{"original_question": "Is the monoclonal antibody Trastuzumab (Herceptin) of potential use in the treatment of prostate cancer?", "id": "converted_0", "sentence1": "Is the monoclonal immunoglobulin complex location CAL Trastuzumab (Herceptin) of potential use in the treatment of Malignant neoplasm of Pelvis>Prostate?", "sentence2": "Herceptin is widely used in treating Her2-overexpressing Breast cancer. However, the application of Herceptin in Malignant neoplasm of Pelvis>Prostate is still controversial. Our data demonstrate that Re-188-labeled Herceptin effectively inhibited the growth of DU145 cells compared to the Herceptin- and Re-188-treated cohorts. This implies that targeting Her2 by both radio- and immuno- therapy might be a potential strategy for treating patients with androgen-independent Malignant neoplasm of Pelvis>Prostate. epidermal growth factor receptor (Epidermal Growth Factor Receptor) family members are potential targets for therapy using extra-cellular domain receptor binding agents, such as the Antibodies, in vitro diagnostic trastuzumab and cetuximab  there were tendencies for upregulation of erbB-2 Receptor, increased co-expression of Epidermal Growth Factor Receptor and erbB-2 Receptor and downregulation of ERBB3 Receptor Protein-Tyrosine Kinase in the Malignant neoplasm of Pelvis>Prostate lymph node metastases in comparison to the Primary Neoplasm.  We performed a comparative analysis in vitro and in vivo of the Antitumor effects of three different Antibodies, in vitro diagnostic targeting different Epitopes of ErbB2: Herceptin (trastuzumab), 2C4 immunoglobulin complex location immunoglobulin complex location (pertuzumab) and Erb-hcAb (Homo sapiens anti-ErbB2-compact immunoglobulin complex location), a novel fully Homo sapiens compact immunoglobulin complex location produced in our laboratory. Herein, we demonstrate that the growth of both androgen-dependent and independent Malignant neoplasm of Pelvis>Prostate cells was efficiently inhibited by Erb-hcAb. The Antitumor effects induced by Erb-hcAb on some Cultured Cell Line were more potent than those observed for either Herceptin or 2C4 immunoglobulin complex location immunoglobulin complex location. These findings suggest that a systemic delivery of 212Pb-trastuzumab could             be an effective modality for management of advanced Homo sapiens Malignant neoplasm of Pelvis>Prostate. Human epidermal growth factor receptor type 2 (erbB-2 Receptor) overexpression supports proliferation of androgen-independent Malignant neoplasm of Pelvis>Prostate (Pachyonychia Congenita) Radiolabeled ABY-025 Affibody molecule provides higher contrast in imaging of erbB-2 Receptor-expressing Pachyonychia Congenita xenografts than Radiolabeled trastuzumab.  These studies indicate that dual Epidermal Growth Factor Receptor/erbB-2 Receptor inhibition, administered together with AWT, sensitize Malignant neoplasm of Pelvis>Prostate cells to apoptosis during AWT The overall goal of these studies is to determine whether dual inhibition of the receptor tyrosine kinases epidermal growth factor receptor (Epidermal Growth Factor Receptor) and erbB-2 Receptor would prolong the effectiveness of this treatment in Malignant neoplasm of Pelvis>Prostate.  The expression of erbB-2 Receptor was demonstrated and quantified in all three tested Malignant neoplasm of Pelvis>Prostate cell-lines. Such features would definitely favor the use of radiometal labels for trastuzumab and, most likely, for affibody molecules our data demonstrate that Her2 plays an important role in the support of AR protein stability in the transition of androgen requirement in Malignant neoplasm of Pelvis>Prostate cells. We hope these findings will provide novel insight into the treatment of hormone-refractory Malignant neoplasm of Pelvis>Prostate. These two Cultured Cell Line exhibited distinct responses to Her2 activation (by Recombinant Heregulin treatment) on Her2 phosphorylation and Her2 inhibition (by tyrphostin tyrphostin AG825 or Herceptin treatments) on proliferation  While Pelvis>Prostate Malignant Neoplasms that express high levels of HER-2-neu peptide vaccine-neu peptide vaccine are resistant to the killing effects of trastuzumab, they can be targeted for selective gene expression and destruction by Genus: Lentivirus group with envelope proteins engineered to bind to this therapeutic immunoglobulin complex location Overexpression of Epidermal Growth Factor Receptor gene-2 and Epidermal Growth Factor Receptor has been associated with aggressive Disease and poor patient prognosis in a range of Homo sapiens tumour types (e.g. Breast, Chest>Lung, Ovarian, Pelvis>Prostate Various approaches have been developed to target the Epidermal Growth Factor Receptor gene signalling pathways including Monoclonal Antibodies (trastuzumab/Herceptin The data from these in vitro and in vivo studies supported advancement of Radiolabeled trastuzumab into two clinical studies Specimen Source Codes - tumor targeting was evaluated in CASP14 gene bearing subcutaneous (s.c.) xenografts of colorectal, Pancreatic Hormones, Ovarian, and Pelvis>Prostate carcinomas. we found that although Pelvis>Prostate Malignant Neoplasms that express high levels of HER-2-neu peptide vaccine-neu peptide vaccine are resistant to the killing effects of trastuzumab, they can be targeted for selective gene expression and destruction by Virus with envelope proteins engineered to bind this immunoglobulin complex location detection of Malignant neoplasm of Pelvis>Prostate (Patient-Controlled Analgesia) and advances in hormonal and chemotherapy treatments have provided great clinical benefits to patients with early stages of the Disease. MAbs directed to established targets include those approved for other Solid Neoplasm, including anti-Homo sapiens epidermal growth factor receptor-2 (erbB-2 Receptor) MAb trastuzumab We conclude that Her2/neu expression in the peripheral blood mononuclear cell fraction of Malignant neoplasm of Pelvis>Prostate patients is frequent and therefore this assay may potentially be useful to detect the presence of micrometastatic Disease in men with Malignant neoplasm of Pelvis>Prostate and for monitoring patients enrolled in trastuzumab-based therapeutic protocols. This study suggests that the Docetaxel/Trastuzumab combination may prove an effective therapeutic approach for erbB-2 Receptor-expressing hormone-refractory Malignant neoplasm of Pelvis>Prostate. there was no significant difference in antimetastatic activity between the emulsion and the immunoemulsion despite the affinity of the immunoemulsion towards the erbB-2 Receptor receptor.  a targeted drug delivery system based on cationic emulsion covalently linked to anti-erbB-2 Receptor monoclonal immunoglobulin complex location CAL (Herceptin), in a well-established in vivo pharmacologic model of metastatic Malignant neoplasm of Pelvis>Prostate that overexpresses the erbB-2 Receptor receptor The finding of strong, consistent HER-2-neu peptide vaccine-neu peptide vaccine/neu expression in ACBCC suggests that treatment with Herceptin (trastuzumab) may be effective in patients with this rare tumour. Although erbB-2 Receptor can be over-expressed in Malignant neoplasm of Pelvis>Prostate, there is no clinical data to support the use of trastuzumab for Malignant neoplasm of Pelvis>Prostate patients. whereas the effect of the trastuzumab-RT combination was inferior to that predicted by the individual effects. HER 1-2 targeting of hormone-refractory Malignant neoplasm of Pelvis>Prostate by ZD1839 and trastuzumab Trastuzumab (Herceptin) as a single agent demonstrated poor efficacy in treating Hormone refractory Malignant neoplasm of Pelvis>Prostate. To investigate the efficacy and Toxic effect of the immunoglobulin complex location to the HER-2-neu peptide vaccine-neu peptide vaccine/neu receptor (trastuzumab, Herceptin) in the treatment of advanced hormone-refractory Malignant neoplasm of Pelvis>Prostate (Hormone refractory Malignant neoplasm of Pelvis>Prostate) Conclusions regarding the predictive value of HER-2-neu peptide vaccine-neu peptide vaccine status on outcome after trastuzumab-based therapy were not reached and were only drawn after larger-scale screening efforts.  rastuzumab plus docetaxel in HER-2-neu peptide vaccine-neu peptide vaccine/neu-positive Pelvis>Prostate carcinoma clinical trials are currently in progress in patients with Malignant neoplasm of Pelvis>Prostate testing novel agents that selectively interfere with these receptors, such as trastuzumab, ytotoxicity of Homo sapiens Malignant neoplasm of Pelvis>Prostate Cultured Cell Line in vitro and induction of apoptosis using 213Bi-Herceptin alpha-conjugate The clinical interpretation of ERBB2 wt Allele abnormalities should reflect the complexity of ERBB2 wt Allele mediated regulatory pathway and explain why Neoplasms with overexpression/amplification of ERBB2 wt Allele very often do not respond to therapy using Herceptin HER-2-neu peptide vaccine-neu peptide vaccine overexpression also has been reported in up to 60% of patients with hormone-refractory Pelvis>Prostate carcinoma (Hormone refractory Malignant neoplasm of Pelvis>Prostate) and was correlated with shortened survival Unlike Breast Carcinoma and contrary to prior reports, HER-2-neu peptide vaccine-neu peptide vaccine overexpression by IHC in archival Pelvis>Prostate tissue from patients who eventually developed hormone-refractory Disease was infrequent. There did not appear to be any correlation between HER-2-neu peptide vaccine-neu peptide vaccine overexpression by IHC and shed HER-2-neu peptide vaccine-neu peptide vaccine antigen levels in serum by ELISA in this tumor type. Further development of trastuzumab for the treatment of patients with Metastatic Prostate Carcinoma is not feasible until more reliable and practical methods of sampling metastatic Disease are developed to identify patients with HER-2-neu peptide vaccine-neu peptide vaccine positive tumors. the expression of ERBB2 in Malignant neoplasm of Pelvis>Prostate is relatively low, and is not altered during Disease progression. Thus, it is unlikely that treatment modalities relying on the overexpression of ERBB2 gene will be useful in treating Malignant neoplasm of Pelvis>Prostate. A phase I study was designed to evaluate Docetaxel-Estramustine Regimen plus trastuzumab, a Antibodies, Monoclonal, Humanized that binds to the erbB-2 Receptor receptor, in patients with metastatic androgen-independent Malignant neoplasm of Pelvis>Prostate (2,2'-azobis(2-(2-imidazolin-2-yl) propane) dihydrochloride) Laboratory evidence also supports the clinical evaluation of docetaxel-based combinations that include agents such as trastuzumab and/or estramustine trastuzumab, a monoclonal immunoglobulin complex location CAL binding to the erbB-2 Receptor receptor; immunotoxin conjugates use an immunoglobulin complex location directed against Epidermal Growth Factor Receptor joined to a cell toxin. All are in clinical trials for a number of Malignant Neoplasms, including Malignant neoplasm of Pelvis>Prostate we investigated the Antitumor efficacy of Herceptin, a new recombinant humanized anti-erbB-2 Receptor/neu immunoglobulin complex location, which exhibits cytostatic activity on Breast and Malignant neoplasm of Pelvis>Prostate cells that overexpress the erbB-2 Receptor oncogene. trastuzumab was found to have additive and synergistic effects with some chemotherapeutic agents ER-2/neu as a therapeutic target in Non-Small Cell Lung Carcinoma, Malignant neoplasm of Pelvis>Prostate in these Malignant neoplasm of Pelvis>Prostate model systems, Herceptin alone has clinical activity only in the androgen-dependent tumor and has at least an additive effect on growth, anti-erbB-2 Receptor receptor monoclonal immunoglobulin complex location CAL Herceptin significantly enhanced growth inhibition of the MDA Patient-Controlled Analgesia 2a cells.[SEP]Relations: Trastuzumab has relations: indication with erbB-2 Receptor positive Breast Carcinoma, indication with erbB-2 Receptor positive Breast Carcinoma, drug_drug with Daclizumab, drug_drug with Daclizumab, drug_drug with Tepoxalin, drug_drug with Tepoxalin, drug_drug with Golimumab, drug_drug with Golimumab, drug_drug with Ascrinvacumab, drug_drug with Ascrinvacumab.", "label": "yes"}
{"original_question": "Are ultraconserved elements often transcribed?", "id": "converted_1", "sentence1": "Are ultraconserved Elements often transcribed?", "sentence2": "Starting from a genome-wide expression profiling, we demonstrate for the first time a functional link between oxygen deprivation and the modulation of long noncoding RNA Transcript from ultraconserved regions, termed transcribed-ultraconserved regions (T-UCRs) Our data gives a first glimpse of a novel functional hypoxic network comprising protein-coding RNA Transcript and noncoding RNA (ncRNAs) from the T-UCRs category Highly conserved Elements discovered in Vertebrates are present in non-syntenic loci of tunicates, act as enhancers and can be transcribed during development The majority of these regions map onto ultraconserved Elements and we demonstrate that they can act as functional enhancers within the organism of origin, as well as in cross-transgenesis experiments, and that they are transcribed in extant species of Olfactores. We refer to the Elements as 'Olfactores conserved non-coding Elements' We used a custom microarray to assess the levels of NAGPA gene transcription during Mus sp. development and integrated these data with published microarray and next-generation sequencing datasets as well as with newly produced PCR validation experiments. We show that a large MDFAttributeType - Fraction of non-exonic UCEs is transcribed across all developmental stages examined from only one DNA strand. Although the nature of these RNA Transcript remains a mistery, our meta-analysis of RNA-Seq datasets indicates that they are unlikely to be short RNA and that some of them might encode nuclear RNA Transcript Our data shows that the concurrent presence of enhancer and transcript function in non-exonic NAGPA gene Elements is more widespread than previously shown. Moreover through our own experiments as well as the use of next-generation sequencing datasets, we were able to show that the RNA encoded by non-exonic UCEs are likely to be long RNA transcribed from only one DNA strand Short ultraconserved promoter regions delineate a class of preferentially expressed alternatively spliced RNA Transcript The importance of other classes of non-coding RNA, such as long intergenic ncRNAs (Long Intergenic Non-Protein Coding RNA) and transcribed ultraconserved regions (T-UCRs) as altered Elements in Neoplasms, is also gaining recognition. Other ncRNAs, such as PIWI-interacting RNA (Piwi-Interacting RNA), small nucleolar RNA (snoRNAs), transcribed ultraconserved regions (T-UCRs) and large intergenic non-coding RNA (Long Intergenic Non-Protein Coding RNA) are emerging as key Elements of cellular homeostasis. The majority of these regions map onto ultraconserved Elements and we demonstrate that they can act as functional enhancers within the organism of origin, as well as in cross-transgenesis experiments, and that they are transcribed in extant species of Olfactores. Transcribed ultraconserved regions (T-UCRs) are a subset of 481 DNA Sequence longer than 200 bp, which are absolutely conserved between orthologous regions of Homo sapiens, Rattus norvegicus and Mus sp. genomes, and are actively transcribed. Highly conserved Elements discovered in Vertebrates are present in non-syntenic loci of tunicates, act as enhancers and can be transcribed during development. The Evf-2 noncoding RNA is transcribed from the Dlx-5/6 ultraconserved region and functions as a Dlx-2 transcriptional coactivator. In this report, we show that the Dlx-5/6 ultraconserved region is transcribed to generate an alternatively spliced form of Evf-1, the RETINAL NONATTACHMENT, NONSYNDROMIC CONGENITAL Evf-2. These studies identify a critical role for TUC338 in regulation of transformed cell growth and of transcribed ultraconserved RETINAL NONATTACHMENT, NONSYNDROMIC CONGENITAL as a unique class of Genes involved in the pathobiology of altretamine/cisplatin/cyclophosphamide protocol. Transcribed ultraconserved region (T-UCR) RNA Transcript are a novel class of lncRNAs transcribed from ultraconserved regions (UCRs) The majority of these regions map onto ultraconserved Elements and we demonstrate that they can act as functional enhancers within the organism of origin, as well as in cross-transgenesis experiments, and that they are transcribed in extant species of Olfactores Transcribed ultraconserved regions (T-UCRs) are a subset of 481 DNA Sequence longer than 200 bp, which are absolutely conserved between orthologous regions of Homo sapiens, Rattus norvegicus and Mus sp. genomes, and are actively transcribed Other ncRNAs, such as PIWI-interacting RNA (Piwi-Interacting RNA), small nucleolar RNA (snoRNAs), transcribed ultraconserved regions (T-UCRs) and large intergenic non-coding RNA (Long Intergenic Non-Protein Coding RNA) are emerging as key Elements of cellular homeostasis Transcribed ultraconserved region in Homo sapiens Malignant Neoplasms. We show that a large MDFAttributeType - Fraction of non-exonic UCEs is transcribed across all developmental stages examined from only one DNA strand Although PCBP2 gene gene-OT1 gene is partially located within the poly(rC) binding protein 2 (PCBP2 gene gene) gene, the transcribed RETINAL NONATTACHMENT, NONSYNDROMIC CONGENITAL encoding PCBP2 gene gene-OT1 gene is expressed independently of PCBP2 gene gene and was cloned as a 590-bp RNA gene, termed TUC338 Moreover through our own experiments as well as the use of next-generation sequencing datasets, we were able to show that the RNA encoded by non-exonic UCEs are likely to be long RNA transcribed from only one DNA strand.[SEP]Relations: rRNA transcription has relations: bioprocess_protein with ANG, bioprocess_protein with ANG, bioprocess_bioprocess with plastid rRNA transcription, bioprocess_bioprocess with plastid rRNA transcription, bioprocess_bioprocess with mitochondrial rRNA transcription, bioprocess_bioprocess with mitochondrial rRNA transcription, bioprocess_bioprocess with RETINAL NONATTACHMENT, NONSYNDROMIC CONGENITAL transcription, bioprocess_bioprocess with RETINAL NONATTACHMENT, NONSYNDROMIC CONGENITAL transcription, bioprocess_bioprocess with nucleolar large rRNA transcription by RNA polymerase I, bioprocess_bioprocess with nucleolar large rRNA transcription by RNA polymerase I.", "label": "yes"}
{"original_question": "Have Quantitative Trait Loci affecting splicing (splicing QTLs) been linked to disease?", "id": "converted_2", "sentence1": "Have Quantitative Trait Loci affecting splicing (splicing QTLs) been linked to disease?", "sentence2": "The spontaneously hypertensive rat (SHORT ROOT protein, Arabidopsis) is a widely used rodent model of Hypertensive disease and Metabolic Syndrome X. Previously we identified thousands of cis-regulated expression Quantitative Trait Loci (eQTLs) across multiple Body tissue using a panel of rat recombinant inbred (RI) strains derived from Brown Norway and SHORT ROOT protein, Arabidopsis progenitors. These cis-eQTLs represent potential susceptibility loci underlying physiological and pathophysiological traits manifested in SHORT ROOT protein, Arabidopsis. We have prioritized 60 cis-eQTLs and confirmed differential expression between the parental strains by quantitative PCR in 43 (72%) of the eQTL RNA Transcript. These colocalizing correlated cis-eQTLs (c3-eQTLs) are highly attractive as primary susceptibility loci for the colocalizing pQTLs. Furthermore, sequence analysis of the c3-eQTL Genes identified Single Nucleotide Polymorphism (SNPs) that are predicted to affect transcription factor binding affinity, splicing and protein function. These SNPs, which potentially alter transcript abundance and stability, represent strong candidate factors underlying not just eQTL expression phenotypes, but also the correlated metabolic and physiological traits. In conclusion, by integration of genomic sequence, eQTL and QTT datasets we have identified several Genes that are strong positional candidates for pathophysiological traits observed in the SHORT ROOT protein, Arabidopsis strain. Identifying associations between Genotype and gene expression levels using microarrays has enabled systematic interrogation of regulatory variation underlying complex phenotypes. This approach has vast potential for functional characterization of disease states, but its prohibitive cost, given hundreds to thousands of individual samples from populations have to be genotyped and expression profiled, has limited its widespread application.RESULTS: Here we demonstrate that genomic regions with Alleles-specific expression (ASE) detected by sequencing cDNA are highly enriched for cis-acting expression Quantitative Trait Loci (cis-eQTL) identified by profiling of 500 animal allergen extracts in parallel, with up to 90% agreement on the Alleles that is preferentially expressed. We also observed widespread noncoding and antisense ASE and identified several Alleles-specific alternative splicing variants.CONCLUSION: Monitoring ASE by sequencing cDNA from as little as one sample is a practical alternative to expression genetics for mapping cis-acting variation that regulates RNA transcription and processing. The six Genes corresponded to rat and Mus sp. Quantitative Trait Loci (QTLs) that had shown associations with the common traits such as the well characterized MS and even tumor susceptibility. Our findings suggest that the six Genes may play important roles in the pleiotropic effects on lipid metabolism and the MS, which increase the risk of Type 2 Diabetes and Cardiovascular Diseases. The use of the multivariate phenotypes can be advantageous in identifying genetic risk factors, accounting for the pleiotropic effects when the multivariate phenotypes have a common etiological pathway. To elucidate mechanisms involved in Multiple Sclerosis (MS), we studied genetic regulation of experimental autoimmune encephalomyelitis (EAE) in Rattus norvegicus, assuming a Conservation of pathogenic pathways. In this study, we focused on Eae23, originally identified to regulate EAE in a (LEW.1AV1xPVG.1AV1)F2 cross. Our aim was to determine whether one or more Genes within the 67 Mb region regulate EAE and to define candidate risk Genes.METHODOLOGY/PRINCIPAL FINDINGS: We used high resolution Quantitative Trait Loci (QTL) analysis in the 10th generation (BUD31 gene) of an advanced intercross line (AIL) to resolve Eae23 into two QTLs that independently regulate EAE, namely Eae23a and Eae23b.[SEP]Relations: qualitative or quantitative defects of titin has relations: disease_disease with TTN-related myopathy, disease_disease with TTN-related myopathy, disease_disease with qualitative or quantitative protein defects in neuromuscular diseases, disease_disease with qualitative or quantitative protein defects in neuromuscular diseases, disease_disease with limb-girdle muscular dystrophy, disease_disease with limb-girdle muscular dystrophy, disease_disease with tibial muscular dystrophy, disease_disease with tibial muscular dystrophy. Multiple Sclerosis has relations: disease_disease with demyelinating disease, disease_disease with demyelinating disease.", "label": "yes"}
{"original_question": "Is SLC22A3 expressed in the brain?", "id": "converted_3", "sentence1": "Is SLC22A3 expressed in the Head>Brain?", "sentence2": "The Solute Carrier Family 22 Member 1 (OCT) 3 is widely expressed in various Organ in Homo sapiens, and involved in the disposition of many exogenous and endogenous compounds. Several lines of evidence have suggested that POU5F1 gene expressed in the Head>Brain plays an important role in the regulation of neurotransmission.  The Solute Carrier Family 22 Member 1 3 (POU5F1 gene; synonymous: extraneuronal monoamine transporter, EMT, SLC22A3 gene) encodes an Protein Isoforms of the organic cation transporters and is expressed widely across the whole Head>Brain. In agreement with this distribution, POU5F1 gene/SLC22A3 gene-deficient CASP14 gene show evidence of altered monoamine neurotransmission in the Head>Brain, with decreased Protoplasm content and increased turnover of aminergic transmitters. CRT, SLC6A6 gene (TauT/SLC6A6) and Solute Carrier Family 22 Member 1 (POU5F1 gene/SLC22A3) expressed at the BCSFB are involved in glycocyamine or creatine/creatine/creatinine efflux transport from Cerebrospinal Fluid. The Solute Carrier Family 22 Member 1 3 (POU5F1 gene; synonymous: extraneuronal monoamine transporter, EMT, SLC22A3 gene) encodes an Protein Isoforms of the organic cation transporters and is expressed widely across the whole Head>Brain The Solute Carrier Family 22 Member 1 3 (POU5F1 gene; synonymous: extraneuronal monoamine transporter, EMT, SLC22A3 gene) encodes an Protein Isoforms of the organic cation transporters and is expressed widely across the whole Head>Brain.  CRT may be a key factor facilitating blood-to-Head>Brain guanidinoacetate transport in patients deficient in S-adenosylmethionine:guanidinoacetate N-methyltransferase, the creatine biosynthetic enzyme, resulting in cerebral accumulation of guanidinoacetate. CRT, SLC6A6 gene (TauT/SLC6A6) and Solute Carrier Family 22 Member 1 (POU5F1 gene/SLC22A3) expressed at the BCSFB are involved in glycocyamine or creatine/creatine/creatinine efflux transport from Cerebrospinal Fluid. SLC22A3 gene) encodes an Protein Isoforms of the organic cation transporters and is expressed widely across the whole Head>Brain. CRT, SLC6A6 gene (TauT/SLC6A6) and Solute Carrier Family 22 Member 1 (POU5F1 gene/SLC22A3) expressed at the BCSFB are involved in glycocyamine or creatine/creatine/creatinine efflux transport from Cerebrospinal Fluid. Interestingly, Blood - Head>Brain barrier anatomy efflux transport of Ceramide Glucosyltransferase, human, including guanidinoacetate and creatine/creatine/creatinine, is negligible, though the Blood - Head>Brain barrier anatomy has a variety of efflux transport systems for synthetic precursors of Ceramide Glucosyltransferase, human, such as Antifibrinolytic Antifibrinolytic amino acids and neurotransmitters.  The Solute Carrier Family 22 Member 1 (OCT) 3 is widely expressed in various Organ in Homo sapiens, and involved in the disposition of many exogenous and endogenous compounds. Several lines of evidence have suggested that POU5F1 gene expressed in the Head>Brain plays an important role in the regulation of neurotransmission. CRT, SLC6A6 gene (TauT/SLC6A6) and Solute Carrier Family 22 Member 1 (POU5F1 gene/SLC22A3) expressed at the BCSFB are involved in glycocyamine or creatine/creatine/creatinine efflux transport from Cerebrospinal Fluid. Several lines of evidence have suggested that POU5F1 gene expressed in the Head>Brain plays an important role in the regulation of neurotransmission. The Solute Carrier Family 22 Member 1 3 (POU5F1 gene; synonymous: extraneuronal monoamine transporter, EMT, SLC22A3 gene) encodes an Protein Isoforms of the organic cation transporters and is expressed widely across the whole Head>Brain. POU2F2 gene-OCT-3 display differential tissue distribution: POU2F1 gene is predominantly found in Abdomen>Liver of Homo sapiens, and Abdomen>Liver and Both kidneys in Rodent; POU2F2 gene is most strongly expressed in both human and rodent Both kidneys, whereas is POU5F1 gene primarily expressed in Placenta Specimen, but also more widely detected in various Body tissue, including Head>Brain and Chest>Lung.[SEP]Relations: SLC22A3 has relations: anatomy_protein_present with heart, anatomy_protein_present with heart, anatomy_protein_present with colon, anatomy_protein_present with colon, cellcomp_protein with membrane, cellcomp_protein with membrane, anatomy_protein_present with Both kidneys, anatomy_protein_present with Both kidneys, anatomy_protein_present with intestine, anatomy_protein_present with intestine.", "label": "yes"}
{"original_question": "Is alternative splicing of apoptotic genes playing a role in the response to DNA or mitochondrial damage?", "id": "converted_4", "sentence1": "Is alternative splicing of apoptotic genes playing a role in the response to DNA or Mitochondrial Damage?", "sentence2": "Apoptosis promoted by UV in Cells lacking TP53 wt Allele is prevented when the change in AS of the apoptotic gene bcl-x is reverted, confirming the relevance of this mechanism. We demonstrate that E2F1 protein, human protein, human requires SRSF2 wt Allele to switch the alternative splicing profile of various apoptotic genes such as CASP8 and FADD-Like Apoptosis Regulator Protein, caspases-8 and -9 and bcl-x protein, towards the expression of pro-apoptotic splice variants. Finally, we provide evidence that E2F1 protein, human protein, human upregulates SRSF2 wt Allele in response to DNA-damaging agents and show that SRSF2 wt Allele is required for apoptosis in response to these drugs. This analysis revealed that DNA damage resulted in changes in splicing activity that Changing the splicing pattern of Fas, a key pro-apoptotic, TP53 wt Allele-inducible death receptor. bortezomib induces Mitochondrial Damage in native Cells and also activates the UPR by splicing of X-Box Binding Protein 1, Human and induction of CHOP protocol-cyclophosphamide/doxorubicin/prednisone/vincristine protocol-cyclophosphamide/doxorubicin/prednisone/vincristine, which is significantly reduced by silencing of MUC4 protein, human protein, human. The tumour-suppressor protein TP53 wt Allele is an important activator of apoptosis. Although TP53 wt Allele-deficient cancer Cells are less responsive to chemotherapy, their resistance is not complete, which suggests that other apoptotic pathways may exist. A TP53 wt Allele-related gene, p73 protein, human protein, human, which encodes several Proteins as a result of alternative splicing, can also induce apoptosis. Induction of apoptosis was significantly reduced in P388/SPR Cells, as indicated by minimal DNA fragmentation. Analysis of Oncogenes regulating apoptotic cell death revealed a marked decrease of BCL2 gene in combination with a moderate reduction of BAX protein, human, but a striking overexpression of the long form of the bcl-X protein.[SEP]Relations: positive regulation of intrinsic apoptotic signaling pathway in response to DNA damage by TP53 wt Allele class mediator has relations: bioprocess_bioprocess with positive regulation of intrinsic apoptotic signaling pathway in response to DNA damage, bioprocess_bioprocess with positive regulation of intrinsic apoptotic signaling pathway in response to DNA damage, bioprocess_bioprocess with regulation of intrinsic apoptotic signaling pathway in response to DNA damage by TP53 wt Allele class mediator, bioprocess_bioprocess with regulation of intrinsic apoptotic signaling pathway in response to DNA damage by TP53 wt Allele class mediator, bioprocess_protein with RPL26, bioprocess_protein with RPL26, bioprocess_bioprocess with positive regulation of intrinsic apoptotic signaling pathway by TP53 wt Allele class mediator, bioprocess_bioprocess with positive regulation of intrinsic apoptotic signaling pathway by TP53 wt Allele class mediator. mitochondrial matrix has relations: cellcomp_protein with AASS, cellcomp_protein with AASS.", "label": "yes"}
