gene, anatomy_protein_present with BMP1 protein, human, anatomy_protein_present with alpha 2 collagen type I, anatomy_protein_present with SERPINH1 gene, anatomy_protein_present with SERPINF1 gene, anatomy_protein_present with TMEM38B gene, anatomy_protein_present with COL1A1 gene, anatomy_protein_present with BMP1 protein, human, anatomy_protein_present with alpha 2 collagen type I, anatomy_protein_present with SERPINH1 gene, anatomy_protein_present with SERPINF1 gene, anatomy_protein_present with TMEM38B gene. Hearing impairment has relations: disease_phenotype_positive with Dentinogenesis imperfecta without osteogenesis imperfecta, disease_phenotype_positive with Dentinogenesis imperfecta without osteogenesis imperfecta. SERPINF1 gene has relations: anatomy_protein_present with Connective Tissue, anatomy_protein_present with Connective Tissue. collagen type I trimer has relations: cellcomp_protein with COL1A1 gene, cellcomp_protein with alpha 2 collagen type I, cellcomp_protein with COL1A1 gene, cellcomp_protein with alpha 2 collagen type I, cellcomp_protein with COL1A1 gene, cellcomp_protein with alpha 2 collagen type I, cellcomp_protein with COL1A1 gene, cellcomp_protein with alpha 2 collagen type I. Autosomal dominant inheritance has relations: disease_phenotype_positive with Dentinogenesis imperfecta without osteogenesis imperfecta, disease_phenotype_positive with Dentinogenesis imperfecta without osteogenesis imperfecta. TMEM38B gene has relations: anatomy_protein_present with Connective Tissue, anatomy_protein_present with Connective Tissue. Hyperextensibility at elbow has relations: disease_phenotype_positive with Dentinogenesis imperfecta without osteogenesis imperfecta, disease_phenotype_positive with Dentinogenesis imperfecta without osteogenesis imperfecta. osteogenesis imperfecta has relations: disease_protein with SERPINF1 gene, disease_protein with COL1A1 gene, disease_protein with SERPINH1 gene, disease_protein with BMP1 protein, human, disease_protein with alpha 2 collagen type I, disease_protein with TMEM38B gene, disease_protein with SERPINF1 gene, disease_protein with COL1A1 gene, disease_protein with SERPINH1 gene, disease_protein with BMP1 protein, human, disease_protein with alpha 2 collagen type I, disease_protein with TMEM38B gene, disease_protein with SERPINF1 gene, disease_protein with COL1A1 gene, disease_protein with SERPINH1 gene, disease_protein with BMP1 protein, human, disease_protein with alpha 2 collagen type I, disease_protein with TMEM38B gene, disease_protein with SERPINF1 gene, disease_protein with COL1A1 gene, disease_protein with SERPINH1 gene, disease_protein with BMP1 protein, human, disease_protein with alpha 2 collagen type I, disease_protein with TMEM38B gene. COL1A1 gene has relations: protein_protein with alpha 2 collagen type I, anatomy_protein_present with Connective Tissue, protein_protein with alpha 2 collagen type I, anatomy_protein_present with Connective Tissue. Blue sclerae has relations: disease_phenotype_positive with Dentinogenesis imperfecta without osteogenesis imperfecta, disease_phenotype_positive with Dentinogenesis imperfecta without osteogenesis imperfecta. SERPINH1 gene has relations: anatomy_protein_present with Connective Tissue, anatomy_protein_present with Connective Tissue.", "label": "yes"}
{"original_question": "Are splicing speckles associated with transcription?", "id": "converted_604", "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: germ cell Cell Nucleus has relations: cellcomp_cellcomp with Cell Nucleus, cellcomp_cellcomp with Cell Nucleus.", "label": "no"}
{"original_question": "Is Tofacitinib effective for Ulcerative Colitis?", "id": "converted_605", "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 na\u00efve 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 JAK1 protein, human PPP1R1A gene, 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 JAK1 protein, human PPP1R1A gene, 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 JAK1 protein, human PPP1R1A gene, 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 JAK1 protein, human PPP1R1A gene, 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 JAK1 protein, human PPP1R1A gene, 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 JAK1 protein, human PPP1R1A gene, 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 JAK1 protein, human PPP1R1A gene, 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 JAK1 protein, human PPP1R1A gene, 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 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 \u03b1 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 tnf\u03b1 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: indication with Rheumatoid Arthritis, indication with Rheumatoid Arthritis. Protein S human has relations: drug_drug with tofacitinib, drug_drug with tofacitinib. ulcerative colitis (disease) has relations: disease_disease with Distal colitis, disease_disease with Distal colitis. Golimumab has relations: drug_drug with tofacitinib, indication with INFLAMMATORY BOWEL DISEASE 2, indication with Rheumatoid Arthritis, drug_drug with tofacitinib, indication with INFLAMMATORY BOWEL DISEASE 2, indication with Rheumatoid Arthritis. 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. Rheumatoid arthritis has relations: disease_phenotype_positive with Rheumatoid Arthritis, disease_phenotype_positive with Rheumatoid Arthritis.", "label": "yes"}
{"original_question": "Is CREB a key memory protein?", "id": "converted_606", "sentence1": "Is Cyclic AMP-Responsive DNA-Binding Protein a key memory protein?", "sentence2": "Homo sapiens cyclic AMP response element Protein Binding (Cyclic AMP-Responsive DNA-Binding Protein) transcription factor which plays a crucial role in memory The activated Cyclic AMP-Responsive DNA-Binding Protein is implicated in the regulation of development, protection, learning, memory and plasticity in the nerve system.  A mouse genetic study showed that ATF2 protein, human (Cyclic AMP-Responsive DNA-Binding Protein)-mediated transcription is required for the formation of social recognition memory. Transcription factor cAMP response element-Protein Binding (Cyclic AMP-Responsive DNA-Binding Protein) plays a critical role in memory formation. It is well known that Molecule like cAMP response element binding (Cyclic AMP-Responsive DNA-Binding Protein) and Protein Binding (1-Chloro-3-bromopropene-1) play a crucial role in memory consolidation.  Cyclic AMP-Responsive DNA-Binding Protein SUMOylation by the ubiquitin-protein ligase PIAS1 protein, human protein, human enhances spatial memory. Therefore, Cyclic AMP-Responsive DNA-Binding Protein phosphorylation may be responsible for signal transduction during the early phase of long-term memory formation, whereas Cyclic AMP-Responsive DNA-Binding Protein SUMOylation sustains long-term memory[SEP]Relations: protein binding has relations: molfunc_protein with PIAS1 protein, human, molfunc_protein with PIAS1 protein, human.", "label": "yes"}