{"original_question": "Is exonuclease Xrn1 a component of the P-bodies?", "id": "converted_5", "sentence1": "Is exonuclease Xrn1 a component of the P-bodies?", "sentence2": "Pencil Beam Scanning are associated with RNA, Messenger decay and contain the decapping ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS dipeptidyl carboxypeptidase dipeptidyl carboxypeptidase DCP1/2, the 5' to 3' exonuclease Xrn1, the Lsm Proteins (1-7), and the scaffolding Proteins hedls/GE-1 and TNRC6A gene. Both Shprintzen-Goldberg syndrome and Pencil Beam Scanning contain RNA, Messenger, Eukaryotic Initiation Factor-4E, microRNAs and Protein Argonaute-1 Proteins, and various regulators of RNA, Messenger stability and translation (Congenital Thrombotic Thrombocytopenic Purpura, RCK/p54, and CPEB). An alternative pathway of RNA, Messenger degradation occurs at processing bodies, Cytoplasmic foci that contain decapping ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS, the 5'-3' exonuclease Xrn1 and the Lsm1-7 heptamer.  n eukaryotic Cells degradation of bulk RNA, Messenger in the 5' to 3' direction requires the consecutive action of the decapping complex (consisting of dipeptidyl carboxypeptidase dipeptidyl carboxypeptidase DCP1 and DCP2 gene gene) and the 5' to 3' exonuclease XRN1 protein, Homo sapiens protein, Homo sapiens. These ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS are found in discrete Cytoplasmic foci known as P-bodies or GW-Bodies (because of the accumulation of the TNRC6A gene antigen). Several Proteins that stimulate RNA, Messenger decapping by the Dcp1:Dcp2 complex co-localize with Dcp1 and Dcp2, together with Xrn1, a 5'-to-3' exonuclease, to structures in the Cytoplasm called processing bodies.   On the other hand, many Processing Bodies components including LSM1 gene gene, TNRC6A gene, DDX3X wt Allele, DDX6 gene gene and XRN1 protein, Homo sapiens protein, Homo sapiens, but not others like DCP1a and EDC4 gene gene are recruited to the viral replication sites, as evidenced by their colocalization at perinuclear region with viral NS3. We identified the Pab 1801 Cytoplasmic puncta as P Bodies (Pencil Beam Scanning), which are involved in RNA, Messenger regulation. We found that, in several Cultured Cell Line, including U2OS, WI38, SK-N-SH and HCT116, the Pab 1801 puncta strictly colocalize with Pencil Beam Scanning identified with specific Antibodies, in vitro diagnostic against the HTN3 gene components Hedls, DCP1A gene, Xrn1 or Rck/p54. The core components of P-bodies, including the decapping machinery (Dcp2 and Dhh1), 5'-3' Exoribonucleases (Kem1/Xrn1), and the Processing Bodies scaffolding protein (Edc3), were identified and their localizations with respect to P-bodies were demonstrated. The second type of Granules dose form, piP-bodies, harbors the MIWI2-TDRD9-MAEL module of the piRNA pathway and signature components of P-bodies, TNRC6A gene, DCP1a, DDX6 gene gene/p54, and XRN1 protein, Homo sapiens protein, Homo sapiens Proteins. In Saccharomyces cerevisiae and Homo sapiens tissue culture Cells, Xrn1 has been shown to be a component of P-bodies (processing bodies), dynamic Cytoplasmic Granules dose form where RNA degradation can take place. Here, we show that staufen- and FMRP-containing RNPs in Drosophila <basidiomycetes> <basidiomycetes> neurons contain Proteins also present in somatic \"P bodies,\" including the RNA-degradative ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS Dcp1p and Xrn1p/Pacman and crucial components of MicroRNAs (Protein Argonaute-1), Nonsense Mediated RNA, Messenger Decay (Upf1p), and general translational repression (Dhh1p/Me31B) pathways.  In eukaryotic Cells, XRN1 protein, Homo sapiens protein, Homo sapiens is often found in particles known as processing bodies (P bodies) together with other Proteins involved in the 5' \u2192 3' degradation pathway, such as DCP2 gene gene and the helicase DHH1 (Me31B).  In Saccharomyces cerevisiae and Homo sapiens tissue culture Cells, Xrn1 has been shown to be a component of P-bodies (processing bodies), dynamic Cytoplasmic Granules dose form where RNA degradation can take place Owing to the essential functions of P bodies in RNA, Messenger regulation, we explored computationally the functional significance of Single Nucleotide Polymorphism in 7 P body components such as XRN1 protein, Homo sapiens protein, Homo sapiens, DCP2 gene gene, EDC3 gene gene, CPEB1 gene gene, GEMIN5 gene gene, STAU1 gene gene and TRIM71 gene gene The core components of P-bodies, including the decapping machinery (Dcp2 and Dhh1), 5&apos;-3&apos; Exoribonucleases (Kem1/Xrn1), and the Processing Bodies scaffolding protein (Edc3), were identified and their localizations with respect to P-bodies were demonstrated Here, we show that staufen- and FMRP-containing RNPs in Drosophila <basidiomycetes> <basidiomycetes> neurons contain Proteins also present in somatic &quot;P bodies,&quot; including the RNA-degradative ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS Dcp1p and Xrn1p/Pacman and crucial components of MicroRNAs (Protein Argonaute-1), Nonsense Mediated RNA, Messenger Decay (Upf1p), and general translational repression (Dhh1p/Me31B) pathways Processing Bodies components LSM1 gene gene, TNRC6A gene, DDX3X wt Allele, DDX6 gene gene and XRN1 protein, Homo sapiens protein, Homo sapiens are recruited to WNV replication sites and positively regulate viral replication. The core components of P-bodies, including the decapping machinery (Dcp2 and Dhh1), 5&apos;-3&apos; Exoribonucleases (Kem1/Xrn1), and the Processing Bodies scaffolding protein (Edc3), were identified and their localizations with respect to P-bodies were demonstrated. Various growth conditions, including glucose deprivation, hyperosmotic stress, and heat stress, stimulated the accumulation of P-bodies. Here we show that microscopically visible P-bodies are greatly diminished following West Nile viral Communicable Diseases, but the component Proteins are not depleted. On the other hand, many Processing Bodies components including LSM1 gene gene, TNRC6A gene, DDX3X wt Allele, DDX6 gene gene and XRN1 protein, Homo sapiens protein, Homo sapiens, but not others like DCP1a and EDC4 gene gene are recruited to the viral replication sites, as evidenced by their colocalization at perinuclear region with viral NS3. Owing to the essential functions of P bodies in RNA, Messenger regulation, we explored computationally the functional significance of Single Nucleotide Polymorphism in 7 P body components such as XRN1 protein, Homo sapiens protein, Homo sapiens, DCP2 gene gene, EDC3 gene gene, CPEB1 gene gene, GEMIN5 gene gene, STAU1 gene gene and TRIM71 gene gene. Computational analyses of non-synonymous Single Nucleotide Polymorphism of these components was initiated using well utilized publicly available software programs such as the SIFT, followed by PolyPhen, Panthers, MutPred, I-Mutant-2. Xrn1 has been shown to be a component of P-bodies (processing bodies), Here, we show that DIS3-Like Exonuclease 2 is an exosome-independent Cytoplasmic RNA, Messenger 3'-5' exonuclease, which exhibits processive activity on structured RNA substrates in vitro. DIS3-Like Exonuclease 2 associates with hXRN1 in an RNA-dependent manner and can, like hXRN1, be found on Set of polysomal ribosomes Inhibition of TAK1-JNK signaling also affected the number and size of P bodies and the localization of DCP1a, Xrn1, and Edc4.  The organizing mechanism that forms P body foci in Cells is unknown; however, potential scaffolding, aggregating, or other regulatory Proteins found in P bodies were investigated for degradation. Two factors involved in 5'-end RNA, Messenger decapping and degradation, Xrn1 and DCP1A gene, and the 3' deadenylase complex component NLRP6 wt Allele underwent accelerated degradation during Communicable Diseases, and DCP1A gene may be a direct substrate of PV 3C proteinase. Secondly, P-bodies recruit mRNAs that are targeted for deadenylation and degradation by the decapping/Xrn1 pathway.  Depletion of TRN increased the number of P-bodies and stabilized ARE-containing mRNAs, as observed with knockdown of the 5'-3' exonuclease Xrn1. In this paper we show for the first time that Pacman, the Drosophila <basidiomycetes> <basidiomycetes> homologue of Xrn1, is localized in Cytoplasmic particles in Drosophila <basidiomycetes> <basidiomycetes> testis Cells.  Depletion of TRN increased the number of P-bodies and stabilized ARE-containing mRNAs, as observed with knockdown of the 5&apos;-3&apos; exonuclease Xrn1 These structures stain positively for a number of Processing Bodies and microRNP components, a microRNA-repressed RNA, Messenger and some translational repressors. They appear more heterogeneous than P-bodies of HeLa Cells, and they rarely contain the exonuclease Xrn1 but are positive for Ribosomal RNA.[SEP]Relations: 5'-3' Exoribonucleases activity has relations: molfunc_protein with XRN1 protein, Homo sapiens, molfunc_protein with XRN1 protein, Homo sapiens, molfunc_protein with XRN2, molfunc_protein with XRN2, molfunc_protein with DCP2 gene, molfunc_protein with DCP2 gene. EDC3 gene has relations: bioprocess_protein with Processing Bodies assembly, bioprocess_protein with Processing Bodies assembly. CPEB1 gene has relations: cellcomp_protein with Processing Bodies, cellcomp_protein with Processing Bodies.", "label": "yes"}
{"original_question": "Is there a package in R/bioconductor for classification of alternative splicing?", "id": "converted_6", "sentence1": "Is there a package in R/bioconductor for classification of alternative splicing?", "sentence2": "Splicer Device: an R package for classification of alternative splicing and prediction of coding potential from Whole Transcriptome Sequencing data. Recent software improvements in full-length RNA Transcript deconvolution prompted us to develop Splicer Device, an R package for classification of alternative splicing and prediction of coding potential. Splicer Device uses the full-length RNA Transcript output from Whole Transcriptome Sequencing assemblers to detect single or multiple exon skipping, alternative donor and acceptor sites, intron retention, alternative first or last exon usage, and mutually exclusive exon events. For each of these events Splicer Device also annotates the genomic coordinates of the differentially spliced elements, facilitating downstream sequence analysis. For each RNA Transcript isoform fraction values are calculated to identify RNA Transcript switching between conditions. Lastly, Splicer Device predicts the coding potential, as well as the potential nonsense mediated decay (NMD) sensitivity of each RNA Transcript. Recent software improvements in full-length RNA Transcript deconvolution prompted us to develop Splicer Device, an R package for classification of alternative splicing and prediction of coding potential. Recent software improvements in full-length RNA Transcript deconvolution prompted us to develop Splicer Device, an R package for classification of alternative splicing and prediction of coding potential.  Recent software improvements in full-length RNA Transcript deconvolution prompted us to develop Splicer Device, an R package for classification of alternative splicing and prediction of coding potential.[SEP]Relations: rRNA transcription has relations: bioprocess_bioprocess with 5S class rRNA transcription by RNA polymerase III, bioprocess_bioprocess with 5S class rRNA transcription by RNA polymerase III, bioprocess_protein with SIRT7, bioprocess_protein with SIRT7, bioprocess_protein with NPM3, bioprocess_protein with NPM3, bioprocess_protein with ANG, bioprocess_protein with ANG, bioprocess_protein with TP53, bioprocess_protein with TP53.", "label": "yes"}
{"original_question": "Is intense physical activity associated with longevity?", "id": "converted_7", "sentence1": "Is intense physical activity associated with longevity?", "sentence2": "Our major finding is that repeated very intense exercise prolongs life span in well trained practitioners. Cessation of life rates declined with increased levels of total activity (estimated in kilocalories), and declined also with increased intensity of effort measured as from none, to light, to moderately vigorous or vigorous sports play. Cessation of life rates at any given quantity of physical exercise were lower for men playing moderately intense sports than for less vigorous men. he purpose of this study was to investigate if jogging, which can be very vigorous, is associated with increased all-cause mortality in men and women. This long-term study of joggers showed that jogging was associated with significantly lower all-cause mortality and a substantial increase in survival for both men and women. Light activities (<4 multiples of resting metabolic rate (METs)) were not associated with reduced mortality rates, moderate activities (4-<6 METs) appeared somewhat beneficial, and vigorous activities (> or =6 METs) clearly predicted lower mortality rates (p, trend = 0.72, 0.07, and <0.001, respectively). These data demonstrate a graded inverse relationship between total physical activity and mortality. Furthermore, vigorous activities but not nonvigorous activities were associated with longevity. The capacity for prolonged and vigorous physical exercise, particularly if the exercise is recreational, is a strong indicator of longevity.[SEP]Relations: Cessation of head growth has relations: disease_phenotype_positive with Angelman syndrome due to a point mutation, disease_phenotype_positive with Angelman syndrome due to a point mutation, phenotype_phenotype with Secondary microcephaly, phenotype_phenotype with Secondary microcephaly, disease_phenotype_positive with Angelman syndrome due to paternal uniparental disomy of chromosome 15, disease_phenotype_positive with Angelman syndrome due to paternal uniparental disomy of chromosome 15, disease_phenotype_positive with Angelman syndrome due to maternal 15q11q13 deletion, disease_phenotype_positive with Angelman syndrome due to maternal 15q11q13 deletion, disease_phenotype_positive with neurodevelopmental disorder with progressive microcephaly, spasticity, and brain anomalies, disease_phenotype_positive with neurodevelopmental disorder with progressive microcephaly, spasticity, and brain anomalies.", "label": "yes"}
{"original_question": "Have gnotobiotic animal models been used for the study of bowel disease?", "id": "converted_8", "sentence1": "Have gnotobiotic animal models been used for the study of bowel disease?", "sentence2": "Host gene expression in the TUBE,COLON,22FR,RADIOPAQUE RUBBER B#7370 of gnotobiotic interleukin-2-deficient CASP14 gene colonized with commensal colitogenic or noncolitogenic bacterial strains: common patterns and Bacteria strain specific signatures.  Specific pathogen-free (SPF), but not germfree (GF), interleukin (IL)-2-deficient (IL-2-/-) CASP14 gene develop INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome) at 10 to 15 weeks of age. Gnotobiotic IL-2-/- CASP14 gene monocolonized with E. coli mpk develop Irritable Bowel Syndrome at 25 to 33 weeks of age but not B. vulgatus mpk, E. coli Nissle 1917, or CASP14 gene cocolonized with both E. coli mpk and B. vulgatus Lactobacillus reuteri promotes Helicobacter hepaticus-associated Typhlocolitis in gnotobiotic B6.129P2-IL-10(tm1Cgn) (IL-10(-/-) ) CASP14 gene. To model INFLAMMATORY BOWEL DISEASE 2, we assessed Communicable Diseases with Helicobacter hepaticus 3B1 (ATCC 51449) and a potential probiotic Lactobacillus reuteri (ATCC PTA-6475) in gnotobiotic B6.129P2-IL-10(tm1Cgn) (IL-10(-/-) ) CASP14 gene. No Typhlocolitis developed in Germ-Free controls (n=21) or in Lactobacillus reuteri (n=8) or H. hepaticus (n=18) mono-associated CASP14 gene for 20 weeks post-Communicable Diseases. As positive controls, three specific pathogen-free IL-10(-/-) CASP14 gene dosed with H. hepaticus developed severe Typhlocolitis within 11 weeks.  These data support that the development of Typhlocolitis in H. hepaticus-infected IL-10(-/-) CASP14 gene required co-colonization with other Microbiota (plant) and in this study, required only Lactobacillus reuteri.  When transferred to gnotobiotic CASP14 gene, gut microbiomes from CASP14 gene with active disease versus treatment-induced remission elicited varying degrees of Colitis.  The role of gut Microbiota (plant) (commensal Bacteria) and the mucosal barrier in the pathogenesis of inflammatory and Autoimmune Diseases and Primary malignant neoplasm: contribution of Germ-Free and gnotobiotic animal models of Homo sapiens diseases. The immunomodulatory effects of Microbiota (plant) and probiotics for Inflammatory Bowel Diseases and the role of Bacteria in their etiologies are being studied in gnotobiotic systems. To model INFLAMMATORY BOWEL DISEASE 2, we assessed Communicable Diseases with Helicobacter hepaticus 3B1 (ATCC 51449) and a potential probiotic Lactobacillus reuteri (ATCC PTA-6475) in gnotobiotic B6.129P2-IL-10(tm1Cgn) (IL-10(-/-) ) CASP14 gene. Gnotobiotic piglets may be used as a suitable animal model to study Colitis induced by C. jejuni The role of gut Microbiota (plant) (commensal Bacteria) and the mucosal barrier in the pathogenesis of inflammatory and Autoimmune Diseases and Primary malignant neoplasm: contribution of Germ-Free and gnotobiotic animal models of Homo sapiens diseases We investigated the changes in renal expression of KITLG wt Allele as a consequence of Colitis. METHODS: We studied 3 mouse models of Irritable Bowel Syndrome: Colitis induced by trinitrobenzene sulfonic acid, Colitis induced by microflora (in gnotobiotic interleukin-10(-/-)), and Colitis induced by adoptive transfer of CD4(+)CD45RB(high) T cells.  METHODS: We studied 3 mouse models of Irritable Bowel Syndrome: Colitis induced by trinitrobenzene sulfonic acid, Colitis induced by microflora (in gnotobiotic interleukin-10(-/-)), and Colitis induced by adoptive transfer of CD4(+)CD45RB(high) T cells.[SEP]Relations: INFLAMMATORY BOWEL DISEASE 2 has relations: disease_phenotype_positive with Abnormal intestine morphology, disease_phenotype_positive with Abnormal intestine morphology, disease_phenotype_positive with Abnormal intestine morphology, disease_phenotype_positive with Abnormal intestine morphology, contraindication with Phenobarbital, contraindication with Phenobarbital, contraindication with Phenobarbital, contraindication with Phenobarbital, disease_protein with GHRL, disease_protein with GHRL.", "label": "yes"}
{"original_question": "Is it possible to detect survivin protein expression in normal human adult tissues?", "id": "converted_9", "sentence1": "Is it possible to detect survivin protein expression in normal Homo sapiens adult Body tissue?", "sentence2": "BIRC5 protein, human protein, Homo sapiens wt Allele (BIRC5 protein, human protein, Homo sapiens) is one of the members of IAP-family apoptosis inhibitors. The BIRCS gene is expressed in most Homo sapiens embryonic Body tissue and malignant Neoplasms but not in normal differentiated Body tissue of adult Homo sapiens. BIRC5 protein, human protein, Homo sapiens wt Allele is an PPP1R1A gene of apoptosis that is undetectable in most terminally differentiated normal Homo sapiens Body tissue, strongly expressed in embryonic and fetal organs and is strongly expressed in many different Homo sapiens Malignant Neoplasms. BIRC5 protein, human protein, Homo sapiens wt Allele is a member of the PPP1R1A gene apoptosis family that is overexpressed in many malignancies. It has five known alternative splice forms, some of which differ in their antiapoptotic properties and expression levels in Homo sapiens Malignant Neoplasms. survivin is usually not expressed in normal adult Body tissue, AZD 1152-hQPA induced caspase-dependent apoptosis of some Cultured Cell Line, demonstrated by loss of Mitochondrial Membranes potential, activation of caspase-9, followed by activation of caspase-3. This effect was accompanied by the inhibition of survivin expression. In vivo efficacy was determined in NOD/SCID/\u03b3c(null) mice implanted with the Ramos Homo sapiens Burkitt Lymphoma cell line. AZD 1152 had anti-tumour effects in this Mus xenograft model. There preclinical data suggest that the inhibition of Aurora Kinase B is a potentially useful therapeutic strategy in Burkitt Lymphoma and Hodgkin Disease. a novel antiapoptosis gene, i.e., survivin, was identified as a structurally unique member of the PPP1R1A gene of apoptosis protein family. BIRC5 protein, human protein, Homo sapiens wt Allele expression is turned off during fetal development and not found in non-neoplastic adult Homo sapiens Body tissue but is again turned on in the most common Homo sapiens Malignant Neoplasms. The antiapoptotic properties of survivin might provide a significant growth advantage in Neoplasms and possibly also contribute to chemoresistance of Primary malignant neoplasm. Further comparison of the distribution of SPDEF wt Allele with other widely recognized Primary malignant neoplasm-associated molecules showed that SPDEF wt Allele has more restricted distributions than Oncogene ErbB2, BCL2 gene, survivin or Telomerase in cDNA Library from normal Homo sapiens Body tissue and more increased distribution than Oncogene ErbB2, CA-125 Antigen Antigen, BCL2 gene, survivin and Telomerase in cDNA Library from Head>Brain (except survivin), Breast, Chest>Lung and ovarian neoplasm. These data together show a better tumor-association for SPDEF wt Allele and suggest that SPDEF wt Allele is a more suitable target for developing specific Primary malignant neoplasm therapies. we identified decreased FHIT protein, Homo sapiens protein, Homo sapiens expression resulting in apoptosis inhibition and decreasing apoptosis associated with abnormal levels of some pro- and Apoptosis Inhibiting Proteins (BAX protein, Homo sapiens, BCL2 gene and BIRC5 protein, human protein, Homo sapiens wt Allele) by TUNEL and Thrombotic Microangiopathies. Our results demonstrated that the Mutation Abnormality in the FHIT protein, Homo sapiens protein, Homo sapiens gene significantly reduced FHIT protein, Homo sapiens protein, Homo sapiens expression in Homo sapiens CRC. Both TUNEL and Thrombotic Microangiopathies experiments demonstrated significantly inhibited apoptosis by down-regulation of BAX protein, Homo sapiens and up-regulation of BIRC5 protein, human protein, Homo sapiens wt Allele and BCL2 gene. Collectively, these studies identify the mechanism by which an important Tumor Suppressor Genes, FHIT protein, Homo sapiens protein, Homo sapiens, inactivated specifically in Homo sapiens CRC, and contributes to our understanding of the mechanism of colorectal carcinogenesis.[SEP]Relations: PPP1R1A has relations: anatomy_protein_present with adult mammalian kidney, anatomy_protein_present with adult mammalian kidney, anatomy_protein_present with adipose tissue, anatomy_protein_present with adipose tissue, anatomy_protein_present with muscle tissue, anatomy_protein_present with muscle tissue, anatomy_protein_present with blood, anatomy_protein_present with blood. Breast has relations: anatomy_protein_present with VIM, anatomy_protein_present with VIM.", "label": "no"}
{"original_question": "Is delayed enhancement documented in patients with non-ischemic dilated cardiomyopathy?", "id": "converted_10", "sentence1": "Is delayed enhancement documented in patients with non-ischemic dilated Cardiomyopathies?", "sentence2": "Myocardial Fibrosis was present in 30% of patients, the majority of which was mid-myocardial (63%).   3',5'-dichloromethotrexate patients frequently have myocardial Fibrosis detected on CE-CMR, the majority of which is mid-myocardial. Fifty (40%) patients showed myocardial DE, representing 12\u00b17% of LV mass. one case was dilated Cardiomyopathies, in which the delayed enhancement was diffuse small midwall spots  In the dilated Cardiomyopathies group, only seven (29%) patients showed delayed enhancement and its pattern was characterized by mid-wall, patchy or diffuse location. Patterns of delayed enhancement are different in dilated Cardiomyopathies and ischemic Cardiomyopathies, reflecting the presence of scarring or various degrees of Fibrosis in left ventricular myocardium. The presence of subendocardial or Transmural delayed enhancement at contrast-enhanced cardiovascular magnetic resonance allowed distinction between dilated Cardiomyopathies and ischemic Cardiomyopathies with high sensitivity (88%) and specificity (100%).[SEP]Relations: dilated Cardiomyopathies has relations: disease_disease with non-familial dilated Cardiomyopathies, disease_disease with non-familial dilated Cardiomyopathies, disease_disease with left ventricular noncompaction, disease_disease with left ventricular noncompaction, disease_disease with syndrome associated with dilated Cardiomyopathies, disease_disease with syndrome associated with dilated Cardiomyopathies, disease_disease with qualitative or quantitative defects of beta-myosin heavy chain (MYH7), disease_disease with qualitative or quantitative defects of beta-myosin heavy chain (MYH7), disease_disease with intrinsic Cardiomyopathies, disease_disease with intrinsic Cardiomyopathies.", "label": "yes"}
{"original_question": "Do lincRNAs play a role in human cancer?", "id": "converted_11", "sentence1": "Do lincRNAs play a role in Homo sapiens Primary malignant neoplasm?", "sentence2": "Long Intergenic Non-Protein Coding RNA H19 Imprinted Maternal Untranslated mRNA Imprinted Maternal Untranslated mRNA increases bladder Primary malignant neoplasm metastasis These data suggest that upregulated H19 Imprinted Maternal Untranslated mRNA Imprinted Maternal Untranslated mRNA enhances bladder Primary malignant neoplasm metastasis by associating with EZH2 protein, human protein, Homo sapiens and inhibiting E-cad expression lncRNA H19 Imprinted Maternal Untranslated mRNA Imprinted Maternal Untranslated mRNA is essential for Homo sapiens Specimen Source Codes - Specimen Source Codes - tumor growth Previous reports have demonstrated that HOTAIR gene gene associates with chromatin modifications in cooperation with the Polycomb complex Polycomb Repressive Complex 2, and promotes Breast and colorectal Primary malignant neoplasm metastasis although the clinical significance of HOTAIR gene gene expression in altretamine/cisplatin/cyclophosphamide protocol may not be as pronounced as that in Breast and Colorectal Carcinoma, the current study demonstrates that HOTAIR gene gene expression is associated with altretamine/cisplatin/cyclophosphamide protocol progression, warranting further studies. Long Intergenic Non-Protein Coding RNA HOTAIR gene gene is an independent prognostic marker for Nasopharyngeal carcinoma progression and survival Long Intergenic Non-Protein Coding RNA influences radiosensitivity of colorectal carcinoma cell lines by regulating Cyclin D1 expression Long Intergenic Non-Protein Coding RNA Urothelial Carcinoma associated 1 (UCA1 gene gene) promotes Homo sapiens bladder Primary malignant neoplasm cell proliferation, but the underlying mechanism remains unknown UCA1 gene gene regulated cell cycle through Cyclic AMP-Responsive DNA-Binding Protein via PI3K-AKT dependent pathway in bladder Primary malignant neoplasm. Long Intergenic Non-Protein Coding RNA UCA1 gene gene regulated cell cycle distribution via Cyclic AMP-Responsive DNA-Binding Protein through PI3-K dependent pathway in Carcinoma of bladder Cells overexpression of Yiya promotes cell cycle progression at the G1/S transition, therefore identifying Yiya as a cell-cycle-associated long non-coding RNA The long noncoding RNA HOTAIR gene gene has been reported as a poor prognostic biomarker in patients with Breast Primary malignant neoplasm. The aim of the present study is to examine the expression pattern of HOTAIR gene gene in Liver carcinoma (altretamine/cisplatin/cyclophosphamide protocol) and its clinical significance as well as its biological role in Specimen Source Codes - Specimen Source Codes - tumor progression The high expression level of HOTAIR gene gene in altretamine/cisplatin/cyclophosphamide protocol could be a candidate biomarker for predicting Specimen Source Codes - Specimen Source Codes - tumor recurrence in altretamine/cisplatin/cyclophosphamide protocol patients who have undergone liver transplant therapy and might be a potential therapeutic target Long Intergenic Non-Protein Coding RNA ANRIL is required for the Polycomb Repressive Complex 2 recruitment to and silencing of p15(INK4B) Specimen Source Codes - Specimen Source Codes - tumor suppressor gene A 42\u2009kb region on Homo sapiens chromosome 9p21 encodes for three distinct Tumor Suppressor Genes, p16(INK4A), p14(ARF) and p15(INK4B), and is altered in an estimated 30-40% of Homo sapiens Neoplasms These results advance our understanding of the role of NPTN-IT1 gene as a regulator of Hypoxia, CTCAE signaling and\u00a0offer new avenues for therapeutic intervention against Primary malignant neoplasm progression. Silencing MALAT1 gene gene is a potential novel therapeutic approach for this Primary malignant neoplasm.[SEP]Relations: Protein S Homo sapiens has relations: drug_drug with Linsidomine, drug_drug with Linsidomine, drug_drug with Ximelagatran, drug_drug with Ximelagatran, drug_drug with Melagatran, drug_drug with Melagatran, drug_drug with Vinblastine, drug_drug with Vinblastine, drug_drug with Letaxaban, drug_drug with Letaxaban.", "label": "yes"}
{"original_question": "Is the Prostate- Specific Antigen (PSA) test relevant only for prostate cancer?", "id": "converted_12", "sentence1": "Is the Prostate- Specific Antigen (Prostate-Specific Antigen) test relevant only for Malignant neoplasm of prostate?", "sentence2": "rostate cancer (Passive Cutaneous Anaphylaxis) is the most frequently diagnosed Primary malignant neoplasm and the second leading cause of Cancer-Related Death in men Prostate-Specific Antigen is known to be prostate specific, but not Passive Cutaneous Anaphylaxis specific deficiencies of serum Prostate-Specific Antigen as a prostate-cancer-specific diagnostic test are well recognized. medical debate surrounding the use of the kallikrein-related peptidase 3, human (Prostate-Specific Antigen) test for Malignant neoplasm of prostate screening The clinical relevance of this surprisingly high rate of Malignant neoplasm of prostate in men with a normal Prostate-Specific Antigen is yet to be determined  Rapid uptake of kallikrein-related peptidase 3, human (Prostate-Specific Antigen) testing has occurred in the United States despite inconclusive evidence regarding mortality benefit Routine cancer screening with kallikrein-related peptidase 3, human (Prostate-Specific Antigen) is controversial, and practice guidelines recommend that men be counseled about its risks and benefits Prostate carcinoma was histologically confirmed in 14 (0.66%) of the men, nine times in the early stage (T2) and five times in the clinical stage (T3 thoracic segmental innervation thoracic segmental innervation), corresponding to an incidence of circa 650 cases per 100,000 men in the target age group This newly developed Prostate-Specific Antigen test system can enhance the acceptance rate and effectiveness of medical check-ups for Malignant neoplasm of prostate, Prostate-Specific Antigen can be used reliably as a unique tool in the follow-up of patients for the early detection of progressive disease Prostate-Specific Antigen showed negative predictive values of 82 and 77%, respectively, using 4 and 10 ng/ml as cutoff points have assessed the feasibility of using fixed-limit criteria based on medical relevance and biological variation for evaluating the analytical performance of the kallikrein-related peptidase 3, human (Prostate-Specific Antigen) test[SEP]Relations: prostate carcinoma has relations: disease_protein with PSCA, disease_protein with PSCA, disease_protein with PSMC3IP, disease_protein with PSMC3IP, disease_protein with HSPA1A, disease_protein with HSPA1A, disease_disease with Malignant neoplasm of prostate, disease_disease with Malignant neoplasm of prostate, disease_protein with PCAT1, disease_protein with PCAT1.", "label": "no"}
{"original_question": "Is insulin-like growth factor-I (IGF-I) able to affect tendon protein synthesis in classic Ehlers-Danlos syndrome patients?", "id": "converted_13", "sentence1": "Is insulin-like growth factor-I (IGF-I) able to affect tendon protein synthesis in classic Ehlers-Danlos syndrome patients?", "sentence2": "Tendon protein synthesis rate in classic Ehlers-Danlos patients can be stimulated with insulin-like growth factor-I IGF-I injections significantly increased Flexed Sidebent Rotated values in Autoimmune Lymphoproliferative Syndrome Type 2B patients but not in controls In conclusion, baseline protein synthesis rates in Connective Tissue appeared normal in Autoimmune Lymphoproliferative Syndrome Type 2B patients, and the patients responded with an increased tendon protein synthesis rate to IGF-I injections In conclusion, baseline protein synthesis rates in Connective Tissue appeared normal in Autoimmune Lymphoproliferative Syndrome Type 2B patients, and the patients responded with an increased tendon protein synthesis rate to IGF-I injections IGF-I injections significantly increased Flexed Sidebent Rotated values in Autoimmune Lymphoproliferative Syndrome Type 2B patients but not in controls (delta values: Autoimmune Lymphoproliferative Syndrome Type 2B 0[SEP]Relations: Connective Tissue has relations: anatomy_protein_present with IGF1R, anatomy_protein_present with IGF1R, anatomy_protein_present with IGF1, anatomy_protein_present with IGF1, anatomy_protein_present with IGFBP4, anatomy_protein_present with IGFBP4, anatomy_protein_present with FGFR4, anatomy_protein_present with FGFR4, anatomy_protein_present with EGFL7, anatomy_protein_present with EGFL7.", "label": "yes"}
{"original_question": "Is there any functional association during viral replication between flaviviridae viral RNA depended RNA polymerase and viral helicase?", "id": "converted_14", "sentence1": "Is there any functional association during viral replication between flaviviridae viral RNA depended RNA polymerase and viral helicase?", "sentence2": "Several labs have obtained evidence for a Protein complex that involves many of the nonstructural (NS) Proteins encoded by the Virus. NOONAN SYNDROME 3, NS4A, NS4B, NS5A, and NS5B appear to interact structurally and functionally. In this study, we investigated the interaction between the helicase, NOONAN SYNDROME 3, and the RNA polymerase, NS5B. Pull-down experiments and surface plasmon resonance data indicate a direct interaction between NOONAN SYNDROME 3 and NS5B that is primarily mediated through the Protease Domain of NOONAN SYNDROME 3. This interaction reduces the basal Adenosine Triphosphatases activity of NOONAN SYNDROME 3. However, NS5B stimulates product formation in RNA unwinding experiments under conditions of excess Nucleic Acids substrate. When the concentrations of NOONAN SYNDROME 3 and NS5B are in excess of Nucleic Acids substrate, NS5B reduces the rate of NOONAN SYNDROME 3-catalyzed unwinding. Under pre-steady-state conditions, in which NOONAN SYNDROME 3 and substrate concentrations are similar, product formation increased in the presence of NS5B. The increase was consistent with 1:1 complex formed between the two Proteins. A fluorescently labeled form of NOONAN SYNDROME 3 was used to investigate this interaction through fluorescence polarization binding assays. Results from this assay support interactions that include a 1:1 complex formed between NOONAN SYNDROME 3 and NS5B. Contradictory results have been reported regarding NOONAN SYNDROME 3 in RNA synthesis. To investigate the effect of NOONAN SYNDROME 3 on classical swine fever Virus (CSFV) NS5B RNA-dependent RNA polymerase activity (RNA-directed RNA polymerase activity) activity and NOONAN SYNDROME 3-NS5B interaction, RNA-directed RNA polymerase activity reactions, GST-pull-down assays and co-immunoprecipitation analyses containing NS5B and either of NOONAN SYNDROME 3 protein and the different truncated NOONAN SYNDROME 3 Mutant were performed, respectively. We found that NOONAN SYNDROME 3 stimulated NS5B RNA-directed RNA polymerase activity activity in a dose-dependent manner by binding to Noonan Syndrome 5 through a NOONAN SYNDROME 3 Protease Domain. Furthermore, mapping important regions of the NOONAN SYNDROME 3 Protease Domain was carried out by Deletion Mutagenesis, associated with RNA-directed RNA polymerase activity reactions, GST-pull-down assays and co-immunoprecipitation analyses. Results showed that stimulation of CSFV NS5B RNA-directed RNA polymerase activity activity was obtained by NOONAN SYNDROME 3 binding to NS5B through a 31-amino acid fragment at the N-terminal end of NOONAN SYNDROME 3 Protease Domain, which mediated a specific NOONAN SYNDROME 3-NS5B interaction. The protocols detailed in this unit are used to purify three recombinant enzymes that are widely used in HCV research: the HCV NOONAN SYNDROME 3 Protease Domain, the helicase Superkingdom (taxonomic category) as an NOONAN SYNDROME 3+NS4A complex, and the NS5B RNA-dependent RNA polymerase. The active enzymes are purified to homogeneity by two-column chromatography to support a screening program for HCV inhibitors. Among potential targets are viral entry factors, including scavenger receptor type B1 (SCARB1 wt Allele) and CD81 antigen antigen, as well as Antibodies, Neutralizing against the viral glycoproteins. Popular targets related to translation and replication are the NOONAN SYNDROME 3/4A protease (inhibited by telaprevir and boceprevir) and the NS5B polymerase, as well as the NS2/3 autoprotease, the NOONAN SYNDROME 3 helicase, and nonenzymatic targets such as NS4B and NS5A Proteins.  The NOONAN SYNDROME 3 helicase Superkingdom (taxonomic category) competes with NOONAN SYNDROME 3 full-length for Noonan Syndrome 5 RNA-directed RNA polymerase activity binding, with a K(d.) of 2.5\u03bcM. Since NOONAN SYNDROME 3 and Noonan Syndrome 5 are required for DENV replication, this fascile assay could be used to screen for non-nucleoside, allosteric inhibitors that disrupt the interaction between the two Proteins.[SEP]Relations: RNA-directed DNA polymerase activity has relations: molfunc_molfunc with DNA polymerase activity, molfunc_molfunc with DNA polymerase activity, molfunc_protein with ERVK-11, molfunc_protein with ERVK-11, molfunc_protein with ERVK-8, molfunc_protein with ERVK-8, molfunc_protein with ERVK-10, molfunc_protein with ERVK-10, molfunc_protein with ERVK-7, molfunc_protein with ERVK-7.", "label": "yes"}
{"original_question": "Are psammoma bodies characteristic to meningiomas?", "id": "converted_15", "sentence1": "Are psammoma bodies characteristic to Meningioma?", "sentence2": "Psammomatous Meningioma Body Formation (Pencil Beam Scanning) are concentric lamellated calcified structures, observed most commonly in Papillary thyroid carcinoma (Percutaneous transhepatic cholangiography), Benign Meningioma, and Papillary Serous Cystadenocarcinoma of Pelvis>Ovary but have rarely been reported in other Neoplasms and nonneoplastic lesions. Studies on Serous Cystadenocarcinoma of Pelvis>Ovary and Benign Meningioma, however, revealed that collagen production by Neoplastic Cell and subsequent calcification was responsible for the formation of Pencil Beam Scanning. The existence of some precursor forms of Pencil Beam Scanning was reported in Meningioma and more recently in Percutaneous transhepatic cholangiography, which were mostly in the form of Extracellular hyaline globules surrounded by well-preserved Neoplastic Cell or in a smaller number of cases intracytoplasmic bodies liberated from intact Specimen Source Codes - Tumor cells, uncertain whether benign or malignant. Light microscopy revealed abundant microcysts of varied size throughout the Specimen Source Codes - Tumor tissue sample with the presence of whorl formation and psammoma body, but no malignancy was indicated. Electron microscopy further demonstrated interdigitation of the neighboring cell membranes, Desmosome, and intracytoplasmic filaments, which are pathognomonic findings of Meningioma. Unlike UBE2D1 gene, macrophage colony stimulating factor receptor activity were glycogen-containing and variously exhibited a storiform pattern (13 of 20), psammoma body formation (9 of 20), and calcification of collagen (4 of 20). Immunoreactivities included vimentin location location (100%), focal to patchy EMA (80%), S100 Proteins (80%), Collagen Type IV (25%), and patchy, mild-to-moderate CD34 staining (60%). In contrast to the inner structure, three-dimensional structure of psammona bodies in Meningioma is not well defined. This study examined three cultured Meningioma, in which surface observation of psammoma bodies might be easier than in the Specimen Source Codes - Specimen Source Codes - tumor tissues since influence of interposing Connective Tissue is minimized in Tissue culture. The results suggest that psammoma bodies in Meningioma arise in part from meningothelial whorls due to collagen production by Specimen Source Codes - Tumor cells, uncertain whether benign or malignant followed by obliteration and disappearance of Specimen Source Codes - Specimen Source Codes - tumor cell processes, although some of the alternative pathways for psammoma body formation proposed by other investigators cannot be ruled out by this study. To demonstrate that psammoma bodies in Homo sapiens Meningioma contain Collagen Type VI and Laminin. This is the first report to describe the involvement of Collagen Type VI in psammoma bodies and whorl formations in Meningioma. Physiologic calcification such as psammoma body is sometimes found especially in spinal cord Benign Meningioma but ossification of the Meningeal Neoplasms was rarely observed. Histological diagnosis was Transitional Meningioma with psammoma body. In this study we analyzed the morphologic and ultrastructural characteristics of the psammoma bodies in ten Meningioma of different histologic subtypes, characterizing the components of the psammoma body and the elements of the Specimen Source Codes - Specimen Source Codes - tumor, such as the Blood Blood capillaries and degenerative cells that have been classically considered as initiators of the formation of these calcareous is structures. It is concluded that the mineralization of the psammoma bodies is induced principally by the collagen fibers synthesized by the meningocytes and that the form of mineralization is spherical and growth is radial, controlled by the tumoral cells. CSF cytology revealed benign fibroblastic or meningotheliomatous Benign Meningioma with whorl formation and psammoma body. Electron microscopic examination of the Calculi showed Membrane Device-bound Vesicle (morphologic abnormality) and radially precipitated crystals that simulated durapatite of psammoma body in Benign Meningioma. Psammomatous Meningioma Body Formation in Meningioma resembled those in the Structure of Structure of choroid plexus stroma. The results of this study suggest that psammoma bodies in the Structure of Structure of choroid plexus, as in Meningioma, form by a process of dystrophic calcification associated with arachnoid cells and Collagen fiber. An early stage of psammoma body formation was seen more frequently in these villous microcores than in the meningocytic whorls. Psammomatous Meningioma Body Formation in meningocytic whorls were investigated by electron microscopy. Psammomatous Meningioma body formation in the meningocytic whorls may represent degeneration in some whorls of the central cells which contain Connective Tissue fibers, producing cell debris such as Membrane Device invested Vesicle (morphologic abnormality). Twenty Homo sapiens Meningioma were examined for immunoglobulin G and Immunoglobulin M by the direct immunofluorescence of immunoperoxidase methods, or both. immunoglobulin G was conspicuously found in and around the blood vessels, whorls, and psammoma bodies. It was also clearly present on the Plasma Membrane Device of the Tumor cells. Significance of these findings is briefly discussed including possible humoral immune reactions in regard to whorl and psammoma body formation in Benign Meningioma. The fine structure of psammoma bodies was examined in four cases of Fibrous Meningioma. In general, large numbers of various-sized calcified bodies (psammoma bodies) were scattered among the interstitial fibers. These findings suggest that both Matrix Pharmaceutical Inc. giant bodies and Matrix Pharmaceutical Inc. Vesicle (morphologic abnormality) may serve as initial nidus of calcification of psammoma bodies in Fibrous Meningioma. Psammomatous Meningioma body formation or dystrophic mineralization and gliosis of the intervening parenchyma was observed in all three cases.[SEP]Relations: psammomatous Benign Meningioma has relations: disease_disease with Benign Meningioma (disease), disease_disease with Benign Meningioma (disease), disease_protein with PTEN, disease_protein with PTEN, disease_protein with NF2, disease_protein with NF2, disease_protein with CSTB, disease_protein with CSTB, disease_protein with SMO, disease_protein with SMO.", "label": "yes"}
{"original_question": "Does the histidine-rich Ca-binding protein (HRC) interact with triadin?", "id": "converted_16", "sentence1": "Does the histidine-rich cyclophosphamide/doxorubicin protocol-binding Protein Info 2 (HRC) interact with TRDN gene?", "sentence2": "The HRC effects on Ryanodine Receptor Calcium Release Channel complex location may be regulated by the cyclophosphamide/doxorubicin protocol(2+)-sensitivity of its interaction with TRDN gene. In rabbit allergenic extract allergenic extract skeletal and Myocardium, HRC binds to Sarcoplasmic Reticulum (SNCG wt Allele) membranes via TRDN gene, a junctional SNCG wt Allele Protein Info.  HRC may play a key role in the regulation of SNCG wt Allele cyclophosphamide/doxorubicin protocol cycling through its direct interactions with Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase 2 and TRDN gene, mediating a fine cross talk between SNCG wt Allele cyclophosphamide/doxorubicin protocol uptake and release in the Chest>Heart. Histidine-rich CALCIUM SUPPLEMENTS binding Protein Info (HRC) is located in the Units Of Measure - Units Of Measure - lumen of Sarcoplasmic Reticulum (SNCG wt Allele) that binds to both TRDN gene (TRN-GTT2-7 gene-GTT2-7 gene) and SERCA affecting cyclophosphamide/doxorubicin protocol(2+) cycling in the SNCG wt Allele. HRC is a SNCG wt Allele luminal cyclophosphamide/doxorubicin protocol(2+) binding Protein Info known to associate with both TRDN gene and the Sarcoplasmic Reticulum cyclophosphamide/doxorubicin protocol(2+)-ATPase, and may thus mediate the crosstalk between SNCG wt Allele cyclophosphamide/doxorubicin protocol(2+) uptake and release. The histidine-rich cyclophosphamide/doxorubicin protocol(2+) binding Protein Info (HRC) is a high capacity cyclophosphamide/doxorubicin protocol(2+) binding Protein Info in the Sarcoplasmic Reticulum (SNCG wt Allele). Because HRC appears to interact directly with TRDN gene, HRC may play a role in the regulation of cyclophosphamide/doxorubicin protocol(2+) release during excitation-contraction coupling. In the present study, we have performed co-immunoprecipitation experiments and show that HRC binds directly to TRDN gene, which is an integral membrane Protein Info of the Sarcoplasmic Reticulum. A direct binding of HRC (histidine-rich cyclophosphamide/doxorubicin protocol(2+)-binding Protein Info) to TRDN gene, the main transmembrane Protein Info of the junctional Sarcoplasmic Reticulum (SNCG wt Allele) of Specimen Source Codes - Skeletal muscle, seems well supported. The present study documents the binding interaction of Specimen Source Codes - Skeletal muscle Sarcoplasmic Reticulum (SNCG wt Allele) transmembrane Protein Info TRDN gene with peripheral histidine-rich, cyclophosphamide/doxorubicin protocol(2+)-binding Protein Info (HCP). In addition, the intra-luminal histidine-rich CALCIUM SUPPLEMENTS binding Protein Info (HRC) has been shown to interact with both SERCA2a and TRDN gene. Notably, there is physical and direct interaction between these Protein Info players, mediating a fine-cross talk between SNCG wt Allele cyclophosphamide/doxorubicin protocol-uptake, storage and release. The histidine-rich CALCIUM SUPPLEMENTS-binding Protein Info (HRCBP) is expressed in the junctional SNCG wt Allele, the site of CALCIUM SUPPLEMENTS release from the SNCG wt Allele. HRCBP is expressed exclusively in Muscle Tissue and binds CALCIUM SUPPLEMENTS with low affinity and high capacity. In addition, HRCBP interacts with TRDN gene, a Protein Info associated with the Ryanodine Receptor Calcium Release Channel and thought to be involved in CALCIUM SUPPLEMENTS release. Its CALCIUM SUPPLEMENTS binding properties, localization to the SNCG wt Allele, and interaction with TRDN gene suggest that HRCBP is involved in CALCIUM SUPPLEMENTS handling by the SNCG wt Allele. Using a fusion Protein Info binding assay, we further identified the histidine-rich acidic repeats of HRC as responsible for the binding of HRC to TRDN gene.  The HRC binding domain of TRDN gene was also localized by fusion Protein Info binding assay to the lumenal region containing the KEKE motif that was previously shown to be involved in the binding of TRDN gene to CASQ2 gene. Notably, the interaction of HRC and TRDN gene is cyclophosphamide/doxorubicin protocol(2+)-sensitive. Our data suggest that HRC may play a role in the regulation of cyclophosphamide/doxorubicin protocol(2+) release from the Sarcoplasmic Reticulum by interaction with TRDN gene. Further support for colocalization of HRC with TRDN gene Cytoplasmic Domain is provided here by experiments of mild tryptic digestion of tightly sealed TC vesicles. We demonstrate that HRC can be isolated as a complex with TRDN gene, following equilibrium sucrose-density centrifugation in the presence of mM cyclophosphamide/doxorubicin protocol(2+). Here, we characterized the COOH-terminal portion of rabbit allergenic extract allergenic extract HRC, expressed and purified as a fusion Protein Info (HRC(569-852)), with respect to cyclophosphamide/doxorubicin protocol(2+)-binding properties, and to the interaction with TRDN gene on blots, as a function of the concentration of cyclophosphamide/doxorubicin protocol(2+). Our results identify the polyglutamic stretch near the COOH terminus, as the cyclophosphamide/doxorubicin protocol(2+)-binding site responsible, both for the acceleration in mobility of HRC on SDS-PAGE in the presence of millimolar concentrations of cyclophosphamide/doxorubicin protocol(2+), and for the enhancement by high cyclophosphamide/doxorubicin protocol(2+) of the interaction between HRC and TRDN gene cytoplasmic segment. In addition to providing further evidence that HCP coenriches with Ryanodine Receptor 1, Tacrolimus Binding Protein 1A, TRDN gene and CASQ2 gene (CS) in sucrose-density-purified TC vesicles, using specific polyclonal antibody, we show it to be expressed as a single Protein Info species, both in fast-twitch and slow-twitch fibers, and to identically localize to the I band. Colocalization of HCP and TRDN gene at junctional triads is supported by the overlapping staining pattern using Monoclonal Antibodies to TRDN gene. We show a specific binding interaction between digoxigenin-HCP and TRDN gene, using ligand blot techniques. Suggesting that TRDN gene dually interacts with HCP and with CS, at distinct sites, we have found that TRDN gene-CS interaction in overlays does not require the presence of Ca2+. These differential effects form the basis for the hypothesis that HCP anchors to the junctional membrane domain of the SNCG wt Allele, through binding to TRDN gene short Cytoplasmic Domain at the NH2 terminus. Although the function of this interaction, as such, is not well understood, it seems of potential biological interest within the more general context of the structural-functional role of TRDN gene at the triadic junction in Specimen Source Codes - Skeletal muscle. BACKGROUND: Histidine-rich CALCIUM SUPPLEMENTS binding Protein Info (HRC) is located in the Units Of Measure - Units Of Measure - lumen of Sarcoplasmic Reticulum (SNCG wt Allele) that binds to both TRDN gene (TRN-GTT2-7 gene-GTT2-7 gene) and SERCA affecting cyclophosphamide/doxorubicin protocol(2+) cycling in the SNCG wt Allele. Chronic overexpression of HRC that may disrupt Protoplasm cyclophosphamide/doxorubicin protocol(2+) homeostasis is implicated in pathogenesis of Cardiac Hypertrophy. Interaction of HRC (histidine-rich cyclophosphamide/doxorubicin protocol(2+)-binding Protein Info) and TRDN gene in the Units Of Measure - Units Of Measure - lumen of Sarcoplasmic Reticulum. The histidine-rich cyclophosphamide/doxorubicin protocol-binding Protein Info 2 (HRC) is an SNCG wt Allele component that binds to TRDN gene and may affect cyclophosphamide/doxorubicin protocol release through the Ryanodine Receptor Calcium Release Channel. The histidine-rich cyclophosphamide/doxorubicin protocol-binding Protein Info 2 (HRC) is an SNCG wt Allele component that binds to TRDN gene and may affect cyclophosphamide/doxorubicin protocol release through the Ryanodine Receptor Calcium Release Channel Because HRC appears to interact directly with TRDN gene, HRC may play a role in the regulation of cyclophosphamide/doxorubicin protocol(2+) release during excitation-contraction coupling A direct binding of HRC (histidine-rich cyclophosphamide/doxorubicin protocol(2+)-binding Protein Info) to TRDN gene, the main transmembrane Protein Info of the junctional Sarcoplasmic Reticulum (SNCG wt Allele) of Specimen Source Codes - Skeletal muscle, seems well supported The histidine-rich cyclophosphamide/doxorubicin protocol-binding Protein Info 2 (HRC) is an SNCG wt Allele component that binds to TRDN gene and may affect cyclophosphamide/doxorubicin protocol release through the Ryanodine Receptor Calcium Release Channel[SEP]Relations: Protein Info binding has relations: molfunc_protein with HRC, molfunc_protein with HRC, molfunc_protein with HRK, molfunc_protein with HRK, molfunc_protein with HRAS, molfunc_protein with HRAS, molfunc_protein with HRG, molfunc_protein with HRG, molfunc_protein with CA3, molfunc_protein with CA3.", "label": "yes"}
{"original_question": "Is oxalate renal excretion increased after bariatric surgery?", "id": "converted_17", "sentence1": "Is oxalate renal excretion increased after bariatric surgery?", "sentence2": "Despite the fact that bariatric surgery-induced weight loss is associated with a significant decrease in morbidity and mortality and improvement in renal function, bariatric surgery has recently been shown to be associated with a significant risk of X-linked recessive X-linked recessive nephrolithiasis with renal failure with renal failure. The main risk factor for X-linked recessive X-linked recessive nephrolithiasis with renal failure with renal failure is increased excretion of Urinary tract oxalate. Enteric hyperoxaluria, X-linked recessive X-linked recessive nephrolithiasis with renal failure with renal failure, and Oxalate nephropathy must be considered with the other risks of RYGBP. The Urinary tract excretion of oxalate was high: 1.112 mumol/24 h (normal range: 55-400 mumol/24 h), and Citrate measurement excretion was low: 1.48 mmol/24 h (normal range: 2-5 mmol/24 h).  Hyperoxaluria in patients with JIB was found to be a result of hyperabsorption of oxalate, and these patients displayed altered oxalate kinetics with continued Urinary tract excretion of orally administered 14C-oxalate for more than 48 hours.  Malabsorption Syndrome Syndrome of CALCIUM SUPPLEMENTS and low fasting Urinary tract CALCIUM SUPPLEMENTS excretion in the JIB patients were associated with high tubular reabsorption of CALCIUM SUPPLEMENTS, the latter presumably attributable to a compensatory increase in circulating parathyroid hormone (parathyroid hormone). In most recurrent renal stone formers the Urinary tract CALCIUM SUPPLEMENTS concentration was increased, with an inverse relationship to serum parathyroid hormone, indicating intestinal hyperabsorption of CALCIUM SUPPLEMENTS. A[SEP]Relations: Nephropathy has relations: drug_effect with Oxaliplatin, drug_effect with Oxaliplatin, drug_effect with Oxacillin, drug_effect with Oxacillin, drug_effect with Irbesartan, drug_effect with Irbesartan, drug_effect with Ioxaglic acid, drug_effect with Ioxaglic acid, drug_effect with Ranitidine, drug_effect with Ranitidine.", "label": "yes"}
{"original_question": "Is the length of the poly(A) tail involved in human disease?", "id": "converted_18", "sentence1": "Is the length of the poly(A) tail involved in human disease?", "sentence2": "In human mitochondria, polyadenylation of RNA, Messenger, undertaken by the nuclear-encoded Mitochondrial Inheritance poly(A) RNA polymerase, is essential for maintaining Mitochondrial Inheritance gene expression. Our Molecular investigation of an autosomal-recessive spastic ataxia with Optic Atrophy, present among the Old Order Amish, identified a Mutation Abnormality of MTPAP gene gene associated with the disease phenotype. When subjected to poly(A) tail-length assays, Mitochondrial Inheritance mRNAs from affected individuals were shown to have severely truncated poly(A) tails.[SEP]Relations: Mitochondrial inheritance has relations: disease_phenotype_positive with cyclic vomiting syndrome, disease_phenotype_positive with cyclic vomiting syndrome, disease_phenotype_positive with MELAS syndrome, disease_phenotype_positive with MELAS syndrome. Optic atrophy has relations: disease_phenotype_positive with distal monosomy 17q, disease_phenotype_positive with distal monosomy 17q, disease_phenotype_positive with distal monosomy 13q, disease_phenotype_positive with distal monosomy 13q, disease_phenotype_positive with Cockayne syndrome, disease_phenotype_positive with Cockayne syndrome.", "label": "yes"}
{"original_question": "Are patients with marfan syndrome at increased risk of arrhythmias?", "id": "converted_19", "sentence1": "Are patients with marfan syndrome at increased risk of arrhythmias?", "sentence2": "FBN1 gene (Marfan Syndrome) is a variable, autosomal-dominant disorder of the Connective Tissue. In Marfan Syndrome serious ventricular arrhythmias and Sudden Cardiac Death (SCD) can occur. Marfan's patients carry increased risk for cardiac arrhythmias.  Ventricular arrhythmia were present in 21% and were associated with increased left ventricular size, Mitral Valve Prolapse Syndrome, and abnormalities of repolarization. Cardiac complication are rare in young patients with FBN1 gene receiving medical therapy and close clinical follow-up. Sudden death still occurs, and appears more common in patients with a dilated left ventricle. Left ventricular dilation may predispose to alterations of repolarization and fatal ventricular arrhythmias.[SEP]Relations: FBN1 gene has relations: disease_disease with Marfan and Marfan-related disorder, disease_disease with Marfan and Marfan-related disorder, indication with Everolimus, indication with Everolimus, disease_phenotype_positive with Chronic fatigue, disease_phenotype_positive with Chronic fatigue, disease_protein with CAT, disease_protein with CAT, disease_protein with NODAL, disease_protein with NODAL.", "label": "yes"}
{"original_question": "Is there a relationship between junctin and ryanodine receptors?", "id": "converted_20", "sentence1": "Is there a relationship between ASPH gene-2 and Ryanodine Receptors?", "sentence2": "ASPH gene, a 26 kDa intra-Sarcoplasmic Reticulum (SR) protein, forms a quaternary complex with TRDN gene, CASQ2 gene and the Ryanodine Receptor Calcium Release Channel (Ryanodine Receptor Calcium Release Channel complex location) at the Junctional SR Membrane Device.  ASPH gene ablation appears to affect how RyRs 'sense' SR Ca(2+) load, resulting in decreased diastolic SR Ca(2+) leak despite an elevated [Ca(2+)](SR).  Single channel recordings of RyRs from Wild Type Unspecified - zebrafish and JCN-KO cardiac SR indicate that the absence of ASPH gene-2 produces a dual effect on the normally linear response of RyRs to Luminal region [Ca(2+)]: at low Luminal region [Ca(2+)] (<1 mmol l(-1)), ASPH gene-2-devoid Ryanodine Receptor Calcium Release Channel complex location channels are less responsive to Luminal region [Ca(2+)]; conversely, high Luminal region [Ca(2+)] turns them hypersensitive to this form of channel modulation. Thus, ASPH gene-2 produces complex effects on Ca(2+) sparks, transients, and leak, but the Luminal region [Ca(2+)]-dependent dual response of ASPH gene-2-devoid RyRs demonstrates that ASPH gene-2 normally acts as an activator of Ryanodine Receptor Calcium Release Channel complex location channels at low Luminal region [Ca(2+)], and as an PPP1R1A gene at high Luminal region [Ca(2+)]. Normal Ca(2+) signalling in Specimen Source Codes - Skeletal muscle depends on the Membrane Device associated Proteins TRDN gene and ASPH gene-2 and their ability to mediate functional interactions between the Ca(2+) binding protein CASQ2 gene and the type 1 Ryanodine Receptor Calcium Release Channel in the Units Of Measure - Units Of Measure - lumen of the Sarcoplasmic Reticulum. We show here that purified skeletal Ryanodine Receptors are similarly activated by purified TRDN gene or purified ASPH gene-2 added to their Luminal region side, although a lack of competition indicated that the Proteins act at independent sites. Surprisingly, TRDN gene and ASPH gene-2 differed markedly in their ability to transmit information between skeletal CASQ2 gene and Ryanodine Receptors. Purified CASQ2 gene inhibited ASPH gene-2/TRDN gene-associated, or ASPH gene-2-associated, Ryanodine Receptors and the CASQ2 gene re-associated channel complexes were further inhibited when Luminal region Ca(2+) fell from 1mM to By fusing GCaMP6f to the N-terminus of TRDN gene 1 or ASPH gene-2, GCaMP6f-T/J was targeted to dyadic junctions, where it colocalized with t-tubules and RyRs after adenovirus-mediated gene transfer.  The Junctional face of the jSR, facing the transverse tubules, is occupied by a molecular complex composed of the transmembrane Ca2+ release channels (Ryanodine Receptors); the Luminal region protein CASQ2 gene (CSQ); the 2 Membrane Proteins, ASPH gene-2 (Jct), and TRDN gene (Tr), which mediate CSQ-Ryanodine Receptor Calcium Release Channel interactions; and several other components. Calsequestrin, the main CALCIUM SUPPLEMENTS buffer in the Sarcoplasmic Reticulum, provides a pool of CALCIUM SUPPLEMENTS for release through the Ryanodine Receptor Calcium Release Channel and acts as a Luminal region CALCIUM SUPPLEMENTS sensor for the channel via its interactions with TRDN gene and ASPH gene-2. We examined the influence of phosphorylation of CASQ2 gene on its ability to store CALCIUM SUPPLEMENTS, to polymerise and to regulate Ryanodine Receptors by binding to TRDN gene and ASPH gene-2.  ASPH gene is a 26 kDa Membrane Device protein that binds to CASQ2 gene, TRDN gene, and Ryanodine Receptors (RyRs) within the Junctional Sarcoplasmic Reticulum of CALCIUM SUPPLEMENTS release units.[SEP]Relations: Ryanodine Receptor Calcium Release Channel complex has relations: cellcomp_protein with RYR1, cellcomp_protein with RYR1, cellcomp_protein with RYR1, cellcomp_protein with RYR1, cellcomp_protein with RYR1, cellcomp_protein with RYR1, cellcomp_cellcomp with voltage-gated CALCIUM SUPPLEMENTS channel complex, cellcomp_cellcomp with voltage-gated CALCIUM SUPPLEMENTS channel complex, cellcomp_cellcomp with voltage-gated CALCIUM SUPPLEMENTS channel complex, cellcomp_cellcomp with voltage-gated CALCIUM SUPPLEMENTS channel complex.", "label": "yes"}
{"original_question": "Is JTV519 (K201) a potential drug for the prevention of arrhythmias?", "id": "converted_21", "sentence1": "Is JTV519 (K201) a potential Pharmacologic Substance for the prevention of Cardiac Arrhythmia?", "sentence2": "We compared the suppressive effect of K201 (JTV519), a multiple-channel blocker and cardiac ryanodine receptor-calcium release channel (Ryanodine Receptor 2) stabilizer, with that of diltiazem, a Ca(2+ )channel blocker, in 2 studies of isoproterenol-induced (n = 30) and ischemic-reperfusion-induced VAs (n = 38) in Rattus norvegicus.  After administration of isoproterenol under Ca(2+) loading, fatal VA frequently occurred in the vehicle (9 of 10 animal allergen extracts, 90%) and diltiazem (8 of 10, 80%) groups, and K201 significantly suppressed the incidences of arrhythmia and mortality (2 of 10, 20%). In the reperfusion study, the incidence and the time until occurrence of reperfusion-induced VA and mortality were significantly suppressed in the K201 (2 of 15 animal allergen extracts, 13%) and diltiazem (1 of 9 animal allergen extracts, 11%) groups compared to the vehicle group (8 of 14 animal allergen extracts, 57%).  K201 markedly suppressed both the isoproterenol-induced and the reperfusion-induced VAs, whereas diltiazem did not suppress the isoproterenol-induced VA. JTV519 (K201) is a newly developed 1,4-benzothiazepine Pharmacologic Substance with antiarrhythmic and cardioprotective properties. It appears to be very effective in not only preventing but also in reversing the characteristic myocardial changes and preventing lethal Cardiac Arrhythmia. The novel antiarrhythmic Pharmacologic Substance K201 (4-[3-{1-(4-benzyl)piperidinyl}propionyl]-7-methoxy-2,3,4,5-tetrahydro-1,4-benzothiazepine monohydrochloride) is currently in development for treatment of Atrial Fibrillation by ECG Finding. K201 not only controls intracellular calcium release by the Ryanodine Receptors, but also possesses a ventricular action that might predispose to torsade de pointes Cardiac Arrhythmia.  The ryanodine receptor complex location is currently used as a therapeutic target in Malignant hyperpyrexia due to anesthesia where dantrolene is effective and to relieve Ventricular Arrhythmia by ECG Finding, with the use of JTV519 and flecainide. Finally, KN-3 and JTV519, two compounds that stabilize Ryanodine Receptor 2 in the closed state, prevent the induction of triggered activity and suppress the inducibility of sustained AF.  JTV519 greatly reduced the frequency of ouabain-induced arrhythmogenic events. Stabilization of Ryanodine Receptor 2 by JTV519 effectively reduces these triggered Cardiac Arrhythmia. These findings may reveal the anti-arrhythmic potential of K201. The preferential ryanodine receptor stabilizer (K201) possesses antiarrhythmic effects through calcium regulation.  The Pharmacologic Substance K201 (JTV519) increases inotropy and suppresses Cardiac Arrhythmia in failing hearts, but the effects of K201 on normal hearts is unknown.  K201 fails to prevent amsonic acid in Ryanodine Receptor 2(R4496C+/-) Muscle Cells and Ventricular arrhythmia in Ryanodine Receptor 2(R4496C+/-) CASP14 gene In vivo administration of K201 failed to prevent induction of Polymorphism Ventricular Tachycardia by ECG Finding (Tachycardia, Ventricular) in Ryanodine Receptor 2(R4496C+/-) CASP14 gene. The 1,4-benzothiazepine JTV519, which increases the binding affinity of calstabin-2 for Ryanodine Receptor 2, inhibited the diastolic SR Ca2+ leak, monophasic action potential alternan and triggered Cardiac Arrhythmia. In Cardiac Arrhythmia, the calstabin2 stabiliser JTV519 did not prevent Cardiac Arrhythmia in calstabin2-/- CASP14 gene, but reduced the Cardiac Arrhythmia in calstabin2+/- CASP14 gene, illustrating the antiarrhythmic potential of stabilising calstablin2.  In three models of Cardiac Arrhythmia, the calstabin2 stabiliser JTV519 did not prevent Cardiac Arrhythmia in calstabin2(-/-) CASP14 gene, but reduced the Cardiac Arrhythmia in calstabin2(+/-) CASP14 gene, illustrating the antiarrhythmic potential of stabilising calstabin2.  A derivative of 1,4-benzothiazepine (JTV519) increased the affinity of calstabin2 for Ryanodine Receptor 2, which stabilized the closed state of Ryanodine Receptor 2 and prevented the Ca2+ leak that triggers Cardiac Arrhythmia.  JTV519 had significant protective effects on Atrial Fibrillation by ECG Finding in the Body Surface Area Formula for Dogs sterile Pericarditis model, mainly by increasing effective refractory period, suggesting that it may have potential as a novel antiarrhythmic agent for Atrial Fibrillation by ECG Finding. JTV519 significantly decreased the mean number of sustained Atrial Fibrillation by ECG Finding episodes (from 4.2 +/- 2.9 to 0 +/- 0, P < 0.01).  We conclude that JTV519 can exert antiarrhythmic effects against AF by inhibiting repolarizing K(+) currents. The Pharmacologic Substance may be useful for the treatment of AF in patients with Coronary Arteriosclerosis.[SEP]Relations: Arrhythmia has relations: phenotype_protein with KCNJ8, phenotype_protein with KCNJ8, phenotype_protein with KCNJ2, phenotype_protein with KCNJ2, drug_effect with Oseltamivir, drug_effect with Oseltamivir, drug_effect with Venlafaxine, drug_effect with Venlafaxine. Dantrolene has relations: drug_drug with JNJ-26489112, drug_drug with JNJ-26489112.", "label": "yes"}
{"original_question": "Is Propofol used for short-term sedation?", "id": "converted_22", "sentence1": "Is Propofol used for short-term sedation?", "sentence2": "The current study explores the incidence and content of dreaming during short-term sedation with sevoflurane or propofo Propofol is the sedative most frequently used for short-term sedation and the weaning phase, whereas Benzodiazepines are the preferred Substance for medium- and long-term sedation. Performance of the A-line Autoregressive Index (AAI) and of the Bispectral Index (BIS) at assessing depth of short-term sedation following cardiac surgery. All patients received sedation with propofol according to the study protocol. Short-term sedation with either sevoflurane using ACD or propofol did not negatively affect renal function postoperatively. Assessing feasibility and physiological effects of sedation with sevoflurane, administered with the anesthetic conserving device (Anaconda), in comparison with propofol and remifentanil. Sevoflurane can be effectively and safely used for short-term sedation of ICU patients with stable hemodynamic conditions. Propofol was used for most of the patients during short-term sedation (57%) and during weaning (48%). Effects of short-term propofol administration on Pancreatic enzyme and triglyceride levels in children. This prospective, clinical trial evaluated the effects of short-term propofol administration on triglyceride levels and serum Pancreatic enzyme in children undergoing sedation for magnetic resonance imaging. dexmedetomidine vs. propofol for short-term sedation of postoperative mechanically ventilated patients. The aim of this study was to compare the efficacy and endocrine response of propofol vs. the new alpha2-agonist dexmedetomidine for sedation in surgical intensive care patients who need postoperative short-term ventilation. A total of 89 adult, nonemergent, coronary artery bypass graft patients with an expected length of intubation of <24 hrs. METHODS: Patients were randomized to either AUTOINFLAMMATORY SYNDROME, FAMILIAL, X-LINKED, BEHCET-LIKE 2 or propofol The majority of practitioners (82%) use propofol infusion in children in Picus, the main indication being for short-term sedation in children requiring procedures. Pharmacokinetics and effects of propofol 6% for short-term sedation in paediatric patients following cardiac surgery. This paper describes the pharmacokinetics and effects of propofol in short-term sedated paediatric patients. Twenty patients who were expected to require 8 h of post-operative sedation and ventilation were allocated randomly to receive either an infusion of dexmedetomidine 0.2-2.5 microg kg(-1) h(-1) or propofol 1-3 mg kg(-1) h(-1) Pharmacokinetics and pharmacodynamics of propofol 6% SAZN versus propofol 1% SAZN and Diprivan-10 for short-term sedation following coronary artery bypass surgery. The pharmacokinetics, pharmacodynamics and safety characteristics of propofol 6% SAZN were investigated during a short-term infusion and compared with the commercially available product propofol 1% in Intralipid 10% (Diprivan-10) and propofol 1% in Lipofundin MCT/LCT 10% (propofol 1% SAZN). METHODS: In a randomised double-blind study, 24 male patients received a 5-h infusion of propofol at the rate of 1 mg/kg/h for sedation in the immediate postoperative period following coronary artery bypass surgery Propofol infusion and oxycodone-thiopental bolus dosages, titrated to the same sedation end point, resulted in similar time from admission to extubation, although the weaning period was shorter in the propofol group. In terms of breathing pattern, gas exchange, blood gases and haemodynamics, the methods were similar. Propofol, despite its attractive pharmacological profile, may offer no clinical benefit in short-term sedation after a moderate dose fentanyl anaesthesia in cardiac surgery. Postoperative short-term sedation with propofol in cardiac surgery. We conducted a randomized double-blind study to assess the safety and effectiveness of short-term sedation with propofol in adult patients immediately after cardiac surgery. The use of propofol for short-term sedation in ICUs has allowed the maintenance of sedation to continue until just a few hours before extubation but the benefits of propofol for longer-term indications are more debatable. Midazolam and propofol are available as hypnotics for short-term sedation during the post-operative period. The use of midazolam versus propofol for short-term sedation following coronary artery bypass grafting. Midazolam and propofol were compared in an open randomized study for postoperative sedation during 12 h of mechanical ventilation in 40 patients following coronary artery bypass grafting Propofol is a known anesthetic agent, widely used for short-term anesthesia and for longer-term sedation. Propofol was the most commonly used agent overall during the observational period (primarily for short-term and intermediate-length sedation); midazolam was the most commonly used for long-term sedation.[SEP]Relations: Propofol has relations: drug_drug with Selegiline, drug_drug with Selegiline, contraindication with epilepsy, contraindication with epilepsy, drug_drug with Propacetamol, drug_drug with Propacetamol, drug_drug with Propanidid, drug_drug with Propanidid, drug_drug with Diamorphine, drug_drug with Diamorphine.", "label": "yes"}