{"original_question": "Is cilengitide effective for treatment of glioblastoma?", "id": "converted_607", "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 av\u03b23 and av\u03b25 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 \u03b23 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\u2009+\u2009RAD 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 \u03b1v\u03b23 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]", "label": "no"}
{"original_question": "Can multiple myeloma patients develop hyperviscosity syndrome?", "id": "converted_608", "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 Waldenstr\u00f6m'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 Waldenstr\u00f6m'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: Cryofibrinogenemia has relations: disease_disease with Cryoglobulinemia, disease_disease with Cryoglobulinemia. Cryoglobulinemia has relations: disease_disease with Cryofibrinogenemia, disease_disease with Cryofibrinogenemia.", "label": "yes"}
{"original_question": "Does the human lncRNA LINC-PINT promote tumorigenesis?", "id": "converted_609", "sentence1": "Does the human lncRNA LINC-PINT promote tumorigenesis?", "sentence2": "The human lncRNA LINC-PINT inhibits Specimen Source Codes - Specimen Source Codes - tumor cell invasion through a highly conserved Sequence - ParameterizedDataType element. Here we characterize the function of the p53-regulated human lncRNA LINC-PINT in Primary malignant neoplasm. We find that LINC-PINT is downregulated in multiple types of Primary malignant neoplasm and acts as a Specimen Source Codes - Specimen Source Codes - tumor suppressor lncRNA by reducing the invasive phenotype of Primary malignant neoplasm cells. A cross-species analysis identifies a highly conserved Sequence - ParameterizedDataType element in LINC-PINT that is essential for its function. This Sequence - ParameterizedDataType mediates a specific interaction with Polycomb Repressive Complex 2, necessary for the LINC-PINT-dependent repression of a pro-invasion signature of Genes regulated by the transcription factor EGR1. We find that LINC-PINT is downregulated in multiple types of Primary malignant neoplasm and acts as a Specimen Source Codes - Specimen Source Codes - tumor suppressor lncRNA by reducing the invasive phenotype of Primary malignant neoplasm cells. These results thus indicate that low plasma LINC-PINT gene expression could serve as a minimally invasive biomarker for early Patient-Controlled Analgesia detection, and that low LINC-PINT gene levels in Patient-Controlled Analgesia tumors could be used for predicting patient prognosis. Our data demonstrate that LINC-PINT gene expression is lower in plasma samples from Patient-Controlled Analgesia patients than from healthy individuals, and indicate that plasma LINC-PINT gene levels are more sensitive than CA-19-9 Antigen for detecting Patient-Controlled Analgesia. Low plasma LINC-PINT gene levels correlate with Specimen Source Codes - Specimen Source Codes - tumor recurrence, while low Specimen Source Codes - Specimen Source Codes - tumor LINC-PINT gene levels correlate with poor prognosis for Patient-Controlled Analgesia patients after pancreatectomy. We find that LINC-PINT is downregulated in multiple types of Primary malignant neoplasm and acts as a Specimen Source Codes - Specimen Source Codes - tumor suppressor lncRNA by reducing the invasive phenotype of Primary malignant neoplasm cells. We find that LINC-PINT is downregulated in multiple types of Primary malignant neoplasm and acts as a Specimen Source Codes - Specimen Source Codes - tumor suppressor lncRNA by reducing the invasive phenotype of Primary malignant neoplasm cells. These results thus indicate that low plasma LINC-PINT gene expression could serve as a minimally invasive biomarker for early Patient-Controlled Analgesia detection, and that low LINC-PINT gene levels in Patient-Controlled Analgesia tumors could be used for predicting patient prognosis.<br> The human lncRNA LINC-PINT inhibits Specimen Source Codes - Specimen Source Codes - tumor cell invasion through a highly conserved Sequence - ParameterizedDataType element.[SEP]Relations: malignant giant cell Specimen Source Codes - tumor has relations: disease_disease with Primary malignant neoplasm, disease_disease with Primary malignant neoplasm.", "label": "no"}
{"original_question": "Is LDB1-mediated enhancer looping dependent on cohesin?", "id": "converted_610", "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": "Is there any link between ERCC1-XPF and cohesin?", "id": "converted_611", "sentence1": "Is there any link between ERCC1-XPF and cohesins?", "sentence2": "ERCC1-XPF cooperates with CTGF protein, human and cohesins to\u00a0facilitate the developmental silencing of imprinted\u00a0Genes. 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\u00a0the 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\u00a0facilitate the developmental silencing of imprinted\u00a0Genes. 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: alpha thalassemia-X-linked intellectual disability syndrome has relations: disease_protein with Alpha thalassemia X-linked intellectual disability syndrome, disease_protein with Alpha thalassemia X-linked intellectual disability syndrome. Heterochromatin has relations: cellcomp_cellcomp with chromatin location, cellcomp_protein with DPEP2 gene, cellcomp_protein with Alpha thalassemia X-linked intellectual disability syndrome, cellcomp_cellcomp with chromatin location, cellcomp_protein with DPEP2 gene, cellcomp_protein with Alpha thalassemia X-linked intellectual disability syndrome.", "label": "yes"}
{"original_question": "Does Evolocumab improve cognitive function?", "id": "converted_612", "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 (\u00b1SD) 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\u00b12.62 in the evolocumab group and -0.29\u00b12.81 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": "Can radius fracture cause carpal tunnel syndrome?", "id": "converted_613", "sentence1": "Can radius Fracture cause Upper extremity>CARPAL TUNNEL SYNDROME 2?", "sentence2": "CARPAL TUNNEL SYNDROME 2 (CTS) 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 (CTS) 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 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 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]", "label": "yes"}
{"original_question": "Can Logic Alignment Free (LAF) be used for bacterial genomes classification?", "id": "converted_614", "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]", "label": "yes"}
{"original_question": "Is Marfan syndrome associated with chordal rupture?", "id": "converted_615", "sentence1": "Is Marfan syndrome associated with chordal Rupture?", "sentence2": "Repair of the mitral valve in children who have Marfan syndrome 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 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 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 Insufficiency.   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 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 Marfan syndrome 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 Marfan syndrome caused by a Gene Deletion Abnormality in exon 29 of the FBN1 gene. Total chordal augmentation in a child with Marfan syndrome and severe mitral insufficiency.[SEP]", "label": "yes"}
{"original_question": "Can canagliflozin cause euglycemic diabetic ketoacidosis?", "id": "converted_616", "sentence1": "Can canagliflozin cause euglycemic Diabetic Ketoacidosis?", "sentence2": "CASE REPORT: We present a case of a 57-year-old Human, Female adult with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder) taking a combination of canagliflozin and metformin who presented with progressive altered mental status over the previous 2\u00a0days. Her work-up demonstrated a Metabolic acidosis with an anion gap of 38 and a venous serum pH of 7.08. The serum glucose was 168\u00a0mg/dL. The urinalysis showed glucose>500\u00a0mg/dL and Ketones of 80\u00a0mg/dL. Further evaluation demonstrated an elevated serum osmolality of 319 mOsm/kg and an acetone concentration of 93\u00a0mg/dL. She was treated with intravenous insulin and Body Fluids and Substances, and the No No metabolic abnormalities and her altered mental status resolved within 36\u00a0h. This was the first episode of diabetic Ketoacidosis (DKA) for this patient. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: diabetic patients on SLC5A2 wt Allele PPP1R1A gene medications are at risk for ketoacidosis. Due to the Kidney glucose-wasting properties of these drugs, they may present with ketoacidosis with only mild elevations in serum glucose, potentially complicating the diagnosis.  Euglycemic diabetic Ketoacidosis with Persistent Diuresis Treated with Canagliflozin. We herein report the case of a 27-year-old Asian Human, Female adult with type 2 diabetes who was treated with a Sodium-Glucose Transporter 1 (SLC5A2 wt Allele) PPP1R1A gene (canagliflozin) who developed euglycemic diabetic Ketoacidosis and persistent diuresis in the absence of Glucose in blood specimen above reference range. Canagliflozin raised the risk of Amputation and the rate of Fracture in the CANVAS trial, although more data are necessary before drawing definite conclusions. The risk of euglycemic diabetic Ketoacidosis seems to be minimal when the drugs are prescribed properly. Severe Ketoacidosis Associated with Canagliflozin (Invokana): A Safety Concern.  However, some serious side effects, including severe anion gap Metabolic acidosis and euglycemic diabetic Ketoacidosis (DKA), have been reported.  At present, the Food and Drug Administration (FDA) has only approved three medications (canagliflozin, dapagliflozin and empagliflozin) in this drug class for the management of Diabetes Mellitus, Non-Insulin-Dependent. In May 2015, the FDA issued a warning of ketoacidosis with use of this drug class. We present a case of euglycemic diabetic Ketoacidosis secondary to canagliflozin in a type 2 diabetic patient. Non-Convulsive Status Epilepticus in Elderly Patients Receiving Selective Serotonin Reuptake Inhibitors; Euglycemic diabetic Ketoacidosis Associated with Canagliflozin Use in a Type 1 diabetic Patient; Duloxetine-Induced Galactorrhea; Canagliflozin-Associated Severe Hypercalcemia and Hypernatremia result result; Vemurafenib-Induced Fanconi Syndrome. Euglycemic diabetic Ketoacidosis in a 27 year-old female patient with type-1-Diabetes treated with sodium-glucose cotransporter-2 (SLC5A2 wt Allele) PPP1R1A gene Canagliflozin. We are reporting a timely case of atypical euglycemic diabetic Ketoacidosis in a type 1 diabetic patient treated with sodium-glucose cotransporter-2 (SGLT-2) PPP1R1A gene canagliflozin. Euglycemic ketoacidosis did not recur in our patient after discontinuing canagliflozin.  Euglycemic diabetic Ketoacidosis With Prolonged Glycosuria Associated With the Sodium-Glucose Cotransporter-2 Canagliflozin. In this article, we present a case of a 50-year-old Human, Female adult with type 2 diabetes who developed euglycemic DKA after initiating therapy with canagliflozin.  SLC5A2 wt Allele inhibitors such as canagliflozin may predispose patients not only to diabetic Ketoacidosis but also to prolonged glucosuria. We present a case of euglycemic diabetic Ketoacidosis secondary to canagliflozin in a type 2 diabetic patient.<br> We present a case of euglycemic diabetic Ketoacidosis secondary to canagliflozin in a type 2 diabetic patient. CONCLUSION Treatment with canagliflozin was associated with development of euglycemic ketoacidosis. Euglycemic diabetic Ketoacidosis with Persistent Diuresis Treated with Canagliflozin. We present a case of euglycemic diabetic Ketoacidosis secondary to canagliflozin in a type 2 diabetic patient.. Euglycemic diabetic Ketoacidosis With Prolonged Glycosuria Associated With the Sodium-Glucose Cotransporter-2 Canagliflozin. Euglycemic diabetic Ketoacidosis in a 27 year-old female patient with type-1-Diabetes treated with sodium-glucose cotransporter-2 (SLC5A2 wt Allele) PPP1R1A gene Canagliflozin.[SEP]Relations: Dapagliflozin has relations: indication with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder), indication with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder). Canagliflozin has relations: indication with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder), indication with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder). Metformin has relations: indication with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder), drug_effect with Ketoacidosis, contraindication with Metabolic acidosis, indication with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder), drug_effect with Ketoacidosis, contraindication with Metabolic acidosis. diabetes mellitus, noninsulin-dependent has relations: disease_disease with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder), disease_disease with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder), disease_disease with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder), disease_disease with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder). Ketoacidosis has relations: disease_phenotype_positive with Diabetic Ketoacidosis, disease_phenotype_positive with Diabetic Ketoacidosis. Empagliflozin has relations: indication with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder), indication with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder). Diabetic Ketoacidosis has relations: disease_disease with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder), disease_phenotype_positive with Ketoacidosis, disease_disease with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder), disease_phenotype_positive with Ketoacidosis.", "label": "yes"}
{"original_question": "Is there an association between Klinefelter syndrome and breast cancer?", "id": "converted_617", "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 tumours 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 tumor, 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 tumours 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: Testosterone has relations: contraindication with Hepatobiliary Disorder, contraindication with prostate Primary malignant neoplasm, contraindication with Gynecomastia, indication with Klinefelter Syndrome, contraindication with Hepatobiliary Disorder, contraindication with prostate Primary malignant neoplasm, contraindication with Gynecomastia, indication with Klinefelter Syndrome. hepatobiliary disease has relations: disease_disease with Hepatobiliary Disorder, disease_disease with Hepatobiliary Disorder. lymphoma, non-Hodgkin, familial has relations: disease_disease with Lymphoma, Non-Hodgkin, Familial, disease_disease with Lymphoma, Non-Hodgkin, Familial.", "label": "yes"}