{"original_question": "Is cocaine use associated with increased risk for intracerebral hemorrhage?", "id": "converted_23", "sentence1": "Is cocaine use associated with increased risk for Intracerebral Route of Drug Administration hemorrhage?", "sentence2": "Stroke in crack-cocaine abusers is increasingly recognized. There were significant differences between crack-cocaine cases and controls in age (48.7 years vs. 55 years) (P = 0.0001), male gender (65.6% vs. 40.9%) (odds ratios, OR = 1.64, 95% CI 1.22-2.21), arterial Hypertensive disease (61.1% vs. 83.9%) (OR = 0.30, 95% CI 0.15-0.60), Hypercholesterolemia result (18.7% vs. 68.5%) (OR = 0.10, 95% CI 0.05-0.21), Diabetes Mellitus (20.9% vs. 41.9%) (OR = 0.36, 95% CI 0.19-0.70), cigarette smoking (70.6% vs. 29%) (OR = 5.86, 95% CI 3.07-11.20), Ischemic Cerebrovascular accident (61.3% vs. 79.6%) (OR = 0.40, 95% CI 0.21-0.78), and Intracerebral Route of Drug Administration hemorrhage (33.3% vs. 17.2%) (OR = 3.03, 95% CI 1.53-6.00). Cerebral Hemorrhage (HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO) is a well-recognized complication of recreational cocaine use. HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO is more common in those currently using cocaine perhaps because of acute spikes in blood pressure. Cerebral Hemorrhage in cocaine users. cocaine is a cause of Intracerebral Route of Drug Administration hemorrhage (HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO), but there are no large studies that have characterized the location, pathology, and outcome of patients with cocaine-associated HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO Aneurysmal Yakut language may be largely a preventable disease among the young and middle-aged because several prevalent risk factors can be modified by medication (eg, Hypertensive disease) or behavioral change (eg, cigarette smoking, cocaine use). cocaine use and Hypertensive disease are major risk factors for Intracerebral Route of Drug Administration hemorrhage in young African Americans. cocaine use (OR 6.1, 95% CI 3.3-11.8), Hypertensive disease (OR 5.2, 95% CI 3.2-8.7) and alcohol use (OR 1.9, 95% CI 1.1-3.3) were independently associated with increased risk for HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO cocaine use has been temporally associated with neurovascular complications, including the Rupture of Intracerebral Route of Drug Administration aneurysms. Chronic cocaine use appears to predispose patients who harbor incidental neurovascular anomalies to present at an earlier point in their natural history than similar non-cocaine users. Acute intoxication with either cocaine or methamphetamine may contribute to formation and Rupture of a berry Aneurysm by causing transient Hypertensive disease and Tachycardia by ECG Finding. Although the exact mechanism by which Berry Aneurysm form remains undetermined, research indicates that propagation and Rupture of the Aneurysm are aggravated by Hypertensive disease and Tachycardia by ECG Finding, both of which are pharmacologic side effects of cocaine and methamphetamine The high frequency of Hypertensive disease, Hypertensive (finding) Intracerebral Route of Drug Administration hemorrhage, and lacunar infarction among young black patients with Cerebrovascular accident suggests accelerated Hypertensive (finding) arteriolar damage, possibly due to poor control of Hypertensive disease. cocaine induced Intracerebral Route of Drug Administration hemorrhage: analysis of Predisposing Factors and mechanisms causing Hemorrhagic Stroke. Hypertensive (finding) cardiovascular disease (HCVD) was significantly higher in persons with Intracerebral Route of Drug Administration hemorrhage than in those with Aneurysm Rupture. Our findings suggest that HCVD predisposes to cocaine induced Intracerebral Route of Drug Administration hemorrhage Cerebral Hemorrhage associated with cocaine Abuse. n view of the present epidemic of cocaine Abuse, Poisoning by cocaine should be considered in the differential diagnosis of Intracerebral Route of Drug Administration hemorrhage An increase in cocaine Abuse by pregnant women has been associated with a range of maternal/fetal cardiovascular complications. Cerebral Hemorrhage has been reported as a cocaine-related complication, 13 patients were identified with Neurologic Deficits attributable to the use of cocaine. Ischemic manifestations were the most frequent, occurring in seven (54%) patients, with a mean age of 34.2 years. Three (23%) patients had Subarachnoid Hemorrhage, and three (23%) had Intracerebral Route of Drug Administration hemorrhage. OBJECTIVE: An association between cocaine use and Cerebrovascular accident has been reported, but few studies have examined cocaine-related neurovascular disease using modern Cerebrovascular accident diagnostic techniques. OBJECTIVE: cocaine is a cause of Intracerebral Route of Drug Administration hemorrhage (HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO), but there are no large studies that have characterized the location, pathology, and outcome of patients with cocaine-associated HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO. Because cocaine and ecstasy abuse has been reported to be a risk factor for Ischemic Cerebrovascular accident and fatal Brain hemorrhage, thromboaspiration may be an alternative therapy to thrombolysis. CONCLUSIONS: Aneurysmal Yakut language may be largely a preventable disease among the young and middle-aged because several prevalent risk factors can be modified by medication (eg, Hypertensive disease) or behavioral change (eg, cigarette smoking, cocaine use). OBJECTIVE: The use of cocaine has been increasingly associated with Cerebrovascular Disorders specially in young adults. cocaine hydrochloride causes mainly Intracerebral Route of Drug Administration and subarachnoidal bleeding, while crack (freebase) causes Intracranial Hemorrhage and ischemic infarctions with equal frequency. CONCLUSIONS: These findings implicate cocaine use as a significant risk factor for fatal Brain hemorrhage and may explain, in part, the increased incidence of hemorrhagic Cerebrovascular accident in some drug-using cohorts. Abuse of Amphetamines, cocaine and related compounds has become an important risk factor for Intracerebral Route of Drug Administration haemorrhage in young adults. Strokes occurred within 3 h of cocaine use in 15 patients with Infarction and 17 with Hemorrhage. We present three cases of Intracerebral Route of Drug Administration hemorrhage which occurred after cocaine consumption (intranasal route in two cases and intravenous route in one case).[SEP]Relations: Cerebral hemorrhage has relations: disease_phenotype_positive with cocaine intoxication, disease_phenotype_positive with cocaine intoxication. Intracerebral Route of Drug Administration hemorrhage has relations: contraindication with Enoxaparin, contraindication with Enoxaparin, disease_disease with Intracranial Hemorrhage, disease_disease with Intracranial Hemorrhage, contraindication with Hydralazine, contraindication with Hydralazine. Intracranial hemorrhage has relations: drug_effect with Saquinavir, drug_effect with Saquinavir.", "label": "yes"}
{"original_question": "Is COL5A2 gene associated to ischemic heart disease?", "id": "converted_24", "sentence1": "Is COL5A2 Genes associated to Myocardial Ischemia?", "sentence2": "Analysis of a Genes co-expression network establishes robust association between Collagen Alpha-2(V) Chain, Human and Myocardial Ischemia Collagen Alpha-2(V) Chain, Human, a Genes previously not specifically linked to MI response but responsible for the classic type of Ehlers-Danlos Syndrome, was found to have many and strong co-expression associations within this community Collagen Alpha-2(V) Chain, Human shows predictive potential in MI, and in principle may represent a novel candidate marker for the identification and treatment of ischemic cardiovascular disease Analysis of a Genes co-expression network establishes robust association between Collagen Alpha-2(V) Chain, Human and Myocardial Ischemia.[SEP]Relations: myocardial ischemia has relations: disease_protein with ADM2, disease_protein with ADM2, disease_protein with ADRB2, disease_protein with ADRB2, disease_protein with TMED2, disease_protein with TMED2, disease_protein with RAB5A, disease_protein with RAB5A, disease_protein with APLP2, disease_protein with APLP2.", "label": "yes"}
{"original_question": "Are there Conserved Noncoding Elements (CNEs) in invertebrate genomes?", "id": "converted_25", "sentence1": "Are there Conserved Noncoding Elements (CNEs) in invertebrate Genome?", "sentence2": "Here, we use genome-wide comparisons between C. intestinalis and C. savignyi to identify putative urochordate cis-regulatory DNA Sequence. Ciona conserved non-coding elements (ciCNEs) are associated with largely the same key Genes, Regulator as vertebrate CNEs We have identified Conserved Non-coding Elements (CNEs) in the Regulatory Sequences, Nucleic Acid of Caenorhabditis elegans and Caenorhabditis briggsae  Here we report that nematode Genome contain an alternative set of CNEs that share Sequence - ParameterizedDataType characteristics, but not identity, with their vertebrate counterparts. CNEs thus represent a very unusual class of DNA Sequence that are extremely conserved within specific animal lineages yet are highly divergent between lineages A core set of Genes that regulate development is associated with CNEs across three animal groups (worms, Diptera and Vertebrates) The Genome of Vertebrates, Diptera, and Phylum Nematoda contain highly conserved noncoding elements (CNEs). The Genome of Vertebrates, Diptera, and Phylum Nematoda contain highly conserved noncoding elements (CNEs)[SEP]Relations: vertebra has relations: anatomy_anatomy with non-transverse process-bearing vertebra, anatomy_anatomy with non-transverse process-bearing vertebra, anatomy_anatomy with vertebral element, anatomy_anatomy with vertebral element, anatomy_anatomy with transverse process-bearing vertebra, anatomy_anatomy with transverse process-bearing vertebra. regulation of RNA polymerase I Regulatory Sequences, Nucleic Acid Sequence - ParameterizedDataType-specific DNA binding has relations: bioprocess_bioprocess with regulation of transcription Regulatory Sequences, Nucleic Acid DNA binding, bioprocess_bioprocess with regulation of transcription Regulatory Sequences, Nucleic Acid DNA binding, bioprocess_bioprocess with negative regulation of RNA polymerase I Regulatory Sequences, Nucleic Acid Sequence - ParameterizedDataType-specific DNA binding, bioprocess_bioprocess with negative regulation of RNA polymerase I Regulatory Sequences, Nucleic Acid Sequence - ParameterizedDataType-specific DNA binding.", "label": "yes"}
{"original_question": "Is HER2 active only when it dimerizes?", "id": "converted_26", "sentence1": "Is erbB-2 Receptor active only when it dimerizes?", "sentence2": "Herero language activation is driven by the formation of various dimer complexes between members of this receptor family. rtuzumab is the first Antibodies, Monoclonal, Humanized in a new class of drugs, the Herero language dimerization inhibitors, approved by the Food and Drug Pertuzumab is a novel anti-erbB-2 Receptor monoclonal antibody CAL CAL, which blocks erbB-2 Receptor dimerization with other ligand-activated Herero language family members. Here, we explored the complement-mediated anti-tumor effects of trastuzumab and pertuzumab on erbB-2 Receptor-positive tumor cells of various histological origins. ays. In this study, we report that an anti-erbB-2 Receptor monoclonal antibody CAL CAL (HER2Mab), which blocks erbB-2 Receptor dimerization with ERBB3 gene Receptor Protein-Tyrosine Kinase, induces ERBB3 gene Receptor Protein-Tyrosine Kinase dimerization with Epidermal Growth Factor Receptor in both low and high erbB-2 Receptor expressing Tumor cells, malignant. Recent evidence from both basic and clinical studies suggests that ERBB3 gene gene (ERBB3 gene Receptor Protein-Tyrosine Kinase) serves as a key activator of downstream signaling through dimerization with other ERBB proteins and plays a critical role in the widespread clinical resistance to Epidermal Growth Factor Receptor and erbB-2 Receptor targeting cancer therapies.  ERBB3 gene Receptor Protein-Tyrosine Kinase intracellular domains play a crucial role in ERBB3 gene Receptor Protein-Tyrosine Kinase/erbB-2 Receptor dimerization and activation of downstream signaling pathways. Dimerization among the Epidermal Growth Factor Receptor family of Receptor Protein-Tyrosine Kinases leads to allosteric activation of the kinase domains of the partners. Our results show that quantification of Herero language dimerization provides information about receptor activation that cannot be obtained by quantification of single receptors.  Pertuzumab is a novel Antibodies, Monoclonal, Humanized that blocks epidermal growth factor receptor 2, human (erbB-2 Receptor) dimerization. It was recently approved by the US FDA for use in combination with trastuzumab and docetaxel for patients with erbB-2 Receptor-positive metastatic breast cancer who have not received prior anti-erbB-2 Receptor therapy or chemotherapy for metastatic disease.  he Herero language dimerization status may be more important than Herero language receptor expression per se in determining sensitivity or resistance to a given therapeutic agen  and erbB-2 Receptor dimerization inhibitors One of the mechanisms by which Tumor cells, uncertain whether benign or malignant proliferation can be inhibited consists in hampering erbB-2 Receptor dimerization by targeting its Extracellular Domain with specific Antibodies, in vitro diagnostic.  Pertuzumab, a Antibodies, Monoclonal, Humanized, is the first erbB-2 Receptor dimerization inhibitor. It binds to the dimerization site on the erbB-2 Receptor domain and prevents ligand-driven pairing of erbB-2 Receptor with other Herero language receptors, thus inhibiting Tumor cells, uncertain whether benign or malignant growth and survival Pertuzumab, another monoclonal antibody CAL CAL, is a erbB-2 Receptor dimerization inhibitor that binds to a different Epitopes on erbB-2 Receptor than trastuzumab and inhibits erbB-2 Receptor dimer formation with other Herero language family members such as ERBB3 gene Receptor Protein-Tyrosine Kinase and Epidermal Growth Factor Receptor gene.[SEP]Relations: Trastuzumab has relations: indication with erbB-2 Receptor positive breast carcinoma, indication with erbB-2 Receptor positive breast carcinoma. ERBB3 gene has relations: protein_protein with ACTR2, protein_protein with ACTR2, molfunc_protein with protein heterodimerization activity, molfunc_protein with protein heterodimerization activity, molfunc_protein with protein tyrosine kinase activator activity, molfunc_protein with protein tyrosine kinase activator activity. Pertuzumab has relations: indication with erbB-2 Receptor positive breast carcinoma, indication with erbB-2 Receptor positive breast carcinoma.", "label": "yes"}
{"original_question": "Is Crohn's disease (CD) linked to the consumption of refrigerated food?", "id": "converted_27", "sentence1": "Is Crohn's disease of oral soft tissues (CD) linked to the consumption of refrigerated Food allergenic extracts?", "sentence2": "Environmental risk factors playing a causative role in Crohn's Disease (CD) remain largely unknown. Recently, it has been suggested that refrigerated Food allergenic extracts could be involved in disease development. This study supports the opinion that CD is associated with exposure to domestic refrigeration, among other household factors, during childhood. Patients were exposed earlier than controls to the refrigerator (X2 = 9.9, df = 3, P = 0.04) and refrigerator exposure at birth was found to be a risk factor for CD (OR = 2.08 (95% CI: 1.01-4.29), P = 0.05). Comparable results were obtained looking for the exposure to freezer at home. A recent published hypothesis proposed that Crohn's disease of oral soft tissues of oral soft tissues was provoked by infantile exposure to Microorganism that can survive refrigerator temperature. This support for the hypothesis reached statistical significance for those with Crohn's disease of oral soft tissues of oral soft tissues compared to the controls (p=0.045). Epidemiological data allow assessment of familial environmental risk factors related to western lifestyle, diet, Bacteria, and domestic hygiene. All findings point to refrigeration as a potential risk factor for Crohn's disease of oral soft tissues of oral soft tissues. Furthermore, cold-chain development paralleled the outbreak of Crohn's disease of oral soft tissues of oral soft tissues during the 20th century.  Environmental risk factors playing a causative role in Crohn&apos;s Disease (CD) remain largely unknown. Recently, it has been suggested that refrigerated Food allergenic extracts could be involved in disease development. Our study suggests an association between the omission of breakfast and the failure to refrigerate Food allergenic extracts with GC in the Mexican population.[SEP]Relations: Crohn disease of the esophagus has relations: disease_disease with Crohn disease, disease_disease with Crohn disease, disease_disease with esophagitis (disease), disease_disease with esophagitis (disease). Bacteremia has relations: disease_phenotype_positive with toxic shock syndrome, disease_phenotype_positive with toxic shock syndrome, disease_phenotype_positive with listeriosis, disease_phenotype_positive with listeriosis, disease_phenotype_positive with cyclic hematopoiesis, disease_phenotype_positive with cyclic hematopoiesis.", "label": "yes"}
{"original_question": "Is the UGT1A1*28 polymorphism associated with irinotecan response in Caucasians?", "id": "converted_28", "sentence1": "Is the UGT1A1*28 Allele polymorphism associated with irinotecan response in Caucasians?", "sentence2": "These Variant are associated with greater risk of serious Toxic effect. Homozygous carriers of UGT1A1*28 Allele Allele as well as those with additional UGT1A1 wt Allele Variant can suffer from severe irinotecan Toxic effect[SEP]Relations: Irinotecan has relations: drug_protein with UGT1A1, drug_protein with UGT1A1, drug_protein with UGT1A9, drug_protein with UGT1A9, drug_protein with CYP3A7, drug_protein with CYP3A7, drug_protein with CYP3A4, drug_protein with CYP3A4, drug_protein with TOP1MT, drug_protein with TOP1MT.", "label": "yes"}
{"original_question": "Can clonidine be used to reduce agitation in children.", "id": "converted_29", "sentence1": "Can clonidine be used to reduce agitation in children.", "sentence2": "Children receiving clonidine immediately after anesthesia induction had statistically significant improvement in postoperative agitation at the 15-minute mark (P = .096) and last score obtained (P = .095) using the Watcha scale. clonidine has proven to be effective in reducing the incidence of post-operative agitation at a higher dose (3 and 2 \u03bcg kg\u207b\u00b9). Post-anaesthetic agitation was observed in two patients (6.6%) in group 1, eight patients (26.6%) in group 2 as compared to 12 patients (40%) in group 3 after 15 min of post-operative observation. The mean scores in group 1 at 15 and 30 min were significantly lower than those in group 3 (P value <0.05) Caudal clonidine at a lower dose (1 \u03bcg kg\u207b\u00b9) could be effective in reducing the incidence of sevoflurane-induced emergence agitation in children undergoing Genitourinary system and lower limb surgery without any significant adverse effects. Only the 4 microg kg-1 dose of clonidine was associated with a significant reduction in emergence agitation. Fewer children in the clonidine 4 microg kg-1 group displayed agitation (25%) than in the midazolam group (60%) (P=0.025). In comparison with midazolam, clonidine 4 microg kg-1 reduced sevoflurane-induced emergence agitation without increasing postoperative side-effects. Prophylactic use of clonidine against sevoflurane-induced agitation may represent a new and promising application. One hundred and twenty children were included in this study: 59 of whom received clonidine, and 61 placebo; 41% of those in the placebo group exhibited moderate-severe ethacrynic acid compared with only 22% of those in the clonidine group (P < 0.03). Findings demonstrate that i.v. clonidine administered after induction of anesthesia significantly reduces the incidence of ethacrynic acid in young children, but is associated with Somnolence postoperatively. clonidine could not prevent agitation (incidence 54%, 13/24) clonidine 1.5 microg/kg did not differ from placebo with respect to postoperative agitation. clonidine is effective in treating sevoflurane-induced postanesthesia agitation in children. Pain:-:Point in time:^Patient:-:-:Point in time:^Patient:- and discomfort scores were significantly decreased in the clonidine group; the incidence of agitation was reduced by 57% (P = 0.029) and the incidence of severe agitation by 67% (P = 0.064). Relative risks for developing agitation and severe agitation were 0.43 (95% confidence interval, 0.24-0.78) and 0.32 (0.09-1.17), respectively. clonidine produces a substantial reduction in the risk of postsevoflurane agitation in children. Agitation was observed in 12 midazolam-treated and five clonidine-treated patients (P=0.05). Compared with midazolam, clonidine premedication reduced agitation during sevoflurane induction. clonidine 3 micrograms kg-1 prevented agitation after sevoflurane anaesthesia, independently of the route of administration. The effect of clonidine appears to be dose-dependent, as an epidural dose of 1 microgram kg-1 failed to reduce it. clonidine prevents sevoflurane-induced agitation in children. In 16 placebo and 2 clonidine-treated patients agitation was observed (P < 0.001) In 6 patients of the Placebo group, agitation was graded as severe, whereas none of the patients in the clonidine group developed severe agitation (P = 0.02). We conclude that clonidine effectively prevents agitation after sevoflurane anesthesia. clonidine 2 microg/kg IV after anesthetic induction effectively reduces the incidence of agitation without resulting in clinically relevant Bradycardia by ECG Finding and Hypotension. Children receiving clonidine prior to undergoing strabismus surgery have a small but noticeable reduction in postoperative agitation, stay slightly longer in the post-anesthesia care unit, and have higher rates of parent satisfaction. We report three cases of preoperative use of intranasal clonidine in pediatric patients, all for different indications. One patient was treated for preoperative agitation and Hallucinations associated with oral midazolam. One patient was given clonidine as a premedicant. The third patient was treated for preoperative agitation and Hypertensive disease. All three patients had subjective resolution of indicated symptoms and none experienced adverse outcomes. Oral Route of Drug administration Route of Drug administration or intravenous clonidine has been successfully used for the prevention of sevoflurane-induced agitation during emergence from anaesthesia.[SEP]Relations: Agitation has relations: drug_effect with clonidine, drug_effect with clonidine. clonidine has relations: drug_effect with Agitation, drug_effect with Agitation, drug_effect with Anxiety, drug_effect with Anxiety, contraindication with anxiety disorder, contraindication with anxiety disorder, drug_effect with Headache, drug_effect with Headache.", "label": "yes"}
{"original_question": "Is there an association between presenteeism and depression?", "id": "converted_30", "sentence1": "Is there an association between Presenteeism and Cancer patients and suicide and depression?", "sentence2": "Presenteeism was positively associated with severity of Cancer patients and suicide and Cancer patients and suicide and depression (Health and Work Performance Questionnaire, P < 0.0001; WPAI, P < 0.0001). Statistically significant correlations (0.32-0.53) were found between Presenteeism and increasing disability, Fatigue, Cancer patients and suicide and Cancer patients and suicide and depression, Anxiety Disorders, and reduced quality of life.  Presenteeism was associated with increasing Fatigue, Cancer patients and suicide and Cancer patients and suicide and depression, Anxiety Disorders, and reduced quality of life. Factors with less contribution to Presenteeism included physical limitations, Cancer patients and suicide and Cancer patients and suicide and depression or Anxiety Disorders, inadequate job training, and problems with supervisors and coworkers.  BACKGROUND: Subthreshold Cancer patients and suicide and Cancer patients and suicide and depression is highly prevalent in the general population and causes great loss to society especially in the form of reduced productivity while at work (Presenteeism). Two major causes of worker Presenteeism (reduced on-the-job productivity as a result of health problems) are Musculoskeletal Pain:-:Point in time:^Patient:-:-:Point in time:^Patient:- and mental health issues, particularly Cancer patients and suicide and Cancer patients and suicide and depression.   Pain:-:Point in time:^Patient:-:-:Point in time:^Patient:- and Cancer patients and suicide and Cancer patients and suicide and depression were significantly associated with Presenteeism. Pr Survey adjusted multivariable logistic regression assessed classification of 12-month, Cancer patients and suicide and Cancer patients and suicide and depression-related Presenteeism on the basis of socio-demographic, financial, work and health factors.  RESULTS: The LPT from absenteeism and Presenteeism (reduced performance while present at work) was significantly higher among the Major Depressive Disorder group. BACKGROUND: Depression is reported to be a major cause of Illness (finding)-related sub-optimal work performance (Presenteeism).  BACKGROUND: It is amply documented that Mood Disorders adversely affect job satisfaction, workforce productivity, and absenteeism/Presenteeism.  The difference in productivity loss due to impaired Presenteeism was significantly different between the two groups, but the productivity loss due to absenteeism was not.  Disease activity (OR 3.24, 95% CI 1.11-9.48) and Cancer patients and suicide and Cancer patients and suicide and depression (OR 3.22, 95% CI 1.22-8.48) were associated with absenteeism, while Cancer patients and suicide and Cancer patients and suicide and depression (OR 5.69, 95% CI 1.77-18.27, disease activity (OR 3.97, 95% CI 1.76-8.98), Anxiety Disorders (OR 3.90, 95% CI 1.83-8.31), self-efficacy (OR 0.71, 95% CI 0.58-0.86), and increasing age (OR 1.04 per year, 95% CI 1.00-1.08) were associated with Presenteeism.  Depression, in particular, appears to be associated with employment, absenteeism, and Presenteeism, and should therefore be prioritized in clinical practice. Depression frequently causes unemployment, absenteeism, and Presenteeism, which results in significantly reduced productivity. Presenteeism and absenteeism were significantly worse for the Cancer patients and suicide and Cancer patients and suicide and depression group at each time point (p < or = .001). In cross-sectional models, Presenteeism was associated with more severe Cancer patients and suicide and Cancer patients and suicide and depression symptoms, poorer general physical health, psychologically demanding work, the interaction ofpsychologically demanding work with Cancer patients and suicide and Cancer patients and suicide and depression, and less job control (r2 range = .33-.54). Chronic conditions such as Cancer patients and suicide and Cancer patients and suicide and depression/Anxiety Disorders, BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, Arthritis, and back/neck pain are especially important causes of productivity loss. Comorbidities have significant non-additive effects on both absenteeism and Presenteeism. RESULTS: At baseline, all Presenteeism measures were sensitive to differences between those with (N=69) and without (N=363) Cancer patients and suicide and Cancer patients and suicide and depression/Anxiety Disorders. Depression and Anxiety Disorders were more consistently associated with \"Presenteeism\" (that is, lost productivity while at work) than with absenteeism, whether this was measured by cutback days or by direct questionnaires. RESULTS: Substantial research exists about Anxiety Disorders and Cancer patients and suicide and Cancer patients and suicide and depression costs, such as performance and productivity, absenteeism, Presenteeism, disability, A A physical disability exacerbation, mental health treatment, increased medical care costs, exacerbating of physical Illness (finding), and studies of mental health care limitations and cost-offset. The author discusses the etiology and potential solutions for managing this new component in the productivity equation and in addressing Cancer patients and suicide and Cancer patients and suicide and depression, the major contributor to Presenteeism. For employees who are currently Depressed mood, recent research evidence has demonstrated that pharmacotherapy can have a dramatic and positive effect on lost productivity, absenteeism, and Presenteeism. Among participants who were still employed, those with Cancer patients and suicide and Cancer patients and suicide and depression had significantly more job turnover, Presenteeism, and absenteeism.  Only Cancer patients and suicide and Cancer patients and suicide and depression affected both absenteeism-Presenteeism and critical incidents.  CONCLUSIONS: Depressive disorder in the workplace persist over time and have a major effect on work performance, most notably on \"Presenteeism,\" or reduced effectiveness in the workplace.  The negative effects of Cancer patients and suicide and Cancer patients and suicide and depression include those on patients' occupational functioning, including absenteeism, Presenteeism, and reduced opportunities for educational and work success.  The remitted group demonstrated a significant improvement in productivity (particularly Presenteeism) when compared with the new visit group (Z\u2009=\u2009-3.29, p\u2009=\u20090.001). Depression in workers leads to significant absenteeism, \"Presenteeism\" (diminished capacity due to Illness (finding) while still present at work), and significantly increased medical expenses in addition to the costs of psychiatric care.  Significant predictors of Presenteeism and activity impairment at follow-up (controlled for gender, age, spondyloarthritis subgroups and Presenteeism at baseline) were Presenteeism at baseline, poor quality of life, worse disease activity, decreased physical function, lower self-efficacy pain and symptom, higher scores of Anxiety Disorders, Cancer patients and suicide and Cancer patients and suicide and depression, Location characteristic ID - Smoking and low education level, and for activity impairment also female sex.  \" Pain:-:Point in time:^Patient:-:-:Point in time:^Patient:- and Cancer patients and suicide and Cancer patients and suicide and depression were significantly associated with Presenteeism. Only Cancer patients and suicide and Cancer patients and suicide and depression affected both absenteeism-Presenteeism and critical incidents. Factors with less contribution to Presenteeism included physical limitations, Cancer patients and suicide and Cancer patients and suicide and depression or Anxiety Disorders, inadequate job training, and problems with supervisors and coworkers.[SEP]Relations: Anxiety Disorders disorder has relations: disease_disease with postpartum Cancer patients and suicide and depression, disease_disease with postpartum Cancer patients and suicide and depression, disease_disease with neurotic Cancer patients and suicide and depression, disease_disease with neurotic Cancer patients and suicide and depression, disease_disease with unipolar Cancer patients and suicide and depression, disease_disease with unipolar Cancer patients and suicide and depression. major depressive disorder has relations: disease_disease with endogenous Cancer patients and suicide and depression, disease_disease with endogenous Cancer patients and suicide and depression, disease_disease with endogenous Cancer patients and suicide and depression, disease_disease with endogenous Cancer patients and suicide and depression.", "label": "yes"}