{"original_question": "Is vorinostat effective for glioblastoma?", "id": "converted_618", "sentence1": "Is vorinostat effective for glioblastoma?", "sentence2": "Conclusions: vorinostat combined with standard chemoradiation had acceptable tolerability in newly diagnosed glioblastoma. 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. 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 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, 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 TMZ in newly diagnosed glioblastoma is underway.[SEP]Relations: Temozolomide has relations: drug_drug with vorinostat, drug_drug with vorinostat. Bevacizumab has relations: drug_drug with vorinostat, drug_drug with vorinostat.", "label": "no"}
{"original_question": "Has ATF4 transcription factor been linked to cancer and neoplastic transformation?", "id": "converted_619", "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 (eIF2\u03b1) 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 factor 4 (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 factor 4 (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 factor 4 (ATF4 protein, human protein, human), a member of the ATF/CREB family, has been reported to be related to tumor angiogenesis[SEP]Relations: malignant giant cell tumor has relations: disease_disease with Primary malignant neoplasm, disease_disease with Primary malignant neoplasm.", "label": "yes"}
{"original_question": "Are patients with Sjogren syndrome at increased risk for lymphoma?", "id": "converted_620", "sentence1": "Are patients with Sjogren's Syndrome at increased risk for lymphoma?", "sentence2": "The heightened risk of Lymphoma, Non-Hodgkin, Familial (Lymphoma, Large-Cell, Follicular) development in primary Sjogren's Syndrome (Supernumerary mandibular right first primary molar) is well established. Primary Kidney Kidney 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 (Kidney Diffuse Large B-Cell Lymphoma).  To our knowledge, the patient described here represents the first reported case of Kidney 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's Syndrome-associated Non-Hodgkin's lymphoma of bone: case series. Five per cent of patients with Primary Sj\u00f6gren's syndrome (Chromosome 11p11.2 Deletion Syndrome) develop Lymphoma, Non-Hodgkin (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's 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 Sj\u00f6gren'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's Syndrome is presented. Furthermore, Rheumatoid Arthritis, Sj\u00f6gren'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 Sj\u00f6gren'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's Syndrome: An easy tool for clinical use. Lymphoma is a very severe complication of primary Sj\u00f6gren'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 Sj\u00f6gren syndrome: clinical and pathophysiologic aspects. Recent results clearly indicate an association between severity of chronic inflammation and lymphoma risk in Rheumatoid Arthritis and Sj\u00f6gren's syndrome. Several Autoimmune Diseases, including primary Sj\u00f6gren'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 Lymphoma, Non-Hodgkin, Familial (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 of bone is highly increased in patients with primary Supernumerary mandibular right first primary molar. Predicting the risk for lymphoma development in Sjogren's 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 Sj\u00f6gren syndrome are at increased risk of lymphoma development. Sjogren's syndrome is an autoimmune disease with a known predisposition for lymphoma development. Certain autoimmune and chronic inflammatory conditions, such as Sj\u00f6gren's syndrome and rheumatoid arthritis (Rheumatoid Arthritis), have consistently been associated with an increased risk of Lymphoma, but it is unclear whether elevated lymphoma risk is a phenomenon that accompanies inflammatory conditions in general.[SEP]Relations: Lymphoma has relations: disease_phenotype_positive with Sjogren's Syndrome, disease_phenotype_positive with Sjogren's Syndrome. Non-Hodgkin lymphoma has relations: phenotype_phenotype with B-Cell Lymphomas, phenotype_phenotype with B-Cell Lymphomas, phenotype_phenotype with B-Cell Lymphomas, phenotype_phenotype with B-Cell Lymphomas. rituximab has relations: indication with Lymphoma, Non-Hodgkin, Familial, indication with lymphoma, indication with Lymphoma, Non-Hodgkin, Familial, indication with lymphoma. lymphoma, non-Hodgkin, familial has relations: indication with rituximab, disease_disease with Lymphoma, Non-Hodgkin, Familial, indication with rituximab, disease_disease with Lymphoma, Non-Hodgkin, Familial. B-Cell Lymphomas has relations: disease_phenotype_positive with Mucosa-Associated Lymphoid Tissue Lymphoma, disease_phenotype_positive with Mucosa-Associated Lymphoid Tissue Lymphoma. Rheumatoid arthritis has relations: disease_phenotype_positive with Sjogren's Syndrome, disease_phenotype_positive with Sjogren's Syndrome.", "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_621", "sentence1": "Down's syndrome occurs when an individual has an extra copy or part of a copy of chromosome 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 Human chromosome 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 chromosome 21, Submicroscopic duplication of chromosome 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 Chromosomes, Human, Pair 21. Down Syndrome is a genetic disorder, occurring when an individual has all or part of an extra copy of chromosome 21. Downs syndrome (DS) occurs due to an extra copy of chromosome 21. Down Syndrome, which arises in individuals carrying an extra copy of chromosome 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 Human chromosome 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 chromosome 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 chromosome 21. Down Syndrome (DS), caused by an extra copy of chromosome 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 Human chromosome 21 and leads to several alterations including intellectual disabilities and locomotor defects. Down's syndrome results from the production of three copies of chromosome 21 within a \"U\" lymphocyte.  Downs syndrome (DS) occurs due to an extra copy of chromosome 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 chromosome 21. n 1959, J. Lejeune, M. Gautier, and R. Turpin demonstrated that the children with Down Syndrome had an extra copy of chromosome 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 chromosome 21 is the most common genetic cause for congenital malformations and Learning Disabilities.[SEP]Relations: congenital Heart Diseases has relations: disease_disease with Heart Diseases, disease_disease with Heart Diseases. Cognitive impairment has relations: disease_phenotype_positive with ALZHEIMER DISEASE 2, disease_phenotype_positive with ALZHEIMER DISEASE 2.", "label": "yes"}