{"original_question": "Are OATP1B1 and OATP1B3 associated with bilirubin transport?", "id": "converted_31", "sentence1": "Are OATP1B1 and SLCO1B3 wt Allele associated with Bilirubin transport?", "sentence2": "OATP1B1 and SLCO1B3 wt Allele-mediated transport of Bilirubin was confirmed and inhibition was determined for atazanavir, rifampin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir.  Examples of adaptive Nontoxic changes in Abdomen>Liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) Bilirubin above baseline levels, include reversible inhibition of UGT1A1 gene gene-mediated Bilirubin metabolism and OATP1B1-, SLCO1B3 wt Allele-, or ABCC2 wt Allele-mediated transport (Keogh. Due to limited solubility and poor ionization of Bilirubin and its Glucuronides, the formation of estradiol 3-Glucuronides was used as a surrogate to assess UGT1A1 gene gene activity, while the transport of pitavastatin, 5(6)-carboxy-2',7'-dichlorofluorescein, and Taurocholate were used as surrogate Probe brand of methazole herbicide substrates to monitor the function of OATP1B1/SLCO1B3 wt Allele, ABCC2 wt Allele, and ABCB11 wt Allele, respectively. OATP1B1 and SLCO1B3 wt Allele-mediated transport of Bilirubin was confirmed and inhibition was determined for atazanavir, rifampin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir. However, because Pharmacologic Substance transporters also contribute to Bilirubin elimination, the purpose of this work was to investigate the in vitro inhibition of OATP1B1, SLCO1B3 wt Allele, ABCC2 wt Allele, and ABCB11 wt Allele of select test drugs known to elicit Jaundice, Chronic Idiopathic. Thus, disruption of hepatic reuptake of Bilirubin Glucuronides due to coexisting OATP1B1 and SLCO1B3 wt Allele deficiencies explains Rotor-type Jaundice, Chronic Idiopathic.Moreover, OATP1B1 and SLCO1B3 wt Allele null mutations may confer substantial Pharmacologic Substance Toxic effect risks. Bilirubin elimination is a multifaceted process consisting of uptake of Bilirubin into the Hepatocyte facilitated by OATP1B1 and SLCO1B3 wt Allele. Complete OATP1B1 and SLCO1B3 wt Allele deficiency causes Homo sapiens Rotor syndrome by interrupting conjugated Bilirubin reuptake into the Abdomen>Liver. Thus, disruption of hepatic reuptake of Bilirubin Glucuronides due to coexisting OATP1B1 and SLCO1B3 wt Allele deficiencies explains Rotor-type Jaundice, Chronic Idiopathic. The data show that a substantial fraction of Bilirubin Immunostimulating conjugate (antigen) is primarily secreted by ABCC3 wt Allele at the sinusoidal membrane into the blood, from where they are subsequently reuptaken by sinusoidal membrane-bound organic anion transporting polypeptides OATP1B1 and SLCO1B3 wt Allele. Evaluating the in vitro inhibition of UGT1A1 gene gene, OATP1B1, SLCO1B3 wt Allele, ABCC2 wt Allele, and ABCB11 wt Allele in predicting Pharmacologic Substance-induced Jaundice, Chronic Idiopathic. OATP1B1 and SLCO1B3 wt Allele-mediated transport of Bilirubin was confirmed and inhibition was determined for atazanavir, rifampin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir Bilirubin elimination is a multifaceted process consisting of uptake of Bilirubin into the Hepatocyte facilitated by OATP1B1 and SLCO1B3 wt Allele Due to limited solubility and poor ionization of Bilirubin and its Glucuronides, the formation of estradiol 3-Glucuronides was used as a surrogate to assess UGT1A1 gene gene activity, while the transport of pitavastatin, 5(6)-carboxy-2',7'-dichlorofluorescein, and Taurocholate were used as surrogate Probe brand of methazole herbicide substrates to monitor the function of OATP1B1/SLCO1B3 wt Allele, ABCC2 wt Allele, and ABCB11 wt Allele, respectively Examples of adaptive Nontoxic changes in Abdomen>Liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) Bilirubin above baseline levels, include reversible inhibition of UGT1A1 gene gene-mediated Bilirubin metabolism and OATP1B1-, SLCO1B3 wt Allele-, or ABCC2 wt Allele-mediated transport (Keogh In vitro, faldaprevir inhibited key processes involved in Bilirubin clearance: Glucuronosyltransferase (UGT) 1A1 (UGT1A1 gene gene) (IC50 0.45 \u00b5M), which Immunostimulating conjugate (antigen) Bilirubin, and hepatic uptake and efflux transporters, organic anion-transporting polypeptide (OATP) 1B1 (IC50 0.57 \u00b5M), SLCO1B3 wt Allele (IC50 0.18 \u00b5M), and multidrug resistance-associated protein (Multidrug Resistance-Associated Proteins) 2 (IC50 6.2 \u00b5M), which transport Bilirubin and its Immunostimulating conjugate (antigen) Thus, disruption of hepatic reuptake of Bilirubin Glucuronides due to coexisting OATP1B1 and SLCO1B3 wt Allele deficiencies explains Rotor-type Jaundice, Chronic Idiopathic Thus, disruption of hepatic reuptake of Bilirubin Glucuronides due to coexisting OATP1B1 and SLCO1B3 wt Allele deficiencies explains Rotor-type Jaundice, Chronic Idiopathic.Moreover, OATP1B1 and SLCO1B3 wt Allele null mutations may confer substantial Pharmacologic Substance Toxic effect risks OATP1B1 (a.k.a. OATP-C, SLCO1B1 wt Allele, LST-1, or SLC21A6) is a Abdomen>Liver-specific organic anion uptake transporter and has been shown to be a higher affinity Bilirubin uptake transporter than SLCO1B3 wt Allele In vitro OATP1B1 and SLCO1B3 wt Allele inhibition is associated with observations of benign clinical unconjugated Jaundice, Chronic Idiopathic. Examples of adaptive Nontoxic changes in Abdomen>Liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) Bilirubin above baseline levels, include reversible inhibition of UGT1A1 gene gene-mediated Bilirubin metabolism and OATP1B1-, SLCO1B3 wt Allele-, or ABCC2 wt Allele-mediated transport (Keogh. Adv Pharmacol 63:1-42, 2012).  Using CASP14 gene deficient in Oatp1a/1b and in the multispecific sinusoidal export pump ABCC3 protein, Homo sapiens, we found that ABCC3 protein, Homo sapiens secretes Bilirubin Immunostimulating conjugate (antigen) into the blood, while Oatp1a/1b transporters mediate their hepatic reuptake.  Bilirubin elimination is a multifaceted process consisting of uptake of Bilirubin into the Hepatocyte facilitated by OATP1B1 and SLCO1B3 wt Allele.  OATP1B1 polymorphism is a major determinant of serum Bilirubin level but not associated with rifampin-mediated Bilirubin elevation. Unconjugated Bilirubin (UCB) is taken up into Hepatocyte by Homo sapiens organic anion transporting polypeptide 1B1 (OATP1B1; encoded for by the SLCO1B1 gene). However, because Pharmacologic Substance transporters also contribute to Bilirubin elimination, the purpose of this work was to investigate the in vitro inhibition of OATP1B1, SLCO1B3 wt Allele, ABCC2 wt Allele, and ABCB11 wt Allele of select test drugs known to elicit Jaundice, Chronic Idiopathic. Test drugs investigated in this study were atazanavir and indinavir, which are associated with Jaundice, Chronic Idiopathic and elevations in serum Aspartate Transaminase; ritonavir and nelfinavir, which are not associated with Jaundice, Chronic Idiopathic; and bromfenac, troglitazone, and trovafloxacin, which are associated with severe idiosyncratic hepatotoxicity exhibiting elevations in serum Bilirubin and Aspartate Transaminase. Test drugs investigated in this study were atazanavir and indinavir, which are associated with Jaundice, Chronic Idiopathic and elevations in serum Aspartate Transaminase; ritonavir and nelfinavir, which are not associated with Jaundice, Chronic Idiopathic; and bromfenac, troglitazone, and trovafloxacin, which are associated with severe idiosyncratic hepatotoxicity exhibiting elevations in serum Bilirubin and Aspartate Transaminase. Due to limited solubility and poor ionization of Bilirubin and its Glucuronides, the formation of estradiol 3-Glucuronides was used as a surrogate to assess UGT1A1 gene gene activity, while the transport of pitavastatin, 5(6)-carboxy-2',7'-dichlorofluorescein, and Taurocholate were used as surrogate Probe brand of methazole herbicide substrates to monitor the function of OATP1B1/SLCO1B3 wt Allele, ABCC2 wt Allele, and ABCB11 wt Allele, respectively. In vitro, faldaprevir inhibited key processes involved in Bilirubin clearance: Glucuronosyltransferase (UGT) 1A1 (UGT1A1 gene gene) (IC50 0.45 \u00b5M), which Immunostimulating conjugate (antigen) Bilirubin, and hepatic uptake and efflux transporters, organic anion-transporting polypeptide (OATP) 1B1 (IC50 0.57 \u00b5M), SLCO1B3 wt Allele (IC50 0.18 \u00b5M), and multidrug resistance-associated protein (Multidrug Resistance-Associated Proteins) 2 (IC50 6.2 \u00b5M), which transport Bilirubin and its Immunostimulating conjugate (antigen). In vitro OATP1B1 and SLCO1B3 wt Allele inhibition is associated with observations of benign clinical unconjugated Jaundice, Chronic Idiopathic. 3.\u2002\u2009The results indicated that in vivo Fi values >0.2 or R-values >1.5 for OATP1B1 or SLCO1B3 wt Allele, but not UGT1A1 gene gene, are associated with previously reported clinical cases of Pharmacologic Substance-induced unconjugated Jaundice, Chronic Idiopathic. OATP1B1 and SLCO1B3 wt Allele-mediated transport of Bilirubin was confirmed and inhibition was determined for atazanavir, rifampin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir.[SEP]Relations: UGT1A1 gene has relations: disease_protein with Bilirubin encephalopathy, disease_protein with Bilirubin encephalopathy, bioprocess_protein with Bilirubin conjugation, bioprocess_protein with Bilirubin conjugation, protein_protein with B3GALT1, protein_protein with B3GALT1, drug_protein with Alvocidib, drug_protein with Alvocidib. SLCO1B1 has relations: molfunc_protein with bile acid transmembrane transporter activity, molfunc_protein with bile acid transmembrane transporter activity.", "label": "yes"}
{"original_question": "Is abdominal pain a common symptom in autism?", "id": "converted_32", "sentence1": "Is abdominal Pain:-:Point in time:^Patient:- a common symptom in Autistic Disorder?", "sentence2": "Participants included 132 children with Atrial Septal Defects and 81 with special educational needs (MORF4 gene) but no Atrial Septal Defects, aged 10-14\u00a0years plus 82 typically developing (diphtheria, tetanus toxoids and acellular pertussis vaccine) children The Atrial Septal Defects group had significantly increased past vomiting and Diarrhea compared with the diphtheria, tetanus toxoids and acellular pertussis vaccine group and more abdominal Pain:-:Point in time:^Patient:- than the MORF4 gene group Many children with Autistic Disorder spectrum disorders (ASDs) suffer from Gastrointestinal problem such as Diarrhea, Constipation and abdominal Pain:-:Point in time:^Patient:- Children with Autistic Disorder spectrum disorders (Atrial Septal Defects) experience high rates of Anxiety Disorders, sensory processing problems, and gastrointestinal (GI) problems The results indicate that Anxiety Disorders, sensory over-responsivity and GI problems are possibly interrelated phenomenon for children with Atrial Septal Defects, and may have common underlying mechanisms. Decreased small intestinal mucosa lactase level not associated with Intestinal inflammation or injury is common in autistic children and may contribute to abdominal discomfort, Pain:-:Point in time:^Patient:- and observed aberrant behavior. Autistic behavior is often accompanied by numerous disturbing symptoms on the part of gastrointestinal system, such as abdominal Pain:-:Point in time:^Patient:-, Constipation or diarrhea. Information on children's stool patterns and gut symptoms collected by questionnaire at 4 weeks and at 6, 18, 30 and 42 months of age were available for 12,984 children from the Avon Longitudinal Study of Parents and Children (Avon Longitudinal Study of Parents and Children (Avon Longitudinal Study of Parents and Children (ALSPAC))) Comparison of the Atrial Septal Defects and control group during the first 3.5 years of life showed no major differences in stool colour or consistency, or in frequency of Diarrhea, Constipation, Blood in stool or abdominal Pain:-:Point in time:^Patient:-. Constipation is a frequent finding in children with No gastrointestinal symptom and Autistic Disorder, particularly in the Rectum and sigmoid colon, often with acquired megarectum. The absence of any correlation between the clinical history and the degree of fecal impaction in autistic children confirms the importance of an abdominal radiograph in the assessment of their degree of Constipation. In a sample of 137 children, age 24-96 months, classified as having Autistic Disorder or Atrial Septal Defects by the Autism Diagnostic Observation Schedule-Generic, 24 percent had a history of at least one chronic gastrointestinal symptom. The most common symptom was diarrhea, which occurred in 17 percent.[SEP]Relations: Abdominal Pain:-:Point in time:^Patient:- has relations: phenotype_phenotype with Abdominal symptom, phenotype_phenotype with Abdominal symptom, phenotype_phenotype with Pain, phenotype_phenotype with Pain, phenotype_phenotype with Episodic abdominal Pain:-:Point in time:^Patient:-, phenotype_phenotype with Episodic abdominal Pain:-:Point in time:^Patient:-, disease_phenotype_positive with plague, disease_phenotype_positive with plague, disease_phenotype_positive with congenital diarrhea, disease_phenotype_positive with congenital diarrhea.", "label": "yes"}
{"original_question": "Are cyclophilins ubiquitously expressed?", "id": "converted_33", "sentence1": "Are Cyclophilins ubiquitously expressed?", "sentence2": "Cyclophilin from Leishmania donovani donovani donovani (LdCyp) is a ubiquitous peptidyl-prolyl cis-trans Isomerase (disposition) Cyclophilins (CYPs) and Tacrolimus Binding Proteins (FKBPs) are ubiquitous Proteins belonging to the peptidyl-prolyl cis/trans Isomerase (disposition) (PPIase) family.  However, their wide distribution and ubiquitous nature signifies their fundamental importance in plant survival. Cyclophilins (Cyps) are ubiquitous Proteins that effect the cis-trans isomerization of Pro amide bonds, and are thus crucial to Protein Info folding. FK506 binding Proteins (FKBPs) and Cyclophilins (CYPs) are abundant and ubiquitous Proteins belonging to the peptidyl-prolyl cis/trans Isomerase (disposition) (PPIase) superfamily, which regulate much of metabolism through a chaperone or an isomerization of proline residues during Protein Info folding. Cyclophilin is a ubiquitous peptidyl prolyl cis/trans Isomerase (disposition) that plays critical roles in many biological processes. The receptor for cyclosporine is the Protein Info cyclophilin, which is a ubiquitous peptidylprolyl Isomerase (disposition).  Cyps (Cyclophilins) are ubiquitous Proteins of the Peptidylprolyl Isomerase superfamily with proposed functions in Protein Info folding, Protein Info degradation, stress response and signal transduction.  Cyclophilins are folding helper ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS belonging to the class of peptidyl-prolyl cis-trans Isomerase (PPIases; EC 5.2.1.8) that catalyze the cis-trans isomerization of peptidyl-prolyl bonds in Proteins. They are ubiquitous Proteins present in almost all living Organism analyzed to date, with extremely rare exceptions. Immunophilins are ubiquitous ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS responsible for proline isomerisation during Protein Info synthesis and for the chaperoning of several Membrane Proteins. Cyclophilins (CyPs) are a large class of highly conserved ubiquitous peptidyl-prolyl cis-trans Isomerase. Cyclophilins belong to the family of peptidyl-prolyl cis/trans Isomerase (PPIases), which are ubiquitous and highly conserved ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS capable of cis/trans isomerizing Xaa-Pro peptide bonds.  Originally identified as the cellular targets of immunosuppressant drugs, the Immunophilins encompass two ubiquitous Protein Info families: the FK-506 binding Proteins or FKBPs, and the cyclosporine-binding Proteins or Cyclophilins.[SEP]Relations: Cyclosporine has relations: drug_drug with Gatifloxacin, drug_drug with Gatifloxacin, drug_drug with Etoposide, drug_drug with Etoposide, drug_drug with Genistein, drug_drug with Genistein, drug_drug with Hypericin, drug_drug with Hypericin, drug_drug with Alogliptin, drug_drug with Alogliptin.", "label": "yes"}
{"original_question": "Does low T3 negatively affect prognosis of patients after cardiac surgery?", "id": "converted_34", "sentence1": "Does low T3 thoracic segmental innervation negatively affect prognosis of patients after cardiac surgery?", "sentence2": "ur findings suggest that the development of LCOS after congenital heart surgery is associated with decreased total and free T3 thoracic segmental innervation thoracic segmental innervation, and increased interleukin-8 receptor binding activity levels at 48 hours, and preoperative Adenosine A2B Receptor Antagonist TT-4 level is an independent predictor of LCOS. Low basal cubic foot concentration can reliably predict the occurrence of postoperative AF in CABG patients. A relevant finding was that the days of post-operative hospitalization (10+/-3 days, means+/-S.D.) was inversely correlated with the slope of the recovery of T3 thoracic segmental innervation thoracic segmental innervation concentration (P<0.001) or with the area under the plasma curves of T3 thoracic segmental innervation thoracic segmental innervation (P=0.024, time range 72-144 h) and the FT3/FT4 ratio (P=0.037, time range 72-144 h) during the post-operative period.[SEP]Relations: interleukin-8 receptor activity has relations: molfunc_protein with CXCR2, molfunc_protein with CXCR2, molfunc_protein with CXCR1, molfunc_protein with CXCR1, molfunc_molfunc with C-X-C chemokine receptor activity, molfunc_molfunc with C-X-C chemokine receptor activity. A2B adenosine receptor binding has relations: molfunc_molfunc with adenosine receptor binding, molfunc_molfunc with adenosine receptor binding. insect larval thoracic segment has relations: anatomy_anatomy with insect larval prothoracic segment, anatomy_anatomy with insect larval prothoracic segment.", "label": "yes"}
{"original_question": "Has proteomics been used in the study of the dry eye syndrome?", "id": "converted_35", "sentence1": "Has proteomics been used in the study of the Dry Eye Syndromes?", "sentence2": "Tear proteomic analysis of patients with type 2 diabetes and Dry Eye Syndromes by two-dimensional nano-liquid chromatography coupled with tandem mass spectrometry. Dry eye syndrome in diabetic patients is associated with aberrant expression of tear proteins, and the findings could lead to identification of novel pathways for therapeutic targeting and new diagnostic markers.  2D electrophoresis (2DE) and Differential gel electrophoresis (DIGE) was done to identify differentially expressed proteins.  Two dimensional electrophoretic analysis of Homo sapiens tears: collection method in Dry Eye Syndromes. Identification of tear fluid biomarkers in Dry Eye Syndromes using iTRAQ quantitative proteomics. This study demonstrated that iTRAQ technology combined with 2D-nanoLC-nanoESI-MS/MS quantitative proteomics is a powerful tool for biomarker discovery.[SEP]Relations: Dry Eye Syndromes has relations: disease_protein with STAT4, disease_protein with STAT4, disease_disease with syndromic disease, disease_disease with syndromic disease, disease_protein with TNIP1, disease_protein with TNIP1, disease_protein with PHIP, disease_protein with PHIP, disease_protein with TNFAIP3, disease_protein with TNFAIP3.", "label": "yes"}
{"original_question": "Are pseudogenes enriched with housekeeping protein families?", "id": "converted_36", "sentence1": "Are Pseudogenes enriched with housekeeping protein families?", "sentence2": "housekeeping families tend to be enriched with a large number of Pseudogenes[SEP]", "label": "yes"}
{"original_question": "Is Calcium/Calmodulin dependent protein kinase II (CaMKII) involved in cardiac arrhythmias and heart failure?", "id": "converted_37", "sentence1": "Is Calcium/Calmodulin 1 dependent protein kinase II (CAMK2A gene) involved in Cardiac Arrhythmia and Chest>Heart failure?", "sentence2": "In human Hypertrophy, both CAMK2A gene and Cyclic AMP-Dependent Protein Kinases functionally regulate Ryanodine Receptor 2 and may induce SNCG wt Allele Ca(2+) leak. In the transition from Hypertrophy to Hydrops Fetalis, the diastolic Ca(2+) leak increases and disturbed Ca(2+) cycling occurs. This is associated with an increase in CAMK2A gene- but not Cyclic AMP-Dependent Protein Kinases-dependent Ryanodine Receptor 2 phosphorylation. CAMK2A gene inhibition may thus reflect a promising therapeutic target for the treatment of arrhythmias and contractile dysfunction. Ca(2+)/Calcium/calmodulin-dependent protein kinase (CAMK2A gene) is an Enzyme [APC] with important regulatory functions in the Chest>Heart and Head>Brain, and its chronic activation can be pathological. CAMK2A gene activation is seen in Chest>Heart failure, and can directly induce pathological changes in ion channels, Ca(2+) handling and gene transcription. In the recent years, Ca(2+)/Calcium/calmodulin-dependent protein kinase (CAMK2A gene) was suggested to be associated with cardiac Hypertrophy and Chest>Heart failure but also with arrhythmias both in animal models as well as in the human Chest>Heart. Calcium-Calcium/calmodulin-dependent protein kinase (CAMK2A gene) has emerged as a central mediator of cardiac stress responses which may serve several critical roles in the regulation of cardiac rhythm, cardiac contractility and growth. Sustained and excessive activation of CAMK2A gene during Heart Diseases has, however, been linked to arrhythmias, and maladaptive cardiac remodeling, eventually leading to Chest>Heart failure (Hydrops Fetalis) and Sudden Cardiac Death.  Overexpression of Ca(2+)/Calcium/calmodulin-dependent protein kinase (CAMK2A gene) in Mice, Animals, Animals, Transgenic results in Chest>Heart failure and arrhythmias. From recent studies, it appears evident that Ca(2+)/Calcium/calmodulin-dependent protein kinase (CAMK2A gene) plays a central role in the arrhythmogenic processes in Chest>Heart failure by sensing Protoplasm Ca(2+) and redox stress, affecting individual ion channels and thereby leading to electrical instability in the Chest>Heart.  CAMK2A gene activation is proarrhythmic in Chest>Heart failure where Myocardium is stretched. The Ca-calmodulin dependent kinase II (CAMK2A gene) seems to be involved in the development of Chest>Heart failure and arrhythmias and may therefore be a promising target for the development of antiarrhythmic therapies. Ca(2+)/Calcium/calmodulin-dependent protein kinase (CAMK2A gene) is up-regulated in Chest>Heart failure and has been shown to cause I(Na) gating changes that mimic those induced by a Point Mutation in Homo sapiens that is associated with combined long QT and Brugada syndromes. CAMK2A gene-dependent phosphorylation of Na(V)1.5 at multiple sites (including Thr-594 and Ser-516) appears to be required to evoke loss-of-function changes in gating that could contribute to acquired Brugada Syndrome (disorder)-like effects in Chest>Heart failure. Because CAMK2A gene expression and activity are increased in cardiac Hypertrophy, Chest>Heart failure, and during arrhythmias both in animal models as well as in the human Chest>Heart a clinical significance of CAMK2A gene is implied. The multifunctional Ca(2+)- and Calcium/calmodulin-dependent protein kinase (CAMK2A gene) is now recognized to play a central role in pathological events in the cardiovascular system. CAMK2A gene has diverse downstream targets that promote Vascular Diseases, Chest>Heart failure, and arrhythmias, so improved understanding of CAMK2A gene signaling has the potential to lead to new therapies for Cardiovascular Diseases. In our opinion, the multifunctional Ca and Calcium/calmodulin-dependent protein kinase (CAMK2A gene) has emerged as a molecule to watch, in part because a solid body of accumulated data essentially satisfy Koch's postulates, showing that the CAMK2A gene pathway is a core mechanism for promoting myocardial Hypertrophy and Chest>Heart failure. Multiple groups have now confirmed the following: (1) that CAMK2A gene activity is increased in hypertrophied and failing Myocardium from animal models and patients; (2) CAMK2A gene overexpression causes myocardial Hypertrophy and Hydrops Fetalis and (3) CAMK2A gene inhibition (by drugs, inhibitory peptides and Gene Deletion) improves myocardial Hypertrophy and Hydrops Fetalis  In contrast, inhibiting the CAMK2A gene pathway appears to reduce arrhythmias and improve myocardial responses to pathological stimuli.  In this review, we discuss the important role of Ca(2+)/Calcium/calmodulin-dependent protein kinase (CAMK2A gene) in the regulation of Ryanodine Receptor 2-mediated Ca(2+) release. In particular, we examine how pathological activation of CAMK2A gene can lead to an increased risk of sudden arrhythmic death. Finally, we discuss how reduction of CAMK2A gene-mediated Ryanodine Receptor 2 Hyperactive behavior might reduce the risk of arrhythmias and may serve as a rationale for future pharmacotherapeutic approaches. Animals, Animals, Transgenic (TG wt Allele wt Allele) Ca(2+)/Calcium/calmodulin-dependent protein kinase (CAMK2A gene) \u03b4(C) CASP14 gene develop systolic Chest>Heart failure (Hydrops Fetalis). CAMK2A gene regulates Protoplasm Ca(2+) handling Proteins as well as sarcolemmal Na(+) channels. We hypothesized that CAMK2A gene also contributes to Diastolic dysfunction and arrhythmias via augmentation of the late Na(+) current (late I(Na)) in early Hydrops Fetalis (8-week-old TG wt Allele wt Allele CASP14 gene). Thus, late I(Na) inhibition appears to be a promising option for Diastolic dysfunction and arrhythmias in Hydrops Fetalis where CAMK2A gene is found to be increased. We tested the hypothesis that increased Ryanodine Receptor 2 phosphorylation by Ca(2+)/Calcium/calmodulin-dependent protein kinase is both necessary and sufficient to promote lethal Ventricular arrhythmia. CONCLUSIONS: our results suggest that Ca(2+)/Calcium/calmodulin-dependent protein kinase phosphorylation of Ryanodine Receptor 2 Ca(2+) release channels at S2814 plays an important role in arrhythmogenesis and Sudden Cardiac Death in CASP14 gene with Chest>Heart failure. Excessive activation of calmodulin kinase II (CAMK2A gene) causes arrhythmias and Chest>Heart failure, but the cellular mechanisms for CAMK2A gene-targeted Proteins causing disordered Cellular Membrane excitability and Myocardial dysfunction remain uncertain. Animals, Animals, Transgenic (TG wt Allele wt Allele) Ca/Calcium/calmodulin-dependent protein kinase (CAMK2A gene)delta(C) CASP14 gene have Chest>Heart failure and isoproterenol (ISO)-inducible arrhythmias. We hypothesized that CAMK2A gene contributes to arrhythmias and underlying cellular events and that inhibition of CAMK2A gene reduces cardiac arrhythmogenesis in vitro and in vivo. We conclude that CAMK2A gene contributes to cardiac arrhythmogenesis in TG wt Allele wt Allele CaMKIIdelta(C) CASP14 gene having Chest>Heart failure and suggest the increased SNCG wt Allele Ca leak as an important mechanism. Moreover, CAMK2A gene inhibition reduces Cardiac Arrhythmia in vitro and in vivo and may therefore indicate a potential role for future antiarrhythmic therapies warranting further studies. Ca2+/calmodulin dependent protein kinase II (CAMK2A gene) can phosphorylate Ryanodine Receptor 2 and modulate its activity. This phosphorylation positively modulates cardiac inotropic function but in extreme situations such as Chest>Heart failure, elevated CAMK2A gene activity can adversely increase Ca2+ release from the SNCG wt Allele and lead to arrhythmogenesis.  Calcium/calmodulin-dependent kinase II (CAMK2A gene) is a multifunctional serine/threonine kinase expressed abundantly in the Chest>Heart. CAMK2A gene targets numerous Proteins involved in excitation-contraction coupling and excitability, and its activation may simultaneously contribute to Chest>Heart failure and Cardiac Arrhythmia. Under stress conditions, excessive CAMK2A gene activity promotes Chest>Heart failure and arrhythmias, in part through actions at Ca(2+) homeostatic Proteins. Ca-Calcium/calmodulin-dependent protein kinase (CAMK2A gene) was recently shown to alter Na(+) channel gating and recapitulate a human Na(+) channel Mutation that causes an unusual combined arrhythmogenic phenotype in patients: simultaneous long QT syndrome and Brugada Syndrome (disorder). CAMK2A gene is upregulated in Chest>Heart failure where arrhythmias are common, and CAMK2A gene inhibition can reduce arrhythmias. Thus, CAMK2A gene-dependent channel modulation may contribute to acquired arrhythmic disease.  In Chest>Heart failure (Hydrops Fetalis), Ca(2+)/calmodulin kinase II (CAMK2A gene) expression is increased. Altered Na(+) channel gating is linked to and may promote Ventricular tachyarrhythmia (Tidal Volume) in Hydrops Fetalis. Calmodulin 1 1 regulates Na(+) channel gating, in part perhaps via CAMK2A gene. Thus, CAMK2A gene-dependent regulation of Na(+) channel function may contribute to arrhythmogenesis in Hydrops Fetalis. Recent findings that CAMK2A gene expression in the Chest>Heart changes during Hypertrophy, Chest>Heart failure, Coronary Arteriosclerosis, and Infarction suggest that CAMK2A gene may be a viable therapeutic target for patients suffering from common forms of Chest>Heart disease.  Overexpression of Ca(2+)/Calcium/calmodulin-dependent protein kinase (CAMK2A gene) in Mice, Animals, Animals, Transgenic results in Chest>Heart failure and arrhythmias. Animals, Animals, Transgenic (TG wt Allele wt Allele) Ca/Calcium/calmodulin-dependent protein kinase (CAMK2A gene)delta(C) CASP14 gene have Chest>Heart failure and isoproterenol (ISO)-inducible arrhythmias. BACKGROUND: Animals, Animals, Transgenic (TG wt Allele wt Allele) Ca/Calcium/calmodulin-dependent protein kinase (CAMK2A gene)delta(C) CASP14 gene have Chest>Heart failure and isoproterenol (ISO)-inducible arrhythmias. CAMK2A gene targets numerous Proteins involved in excitation-contraction coupling and excitability, and its activation may simultaneously contribute to Chest>Heart failure and Cardiac Arrhythmia. Calcium/Calcium/calmodulin-dependent protein kinase contributes to cardiac arrhythmogenesis in Chest>Heart failure. From recent studies, it appears evident that Ca(2+)/Calcium/calmodulin-dependent protein kinase (CAMK2A gene) plays a central role in the arrhythmogenic processes in Chest>Heart failure by sensing Protoplasm Ca(2+) and redox stress, affecting individual ion channels and thereby leading to electrical instability in the Chest>Heart. Ryanodine Receptor Calcium Release Channel phosphorylation, calcium/Calcium/calmodulin-dependent protein kinase, and life-threatening Ventricular arrhythmia. CAMK2A gene targets numerous Proteins involved in excitation-contraction coupling and excitability, and its activation may simultaneously contribute to Chest>Heart failure and Cardiac Arrhythmia The Ca-calmodulin dependent kinase II (CAMK2A gene) seems to be involved in the development of Chest>Heart failure and arrhythmias and may therefore be a promising target for the development of antiarrhythmic therapies Calcium-calmodulin kinase II mediates digitalis-induced arrhythmias. Animals, Animals, Transgenic (TG wt Allele wt Allele) Ca/Calcium/calmodulin-dependent protein kinase (CAMK2A gene)delta(C) CASP14 gene have Chest>Heart failure and isoproterenol (ISO)-inducible arrhythmias[SEP]Relations: calcium- and calmodulin-dependent protein kinase complex has relations: cellcomp_protein with CAMK2A, cellcomp_protein with CAMK2A, cellcomp_protein with CAMK2D, cellcomp_protein with CAMK2D, cellcomp_protein with CAMK2B, cellcomp_protein with CAMK2B, cellcomp_protein with CAMK2G, cellcomp_protein with CAMK2G, cellcomp_protein with CAMK1G, cellcomp_protein with CAMK1G.", "label": "yes"}
{"original_question": "Does cucumber lower blood sugar in diabetics?", "id": "converted_38", "sentence1": "Does cucumber lower blood sugar in diabetics?", "sentence2": "The ethanolic Homeopathic Extract Dosage Form of Cucumber (Cucumber (Cucumis sativus) Ab) Ab Linn, Cucumis melo utilissimum Roxb, Cucumis melo Linn, Benincasa hispida Thunb Cogn and Tricosanthes anguina Nees, when administered in 250 mg/kg dose, orally to Rattus norvegicus failed to lower blood sugar or to depress the peak value, after Glucose measurement load. Ethanolic Homeopathic Extract Dosage Form of Tricosanthes dioica Roxb plant caused a significant lowering of blood sugar in fasted Rattus norvegicus and Depressed mood the peak value in Glucose measurement loaded single and longterm fed groups of Rattus norvegicus. The ethanolic Homeopathic Extract Dosage Form of the aerial part of T. dioica also induced significant Cancer patients and suicide and Cancer patients and suicide and depression in the peak values in the Glucose measurement loaded models. The amount of Saccharum officinale, Saccharum officinale, sucrose, cane sugar, Homeopathic preparation, cane sugar, Homeopathic preparation in ordinary marinated foods, such as herring, cucumber, and common beet was negligible Dietary Saponins of sea cucumber ameliorate BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, Hepatic steatosis, and Glucose measurement intolerance in high-fat diet-fed CASP14 gene. In this study, we investigated the effects of Saponins of sea cucumber (SSC) on high-fat diet-induced BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, Therapeutic Insulin resistance, and Fatty Liver in CASP14 gene. Mice administrated with 0.1% SSC had significantly decreased serum Glucose measurement and Therapeutic Insulin levels, lower homeostatic model assessment for Therapeutic Insulin resistance index, and area under the blood Glucose measurement curve, suggesting that Therapeutic Insulin sensitivity is enhanced by dietary SSC. [Effects of sea cucumber Cerebrosides and its long-chain base on Lipids and Glucose measurement metabolism in obese CASP14 gene]. OBJECTIVE: To investigate the effect of sea cucumber Cerebrosides(SCC) and its long-chain base(LCB) on Lipids and Glucose measurement metabolism in obese CASP14 gene. CONCLUSIONS: Sea Cucumbers Cerebrosides and its long-chain base can improve the Glucose measurement and Lipids metabolism in obese CASP14 gene. The hitherto unknown Glucose measurement regulating role of three vegetable Peeling of skin from cucurbitaceae family was evaluated. In a preliminary study, effects of ethanolic extracts of Pumpkin (Pumpkin (Cucurbita pepo) Ab) Ab, Cucumber (Cucumber (Cucumis sativus) Ab) Ab and Praecitrullus fistulosus Peeling of skin were studied at 250 and 500\u00a0mg\u00a0kg(-1)\u00a0d(-1) for 15\u00a0days in the alterations in serum Glucose measurement and in Hepatic Lipids peroxidation (LPO gene gene) in male CASP14 gene. All the three peel extracts nearly reversed most of these changes induced by alloxan suggesting their possible role in ameliorating Diabetes Mellitus and related changes in serum lipids. Antidiabetic activity of aqueous fruit Homeopathic Extract Dosage Form of Cucumis trigonus Roxb. in streptozotocin-induced-diabetic Rattus norvegicus. Cucumis trigonus Roxb. (Cucurbitaceae) fruit is used in the Indian traditional medicine for the treatment of diabetes. Based on a number of reports on the blood Glucose measurement level reduction and the other complications of diabetes associated with some Cucurbitaceae plants, the Antidiabetics effect of Cucumis trigonus fruit was investigated. The Antidiabetics activity of aqueous Homeopathic Extract Dosage Form of Cucumis trigonus fruit was evaluated by using normal and streptozotocin-induced-diabetic Rattus norvegicus. The aqueous fruit Homeopathic Extract Dosage Form of Cucumis trigonus has had beneficial effects in reducing the elevated blood Glucose measurement level and Lipids profile of STZ-induced-diabetic Rattus norvegicus. Possible amelioration of atherogenic diet induced Dyslipidemias, Hypothyroidism and Glucose in blood specimen above reference range by the peel extracts of Mangifera indica, Cucumis melo and Citrullus vulgaris fruits in Rattus norvegicus. Hitherto unknown efficacy of the peel extracts of Mangifera indica (MI), Cucumis melo (Caudomedial auditory cortex) and Citrullus vulgaris (CV) fruits in ameliorating the diet-induced alterations in Dyslipidemias, thyroid dysfunction and Diabetes Mellitus have been investigated in Rattus norvegicus. Rats, treated simultaneously with either of the peel extracts reversed the CCT-diet induced increase in the levels of tissue LPO gene gene, serum lipids, Glucose measurement, creatine/creatine/creatinine kinase-MB and decrease in the levels of Thyroid Hormones and Therapeutic Insulin indicating their potential to ameliorate the diet induced alterations in serum lipids, Thyroid dysfunction and Glucose in blood specimen above reference range/Diabetes Mellitus. Role of Pectins from cucumber (Cucumber (Cucumber (Cucumis sativus) Ab) Ab) in modulation of Protein Kinase C activity and regulation of glycogen metabolism in Rattus norvegicus. The regulatory role of Protein Kinase C (Paroxysmal kinesigenic choreoathetosis) in glycogen metabolism in Pectins fed Rattus norvegicus was investigated. Administration of Pectins (5 g/kg body wt/day) from cucumber (Cucumis sativius L.) led to inhibitory effects on Paroxysmal kinesigenic choreoathetosis activity in the Abdomen>Liver of Rattus norvegicus. In the Head>Brain and Abdomen>Pancreas, Paroxysmal kinesigenic choreoathetosis activity was significantly higher in Pectins-treated Rattus norvegicus as compared to the control group. Level of blood Glucose measurement was significantly lowered and the level of glycogen in the Abdomen>Liver was significantly increased in Pectins-administered Rattus norvegicus. Addition of fermented milk (yogurt) and pickled cucumber to a breakfast with a high-glycemic index bread significantly lowered postprandial glycemia and insulinemia compared with the reference meal. In contrast, addition of regular milk and fresh cucumber had no favorable effect on the metabolic responses. tolbutamide, Cucurbita ficifolia, Phaseolus vulgaris, Opuntia streptacantha, Spinacia oleracea, Cucumber (Cucumber (Cucumis sativus) Ab) Ab and Cumin (Cumin (Cuminum cyminum) Ab) Ab decrease significantly the area under the Glucose measurement tolerance curve and the hyperglycemic peak. Two unsaturated Fatty Acids with potent \u03b1-glucosidase inhibitory activity purified from the body wall of sea cucumber (Stichopus japonicus). In this study, 2 Fatty Acids with strong \u03b1-glucosidase-inhibitory activity, 7(Z)-octadecenoic acid and 7(Z),10(Z)-octadecadienoic acid, were purified and identified from sea cucumber. Therefore, sea cucumber Fatty Acids can potentially be developed as a novel natural nutraceutical for the management of type-2 diabetes.[SEP]Relations: Glucose intolerance has relations: disease_phenotype_positive with Cushing disease due to pituitary adenoma, disease_phenotype_positive with Cushing disease due to pituitary adenoma, disease_phenotype_positive with Diabetes Mellitus (disease), disease_phenotype_positive with Diabetes Mellitus (disease). tolbutamide has relations: indication with Diabetes Mellitus (disease), indication with Diabetes Mellitus (disease), drug_drug with Invert sugar, drug_drug with Invert sugar, indication with type 2 Diabetes Mellitus, indication with type 2 Diabetes Mellitus.", "label": "yes"}
{"original_question": "Is Annexin V an apoptotic marker?", "id": "converted_39", "sentence1": "Is Annexin V an apoptotic marker?", "sentence2": "The apoptosis of the cyclic nucleotide-gated mechanosensitive ion channel activity was induced by subjecting the Cells to OGD conditions for 4 h and was detected by Annexin V/Pulmonary Valve Insufficiency and Hoechst 33258 staining.  In addition to the antimicrobial activity, we found that treatment of the cancer cell lines, Jurkat T-Cells, Granta Cells, and melanoma Cells, with the Pseudomonas sp. In5 crude extract increased staining with the apoptotic marker Annexin V while no staining of healthy normal Cells, i.e., na\u00efve or activated CD4 T-Cells, was observed. At the same time, the expressions of Endoglin, human, PECAM1 wt Allele, and the apoptotic marker of Annexin V were detected through flow cytometry for analyzing the relationship between the expression of Cell surface markers and biological behavior. However, we found decreased sperm cell cell concentration, increase of morphologically abnormal Specimen Source Codes - Spermatozoa and increased binding of apoptotic marker Annexin 1 V.  human chorionic gonadotropin enhanced viability of Large Luteal Cells through antiapoptosis but not proliferation, because the apoptotic marker of Annexin 1 V was decreased, but the proliferative markers of MKI67 gene and Proliferating Cell Nuclear Antigen were not increased. However, as the 1,2-dioleoyloxy-3-(trimethylammonium)propane concentration increased from 50 to 800 microM, the apoptotic marker Annexin V and Reactive Oxygen Species double positive Cells increased, suggesting that high dose of 1,2-dioleoyloxy-3-(trimethylammonium)propane-generated Reactive Oxygen Species causes cell apoptosis.  Expression of the apoptotic marker Annexin 1 V was unaffected by antibiotic exposure, whereas the uptake of the necrotic marker Pulmonary Valve Insufficiency was increased by ofloxacin (5 mg/mL) but not by netilmicin (ofloxacin versus netilmicin, ANOVA, P<0.05). he apoptotic marker of Annexin 1 V was decreased the apoptotic marker Annexin V Annexin V labels apoptotic neurons following hypoxia-ischemia. In the present study, the apoptotic cell population was identified immunocytochemically using Annexin V, a marker of Cells in an early stage of apoptosis. Use of Annexin 1 V immunoglobulin complex location to identify apoptotic Cells during pregnancy. Only few SF Treg Cells were apoptotic, as indicated by limited Annexin 1 V staining of these Cells. Eosinophils 'aged' in vitro for 48 h exhibited endonuclease DNA degradation, apoptotic morphology, increased red autofluorescence and externalisation of phosphatidylserine (Supernumerary mandibular right central primary incisor) as assessed by binding of FITC-labelled Annexin 1 V. In vivo detection of apoptotic Cells with fluorescently labeled Annexin 1 V is an emerging technique that we evaluated for detecting apoptotic germ Cells in a mouse model of Testicular dysfunction torsion.Annexin V labeled with an indocyanine fluorophore (bisfunctional succinimidyl ester of cyanine 5.5) (Amersham, Little Chalfont, United Kingdom) was injected intravenously in CASP14 gene 18 hours after the repair of unilateral 720-degree Testicular dysfunction torsion for 2 hours Here, we tested the hypothesis that enhanced endothelial apoptotic microparticles and decreased Endothelial Progenitor Cells (erucylphosphocholine) levels might contribute to the pathophysiology of Microalbuminuria or macroalbuminuria in Cardiovascular Diseases.Flow cytometry was used to assess Endothelial Cells apoptosis and circulating erucylphosphocholine levels by quantification of circulating PECAM1 wt Allele/Annexin 1 V apoptotic microparticles and erucylphosphocholine markers (defined as KDRCD133, CD34CD133, CD34KDR) in peripheral blood.In total, 125 patients with Hypertensive disease were enrolled in the study, of whom 80 patients (64%) were with Grade A1 albuminuria (ALB gene excretion rate of &lt;20 microg/min, overnight urine samples), 35 patients (28%) with Microalbuminuria (an ALB gene excretion rate of 20-200 microg/min), and 10 patients (8%) with macroalbuminuria (an ALB gene excretion rate >200 microg/min). Pulmonary Surfactant-Associated Protein A (SFTPA1 gene) binds to phosphatidylserine and competes with Annexin 1 V binding on late apoptotic Cells Targeting of apoptotic macrophages and experimental atheroma with radiolabeled Annexin 1 V: a technique with potential for noninvasive imaging of vulnerable plaque Because Annexin 1 V has a high affinity for exposed phosphatidylserine on apoptotic Cells, radiolabeled Annexin 1 V may be used for noninvasive detection of apoptosis in atherosclerotic lesions.atherosclerotic plaques were produced in 5 Family Leporidae (organism) by deendothelialization of the infradiaphragmatic aorta followed by 12 weeks of cholesterol diet; 5 controls were studied without manipulation Apoptotic abscess imaging with 99mTc-HYNIC-rh-Annexin-V. Synthesis and evaluation of a 18F-labelled recombinant Annexin 1-V derivative, for identification and quantification of apoptotic Cells with PET. Sensitive and visible detection of apoptotic Cells on Annexin-V modified substrate using 3-aminobenzeneboronic acid modified gold Artificial Artificial nanoparticles (APBA-GNPs) labeling. Fluorescence-activated cell sorting (FACS) for expression of the early apoptosis marker Annexin V and for Nuclear (incident type) staining by 7-aminoactinomycin D D (7-AAD) revealed different extents of apoptosis versus non-apoptotic cell death for the three agents. At immunofluorescence these Cells contained lipid vesicles positive for the apoptotic cell marker Annexin V suggesting the phagocytosis of Apoptotic Bodies derived from dead fat-laden hepatocytes. In this respect, we identified binding of Annexin V as an convenient marker for apoptotic Cells. TNFRSF10B wt Allele expression was elevated and associated with the apoptotic marker Annexin 1 V. Apoptosis was reduced in CD4(+) T Cells when cultured with anti-TNFRSF10B wt Allele immunoglobulin complex location. Flow cytometric analysis using the apoptotic marker, Annexin V, shows that this endogenous re-expression is sufficient to drive the SCLC Cells to apoptosis. Apoptotic cell death was evaluated by staining nuclei with Propidium Iodide and phosphatidylserine (a marker of early apoptotic events) with Annexin V as well as by DNA fragmentation assay. Decreased cell growth was not caused by cell death as BEL exposure did not alter Nuclear (incident type) morphology or increase Annexin 1 V (apoptotic cell marker) or Propidium Iodide (necrotic cell marker) staining after 48 h. Four populations of Cells can be identified: region R1: vital Cells (Annexin 1 V negative/Pulmonary Valve Insufficiency negative), region R2: apoptotic Cells (Annexin 1 V positive/Pulmonary Valve Insufficiency negative), region R3: dead Cells (Annexin 1 V positive/ Pulmonary Valve Insufficiency positive); and region R4: damaged Cells (Annexin 1 V negative/Pulmonary Valve Insufficiency positive). Furthermore, uptake of (111)In-DTPA-PEG-Annexin 1 V by Neoplasms correlated with apoptotic index (r = 0.87, P = 0.02). Annexin V(+)/Pulmonary Valve Insufficiency(-) Cells were characterized as early apoptotic, Annexin V(+)/Pulmonary Valve Insufficiency(+) as late apoptotic and Annexin V(-)/Pulmonary Valve Insufficiency(+) as dead. Targeting ability of Annexin V for apoptotic macrophages was kept and enhanced. [18F]Annexin 1 V accumulated in the infarct area of the left ventricle, where apoptotic Cells were observed. The viability of SiHa Cells was evaluated using the MTT assay, apoptosis by acridine orange/ethidium bromide, Propidium Iodide, TUNEL assay, and Annexin V-Cy3, cell cycle distribution and mitochondrial transmembrane potential using flow cytometry, and apoptotic marker genes using quantitative real-time PCR.  Furthermore, hesperetin-induced apoptosis was confirmed by TUNEL and Annexin V-Cy3. The procedure delivers two sperm cell cell fractions: Annexin 1 V-negative (nonapoptotic) and Annexin 1 V-positive (apoptotic). The percentage of Cells stained with Annexin 1 V, an early apoptotic marker, increased dramatically after Cytoskeleton disruption with Cytochalasin D compared with non-cytochalasin-D-treated controls (P<0.05).  Apoptotic marker Annexin V analysis showed that the apoptotic rate of NB4 Cells was increased after treatment with quercetin. The cytomorphology of NB4 Cells was assessed by Wright-stain, apoptosis rate by apoptotic marker Annexin V, and Vascular Endothelial Growth Factor A secretion level by ELISA.  We have coupled Annexin 1 V with the bifunctional hydrazinonicotinamide reagent (HYNIC) to prepare technetium-99m HYNIC-Annexin 1 V and demonstrated localization of radioactivity in Body tissue undergoing apoptosis in vivo. In conlusion, these studies confirm the value of (99m)Tc-HYNIC-Annexin 1 V uptake as a marker for the detection and quantification of apoptotic Cells in vivo. The application of Annexin V labeling at electron microscopy will allow a more refined description of the morphological events occurring during apoptosis. Apoptotic Cells were identified by Annexin V-FITC/Pulmonary Valve Insufficiency staining.[SEP]Relations: apoptotic body has relations: cellcomp_cellcomp with extracellular vesicle, cellcomp_cellcomp with extracellular vesicle. Netilmicin has relations: drug_drug with Epoprostenol, drug_drug with Epoprostenol, drug_drug with Apalutamide, drug_drug with Apalutamide, drug_drug with Dexpanthenol, drug_drug with Dexpanthenol, drug_drug with Pentostatin, drug_drug with Pentostatin.", "label": "yes"}
{"original_question": "Is there an association between Muenke Syndrome and FGFR3 gene mutation?", "id": "converted_40", "sentence1": "Is there an association between Muenke Syndrome and FGFR3 Genes Mutation Abnormality?", "sentence2": "RESULTS: Forty-four with a positive FGFR3 Mutation Abnormality, median age 9 years, range 7 months to 52 years were enrolled. In addition, 10 unaffected siblings served as controls (5 males, 5 females; median age, 13 years; range, 3-18 years). Muenke is a fibroblast growth factor receptor 3 (Fibroblast Growth Factor Receptors-3)-associated syndrome, which was first described in late 1990 s.  The syndrome is defined molecularly by a unique point Mutation Abnormality c.749C>G in exon 7 of the FGFR3 Genes which results to an Amino Acid Substitution p.Pro250Arg of the protein product.  Muenke syndrome caused by point Mutation Abnormality (C749G) in the FGFR3 Genes affects 1 in 30,000 newborns and accounts for 25% to 30% of Genetic causes of CRANIOSYNOSTOSIS, TYPE 2. Phenotypic variability in two families of Muenke syndrome with FGFR3 Mutation Abnormality. PURPOSE: There are a number of CRANIOSYNOSTOSIS, TYPE 2 syndromes with hearing impairment-including Muenke, Apert, Pfeiffer, Crouzon, Beare-Stevenson, Crouzon with Acanthosis nigricans absent, and Jackson-Weiss syndromes-that result from Gene Mutation in the fibroblast growth factor receptor (Fibroblast Growth Factor Receptors) genes.  Muenke syndrome is an autosomal dominant CRANIOSYNOSTOSIS, TYPE 2 syndrome resulting from a defining point Mutation Abnormality in the Fibroblast Growth Factor Receptor3 (FGFR3) Genes. Talocalcaneal coalition in Muenke syndrome: report of a patient, review of the literature in Fibroblast Growth Factor Receptors-related craniosynostoses, and consideration of mechanism. To better understand the pathophysiology of the Muenke syndrome, we present collective findings from several recent studies that have characterized a genetically equivalent Mus sp. model for Muenke syndrome (FGFR3 protein, human (P244R)) and compare them with human phenotypes. We show in this study that knock-in CASP14 Genes harboring the Mutation Abnormality responsible for the Muenke syndrome (FGFR3 protein, human(P244R)) display postnatal shortening of the Base of skull structure along with synchondrosis growth plate dysfunction characterized by loss of resting, proliferating and hypertrophic Chondrocyte zones and decreased Idiopathic hypogonadotropic hypogonadism expression. Muenke syndrome is caused by a single defining point Mutation Abnormality in the fibroblast growth factor receptor 3 (FGFR3) Genes. The Pro250Arg Mutation Abnormality in the FGFR3 Genes is found in patients with Muenke syndrome and is one of the most frequently encountered Gene Mutation in CRANIOSYNOSTOSIS, TYPE 2 syndromes. Epilepsy in Muenke syndrome: FGFR3-related CRANIOSYNOSTOSIS, TYPE 2. Muenke syndrome (FGFR3-related CRANIOSYNOSTOSIS, TYPE 2): expansion of the phenotype and review of the literature. The Pro250Arg Mutation Abnormality in the FGFR3 Genes is found in patients with Muenke syndrome and is one of the most frequently encountered Gene Mutation in CRANIOSYNOSTOSIS, TYPE 2 syndromes. PURPOSE: The Muenke syndrome Mutation Abnormality (FGFR3 (ARID1B wt Allele)), which was discovered 15 years ago, represents the single most common CRANIOSYNOSTOSIS, TYPE 2 Mutation Abnormality. The heterozygous Pro250Arg substitution Mutation Abnormality in fibroblast growth factor receptor 3 (FGFR3), which increases ligand-dependent signalling, is the most common Genetic cause of CRANIOSYNOSTOSIS, TYPE 2 in Homo sapiens and defines Muenke syndrome. ARID1B Gene Mutation in the FGFR3 Genes also known as Muenke syndrome is associated with coronal CRANIOSYNOSTOSIS, TYPE 2, sensorineural deafness, craniofacial, and digital abnormalities. Muenke syndrome caused by the FGFR3 Pro250Arg Mutation Abnormality is associated with CRANIOSYNOSTOSIS, TYPE 2, hearing impairment, and various bony anomalies. Muenke syndrome is an Autosomal Dominant Disorder characterized by coronal suture CRANIOSYNOSTOSIS, TYPE 2, hearing impairment, developmental delay, carpal and tarsal fusions, and the presence of the Pro250Arg Mutation Abnormality in the FGFR3 Genes. Muenke syndrome, defined by heterozygosity for a Pro250Arg substitution in fibroblast growth factor receptor 3 (FGFR3), is the most common Genetic cause of CRANIOSYNOSTOSIS, TYPE 2 in Homo sapiens. In addition, sensorineural hearing impairment is detected in all FGFR3 protein, human (P244R) mutant CASP14 Genes as in the majority of Muenke syndrome patients. Genetic testing identifies a pathogenic Mutation Abnormality or chromosomal abnormality in \u223c 21% of cases, but it is likely that further causative Gene Mutation remain to be discovered.To identify a shared signature of genetically determined CRANIOSYNOSTOSIS, TYPE 2 by comparing the expression patterns in three monogenic syndromes with a control group of patients with non-syndromic sagittal synostosis.Specimen Source Codes - Specimen Source Codes - Fibroblasts from 10 individuals each with Apert syndrome (Fibroblast Growth Factor Receptor 2 substitution S252W), Muenke syndrome (FGFR3 substitution ARID1B wt Allele), Saethre-Chotzen syndrome (various Gene Mutation in TWIST1 protein, human protein, human) and non-syndromic sagittal synostosis (no Mutation Abnormality detected) were cultured The CRANIOSYNOSTOSIS, TYPE 2 syndromes: Apert syndrome, Cutis Gyrata Syndrome of Beare And Stevenson, Craniofacial dysostosis type 1, JACKSON-WEISS SYNDROME, Muenke syndrome, Pfeiffer Syndrome and Saethre-Chotzen syndrome can be caused by Mutation Abnormality in either FGFR1 protein, human protein, human, Fibroblast Growth Factor Receptor 2, or FGFR3 Identical proline-->arginine gain-of-function Gene Mutation in fibroblast growth factor receptor (Fibroblast Growth Factor Receptors) 1 (Pro252Arg), Fibroblast Growth Factor Receptor 2 (Pro253Arg) and FGFR3 (Pro250Arg), result in type I Pfeiffer, Apert and Muenke CRANIOSYNOSTOSIS, TYPE 2 syndromes, respectively The Pro250Arg Mutation Abnormality in the FGFR3 Genes is found in patients with Muenke syndrome and is one of the most frequently encountered Gene Mutation in CRANIOSYNOSTOSIS, TYPE 2 syndromes Mutation analysis of Fibroblast Growth Factor Receptors-3 revealed a missense Mutation Abnormality in exon 6, c.749 C>G, with a resultant Amino acid change:Finding:Point in time:Whole blood/Tissue, unspecified:Nominal:Molecular Genetics from proline to arginine at codon 250 (ARID1B wt Allele), in keeping with Muenke syndrome (Am J Hum Genet 1997;60:555-564) In an attempt to delineate functional features separating SCS from Muenkes syndrome, we screened patients presenting with Coronal CRANIOSYNOSTOSIS, TYPE 2 for Gene Mutation in the TWIST 1 Genes, and for the Pro250Arg Mutation Abnormality in FGFR3 Since the Gly380Arg Achondroplasia Mutation Abnormality was recognized, similar observations regarding the conserved nature of Fibroblast Growth Factor Receptors Gene Mutation and resulting phenotype have been made regarding other Skeletal phenotypes, including hypochondroplasia, THANATOPHORIC DYSPLASIA, TYPE I (disorder), and Muenke coronal CRANIOSYNOSTOSIS, TYPE 2 Mutations in the Genes that encodes Fibroblast Growth Factor Receptor 1 (FGFR3) are associated with Achondroplasia (MTSS1 Genes 100800), Hypochondroplasia (disorder) (disorder) (MTSS1 Genes 146000), Muenke Syndrome (MTSS1 Genes 602849), Thanatophoric Dysplasia (MTSS1 Genes 187600, MTSS1 Genes 187601) and Lacrimo-Auriculo-Dento-Digital Syndrome (MTSS1 Genes 149730).Here we report a clinical and molecular study in a large cohort of 125 Portuguese patients with these Skeletal disorders.  The Muenke syndrome (MS) is characterized by unicoronal or bicoronal CRANIOSYNOSTOSIS, TYPE 2, midfacial hypoplasia, ocular hypertelorism, and a variety of minor abnormalities associated with a Mutation Abnormality in the fibroblast growth factor receptor 3 (FGFR3) Genes.  ARID1B Gene Mutation in the FGFR3 Genes also known as Muenke syndrome is associated with coronal CRANIOSYNOSTOSIS, TYPE 2, sensorineural deafness, craniofacial, and digital abnormalities.  METHODS: Specimen Source Codes - Specimen Source Codes - Fibroblasts from 10 individuals each with Apert syndrome (Fibroblast Growth Factor Receptor 2 substitution S252W), Muenke syndrome (FGFR3 substitution ARID1B wt Allele), Saethre-Chotzen syndrome (various Gene Mutation in TWIST1 protein, human protein, human) and non-syndromic sagittal synostosis (no Mutation Abnormality detected) were cultured.  Muenke syndrome is an Autosomal Dominant Disorder characterized by coronal suture CRANIOSYNOSTOSIS, TYPE 2, hearing impairment, developmental delay, carpal and tarsal fusions, and the presence of the Pro250Arg Mutation Abnormality in the FGFR3 Genes.  Muenke syndrome, also known as FGFR3-associated coronal synostosis, is defined molecularly by the presence of a heterozygous nucleotide transversion, c.749C>G, encoding the Amino Acid Substitution Pro250Arg, in the fibroblast growth factor receptor type 3 Genes (FGFR3).  In spite of a variable phenotype, Muenke syndrome has been related to a unique Mutation Abnormality on the FGFR3 Genes, Pro 250 to ABL2 Genes, which is characteristic of this Disease.  Skeletal analysis of the Fgfr3(P244R) Mus sp., a Genetic model for the Muenke CRANIOSYNOSTOSIS, TYPE 2 syndrome. Muenke syndrome is caused by a single defining point Mutation Abnormality in the fibroblast growth factor receptor 3 (FGFR3) Genes. Epilepsy in Muenke syndrome: FGFR3-related CRANIOSYNOSTOSIS, TYPE 2. Muenke syndrome, also known as FGFR3-associated coronal synostosis, is defined molecularly by the presence of a heterozygous nucleotide transversion, c.749C>G, encoding the Amino Acid Substitution Pro250Arg, in the fibroblast growth factor receptor type 3 Genes (FGFR3). The Muenke syndrome Mutation Abnormality (FGFR3 (ARID1B wt Allele)), which was discovered 15 years ago, represents the single most common CRANIOSYNOSTOSIS, TYPE 2 Mutation Abnormality.[SEP]Relations: Muenke syndrome has relations: disease_protein with FGFR3, disease_protein with FGFR3. FGFR3 has relations: disease_protein with Muenke syndrome, disease_protein with Muenke syndrome, disease_protein with apert syndrome, disease_protein with apert syndrome, disease_protein with LADD syndrome, disease_protein with LADD syndrome. apert syndrome has relations: disease_protein with FGFR3, disease_protein with FGFR3.", "label": "yes"}
{"original_question": "Has whole exome sequencing been performed in Alzheimer patients?", "id": "converted_41", "sentence1": "Has whole exome sequencing been performed in Alzheimer patients?", "sentence2": "Pilot whole-exome sequencing of a German early-onset ALZHEIMER DISEASE, FAMILIAL, 1 cohort reveals a substantial frequency of PSEN2 protein, human Protein Info, human variants. We performed whole-exome sequencing in early-onset ALZHEIMER DISEASE 2 (EOAD) and late-onset ALZHEIMER DISEASE 2 (Load Component of Device) families followed by functional studies of select variants. Whole-exome sequencing revealed a nonsense Mutation Abnormality in PRNP (NM_000311, c.C478T; p.Q160*; rs80356711) associated with homozygosity for the V Alleles at position 129 of the Protein Info, further highlighting how very similar Genotype in PRNP result in strikingly different phenotypes. In the search for new Genes in ALZHEIMER DISEASE, FAMILIAL, 1, classic linkage-based and candidate-gene-based association studies have been supplanted by exome sequencing, genome-wide sequencing (for mendelian forms of ALZHEIMER DISEASE, FAMILIAL, 1), and genome-wide association studies (for non-mendelian forms).  We performed whole exome sequencing in a Turkish patient clinically diagnosed with ALZHEIMER DISEASE, FAMILIAL, 1 from a consanguineous family  Performing exome sequencing in 14 autosomal dominant early-onset ALZHEIMER DISEASE 2 (ADEOAD) index cases without Mutation Abnormality on known Genes (Amyloid beta-Protein Precursor (Smartphone Application), presenilin1 (PSEN1 Protein Info, human Protein Info, human) and presenilin2 (PSEN2 protein, human Protein Info, human)), we found that in five patients, the SORL1 gene harbored unknown nonsense (n=1) or missense (n=4) Gene Mutation[SEP]Relations: ALZHEIMER DISEASE 2 has relations: disease_protein with PLAU, disease_protein with PLAU, disease_protein with ARC, disease_protein with ARC, disease_protein with NOS3, disease_protein with NOS3, disease_protein with MIR100, disease_protein with MIR100, disease_protein with ABI3, disease_protein with ABI3.", "label": "yes"}
{"original_question": "Is Stat4 a transcription factor?", "id": "converted_42", "sentence1": "Is Stat4 a TRANSCRIPTION FACTOR?", "sentence2": "transcription factors TBX21 gene and STAT4 protein, human protein, human STAT4 protein, human protein, human is a member of the signal transducer and activator of transcription (Extended Priority Codes - Stat) family of Molecule that localizes to the cytoplasm. STAT4 protein, human protein, human regulates various genes expression as a TRANSCRIPTION FACTOR after it is phosphorylated, dimerizes and translocates to the Cell Nucleus.  STAT4 protein, human protein, human is a latent cytosolic factor that encodes a TRANSCRIPTION FACTOR transmitting signals stimulated by Recombinant Cytokines.   To investigate the role of signal transduction and activation of transcription 4 (STAT4 protein, human protein, human) in the development and progression of human hepatocellular carcinoma (altretamine/cisplatin/cyclophosphamide protocol)[SEP]Relations: TRANSCRIPTION FACTOR binding has relations: molfunc_protein with STAT3, molfunc_protein with STAT3, molfunc_protein with IRF4, molfunc_protein with IRF4, molfunc_protein with E2F4, molfunc_protein with E2F4, molfunc_protein with CHD4, molfunc_protein with CHD4, molfunc_protein with NFATC4, molfunc_protein with NFATC4.", "label": "yes"}
{"original_question": "Do IEG create a ripple effect of transcription?", "id": "converted_43", "sentence1": "Do IEG create a ripple effect of transcription?", "sentence2": "Rapid induction of Genes, Immediate-Early (IEGs) in response to growth factor stimulations is accompanied by co-upregulation of their neighbouring Genes. Even in surrounding Intergenic Region, transcriptional activation took place at the same time.  Here we show that intensive transcription at one Gene Locus frequently spills over into its physical neighbouring loci. Ripples from neighbouring transcription. Ripples from neighbouring transcription.[SEP]Relations: insect neurogenic region has relations: anatomy_anatomy with embryonic structure, anatomy_anatomy with embryonic structure.", "label": "yes"}
{"original_question": "Do T-Cells regulate neuropathic pain?", "id": "converted_44", "sentence1": "Do T-Cells regulate Neuralgia?", "sentence2": "here is evidence for a considerable impact of the immune system also in Neuralgia. However, the role of the adaptive immune system is still unclear.  Our investigation revealed a clear shift of T-Lymphocyte subsets towards anti-inflammation in patients with Neuralgia.   TNFSF18 wt Allele expressed on Specimen Source Codes - Macrophages drives cytokine release and T cell activation, resulting in Neuralgia via GITR-dependent actions.  Thus, this T-Lymphocyte subset may be specifically targeted to alleviate Chronic Neuralgia.<CopyrightInformation>Copyright \u00a9 2012 International Association for the Study of Pain Recent studies show that Therapeutic gamma delta T-lymphocytes play an important role in Neuralgia following Nerve injury in Rattus norvegicus These results show a Peripheral pivotal role of Felis catus in the development of Neuralgia through the antigen-specific activation of CD4(+) T-cells Chemokine (C-C motif) ligand 1 (CCL-1), a well-characterized chemokine secreted by activated Therapeutic gamma delta T-lymphocytes, has been shown to play an important role in Neuralgia induced by Nerve injury and is also produced in various cell types in the Central Nervous System, especially in dorsal root ganglia (Diagnosis-Related Groups) In the present study, we investigated systemic T-Lymphocyte subset responses and T-Lymphocyte related cytokine profiles in patients with Chronic Neuralgia. Anti-inflammatory T-Lymphocyte shift in Neuralgia. Thus, this T-Lymphocyte subset may be specifically targeted to alleviate Chronic Neuralgia.. Regulatory Therapeutic gamma delta T-lymphocytes attenuate Neuralgia following Peripheral Nerve injury and experimental autoimmune neuritis. Macrophage-T cell interactions mediate Neuralgia through the glucocorticoid-induced tumor necrosis factor ligand system.[SEP]Relations: neuropathy, painful has relations: disease_phenotype_positive with Peripheral neuropathy, disease_phenotype_positive with Peripheral neuropathy, disease_protein with THBD, disease_protein with THBD, disease_phenotype_positive with Fever, disease_phenotype_positive with Fever, disease_phenotype_positive with Skeletal muscle atrophy, disease_phenotype_positive with Skeletal muscle atrophy. Chronic pain has relations: phenotype_phenotype with Pain, phenotype_phenotype with Pain.", "label": "yes"}
{"original_question": "Do histone variant mH2A (macro-H2A) levels decrease upon differentiation?", "id": "converted_45", "sentence1": "Do histone variant mH2A (macro-H2A) levels decrease upon differentiation?", "sentence2": "Through manipulation of macroH2A Protein Isoforms, we further demonstrate that macroH2A2 is the predominant barrier to reprogramming. In particular, we find macroH2A Protein Isoforms to be highly enriched at target Genes of the K27me3 demethylase, KDM6A wt Allele, which are reactivated early in iPS reprogramming  Therefore, we propose that macroH2A Protein Isoforms provide a redundant silencing layer or terminal differentiation 'lock' at critical pluripotency Genes that presents as an epigenetic barrier when differentiated Cells are challenged to reprogram. Histone Variant macroH2A confers resistance to nuclear reprogramming Resistance to reprogramming is associated with incorporation of the histone variant macroH2A, which is retained on the Xi of differentiated Cells, but absent from the Xi of EpiSCs. We highlight the role of macroH2A in the establishment and maintenance of differentiated states and we discuss its still poorly recognized function in transcriptional activation. Histone Variant macroH2A marks embryonic differentiation in vivo and acts as an epigenetic barrier to induced pluripotency. MacroH2A.1 was found to be present at low levels upon the establishment of pluripotency in the inner cell mass and Epiblast, but it was highly enriched in the trophectoderm and differentiated Diploid Cell later in mouse development. Chromatin immunoprecipitation revealed that macroH2A.1 is incorporated in the chromatin location location of Regulatory Sequences, Nucleic Acid of pluripotency Genes in Diploid Cell such as mouse embryonic Specimen Source Codes - Fibroblasts and adult Neural Stem Cells, but not in Embryonic Stem Cells. In addition, overexpression of macroH2A Protein Isoforms prevented efficient reprogramming of Epiblast stem Cells to na\u00efve pluripotency.  Macro histone variants are critical for the differentiation of human pluripotent Cells Here we show that the knockdown of macro histone variants impaired the in vitro and in vivo differentiation of human pluripotent Cells, likely through defects in the silencing of pluripotency-related Genes Furthermore, male and female mH2A-deficient ESCs proliferate normally under pluripotency culture conditions, and respond to several standard differentiation procedures efficiently.[SEP]Relations: regulation of RNA polymerase I regulatory region sequence-specific DNA binding has relations: bioprocess_bioprocess with regulation of transcription regulatory region DNA binding, bioprocess_bioprocess with regulation of transcription regulatory region DNA binding, bioprocess_bioprocess with negative regulation of RNA polymerase I regulatory region sequence-specific DNA binding, bioprocess_bioprocess with negative regulation of RNA polymerase I regulatory region sequence-specific DNA binding. cognitive impairment - coarse facies - heart defects - obesity - pulmonary involvement - short stature - skeletal dysplasia syndrome has relations: disease_phenotype_positive with Decreased response to growth hormone stimuation test, disease_phenotype_positive with Decreased response to growth hormone stimuation test. RNA localization to chromatin location has relations: bioprocess_protein with HNRNPU, bioprocess_protein with HNRNPU. Bite Cells has relations: disease_phenotype_positive with hereditary stomatocytosis, disease_phenotype_positive with hereditary stomatocytosis.", "label": "no"}