{"original_question": "Is creatinine assessment included in the MELD score?", "id": "converted_622", "sentence1": "Is creatine/creatinine assessment included in the MELD score?", "sentence2": "Model For End-Stage Hepatobiliary Disorder (MELD) scores were calculated as 3.78\u00d7ln[TB]\u00a0+\u00a011.2\u00d7ln[Integrated Neuromusculoskeletal Release]\u00a0+\u00a09.57\u00d7ln[creatine/creatine/creatinine]\u00a0+\u00a06.43.  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 \u00b1 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]", "label": "yes"}
{"original_question": "Is celiac disease caused by gliadin-induced transglutaminase-2 (TG2)-dependent events ?", "id": "converted_623", "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 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 Transglutaminase 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). Protein Glutamine gamma Glutamyltransferase 2 (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]", "label": "yes"}
{"original_question": "Does wheat belongs to the genus Avena, yes or no?", "id": "converted_624", "sentence1": "Does Triticum aestivum belongs to the genus Avena, yes or no?", "sentence2": "oat seedlings (oat allergenic extract preparation) wild green-oat (oat allergenic extract preparation)   Oat (oat allergenic extract preparation L.) Oat (oat allergenic extract preparation L.) Avena (Oats) wild oat allergenic extract (Avena fatua L.) oat allergenic extract (genus Avena) oat allergenic extract preparation L. and A. byzantina C. Koch)   oat (oat allergenic extract preparation L.). oat (oat allergenic extract preparation L.) and Wheat (Triticum aestivum) Ab (Wheat (Wheat (Triticum aestivum) Ab) Ab[SEP]", "label": "no"}
{"original_question": "Does Uc.160 promote cancer?", "id": "converted_625", "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.", "label": "no"}
{"original_question": "Can doxycycline cause photosensitivity?", "id": "converted_626", "sentence1": "Can doxycycline cause Photosensitivity of Skin Specimen Source Code?", "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: Tetracycline has relations: drug_drug with doxycycline, drug_drug with doxycycline. Amiodarone has relations: drug_drug with doxycycline, drug_drug with doxycycline. Erythema has relations: drug_effect with doxycycline, drug_effect with doxycycline. Anxiety Disorders disorder has relations: disease_disease with Anxiety Disorders, disease_disease with Anxiety Disorders. Ceftriaxone has relations: drug_drug with doxycycline, drug_drug with doxycycline. Quinine has relations: drug_drug with doxycycline, drug_drug with doxycycline. Mefenamic acid has relations: drug_drug with doxycycline, drug_drug with doxycycline. Vomiting has relations: drug_effect with doxycycline, drug_effect with doxycycline. Diclofenac has relations: drug_drug with doxycycline, drug_drug with doxycycline. Prochlorperazine has relations: drug_drug with doxycycline, drug_drug with doxycycline.", "label": "yes"}
{"original_question": "Are paralog genes co-regulated?", "id": "converted_627", "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]", "label": "yes"}
{"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_628", "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 Dinophyceae. 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: germ cell Cell Nucleus has relations: cellcomp_cellcomp with Cell Nucleus, cellcomp_cellcomp with Cell Nucleus.", "label": "no"}
{"original_question": "Are stress granules membraneous?", "id": "converted_629", "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]", "label": "no"}
{"original_question": "Is the consumption of chocolate associated with an increase in cardiovascular disease?", "id": "converted_630", "sentence1": "Is the consumption of chocolate associated with an increase in Cardiovascular system disease?", "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 Arteriosclerosis and Cerebrovascular accident. 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 system disease. Chocolate consumption may have a beneficial effect on Cardiovascular system health, Data currently available indicate that daily consumption of CALCOCO1 gene-rich chocolate (rich in polyphenols) may at least partially lower Cardiovascular system disease risk. CONCLUSIONS The blood pressure and cholesterol lowering effects of dark chocolate consumption are beneficial in the prevention of Cardiovascular system events in a population with Metabolic Syndrome X. Daily dark chocolate consumption could be an effective Cardiovascular system preventive strategy in this population. BACKGROUND The consumption of chocolate and CALCOCO1 gene has established Cardiovascular system benefits. CONCLUSIONS Chocolate consumption is associated with lower risk of MI and ischaemic heart disease. Chocolate consumption was inversely associated with MI risk. Chocolate consumption is associated with lower risk of MI and ischaemic heart disease. The consumption of 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 Arteriosclerosis: the National Heart, Chest>Chest>Lung, and Blood Institute Family Heart Study. Daily 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 system disease risk. The consumption of CALCOCO1 gene and dark 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 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 chocolate/CALCOCO1 gene on the risk of cardio vascular disease (Cerebrovascular Disorders).[SEP]Relations: heart disease has relations: disease_disease with Cardiovascular system disease, disease_disease with Cardiovascular system disease. Metabolic Syndrome X X has relations: disease_disease with Metabolic Syndrome X, disease_disease with Metabolic Syndrome X.", "label": "no"}
{"original_question": "Is the gene CDKN2A nevogenic?", "id": "converted_631", "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. melanocytic neoplasm has relations: disease_disease with Melanocytic neoplasm, disease_disease with Melanocytic neoplasm.", "label": "yes"}
{"original_question": "Are there ways of joint Bayesian inference of risk variants?", "id": "converted_632", "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]", "label": "yes"}
{"original_question": "Has intepirdine been evaluated in clinical trials? (November 2017)", "id": "converted_633", "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": "Is subacute sclerosing panencephalitis caused by the Measles vaccine?", "id": "converted_634", "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 Encephalitis, disease_disease with Encephalitis. inherited neurodegenerative disorder has relations: disease_disease with Neurodegenerative Disorders, disease_disease with Neurodegenerative Disorders. Nipah Virus disease has relations: disease_disease with Encephalitis, disease_disease with Encephalitis.", "label": "no"}