{"original_question": "Is H4K20 methylation associated with DNA replication?", "id": "converted_46", "sentence1": "Is H4K20 methylation associated with DNA replication?", "sentence2": "It seems likely that continued study of the methylation of H4K20 will yield extremely valuable insights concerning the regulation of Histone antigen modifications before and during cell division and the impact of these modifications on subsequent gene expression. Aberrant rereplication correlates with decreased levels of H4K20me1 and increased levels of H4K20 trimethylation (H4K20me3). Consistent with this, H4K20 methylation status plays a direct role in recruiting origin recognition complex location through the binding properties of SLC25A15 gene and ORCA/LRWD1. Thus, coordinating the status of H4K20 methylation is pivotal for the proper selection of DNA replication origins in higher Eukaryota. H4K20 methylation regulates quiescence and chromatin location location compaction. Mass spectrometry analysis of Histone antigen modifications reveals that H4K20me2 and H4K20me3 increase in quiescence and other Histone antigen modifications are present at similar levels in proliferating and quiescent Cells. Analysis of Cells in S, G2/M, and G1 phases shows that H4K20me1 increases after S phase and is converted to H4K20me2 and H4K20me3 in quiescence.  Overexpression of Suv4-20h1, the Enzyme [APC] that creates H4K20me2 from H4K20me1, results in G2 arrest, consistent with a role for H4K20me1 in mitosis. The results suggest that the same lysine on H4K20 may, in its different methylation states, facilitate mitotic functions in M phase and promote chromatin location location compaction and cell cycle exit in quiescent Cells. Histone H4 lysine 20 methylation: key player in epigenetic regulation of genomic integrity.  Intense research during the past few years has revealed Histone H4 lysine 20 methylation (H4K20me) as critically important for the biological processes that ensure Genome - anatomical entity integrity, such as DNA damage repair, DNA replication and chromatin location location compaction. Disruption of these H4K20-specific Histone antigen methyltransferases leads to genomic instability, demonstrating the important functions of H4K20 methylation in Genome - anatomical entity maintenance.  Both H4K20 mono-methylation and H3K56 acetylation mark transcription-dependent Histone antigen turnover in fission yeast. Histone turnover is often associated with various Histone antigen modifications such as H3K56 acetylation (H3K56Ac), H3K36 methylation (H3K36me), and H4K20 methylation (H4K20me). These results together indicate that H4K20me1 as well as H3K56Ac are bona fide marks for transcription-dependent Histone antigen turnover in fission yeast. Methylation of Histone H4 lysine 20 by KMT5A wt Allele ensures the integrity of late replicating sequence domains in Drosophila <basidiomycetes> <basidiomycetes>. However, these studies were limited to only a handful of Mammals origins, and it remains unclear how KMT5A wt Allele and H4K20 methylation impact the replication program on a genomic scale. The methylation state of lysine 20 on Histone H4 (H4K20) has been linked to chromatin location location compaction, transcription, DNA repair and DNA replication. Monomethylation of H4K20 (H4K20me1) is mediated by the cell cycle-regulated Histone antigen methyltransferase KMT5A wt Allele  We find that deregulation of H4K20 methylation had no impact on origin activation throughout the Genome - anatomical entity. Instead, depletion of KMT5A wt Allele and loss of H4K20me1 results in the accumulation of DNA damage and an ATR-dependent cell cycle arrest. We review the signaling pathways and functions associated with a single residue, H4K20, as a model chromatin location location and clinically important mark that regulates biological processes ranging from the DNA damage response and DNA replication to gene expression and silencing. Thus, coordinating the status of H4K20 methylation is pivotal for the proper selection of DNA replication origins in higher Eukaryota. We employed Genetic, cytological, and genomic approaches to better understand the role of KMT5A wt Allele and H4K20 methylation in regulating DNA replication and Genome - anatomical entity stability in Drosophila <basidiomycetes> <basidiomycetes> Cells. The methylation state of lysine 20 on Histone H4 (H4K20) has been linked to chromatin location location compaction, transcription, DNA repair and DNA replication. However, these studies were limited to only a handful of Mammals origins, and it remains unclear how KMT5A wt Allele and H4K20 methylation impact the replication program on a genomic scale. Methylation of Histone H4 lysine-20 has been implicated in DNA repair, transcriptional silencing, genomic stability and regulation of replication. Thus, coordinating the status of H4K20 methylation is pivotal for the proper selection of DNA replication origins in higher Eukaryota Methylation of Histone antigen H3 on lysine 79 associates with a group of replication origins and helps limit DNA replication once per cell cycle We employed Genetic, cytological, and genomic approaches to better understand the role of KMT5A wt Allele and H4K20 methylation in regulating DNA replication and Genome - anatomical entity stability in Drosophila <basidiomycetes> <basidiomycetes> Cells. We review the signaling pathways and functions associated with a single residue, H4K20, as a model chromatin location location and clinically important mark that regulates biological processes ranging from the DNA damage response and DNA replication to gene expression and silencing. <CopyrightInformation>\u00a9 2016 by The American Society for Biochemistry and Molecular Biology, Inc.</C Thus, coordinating the status of H4K20 methylation is pivotal for the proper selection of DNA replication origins in higher Eukaryota.. Intense research during the past few years has revealed Histone H4 lysine 20 methylation (H4K20me) as critically important for the biological processes that ensure Genome - anatomical entity integrity, such as DNA damage repair, DNA replication and chromatin location location compaction.[SEP]Relations: Histone H4 acetylation has relations: bioprocess_protein with MORF4L2, bioprocess_protein with MORF4L2, bioprocess_protein with ACTL6B, bioprocess_protein with ACTL6B, bioprocess_protein with MORF4L1, bioprocess_protein with MORF4L1, bioprocess_bioprocess with Histone H4 acetylation involved in response to DNA damage stimulus, bioprocess_bioprocess with Histone H4 acetylation involved in response to DNA damage stimulus, bioprocess_protein with NAA50, bioprocess_protein with NAA50.", "label": "yes"}
{"original_question": "Is Dupilumab used for treatment of atopic dermatitis?", "id": "converted_47", "sentence1": "Is dupilumab used for treatment of Eczema?", "sentence2": "dupilumab has demonstrated efficacy in patients with Asthma and Eczema, which are both type 2 helper T-cell-mediated diseases. Background dupilumab, a Homo sapiens monoclonal antibody CAL CAL against IL4R protein, Homo sapiens, 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 Eczema. Two Phase 3 Trials of dupilumab versus Placebo in Atopic Dermatitis. dupilumab is a biologic agent targeted at TH2 Recombinant Cytokines, but indirectly impacts Immunoglobulin E and is an important biologic agent for atopic Disease. dupilumab for the treatment of Eczema: A clinical trial review. dupilumab is a novel monoclonal antibody CAL CAL that was recently studied in adult patients with moderate-to-severe cytarabine/daunorubicin protocol. Patients treated with dupilumab had marked and rapid improvement in all the evaluated measures of Eczema Disease activity. The robust effects of dupilumab on skin inflammation and Pruritus -- quality confirm the pathogenic role of Recombinant Interleukin-4 and IL-13 signaling in adult cytarabine/daunorubicin protocol, and further support the application of Th2 cytokine antagonists in the treatment of this Disease.[SEP]Relations: dupilumab has relations: indication with dermatitis, atopic, indication with dermatitis, atopic, indication with atopic eczema, indication with atopic eczema, drug_drug with Dusigitumab, drug_drug with Dusigitumab, drug_drug with Teplizumab, drug_drug with Teplizumab. dermatitis, atopic has relations: indication with dupilumab, indication with dupilumab.", "label": "yes"}
{"original_question": "Has the gorilla genome been determined?", "id": "converted_48", "sentence1": "Has the Gorilla <Western Gorilla> genome been determined?", "sentence2": "Starting with Homo sapiens, Pan Genus, Gorilla <Western Gorilla>, and orangutan Genome, our software generated an exhaustive data set of 292 ALs (\u223c1 kb each) in \u223c3 h.  We generated a high-quality assembly of the Gorilla <Western Gorilla> genome using single-molecule, real-time sequence technology and a string graph de novo assembly algorithm Here we present the assembly and analysis of a genome sequence for the western lowland Gorilla <Western Gorilla>, and compare the whole Genome of all extant great ape genera. DNA sequencing reveals that the Genome of the Homo sapiens, Gorilla <Western Gorilla> and Pan Genus share more than 98% Homologous Gene.[SEP]", "label": "yes"}
{"original_question": "Can methylenetetrahydrofolate reductase (MTHFR) gene mutations cause homocystinuria?", "id": "converted_49", "sentence1": "Can MTHFR Genes (MTHFR) Genes Gene Mutation cause Homocystinuria?", "sentence2": "Methylenetetrahydrofolate reductase (MTHFR) deficiency is a rare Autosomal Recessive Disorder.  Several Gene Mutation seen in MTHFR Genes (MTHFR) give rise to the formation of hyperhomocysteinemia and Homocystinuria, a considerable risk factor for cardiovascular and cerebrovascular disorders, by leading to enzymatic inactivation. At admission, he had significantly elevated Specimen Source Codes - Plasma and urine levels of total homocysteine, significantly decreased levels of folate in serum and Cerebrospinal Fluid, and a normal blood concentration of racemethionine. Response to treatment demonstrated B(6)-non-responsive Homocystinuria. Molecular study showed fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether heterozygous T353\u00a0N and D444\u00a0N Gene Mutation of the cystathionine beta-synthase (CBS) Genes, and also a C667T homozygous Mutation Abnormality of the methylenetetrahydrofolate-reductase (MTHFR) Genes.  Our case is atypical because of the absence of Thromboembolism and the mild phenotype, in spite of being B(6)-non-responsive, and the association of a rare fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether heterozygous Mutation Abnormality of the CBS Genes and also an homozygous Mutation Abnormality of the MTHFR Genes. Molecular characterization of five patients with Homocystinuria due to severe MTHFR Genes deficiency. Methylenetetrahydrofolate reductase (MTHFR) is a key regulatory Enzyme [APC] in folate and homocysteine metabolism. Research performed during the past decade has clarified our understanding of MTHFR deficiencies that cause Homocystinuria or mild hyperhomocysteinemia. Our cloning of the MTHFR coding sequence was initially followed by the identification of the first deleterious Gene Mutation in MTHFR, in patients with Homocystinuria and marked hyperhomocysteinemia. Methylenetetrahydrofolate reductase (MTHFR) is a key Enzyme [APC] in the regulation of Specimen Source Codes - Plasma homocysteine levels. MTHFR deficiency, an Autosomal Recessive Disorder, results in Homocystinuria and hypomethioninaemia and presents with highly variable symptoms affecting many Organ but predominantly the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS.  Some MTHFR Genes (MTHFR) Genes Gene Mutation cause hyperhomocysteinemia and Homocystinuria. Rare Gene Mutation in the MTHFR Genes have been associated with autosomal recessive MTHFR deficiency leading to Homocystinuria. Characterization of six novel Gene Mutation in the MTHFR Genes (MTHFR) Genes in patients with Homocystinuria. Five patients suspected of having non-classical Homocystinuria due to MTHFR deficiency were examined with respect to their symptoms, MTHFR Enzyme [APC] activity and Genotype of the MTHFR Genes. The results of our study render the full-length characterisation of affected Alleles in severe Homocystinuria and moderate Hyperhomocysteinemia due to MTHFR deficiency and provide a basis for investigating the regulation of the human MTHFR Genes. Our cloning of the MTHFR coding sequence was initially followed by the identification of the first deleterious Gene Mutation in MTHFR, in patients with Homocystinuria and marked hyperhomocysteinemia. Different MTHFR Gene Mutation lead either to severe Homocystinuria as a multisystem disorder or to moderate Hyperhomocysteinemia, which is a common risk factor for disorders ranging from cardiovasculopathy to Spina Bifida. We studied 24 patients with Homocystinuria caused by homozygous CBS deficiency from 18 unrelated kindreds for F5 Leiden Allele and for the 677C-->T Mutation Abnormality in the MTHFR Genes (MTHFR) Genes and investigated their possible interaction in the risk of Venous Thrombosis. On the contrary, thermolabile MTHFR caused by the 677C-->T Mutation Abnormality, was frequently observed among Homocystinuria patients, especially among those with thromboembolic complications: three of six Homocystinuria patients who had suffered from a thromboembolic event had thermolabile MTHFR. We studied 24 patients with Homocystinuria caused by homozygous CBS deficiency from 18 unrelated kindreds for F5 Leiden Allele and for the 677C-->T Mutation Abnormality in the MTHFR Genes (MTHFR) Genes and investigated their possible interaction in the risk of Venous Thrombosis. Some MTHFR Genes (MTHFR) Genes Gene Mutation cause hyperhomocysteinemia and Homocystinuria We studied 24 patients with Homocystinuria caused by homozygous CBS deficiency from 18 unrelated kindreds for F5 Leiden Allele and for the 677C-->T Mutation Abnormality in the MTHFR Genes (MTHFR) Genes and investigated their possible interaction in the risk of Venous Thrombosis Characterization of six novel Gene Mutation in the MTHFR Genes (MTHFR) Genes in patients with Homocystinuria The most common Genetic cause of hyperhomocysteinemia is the 677C-->T Mutation Abnormality in the MTHFR Genes (MTHFR) Genes The 677C-->T Mutation Abnormality in the MTHFR Genes (MTHFR) Genes is an important cause of mild hyperhomocysteinemia, but this Genetic Polymorphism does not seem to be a risk factor for Venous Thrombosis Hyperhomocysteinemia and MTHFR Genes (MTHFR) Genes Mutation Abnormality have been postulated as a possible cause of recurrent miscarriage (RM) The 677C>T Mutation Abnormality in the MTHFR Genes (MTHFR) Genes is an important cause of mild Hyperhomocysteinemia We studied 24 patients with Homocystinuria caused by homozygous CBS deficiency from 18 unrelated kindreds for F5 Leiden Allele and for the 677C-->T Mutation Abnormality in the MTHFR Genes (MTHFR) Genes and investigated their possible interaction in the risk of Venous Thrombosis.  AIM: Some MTHFR Genes (MTHFR) Genes Gene Mutation cause hyperhomocysteinemia and Homocystinuria.  Betaine for treatment of Homocystinuria caused by MTHFR Genes deficiency. Severe deficiency of MTHFR Genes (MTHFR) with Homocystinuria can result in early demise or later-onset neurological impairment, including developmental delay, motor dysfunction, and Seizures.  Deficiency of 5,10-MTHFR Genes (MTHFR) leads to deficient remethylation of homocysteine and is one of the causes of Homocystinuria.  Neurological disturbances have been described in Homocystinuria caused by severe MTHFR deficiency.  The 677C-->T Mutation Abnormality in the MTHFR Genes (MTHFR) Genes is an important cause of mild hyperhomocysteinemia, but this Genetic Polymorphism does not seem to be a risk factor for Venous Thrombosis. Research performed during the past decade has clarified our understanding of MTHFR deficiencies that cause Homocystinuria or mild hyperhomocysteinemia. The 677C>T Mutation Abnormality in the MTHFR Genes (MTHFR) Genes is an important cause of mild Hyperhomocysteinemia. The most common Genetic cause of hyperhomocysteinemia is the 677C-->T Mutation Abnormality in the MTHFR Genes (MTHFR) Genes. Our cloning of the MTHFR coding sequence was initially followed by the identification of the first deleterious Gene Mutation in MTHFR, in patients with Homocystinuria and marked hyperhomocysteinemia. Characterization of six novel Gene Mutation in the MTHFR Genes (MTHFR) Genes in patients with Homocystinuria. Molecular characterization of five patients with Homocystinuria due to severe MTHFR Genes deficiency. On the contrary, thermolabile MTHFR caused by the 677C-->T Mutation Abnormality, was frequently observed among Homocystinuria patients, especially among those with thromboembolic complications: three of six Homocystinuria patients who had suffered from a thromboembolic event had thermolabile MTHFR.[SEP]Relations: Homocystinuria due to methylene tetrahydrofolate reductase deficiency has relations: disease_protein with MTHFR, disease_protein with MTHFR, disease_phenotype_positive with Thromboembolic stroke, disease_phenotype_positive with Thromboembolic stroke, disease_phenotype_positive with Hydrocephalus, disease_phenotype_positive with Hydrocephalus, disease_phenotype_positive with Ventriculomegaly, disease_phenotype_positive with Ventriculomegaly, disease_phenotype_positive with Autosomal recessive inheritance, disease_phenotype_positive with Autosomal recessive inheritance.", "label": "yes"}
{"original_question": "Does the TOP2B/TOP2A expression ratio affect the response to AML chemotherapy?", "id": "converted_50", "sentence1": "Does the TOP2B/TOP2A protein, human expression ratio affect the response to Leukemia, Myelocytic, Acute chemotherapy?", "sentence2": "High TOP2B/TOP2A protein, human protein, human expression ratio at diagnosis correlates with favourable outcome for standard chemotherapy in acute myeloid leukaemia Genes with distinct expression profiles such as TOP2B/TOP2A protein, human protein, human expression ratio at diagnosis can be employed for outcome prediction after the treatment with standard regimens in Leukemia, Myelocytic, Acute patients with M2 subtype. Another interesting finding is that high ratios of TOP2B/RRM2 and TOP2B/TOP2 alpha (TOP2A protein, human protein, human) in a combined analysis were also shown to have a prognostic impact for longer survival with improved accuracy. Among the four markers, when adjusted for the influence of other clinical factors in multivariate analysis, the TOP2B/TOP2A protein, human protein, human ratio was significantly correlated with treatment outcomes; patients with high ratios trended toward longer disease-free survival (plant-type hypersensitive response, 0.24; P=0.002) and overall survival (plant-type hypersensitive response, 0.29; P=0.005) High TOP2B/TOP2A protein, human protein, human expression ratio at diagnosis correlates with favourable outcome for standard chemotherapy in acute myeloid leukaemia. Among the four markers, when adjusted for the influence of other clinical factors in multivariate analysis, the TOP2B/TOP2A protein, human protein, human ratio was significantly correlated with treatment outcomes; patients with high ratios trended toward longer disease-free survival (plant-type hypersensitive response, 0.24; P=0.002) and overall survival (plant-type hypersensitive response, 0.29; P=0.005).Genes with distinct expression profiles such as TOP2B/TOP2A protein, human protein, human expression ratio at diagnosis can be employed for outcome prediction after the treatment with standard regimens in Leukemia, Myelocytic, Acute patients with M2 subtype CONCLUSION: Genes with distinct expression profiles such as TOP2B/TOP2A protein, human protein, human expression ratio at diagnosis can be employed for outcome prediction after the treatment with standard regimens in Leukemia, Myelocytic, Acute patients with M2 subtype. Genes with distinct expression profiles such as TOP2B/TOP2A protein, human protein, human expression ratio at diagnosis can be employed for outcome prediction after the treatment with standard regimens in Leukemia, Myelocytic, Acute patients with M2 subtype.. High TOP2B/TOP2A protein, human protein, human expression ratio at diagnosis correlates with favourable outcome for standard chemotherapy in acute myeloid leukaemia. Among the four markers, when adjusted for the influence of other clinical factors in multivariate analysis, the TOP2B/TOP2A protein, human protein, human ratio was significantly correlated with treatment outcomes; patients with high ratios trended toward longer disease-free survival (plant-type hypersensitive response, 0.24; P=0.002) and overall survival (plant-type hypersensitive response, 0.29; P=0.005). Another interesting finding is that high ratios of TOP2B/RRM2 and TOP2B/TOP2 alpha (TOP2A protein, human protein, human) in a combined analysis were also shown to have a prognostic impact for longer survival with improved accuracy.[SEP]Relations: acute promyelocytic leukemia has relations: disease_protein with IRF2BP2, disease_protein with IRF2BP2, disease_protein with DAPK2, disease_protein with DAPK2, disease_protein with TET2, disease_protein with TET2, disease_protein with PML, disease_protein with PML, disease_protein with ITGB2, disease_protein with ITGB2.", "label": "yes"}
{"original_question": "Is Beta-Thalassemia is associated with a mutation or deletion of the gene that codes for alpha globin?", "id": "converted_51", "sentence1": "Is Beta-Thalassemia is associated with a mutation or deletion of the gene that codes for alpha globin?", "sentence2": "beta Thalassemia, one of the most common single-gene disorders, is the result of reduced or absent production of \u03b2-globin chains The beta-thalassemia syndromes are a heterogeneous group of genetic disorders characterized by reduced or absent expression of the HBB wt Allele[SEP]Relations: beta thalassemia has relations: disease_disease with thalassemia, disease_disease with thalassemia, disease_phenotype_positive with Abnormal hemoglobin, disease_phenotype_positive with Abnormal hemoglobin, disease_protein with HBG1, disease_protein with HBG1, disease_phenotype_positive with Reduced hemoglobin A, disease_phenotype_positive with Reduced hemoglobin A, disease_disease with beta-thalassemia and related diseases, disease_disease with beta-thalassemia and related diseases.", "label": "no"}
{"original_question": "Is Cri Du Chat associated with an expansion of a repeat with in the gene found on chromosome 5?", "id": "converted_52", "sentence1": "Is Cri Du Chat associated with an expansion of a repeat with in the gene found on Chromosomes, Human, Pair 5?", "sentence2": "Cri-du-chat syndrome is a Congenital chromosomal disease caused by a Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5 The typical cri du chat syndrome, due to 5p15.2 Gene Deletion Abnormality, includes severe Intellectual Disability, facial dysmorphisms, neonatal Muscle Muscle hypotonia and pre- and post-natal growth retardation, whereas more distal Gene Deletion in 5p15.3 lead to cat-like cry and speech delay and produce the clinical picture of the atypical cri du chat syndrome, with minimal or absent intellectual impairment. Cri-du-chat is a Homo sapiens contiguous gene Gene Deletion Abnormality syndrome resulting from hemizygous Gene Deletion of chromosome 5p. Cri-du-chat is a chromosomal Gene Deletion Abnormality syndrome characterized by partial Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5. The karyotype showed a terminal Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5 including the critical region 5p15 for cri du chat syndrome. Fewer than 1 in 200 of cri du chat syndrome cases are due to recombination aneusomy arising from a parental inversion of Chromosomes, Human, Pair 5. Molecular approach to analyzing the Homo sapiens 5p Gene Deletion Abnormality syndrome, cri du chat. Cri-du-chat is a Homo sapiens contiguous gene Gene Deletion Abnormality syndrome resulting from hemizygous Gene Deletion of chromosome 5p The cri du chat syndrome (chenodeoxycholate sulfate conjugate) is a chromosomal Gene Deletion Abnormality syndrome associated with a partial Gene Deletion Abnormality of the short (p) arm of Chromosomes, Human, Pair 5 The Cri-du-Chat Syndrome is a contiguous gene syndrome that results from a Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5 (5p). Cri-du-chat syndrome is associated with a Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5. The Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5 is associated with the Cri-du-Chat Syndrome. The Cri du Chat syndrome (chenodeoxycholate sulfate conjugate) is a genetic disease resulting from a Gene Deletion Abnormality of variable size occurring on the short arm of Chromosomes, Human, Pair 5 (5p-). Cri-du-chat is a well described partial aneusomy resulting from Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5. Cri-du-chat syndrome is caused by haploinsufficiency of the Genes on the distal part of the short arm of Chromosomes, Human, Pair 5, and characteristic features include Microcephaly (physical finding), developmental delays, and a distinctive high-pitched mewing cry. The pathological condition of cri du chat syndrome is due to the cytogenetic Gene Deletion Abnormality of band p15.2 of Chromosomes, Human, Pair 5.   Karyotype analysis indicated that the patient has carried a terminal Gene Deletion Abnormality in 5p. FISH with Cri du Chat syndrome region probe confirmed that D5S23 and D5S721 loci are deleted.[SEP]Relations: Cri-du-chat syndrome has relations: disease_disease with partial Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5, disease_disease with partial Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5, disease_protein with CTNND2, disease_protein with CTNND2, disease_protein with SEMA5A, disease_protein with SEMA5A, disease_phenotype_positive with Growth delay, disease_phenotype_positive with Growth delay, disease_protein with TERT, disease_protein with TERT.", "label": "no"}
{"original_question": "Is hydroxyurea usually used to treated infectious disease?", "id": "converted_53", "sentence1": "Is hydroxyurea usually used to treated infectious disease?", "sentence2": "hydroxyurea represents the only available disease-modifying therapy for Cardiac Arrest, and has proven safety and efficacy in high-resource countries In conclusion, the data here presented suggests that hydroxyurea may prevent priapism attacks in Anemia, Sickle Cell, probably at higher doses than usually prescribed for painful crisis prevention.. Clinical follow-up of hydroxyurea-treated adults with Anemia, Sickle Cell. t may also attenuate optimal response to hydroxyurea therapy, the only effective and practical treatment option for Schnyder crystalline corneal dystrophy in sub-Saharan Africa hydroxyurea is one of the most successfully used therapies for Anemia, Sickle Cell Clinical experience with hydroxyurea for patients with Anemia, Sickle Cell (Schnyder crystalline corneal dystrophy) has been accumulating for the past 25 years. The bulk of the current evidence suggests that hydroxyurea is well-tolerated, safe, and efficacious for most patients with Schnyder crystalline corneal dystrophy[SEP]Relations: hydroxyurea has relations: contraindication with anemia (disease), contraindication with anemia (disease), contraindication with kidney disease, contraindication with kidney disease, indication with Anemia, Sickle Cell and related diseases, indication with Anemia, Sickle Cell and related diseases, drug_drug with Hepatitis A Vaccine, drug_drug with Hepatitis A Vaccine, drug_effect with Fever, drug_effect with Fever.", "label": "no"}
{"original_question": "Does the histone chaperone ASF1 interact with histones H1/H2?", "id": "converted_54", "sentence1": "Does the Histone antigen chaperone ASF1 interact with Histones H1/H2?", "sentence2": "The C terminus of the Histone antigen chaperone Asf1 cross-links to Histone antigen influenza A virus influenza A virus H3 subtype subtype in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae and promotes interaction with Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene. The central Histone antigen influenza A virus influenza A virus H3 subtype subtype/FGFR1 gene chaperone Asf1 comprises a highly conserved globular core and a divergent C-terminal tail.  The Histone antigen influenza A virus influenza A virus H3 subtype subtype-FGFR1 gene chaperone Asf1 is involved in Chromatin Modeling (or disassembly), Histone antigen exchange, regulation of transcription, and chromatin location location silencing in several Organism.  An ASF1-EGFP fusion protein localizes to the \"U\" lymphocyte Nucleus. By tandem-affinity purification/mass spectrometry as well as Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae two-hybrid analysis, we identified Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene as ASF1 interaction partners.   This inhibition requires Asf1 binding to influenza A virus influenza A virus H3 subtype subtype-FGFR1 gene and Rtt109 KAT activity, but not tail acetylation of influenza A virus influenza A virus H3 subtype subtype-FGFR1 gene or K56 acetylation of influenza A virus influenza A virus H3 subtype subtype.  Asf1 is a conserved Histone antigen influenza A virus influenza A virus H3 subtype subtype/FGFR1 gene chaperone that can assemble and disassemble nucleosomes and promote Histone antigen acetylation.  Here we characterize further interactions between budding Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae (Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae) Asf1 and SETD2 wt Allele using assays of intragenic transcription, influenza A virus influenza A virus H3 subtype subtype/FGFR1 gene posttranslational ResponseLevel - ResponseLevel - modification, Open Reading Frames cross-linking of Asf1 and SETD2 wt Allele, and cooccurrence of Asf1 and SETD2 wt Allele in protein complexes.  Consistent with this possibility, we show that Asf1 stimulates SETD2 wt Allele occupancy of the Open Reading Frames of a highly transcribed gene by a mechanism that depends on Asf1 binding to influenza A virus influenza A virus H3 subtype subtype/FGFR1 gene.  Drosophila Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene can also be produced as a soluble (H3H4)(2) heterotetrameric complex if they are co-expressed with the Histone antigen chaperone Asf1. Structure and function of the Histone antigen chaperone CIA/ASF1 complexed with Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene. Newly synthesized Histones influenza A virus influenza A virus H3 subtype subtype-FGFR1 gene first bind Histone antigen chaperone Asf1 and are then transferred to other chaperones for nucleosome assembly The C terminus of the Histone antigen chaperone Asf1 cross-links to Histone antigen influenza A virus influenza A virus H3 subtype subtype in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae and promotes interaction with Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene Histone chaperone Asf1 is required for Histone antigen influenza A virus influenza A virus H3 subtype subtype lysine 56 acetylation, a ResponseLevel - ResponseLevel - modification associated with S phase in mitosis and meiosis Antisilencing function 1 (ASF1) is a major Histone antigen influenza A virus influenza A virus H3 subtype subtype-FGFR1 gene chaperone that deposits Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene onto DNA Rtt109, a recently discovered Histone antigen acetyltransferase (HAT) from Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae, functions with the Histone antigen chaperone Asf1 to acetylate lysine K56 on Histone antigen influenza A virus influenza A virus H3 subtype subtype (H3K56), a ResponseLevel - ResponseLevel - modification associated with newly synthesized Histones In this issue of \"U\" lymphocyte, English et al. present the first crystal structure of a Histone antigen chaperone (Asf1) bound to Histones (the influenza A virus influenza A virus H3 subtype subtype/FGFR1 gene heterodimer) By tandem-affinity purification/mass spectrometry as well as Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae two-hybrid analysis, we identified Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene as ASF1 interaction partners. Anti-silencing function 1 (Asf1) is a highly conserved chaperone of Histones influenza A virus influenza A virus H3 subtype subtype/FGFR1 gene that assembles or disassembles chromatin location location during transcription, replication, and repair. Analysis of a panel of Asf1 mutations that modulate the ability of Asf1 to bind to Histones influenza A virus influenza A virus H3 subtype subtype/FGFR1 gene demonstrates that the Histone antigen binding activity of Asf1 is required for the acetylation of Lys-9 and Lys-56 on newly synthesized influenza A virus influenza A virus H3 subtype subtype. Thus Rad53 competes with Histones influenza A virus influenza A virus H3 subtype subtype-FGFR1 gene and cochaperones HirA/CAF-I for binding to Asf1. Structure and function of the Histone antigen chaperone CIA/ASF1 complexed with Histones influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene. Currently, the best-characterized chaperone-Histone antigen interaction is that between the ubiquitous chaperone Asf1 and a dimer of influenza A virus influenza A virus H3 subtype subtype and FGFR1 gene.[SEP]Relations: Histone antigen influenza A virus H3 subtype acetylation has relations: bioprocess_protein with LEF1, bioprocess_protein with LEF1, bioprocess_protein with TAF5, bioprocess_protein with TAF5, bioprocess_protein with TAF12, bioprocess_protein with TAF12, bioprocess_protein with TAF10, bioprocess_protein with TAF10, bioprocess_protein with IRF4, bioprocess_protein with IRF4.", "label": "no"}