{"original_question": "Does armodafinil improve fatigue of glioma patients?", "id": "converted_635", "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]", "label": "no"}
{"original_question": "Can gas vesicles be detected by ultrasound?", "id": "converted_636", "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]", "label": "yes"}
{"original_question": "Is Citrobacter rodentium pathogenic?", "id": "converted_637", "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]", "label": "yes"}
{"original_question": "Can CD55 deficiency cause thrombosis?", "id": "converted_638", "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 HYPERACTIVATION, ANGIOPATHIC THROMBOSIS, AND PROTEIN-LOSING ENTEROPATHY, 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 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 HYPERACTIVATION, ANGIOPATHIC THROMBOSIS, AND PROTEIN-LOSING ENTEROPATHY, Early-Onset Protein-Losing Enteropathy, and Thrombosis.[SEP]Relations: paroxysmal nocturnal hemoglobinuria has relations: disease_disease with hemolytic Genus Anemia, disease_protein with CD59 Antigen, disease_disease with hemolytic Genus Anemia, disease_protein with CD59 Antigen.", "label": "yes"}
{"original_question": "Are sleep apnea and snoring associated with cardiac arrhythmias?", "id": "converted_639", "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 (OSA), 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 (OSA) and Cardiovascular system (CVD) conditions and events, including coronary artery disease, Hypertensive disease, arrhythmia, heart failure, and sudden Cardiac - anatomy qualifier 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 (OSA) 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 Arteriosclerosis, 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 (OSA), reportedly as a consequence of the autonomic effects of recurrent apnea with subsequent oxygen desaturation. Obstructive apnea is associated with myocardial ischemia (silent or symptomatic), acute coronary events, Cerebrovascular accident and transient ischemic attacks, Cardiac - anatomy qualifier arrhythmia, Pulmonary Hypertension and heart failure. Obstructive Sleep Apnea Syndromes (OSA) 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 OSA; these include Hypertensive disease, coronary artery disease, Cerebrovascular accident, congestive heart failure, Pulmonary Hypertension, 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 - anatomy qualifier arrhythmia.  Obstructive Sleep Apnea Syndromes (OSA) affects approximately 4% of middle-aged men and 2% of middle-aged women. Cardiac Arrhythmia are common problems in patients with OSA, even though the true prevalence and clinical relevance of Cardiac - anatomy qualifier arrhythmias remains to be determined.  Cardiac Arrhythmia 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 (OSA) 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 Arrhythmia are common problems in OSA 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 OSA are frequently Hypertensive (finding) and can have dangerous Cardiac - anatomy qualifier arrhythmias. Patients with stable Cardiac - anatomy qualifier failure who snore may present sleep hypopnea and Cardiac - anatomy qualifier arrhythmias.   Obstructive Sleep Apnea Syndromes (OSA) is associated with increased Cardiovascular system morbidity and mortality. Cardiac Arrhythmia are common in patients with OSA.  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: Hypertensive (finding) Heart Diseases has relations: disease_disease with Heart Diseases, disease_disease with Heart Diseases.", "label": "yes"}
{"original_question": "Are osteoclasts specialized in bone degradation?", "id": "converted_640", "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]", "label": "yes"}
{"original_question": "Does temsirolimus improve survival of glioblastoma patients?", "id": "converted_641", "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 tumors. 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: Imatinib has relations: drug_drug with temsirolimus, drug_drug with temsirolimus. Bevacizumab has relations: drug_drug with temsirolimus, drug_drug with temsirolimus. Vandetanib has relations: drug_drug with temsirolimus, drug_drug with temsirolimus. Temozolomide has relations: drug_drug with temsirolimus, drug_drug with temsirolimus. Dasatinib has relations: drug_drug with temsirolimus, drug_drug with temsirolimus. Erlotinib has relations: drug_drug with temsirolimus, drug_drug with temsirolimus.", "label": "no"}
{"original_question": "Are there sex differences in the transcriptome of the mouse hippocampus?", "id": "converted_642", "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]", "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_643", "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-\u03b1-1,3-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-\u03b1-1,3-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]", "label": "yes"}
{"original_question": "Is Rucaparib effective for ovarian cancer?", "id": "converted_644", "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\u2122) is an oral, small molecule, Poly(ADP-ribose) Polymerase Inhibitors 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: indication with Ovarian cancer, drug_drug with olaparib, indication with Ovarian cancer, drug_drug with olaparib. olaparib has relations: drug_drug with rucaparib, indication with Ovarian cancer, drug_drug with rucaparib, indication with Ovarian cancer.", "label": "yes"}
{"original_question": "Does verubecestat activate BACE?", "id": "converted_645", "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]", "label": "no"}
{"original_question": "Is there a link between nuclear position and DNA repair pathway choice?", "id": "converted_646", "sentence1": "Is there a link between Nuclear (incident type) position and DNA repair pathway choice?", "sentence2": "Nuclear position dictates DNA repair pathway choice. We demonstrate that DSBs induced at the Nuclear (incident type) membrane (but not at Nuclear (incident type) pores or Nuclear (incident type) interior) fail to rapidly activate the DNA damage response (DDR) and repair by homologous recombination (HR). Real-time and superresolution imaging reveal that DNA DSBs within lamina-associated domains do not migrate to more permissive environments for HR, like the Nuclear (incident type) pores or the Nuclear (incident type) interior, but instead are repaired in situ by alternative end-joining. Our results are consistent with a model in which Nuclear (incident type) position dictates the choice of DNA repair pathway, thus revealing a new level of regulation in 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione repair controlled by spatial organization of DNA within the Cell Nucleus. Our results are consistent with a model in which Nuclear (incident type) position dictates the choice of DNA repair pathway, thus revealing a new level of regulation in 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione repair controlled by spatial organization of DNA within the Cell Nucleus. Nuclear position dictates DNA repair pathway choice. Our results are consistent with a model in which Nuclear (incident type) position dictates the choice of DNA repair pathway, thus revealing a new level of regulation in 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione repair controlled by spatial organization of DNA within the Cell Nucleus.[SEP]Relations: germ cell Cell Nucleus has relations: cellcomp_cellcomp with Cell Nucleus, cellcomp_cellcomp with Cell Nucleus.", "label": "yes"}
{"original_question": "Can non ubiquitinated Tomm20 promote mitophagy?", "id": "converted_647", "sentence1": "Can non ubiquitinated Tomm20 promote mitophagy?", "sentence2": "A total of 338 new targets were identified and from these we validated NEK3 gene (Gsk3\u03b2), which can phosphorylate \u03b1-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 Gsk3\u03b2 using K63 linkages.[SEP]", "label": "no"}
{"original_question": "Does SARM1 deletion cause neurodegeneration?", "id": "converted_648", "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.", "label": "no"}
{"original_question": "Is DNA polymerase \u03b8 involved in DNA repair?", "id": "converted_649", "sentence1": "Is DNA polymerase \u03b8 involved in DNA repair?", "sentence2": "DNA polymerase \u03b8 (Pol \u03b8) is implicated in various cellular processes including double-strand break repair and apurinic/apyrimidinic site bypass.  Pol \u03b8 is the defining Enzyme [APC] for a pathway of DSB repair termed \"alternative end-joining\" (altEJ) or \"theta-mediated end-joining.\" DNA polymerase \u03b8 is a key player in PARP-mediated DNA damage repair and essential for the survival of Tumor cells, malignant where homologous recombination is compromised.  DNA polymerase \u03b8 protects against genomic instability via an alternative end-joining repair pathway for DNA double-strand breaks.[SEP]", "label": "yes"}
{"original_question": "Can nanoparticles be used for afterglow imaging?", "id": "converted_650", "sentence1": "Can Artificial nanoparticles be used for afterglow imaging?", "sentence2": "Ultralong Phosphorescence of Water-Soluble Organic Nanoparticles for In Vivo Afterglow Imaging Afterglow or persistent luminescence eliminates the need for light excitation and thus circumvents the issue of autofluorescence, holding promise for molecular imaging. However, current persistent luminescence agents are rare and limited to Inorganic Artificial Artificial nanoparticles. This study reports the design principle, synthesis, and proof-of-concept application of organic semiconducting Artificial Artificial nanoparticles (OSNs) with ultralong phosphorescence for in vivo afterglow imaging.  This study not only introduces the first category of water-soluble ultralong phosphorescence organic Artificial Artificial nanoparticles but also reveals a universal design principle to prolong the lifetime of phosphorescent molecules to the level that can be effective for molecular imaging.[SEP]", "label": "yes"}
{"original_question": "Is there any role of interleukin-11 in cardiovascular fibrosis?", "id": "converted_651", "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 Il11 transgene expression or Il11 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.", "label": "yes"}
{"original_question": "Is there a disease or condition called Exploding Head Syndrome?", "id": "converted_652", "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]", "label": "yes"}
{"original_question": "Is Enlimomab effective for stroke treatment?", "id": "converted_653", "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]", "label": "no"}
{"original_question": "Does International Citicoline Trial on acUte Stroke trial supports efficacy of citicoline for stroke treatment?", "id": "converted_654", "sentence1": "Does International Citicoline Trial on acUte Stroke trial supports efficacy of citicoline for Cerebrovascular accident treatment?", "sentence2": "The meta-analysis showed that no significant differences were found in the long-term mortality (OR=0.91, 95% CI 0.07 to 1.09, P=0.30), the rate of dependency (OR=1.02, 95% CI 0.87 to 1.24, P=0.85), and the effective rate (OR=0.98, 95% CI 0.84 to 1.14, P=0.82) between citicoline group and control group.   In conclusion, citicolne cannot reduce long-term mortality and dependence rate in the treatment of acute Cerebrovascular accident, and the effective rate of citivoline may be not better than that of controls but with reliable safety. In Homo sapiens, although a recent trial International Citicoline Trial on Acute Stroke (ICTUS) has shown that global recovery is similar in citicoline and placebo groups, citicoline was shown to be more beneficial in some patients, such as those with moderate Cerebrovascular accident severity and not treated with PLAT protein, human.  INTERPRETATION: Under the circumstances of the ICTUS trial, citicoline is not efficacious in the treatment of moderate-to-severe acute ischaemic Cerebrovascular accident. The trial was stopped for futility at the third interim analysis on the basis of complete data from 2078 patients. Global recovery was similar in both groups (odds ratio 1\u00b703, 95% CI 0\u00b786-1\u00b725; p=0\u00b7364). INTERPRETATION Under the circumstances of the ICTUS trial, citicoline is not efficacious in the treatment of moderate-to-severe acute ischaemic Cerebrovascular accident. In Homo sapiens, although a recent trial International Citicoline Trial on Acute Stroke (ICTUS) has shown that global recovery is similar in citicoline and placebo groups, citicoline was shown to be more beneficial in some patients, such as those with moderate Cerebrovascular accident severity and not treated with PLAT protein, human. Several mechanisms have been proposed to explain the beneficial actions of citicoline. In Homo sapiens, although a recent trial International Citicoline Trial on Acute Stroke (ICTUS) has shown that global recovery is similar in citicoline and placebo groups, citicoline was shown to be more beneficial in some patients, such as those with moderate Cerebrovascular accident severity and not treated with PLAT protein, human.[SEP]", "label": "no"}
{"original_question": "Is human lysyl oxidase-like 2 a glycoprotein?", "id": "converted_655", "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]", "label": "yes"}
{"original_question": "Can GDF15 be a biomarker for metformin treatment?", "id": "converted_656", "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]", "label": "yes"}
{"original_question": "Has rituximab been considered as a treatment for chronic fatigues syndrome? (November 2017)", "id": "converted_657", "sentence1": "Has rituximab been considered as a treatment for chronic fatigues syndrome? (November 2017)", "sentence2": "The use of Rintatolimod and rituximab as well as counselling, behavioural and rehabilitation therapy programs may be of benefit for CFS/ME, but the evidence of their effectiveness is still limited.[SEP]", "label": "yes"}
{"original_question": "Does oncogene-induced DNA replication stress inhibit genomic instability?", "id": "converted_658", "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]", "label": "no"}
{"original_question": "Is the petrous bone used in ancient DNA sampling?", "id": "converted_659", "sentence1": "Is the petrous bone used in ancient DNA sampling?", "sentence2": "Large-scale genomic analyses of ancient Homo sapiens populations have become feasible partly due to refined sampling methods. The inner part of Structure of petrous part of temporal bone and the cementum layer in teeth roots are currently recognized as the best substrates for such research. Ancient DNA (aDNA) research involves invasive and destructive sampling procedures that are often incompatible with anthropological, anatomical, and bioarcheological analyses requiring intact skeletal remains. The osseous Labyrinth inside the petrous bone has been shown to yield higher amounts of endogenous DNA than any other skeletal element; however, accessing this Labyrinth in cases of a complete or reconstructed skull involves causing major structural damage to the Calvaria or base. first genome-wide ancient DNA from Anatolian Neolithic farmers, whose Genetic Materials we obtained by extracting from Structure of petrous part of temporal bone,[SEP]", "label": "yes"}
{"original_question": "Is recursive splicing more common in short introns?", "id": "converted_660", "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 intron 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 intron 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 intron than for the 3' splice site of the shorter alternative intron 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]", "label": "no"}
{"original_question": "Is Lysyl oxidase crosslinking collagen?", "id": "converted_661", "sentence1": "Is LOX protein, human gene crosslinking collagen?", "sentence2": "LOX protein, human 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.  LOXL4 gene, a crosslinking Enzyme [APC] implicated in collagen and ELN protein, human 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 LOX protein, human, molfunc_protein with LOX protein, human.", "label": "yes"}
{"original_question": "Is sternotomy closure done using either a sternal ZipFix\u2122 implant  or conventional steel wire following cardiac surgery?", "id": "converted_662", "sentence1": "Is sternotomy closure done using either a Sternum ZipFix\u2122 implant  or conventional steel wire following cardiac surgery?", "sentence2": "o determine the difference in Sternum Communicable Diseases and other infectious events between conventional wire and cable-tie-based closure techniques post-sternotomy in a collective of patients after cardiac surgery. Our study underlines a neutral effect of the Sternum ZipFix\u2122 system in patients regarding Sternum Communicable Diseases. Postoperative complications are similar in both Sternum closure methods. The cable-tie-based system is fast, easy to use, reliable and safe.  Wire closure still remains the preferred technique despite reasonable disadvantages. Associated complications, such as Communicable Diseases and Sternum instability, cause time- and cost-consuming therapies. We present a new tool for Sternum closure with its first clinical experience and results.METHODS: The Sternum ZipFix(TM) System is based on the cable-tie principle.  In our initial evaluation, the short-term results have shown that the Sternum ZipFix(TM) can be used safely and effectively. It is fast, easy to use and serves as a potential alternative for traditional wire closure. To determine the difference in Sternum Communicable Diseases and other infectious events between conventional wire and cable-tie-based closure techniques post-sternotomy in a collective of patients after cardiac surgery.[SEP]", "label": "yes"}
{"original_question": "Is transcription of eRNA bidirectional?", "id": "converted_663", "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 RNA (eRNAs). Kallikrein (kallikrein-related peptidase 3, human), which codes for prostate-specific antigen (Prostate-Specific Antigen), is a well-known AR-regulated gene and its upstream enhancers produce bidirectional enhancer RNA (eRNAs), termed KLK3e. The distal enhancer of the gonadotropin hormone \u03b1-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 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 RNA (eRNA) production at enhancers XR-seq maps capture transcription-coupled repair at Site of divergent gene Promoter and bidirectional enhancer RNA (eRNA) production at enhancers. The distal enhancer of the gonadotropin hormone \u03b1-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 \u223c3-5 kb. XR-seq maps capture transcription-coupled repair at Site of divergent gene Promoter and bidirectional enhancer RNA (eRNA) production at enhancers. We identify 76 enhancer 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 RNA (eRNA) production at enhancers. Instead, communication between Promoter and enhancers can be bidirectional with Promoter required to activate Enhancer of 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]", "label": "yes"}
{"original_question": "Is the protein pelota a ribosomal rescue factor?", "id": "converted_664", "sentence1": "Is the protein pelota a ribosomal rescue factor?", "sentence2": "a novel binding partner of the Ribosomes recycling protein Pelota n Eukaryota, Pelota (Dom34 in Saccharomyces cerevisiae) and HBS1L gene are responsible for solving general problems of ribosomal stall in translation.  In Eukaryota, the protein complex of Pelota (Saccharomyces cerevisiae Dom34) and HBS1L gene translational Guanosine Triphosphate Phosphohydrolases recognizes the stalled Ribosomes containing the defective RNA, Messenger.[SEP]", "label": "yes"}
{"original_question": "Is CXCL7 a chemokine?", "id": "converted_665", "sentence1": "Is PPBP wt Allele a chemokine?", "sentence2": "PPBP wt Allele, a chemokine highly expressed in Blood Platelets,  Chemokine PPBP wt Allele Heterodimers[SEP]", "label": "yes"}
{"original_question": "The TRPM2 gene is associated with development of spontaneous thromboembolism?", "id": "converted_666", "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 Cells 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 toxicity 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]", "label": "no"}
{"original_question": "Is a mutation of the  ZIKV's membrane protein prM responsible for the microcephaly in new-born infants?", "id": "converted_667", "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\u2192Asn139(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 lumican a secreted protein?", "id": "converted_668", "sentence1": "Is LUM protein, Homo sapiens a secreted protein?", "sentence2": "Specimen Source Codes - Fibroblasts stimulated with the fibrocyte-secreted inflammatory signal tumor necrosis factor-\u03b1 secrete the small leucine-rich Proteoglycan LUM protein, Homo sapiens TNF-\u03b1-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]", "label": "yes"}
{"original_question": "Is p53 a transcription factor?", "id": "converted_669", "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 (miRNAs) and long noncoding RNAs (lncRNAs).  TP53 wt Allele is a TRANSCRIPTION FACTOR[SEP]", "label": "yes"}