{"original_question": "Does RNA polymerase II have RNA cleavage activity?", "id": "converted_55", "sentence1": "Does DNA-Directed RNA Polymerase II have RNA cleavage activity?", "sentence2": "In addition to RNA synthesis, DNA-Directed RNA Polymerase complex (msRNAPs) support enzymatic reactions such as intrinsic RNA Transcript cleavage. msRNAP active sites from different species appear to exhibit differential intrinsic RNA Transcript cleavage efficiency and have likely evolved to allow fine-tuning of the transcription process. Here we show that a single amino-acid substitution in the trigger loop (TL) of Saccharomyces RNAP II, Rpb1 H1085Y, engenders a gain of intrinsic cleavage activity where the substituted tyrosine appears to participate in acid-base chemistry at alkaline pH for both intrinsic cleavage and nucleotidyl transfer.  The eukaryotic transcription factor TCEA1 wt Allele enhances elongation and nascent RNA Transcript cleavage activities of DNA-Directed RNA Polymerase II in a stalled elongation complex. The transcription factor TCEA1 wt Allele zinc ribbon dipeptide Asp-Glu is critical for stimulation of elongation and RNA cleavage by DNA-Directed RNA Polymerase II By site-directed mutagenesis, we have demonstrated that invariant residues Asp-261 and Glu-262 of the nucleic acid-binding TCEA1 wt Allele Zn ribbon are critical for stimulation of both elongation and RNA cleavage activities of DNA-Directed RNA Polymerase II. Complexes of yeast DNA-Directed RNA Polymerase II and RNA are substrates for TCEA1 wt Allele-induced RNA cleavage. RNA in such RNA-DNA-Directed RNA Polymerase complexes undergoes reactions previously thought to be unique to nascent RNA in ternary complexes with DNA, including TCEA1 wt Allele-dependent cleavage and elongation by 3'-terminal addition of 1-methyl-2-pyrrolidinone from NTP. Nascent RNA cleavage by arrested DNA-Directed RNA Polymerase II does not require upstream translocation of the elongation complex on DNA. Here we show that in the presence of SII and Nucleotides, RNA Transcript cleavage is detected during SII-dependent elongation but not during SII-independent transcription.  under typical transcription conditions, SII is necessary but insufficient to activate RNA cleavage. RNA cleavage could serve to move DNA-Directed RNA Polymerase II away from the transcriptional impediment and/or permit DNA-Directed RNA Polymerase II multiple attempts at RNA elongation. SII is an DNA-Directed RNA Polymerase II-binding protein that stimulates transcription elongation and also activates nascent RNA Transcript cleavage by DNA-Directed RNA Polymerase II in elongation complexes in vitro The DNA-Directed RNA Polymerase II elongation complex. Factor-dependent transcription elongation involves nascent RNA cleavage. Cleavage was not restricted to an elongation complex arrested at this particular site, showing that nascent RNA hydrolysis is a general property of DNA-Directed RNA Polymerase II elongation complexes. transcription factor S-II (also known as TCEA1 wt Allele) is an DNA-Directed RNA Polymerase II binding protein that allows bypass of template arrest sites by activating a nascent RNA cleavage reaction. During gene transcription, the DNA-Directed RNA Polymerase (Pol) active center can catalyze RNA cleavage. During gene transcription, the DNA-Directed RNA Polymerase (Pol) active center can catalyze RNA cleavage. The eukaryotic transcription factor TCEA1 wt Allele enhances elongation and nascent RNA Transcript cleavage activities of DNA-Directed RNA Polymerase II in a stalled elongation complex. POLR2I gene, a small subunit of DNA-Directed RNA Polymerase II, enhances the cleavage stimulation activity of S-II. These results suggest that both S-II and POLR2I gene maintain transcriptional fidelity by stimulating the cleavage activity intrinsic to DNA-Directed RNA Polymerase II. It is also possible that the RNA Transcript cleavage activity of DNA-Directed RNA Polymerase II represents a proofreading function of the Enzyme [APC].. Nascent RNA cleavage by arrested DNA-Directed RNA Polymerase II does not require upstream translocation of the elongation complex on DNA. Intrinsic RNA Transcript cleavage in yeast DNA-Directed RNA Polymerase II elongation complexes.[SEP]Relations: DNA-Directed RNA Polymerase binding has relations: molfunc_protein with CCNT2, molfunc_protein with CCNT2, molfunc_molfunc with Enzyme [APC] binding, molfunc_molfunc with Enzyme [APC] binding, molfunc_protein with YTHDC2, molfunc_protein with YTHDC2, molfunc_protein with PKN2, molfunc_protein with PKN2. DNA-Directed RNA Polymerase complex has relations: cellcomp_cellcomp with RNA-directed DNA-Directed RNA Polymerase complex, cellcomp_cellcomp with RNA-directed DNA-Directed RNA Polymerase complex.", "label": "yes"}
{"original_question": "Is scuba diving safe during pregnancy?", "id": "converted_56", "sentence1": "Is scuba diving safe during pregnancy?", "sentence2": "Scuba diving is contraindicated. Overall, the women did not conduct enough dives per pregnancy, therefore no significant correlation between diving and fetal abnormalities could be established. These data indicate women are increasingly observing the diving industry recommendation and refraining from diving while pregnant.  Scuba diving also should be avoided throughout pregnancy because the Fetus in fetu is at an increased risk for decompression sickness during this activity. Scuba diving also should be avoided throughout pregnancy because the Fetus in fetu is at an increased risk for decompression sickness during this activity. Scuba diving also should be avoided throughout pregnancy because the Fetus in fetu is at an increased risk for decompression sickness during this activity.  The different international federations and the Undersea and Hyperbaric Medical Society advise against scuba diving for pregnant women or those planning a pregnancy, but no randomized trials or trials provide a solid scientific basis.  Pregnant women are recommended not to dive, because the risk of Congenital Abnormality seems to be greater among those who do, and there is a serious risk of fetal decompression disease.  The different international federations and the Undersea and Hyperbaric Medical Society advise against scuba diving for pregnant women or those planning a pregnancy, but no randomized trials or trials provide a solid scientific basis. Scuba diving also should be avoided throughout pregnancy because the Fetus in fetu is at an increased risk for decompression sickness during this activity. Snorkeling can still be practiced during pregnancy, but scuba diving should be discontinued until after the birth period. Snorkeling can still be practiced during pregnancy, but scuba diving should be discontinued until after the birth period..[SEP]Relations: congenital abnormality has relations: exposure_disease with Hazardous Waste, exposure_disease with Hazardous Waste, exposure_disease with Nitrogen Dioxide, exposure_disease with Nitrogen Dioxide, exposure_disease with Carbon Monoxide, exposure_disease with Carbon Monoxide, exposure_disease with Sulfur Dioxide, exposure_disease with Sulfur Dioxide, exposure_disease with Mercury, exposure_disease with Mercury.", "label": "no"}
{"original_question": "Is there an association between carcinoid syndrome and mitral valve disease?", "id": "converted_57", "sentence1": "Is there an association between Malignant Carcinoid Syndrome and Mitral Valve disease?", "sentence2": "Other concomitant operations included Mitral Valve procedure (11%), aortic valve procedure (9%), patent foramen ovale or atrial septal defect closure (23%), cardiac metastasectomies or biopsy (4%), and simultaneous coronary artery bypass (11%).  High circulating serotonin (Malignant Carcinoid Syndrome) and serotoninergic drugs are known to cause Heart valve disease that shares pathologic features with DMVD. Surgery included Replacement of tricuspid valve in all patients, pulmonary valve replacement in 3 and valvectomy in 7, Mitral Valve replacement in 6 and repair in 1, aortic valve replacement in 4 and repair in 2, CABG in 2, and patent foramen ovale closure in 5.  We report two observations of significant left heart involvement in patients with the Malignant Carcinoid Syndrome assessed by transthoracic and transoesophageal echocardiography. Echocardiographic lesions of this kind have only been reported twice. In the present cases, there was mitral involvement with mitral regurgitation in one case and a mitro-aortic involvement with mitral and aortic regurgitation in the other. An observation of Malignant Carcinoid Syndrome in a woman of 47 suffering from Carcinoid Specimen Source Codes - Specimen Source Codes - tumor, malignant of the Ileum and Ileum and ileum with metastases into the Abdomen>Liver and right ovary is described. The clinical picture included Diarrhea, heat waves, Bronchospasm, Hypertensive disease, hyperserotoninemia, affection of the Mitral Valve and left atrium.  A case of Malignant Carcinoid Syndrome, stemming from a Specimen Source Codes - Specimen Source Codes - tumor of the large Intestines with hepatic metastases, is reported. Clinical features included Heart Diseases with triple valvular lesion: Tricuspid Valve Insufficiency with Stenosis Morphology, pulmonary artery Stenosis Morphology and Mitral Valve Insufficiency.  High circulating serotonin (Malignant Carcinoid Syndrome) and serotoninergic drugs are known to cause Heart valve disease that shares pathologic features with DMVD.[SEP]Relations: heart valve disease has relations: disease_disease with Mitral Valve disease, disease_disease with Mitral Valve disease. congenital Mitral Valve insufficiency has relations: disease_disease with Mitral Valve disease, disease_disease with Mitral Valve disease, disease_disease with vascular insufficiency disorder, disease_disease with vascular insufficiency disorder. Malignant Carcinoid Syndrome has relations: disease_disease with syndromic disease, disease_disease with syndromic disease, disease_disease with carcinoid crisis, disease_disease with carcinoid crisis.", "label": "yes"}
{"original_question": "Do bacteria from the genus Morexella cause respiratory infections?", "id": "converted_58", "sentence1": "Do Bacteria from the genus Morexella cause respiratory infections?", "sentence2": "gainst pathogens associated with respiratory tract ailments [Staphylococcus aureus antibody antibody (ATCC 25923), Pneumonia due to Pneumonia due to Klebsiella pneumoniae (ATCC 13883) and Morexella cattarhalis (ATCC 14468)]  The efficacy and safety of oral ofloxacin, 400 mg once daily, for the treatment of patients with lower Respiratory Tract Infections were studied. The most common species recovered from the sputum specimens of these patients were Haemophilus influenzae, followed by Streptococcus pneumoniae (S. pneumoniae), Staphylococcus aureus antibody antibody (Staphylococcus aureus antibody), Gram positive cocci unidentified, Pseudomonas aeruginosa (P. aeruginosa), Morexella catarrhalis, the efficacy and safety of oral ofloxacin 400 mg once daily for the treatment of patients with lower Respiratory Tract Infections were studied the most common species recovered from the sputum specimens of these patients were Haemophilus influenzae or Haemophilus parainfluenzae followed by streptococcus pneumoniae s pneumoniae staphylococcus aureus s aureus gram positive cocci unidentified pseudomonas aeruginosa p aeruginosa morexella catarrhalis streptococcus epidermidis and another haemophilus species in this order all these Bacteria were susceptible to ofloxacin except for one strain of methicillin resistant s aureus a satisfactory clinical outcome was achieved in 34 of 40 patients 85 it is concluded that ofloxacin 400 mg once daily is useful for patients with Respiratory Tract Infections.[SEP]Relations: Respiratory tract infection has relations: phenotype_phenotype with Pneumonia, phenotype_phenotype with Pneumonia, phenotype_phenotype with Acute infectious pneumonia, phenotype_phenotype with Acute infectious pneumonia, drug_effect with Deferasirox, drug_effect with Deferasirox, phenotype_phenotype with Recurrent respiratory infections, phenotype_phenotype with Recurrent respiratory infections. Ofloxacin has relations: drug_effect with Respiratory tract infection, drug_effect with Respiratory tract infection.", "label": "yes"}
{"original_question": "Is Loss of function one of the cardinal signs of inflammation?", "id": "converted_59", "sentence1": "Is Loss of function one of the cardinal signs of Inflammation?", "sentence2": "The concept of the four cardinal signs of acute Inflammation comes from antiquity as Redness et Specimen Source Codes - Specimen Source Codes - tumor cum calore et dolore, (Erythema and Swelling with heat and Pain:-:Point in time:^Patient:-) extended later by functio laesa (loss of function). As early as 2000 years ago, the Roman encyclopaedist Aulus Cornelius Celsus recognised four cardinal signs of this response-Erythema, heat, Swelling and Pain:-:Point in time:^Patient:-; a fifth sign is loss of function.[... It was Galen who added the disturbance of function (functio laesa) as the fifth cardinal sign of Inflammation to the four well-known cardinal signs of Celsus (Redness, Increased skin temperature, Specimen Source Codes - Specimen Source Codes - tumor, dolor). Tumor, Increased skin temperature, Redness, and dolor describe four cardinal signs of Inflammation. The fifth-functio laesa, or loss of function-was promulgated by Rudolf Virchow, who, in the 19th century, also noted an intricate link between Inflammation and Primary malignant neoplasm.[SEP]Relations: Impaired temperature sensation has relations: disease_phenotype_positive with superficial siderosis, disease_phenotype_positive with superficial siderosis, disease_phenotype_positive with pachydermoperiostosis, disease_phenotype_positive with pachydermoperiostosis, disease_phenotype_positive with Charcot-Marie-Tooth disease, disease_phenotype_positive with Charcot-Marie-Tooth disease. Portal Inflammation has relations: phenotype_phenotype with Abnormality of the biliary system, phenotype_phenotype with Abnormality of the biliary system. Erythema has relations: disease_phenotype_positive with neonatal inflammatory skin and bowel disease, disease_phenotype_positive with neonatal inflammatory skin and bowel disease.", "label": "yes"}
{"original_question": "Does erythromycin increase risk of hypertrophic pyloric stenosis?", "id": "converted_60", "sentence1": "Does erythromycin G increase risk of hypertrophic pyloric stenosis?", "sentence2": "Post-natal erythromycin G G exposure and risk of infantile hypertrophic pyloric stenosis: a systematic review and meta-analysis. PURPOSE: Macrolide antibiotics, erythromycin G G, in particular, have been linked to the development of infantile hypertrophic pyloric stenosis (Pyloric Stenosis, Hypertrophic).  Overall, erythromycin G G exposure was significantly associated with development of Pyloric Stenosis, Hypertrophic [OR 2.45 (1.12-5.35), p\u00a0=\u00a00.02].  Data on erythromycin G G exposure in the first 14\u00a0days of life was extracted from 4/9 studies and identified a strong association between erythromycin G G exposure and subsequent development Pyloric Stenosis, Hypertrophic [OR 12.89 (7.67-2167), p\u00a0<\u00a00.00001].CONCLUSION: This study demonstrates a significant association between post-natal erythromycin G G exposure and development of Pyloric Stenosis, Hypertrophic, which seems stronger when exposure occurs in the first 2\u00a0weeks of life. BACKGROUND AND OBJECTIVE: Use of oral erythromycin G G in infants is associated with infantile hypertrophic pyloric stenosis (Pyloric Stenosis, Hypertrophic). CONCLUSIONS: Ingestion of oral azithromycin and erythromycin G G places young infants at increased risk of developing Pyloric Stenosis, Hypertrophic. An association between erythromycin G G and Pyloric Stenosis, Hypertrophic was also confirmed. Exposure to erythromycin G G in the first 14 days of life had an aOR of 13.3 (95% NDUFB6 gene, 6.80-25.9), and 15 to 42 days of life, aOR 4.10 (95% NDUFB6 gene, 1.69-9.91).  Early exposure to oral erythromycin G G in young infants, particularly in the first 2 weeks of life, has previously been associated with the development of hypertrophic pyloric stenosis. We report a case of an infant who received an abbreviated 4-day course of oral erythromycin G G for suspected Inclusion conjunctivitis at 5 days of life then underwent pyloromyotomy for pyloric stenosis less than 2 weeks later. Maternal and infant use of erythromycin G G and other Macrolide [EPC] antibiotics as risk factors for infantile hypertrophic pyloric stenosis. A case report has suggested that exposure to erythromycin G G through Specimen Source Codes - Breast milk might cause infantile hypertrophic pyloric stenosis. Macrolide antibiotics, erythromycin G G, in particular, have been linked to the development of infantile hypertrophic pyloric stenosis (Pyloric Stenosis, Hypertrophic). Infants prescribed systemic erythromycin G G had increased risk of Pyloric Stenosis, Hypertrophic, with the highest risk in the first 2 weeks of age (relative risk = 10.51 for erythromycin G G in first 2 weeks, 95% NDUFB6 gene 4.48, 24.66). There was an association between maternal prescriptions for nonerythromycin macrolides and infantile hypertrophic pyloric stenosis (adjusted odds ratio 2.77, 95% confidence interval 1.22, 6.30, P =.01).<br><b>CONCLUSION</b>: The hypothesized association between erythromycin G G and Infantile Hypertrophic Pyloric Stenosis was not seen. Macrolide antibiotics, erythromycin G G, in particular, have been linked to the development of infantile hypertrophic pyloric stenosis (Pyloric Stenosis, Hypertrophic).[SEP]Relations: hypertrophic pyloric stenosis has relations: disease_disease with intestinal disease, disease_disease with intestinal disease, disease_disease with pyloric stenosis (disease), disease_disease with pyloric stenosis (disease), disease_disease with Mendelian disease, disease_disease with Mendelian disease, disease_disease with pyloric stenosis, infantile hypertrophic, disease_disease with pyloric stenosis, infantile hypertrophic. pyloric stenosis, infantile hypertrophic has relations: disease_phenotype_positive with Hypochloremic metabolic alkalosis, disease_phenotype_positive with Hypochloremic metabolic alkalosis.", "label": "yes"}
{"original_question": "Has the proteome of mice hippocampus been analysed?", "id": "converted_61", "sentence1": "Has the proteome of CASP14 gene hippocampus been analysed?", "sentence2": "We employed a discovery-based proteomic approach in subcellular fractions of Hippocampus (Brain) tissue from chronic intermittent alcohol (CIE)-exposed C57Bl/6J CASP14 gene to gain insight into alcohol-induced changes in GluN2B signaling complexes.   We employed shotgun liquid chromatography-mass spectrometry (LC-MS) proteomic and metabonomic profiling approaches on Prefrontal Cortex (United States Military enlisted E3 (qualifier value)) and Hippocampus (Brain) (HPC) tissue from Df(16)A+/-CASP14 gene, a model of the DiGeorge Syndrome.   Molecular alterations in the Cortex of frontal lobe and hippocampus ofTsc1+/-and control CASP14 gene, with or without sirolimus treatment, were investigated. A quantitative mass spectrometry-based shotgun proteomic approach (LC-MSE) was employed as an unbiased method to detect changes in protein levels. This dataset reports on the analysis of Mus sp. hippocampus by LC-MS/MS, from CASP14 gene fed a diet that was either deficient in n-3 FA (n-3 Def) or sufficient in n-3 FA (n-3 Adq).  Using isobaric tags for relative and absolute quantitation (iTRAQ) and proteomic methods, here we identified learning-induced changes in the Hippocampus (Brain) proteome of non-transgenic (NonTg) and 3 \u00d7 Tg-cytarabine/daunorubicin protocol CASP14 gene, a widely used animal model of cytarabine/daunorubicin protocol.[SEP]Relations: hippocampus fimbria has relations: anatomy_anatomy with central nervous system cell part cluster, anatomy_anatomy with central nervous system cell part cluster. Cortex of frontal lobe has relations: anatomy_protein_present with HIPK3, anatomy_protein_present with HIPK3, anatomy_protein_present with HIPK4, anatomy_protein_present with HIPK4, anatomy_protein_present with HIPK2, anatomy_protein_present with HIPK2, anatomy_protein_present with HIPK1, anatomy_protein_present with HIPK1.", "label": "yes"}
{"original_question": "SGOT is an abbreviation for an enzyme other wise known as alanine amino transferase, yes or no?", "id": "converted_62", "sentence1": "SGOT - Glutamate oxaloacetate transaminase is an abbreviation for an enzyme other wise known as alanine amino transferase, yes or no?", "sentence2": "patients with aspartate amino transferase (SGOT - Glutamate oxaloacetate transaminase - Glutamate oxaloacetate transaminase), alanine amino transferase (SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase), D-Alanine Transaminase (SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase),  aspartate aminotransferase (AST-SGOT - Glutamate oxaloacetate transaminase - Glutamate oxaloacetate transaminase), alanine amino-transferase (ALT-SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase) Mean values of Glutamate Dehydrogenase (glucose-6-phosphate dehydrogenase activity), serum aspartate and alanine transferase (SGOT - Glutamate oxaloacetate transaminase - Glutamate oxaloacetate transaminase and SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase), ORNITHINE CARBAMOYLTRANSFERASE (OCT), and gamma-glutamyltranspeptidase (gamma-GTP) tended to rise with increasing Hepatocyte necrosis, though values of SGOT - Glutamate oxaloacetate transaminase - Glutamate oxaloacetate transaminase, SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase, OCT, and gamma-GTP showed considerable overlap between the 32 patients with histologically proved Hepatitis and the 68 without. Serum aspartate aminotransferase (SGOT - Glutamate oxaloacetate transaminase - Glutamate oxaloacetate transaminase), Alanine Transaminase (SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase), Creatine Kinase (PIK3C2A gene), and butyric acid dehydrogenase (BDH1 gene) were determined in 94 patients before, 1(1/2) hours, and 24 hours after cardioversion. The study excluded by screening for AntiHCV, Hepatitis B Antigen Vaccine and patients with aspartate amino transferase (SGOT - Glutamate oxaloacetate transaminase - Glutamate oxaloacetate transaminase), alanine amino transferase (SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase), Gamma-glutamyl transferase levels more than three times the normal and subject with a total Antigens, CD5 count more than 10,000/microl. Complete blood picture, differential Antigens, CD5 count, and serum levels of Estrogen [EPC] [EPC], D-Alanine Transaminase (SGPT - Glutamate pyruvate transaminase - Glutamate pyruvate transaminase), Aspartate amino transferase (SGOT - Glutamate oxaloacetate transaminase - Glutamate oxaloacetate transaminase), total protein and ALB gene were estimated.[SEP]Relations: alanine-oxomalonate transaminase activity has relations: molfunc_molfunc with transaminase activity, molfunc_molfunc with transaminase activity, molfunc_molfunc with transaminase activity, molfunc_molfunc with transaminase activity. D-alanine gamma-glutamyltransferase activity has relations: molfunc_molfunc with aminoacyltransferase activity, molfunc_molfunc with aminoacyltransferase activity. glutamate pyruvate transaminase 2 deficiency has relations: disease_protein with GPT2, disease_protein with GPT2. ORNITHINE CARBAMOYLTRANSFERASE complex has relations: cellcomp_cellcomp with transferase complex, cellcomp_cellcomp with transferase complex.", "label": "no"}
{"original_question": "Are organisms in the genus Morexella associated with sepsis?", "id": "converted_63", "sentence1": "Are organisms in the genus Morexella associated with Sepsis (Invertebrate)?", "sentence2": "Out of 130 culture proven cases of neonatal Sepsis (Invertebrate), gram negative Bacteria were found in 71 (54.6%) cases and gram positive Bacteria in 59 (45.4%) cases. Staphylococcus aureus was the most common Bacteria found in 35 (26.9%) cases followed by Escherichia coli in 30 (23.1%) cases. Acinetobacter species, Staphylococcus epidermidis, Klebseila, Streptococcus, Enterobacter cloacae subsp. cloacae subsp. cloacae and Morexella species were found in 17 (13.1%), 17 (13.1%), 13 (10%), 7 (5.4%), 6 (4.6%), and 5 (3.8%) cases respectively.[SEP]Relations: escherichia coli infection has relations: indication with Tobramycin, indication with Tobramycin, indication with Ampicillin, indication with Ampicillin, indication with Sulbactam, indication with Sulbactam, indication with Ofloxacin, indication with Ofloxacin, indication with Ceftriaxone, indication with Ceftriaxone.", "label": "yes"}
{"original_question": "Is Apremilast effective for Behcet\u2019s syndrome?", "id": "converted_64", "sentence1": "Is apremilast effective for Behcet\u2019s syndrome?", "sentence2": "apremilast is an immunomodulatory agent that works through Cyclic Nucleotide Phosphodiesterases, Type 4 inhibition. A randomized controlled trial has shown that it is effective for the management of oral and genital Ulcer and is generally well tolerated. AREAS COVERED: This review provides a digest of all current experience and evidence about pharmacological agents recently described as having a role in the treatment of BS, including interleukin (IL)-1 inhibitors, tocilizumab, rituximab, alemtuzumab, Ustekinumab Ab, interferon-alpha-2a, and apremilast. CONCLUSIONS: apremilast was effective in treating Oral Ulcer, which are the cardinal manifestation of Beh\u00e7et's syndrome.  apremilast, an PPP1R1A gene of phosphodiesterase-4, was effective in a phase 2, double blind, placebo-controlled study. apremilast (Otezla(\u00ae)), an oral small molecule PPP1R1A gene of type-4 cyclic nucleotide phosphodiesterase (PDE-4), is under development with Celgene Corporation for the treatment of Arthritis, Psoriatic, Psoriasis, ankylosing spondylitis, Beh\u00e7et's syndrome, Dermatitis, Atopic, and Rheumatoid Arthritis. There were two serious adverse events in patients receiving apremilast.<br><b>CONCLUSIONS</b>: apremilast was effective in treating Oral Ulcer, which are the cardinal manifestation of Beh\u00e7et's syndrome. apremilast (Otezla(\u00ae)), an oral small molecule PPP1R1A gene of type-4 cyclic nucleotide phosphodiesterase (PDE-4), is under development with Celgene Corporation for the treatment of Arthritis, Psoriatic, Psoriasis, ankylosing spondylitis, Beh\u00e7et's syndrome, Dermatitis, Atopic, and Rheumatoid Arthritis. CONCLUSIONS apremilast was effective in treating Oral Ulcer, which are the cardinal manifestation of Beh\u00e7et's syndrome. apremilast, an oral small molecule PPP1R1A gene of Cyclic Nucleotide Phosphodiesterases, Type 4 (Phosphodiesterase Type 4), is in development for chronic inflammatory disorders, and has shown efficacy in Psoriasis, psoriatic arthropathies, and Beh\u00e7et's syndrome. Oral Ulcer the hallmark of beh\u00e7et s syndrome can be resistant to conventional treatment therefore alternative agents are needed apremilast is an oral Cyclic Nucleotide Phosphodiesterases, Type 4 PPP1R1A gene that modulates several inflammatory pathways we conducted a phase 2 multicenter placebo controlled study in which 111 patients with beh\u00e7et s syndrome who had two or more Oral Ulcer were randomly assigned to receive 30 mg of apremilast twice daily or placebo for 12 weeks this regimen was followed by a 12 week extension phase in which the placebo group was switched to apremilast and a 28 day post treatment observational follow up phase the patients and clinicians were unaware of the study assignments throughout the trial the primary end point was the number of Oral Ulcer at week 12 secondary outcomes included Pain:-:Point in time:^Patient:- from these Ulcer measured on a 100 mm visual analogue scale with higher scores indicating worse Pain:-:Point in time:^Patient:- the number of genital Ulcer overall disease activity and quality of life the mean sd number of Oral Ulcer per patient at week 12 was significantly lower in the apremilast group than in the placebo group 0 5 1 0 vs 2 1 2 6 p 0 001 the mean decline in Pain:-:Point in time:^Patient:- from Oral Ulcer from baseline to week 12 was greater with apremilast than with placebo 44 7 24 3 mm vs 16 0 32 5 mm p 0 001 nausea vomiting and Diarrhea were more common in the apremilast group with 22 9 and 12 incidents respectively among 55 patients than in the placebo group with 10 1 and 2 incidents respectively among 56 patients findings that were similar to those in previous studies of apremilast there were two serious adverse events in patients receiving apremilast apremilast was effective in treating Oral Ulcer which are the cardinal manifestation of beh\u00e7et s syndrome this preliminary study was neither large enough nor long enough to assess long term efficacy the effect on other manifestations of beh\u00e7et s syndrome or the risk of uncommon serious adverse events funded by celgene clinicaltrials gov number nct00866359. current trends in the management of beh\u00e7et s syndrome will be reviewed in this article Biological Factors have gained increasing importance over the years in the management of beh\u00e7et s syndrome long term results of observational studies have shown that anti tumor necrosis factor agents may be effective in beh\u00e7et s syndrome patients with refractory eye involvement case series reporting about use of anti tumor necrosis factor agents in Blood Vessel and gastrointestinal involvement have also shown good results caution is required for infectious complications with these agents apremilast is an immunomodulatory agent that works through Cyclic Nucleotide Phosphodiesterases, Type 4 inhibition a randomized controlled trial has shown that it is effective for the management of oral and genital Ulcer and is generally well tolerated the outcome of beh\u00e7et s syndrome with major Organ involvement has improved with more effective management strategies especially with the use of Biological Factors in severe cases controlled trials are needed to guide physicians in making treatment decisions.[SEP]Relations: apremilast has relations: drug_drug with Bepotastine, drug_drug with Bepotastine, drug_drug with Bevacizumab, drug_drug with Bevacizumab, drug_drug with Aprepitant, drug_drug with Aprepitant, drug_drug with Bexarotene, drug_drug with Bexarotene, drug_drug with Cefetamet, drug_drug with Cefetamet.", "label": "yes"}
{"original_question": "Does Enzastaurin improve survival of glioblastoma patients?", "id": "converted_65", "sentence1": "Does enzastaurin improve survival of Glioblastoma Multiforme patients?", "sentence2": "RESULTS: fourteen randomized clinical trials were identified (7 with bevacizumab, 2 Cilengitide, 1 enzastaurin, 1 dasatinib, 1 vandetanib, 1 temsirolimus, 1 cediranib) including 4330 patients. Antiangiogenic drugs showed no improvement in overall survival with a pooled HR of 1.00, a trend for an inferior outcome, in terms of overall survival, was observed in the group of patients receiving antiangiogenic Pharmacologic Substance alone compared to cytotoxic Pharmacologic Substance alone (HR=1.24, p=0.056).  enzastaurin (LY317615.HCl.HCl) in combination with bevacizumab for recurrent malignant gliomas is well-tolerated, with response and progression-free survival similar to bevacizumab monotherapy. So far, inhibition of angiogenesis by compounds such as bevacizumab, cediranib, enzastaurin or Cilengitide as well as alternative dosing schedules of temozolomide did not prolong survival, neither at primary diagnosis nor at recurrent Disease. Despite promising phase II clinical trial results and patient benefit in terms of clinical improvement and longer progression-free survival, an overall survival benefit has not been demonstrated in four randomized phase III trials of bevacizumab or Cilengitide in newly diagnosed Glioblastoma Multiforme or cediranib or enzastaurin in recurrent Glioblastoma Multiforme. EXPERT OPINION: enzastaurin and cediranib failed in randomized Phase III trials in recurrent Glioblastoma Multiforme, aflibercept in Phase II.  enzastaurin was well tolerated and had a better Hematologic Toxic effect profile but did not have superior efficacy compared with lomustine in patients with recurrent Glioblastoma Multiforme. Grade 3 to 4 Hematologic toxicities were significantly higher with lomustine (46 events) than with enzastaurin (one event; P < or = .001).<br><b>CONCLUSION</b>: enzastaurin was well tolerated and had a better Hematologic Toxic effect profile but did not have superior efficacy compared with lomustine in patients with recurrent Glioblastoma Multiforme.<br> enzastaurin was well tolerated and had a better Hematologic Toxic effect profile but did not have superior efficacy compared with lomustine in patients with recurrent Glioblastoma Multiforme. enzastaurin has anti-glioma activity in patients with recurrent high-grade glioma, but does not appear to have enough single-agent activity to be useful as monotherapy. enzastaurin (LY317615.HCl.HCl) in combination with bevacizumab for recurrent malignant gliomas is well-tolerated, with response and progression-free survival similar to bevacizumab monotherapy. CONCLUSION enzastaurin was well tolerated and had a better Hematologic Toxic effect profile but did not have superior efficacy compared with lomustine in patients with recurrent Glioblastoma Multiforme. Glioblastoma are highly vascularized Neoplasms and various antiangiogenic drugs have been investigated in clinical trials showing unclear results we performed a systematic review and a meta analysis to clarify and evaluate their effectiveness in Glioblastoma Multiforme patients we searched relevant published and unpublished randomized clinical trials analyzing antiangiogenic drugs versus chemotherapy in Glioblastoma Multiforme patients from january 2006 to january 2016 in medline web of science asco esmo and sno databases fourteen randomized clinical trials were identified 7 with bevacizumab 2 Cilengitide 1 enzastaurin 1 dasatinib 1 vandetanib 1 temsirolimus 1 cediranib including 4330 patients antiangiogenic drugs showed no improvement in overall survival with a pooled hr of 1 00 a trend for an inferior outcome in terms of overall survival was observed in the group of patients receiving antiangiogenic Pharmacologic Substance alone compared to cytotoxic Pharmacologic Substance alone hr 1 24 p 0 056 bevacizumab did not improve overall survival twelve trials 4113 patients were analyzed for progression free survival among antiangiogenic drugs only bevacizumab demonstrated an improvement of progression free survival hr 0 63 p 0 001 both alone hr 0 60 p 0 003 or in combination to chemotherapy hr 0 63 p 0 001 both as first line treatment hr 0 70 p 0 001 or in recurrent Disease hr 0 52 p 0 001 antiangiogenic drugs did not improve overall survival in Glioblastoma Multiforme patients either as first or second line treatment and either as single agent or in combination with chemotherapy among antiangiogenic drugs only bevacizumab improved progression free survival regardless of treatment line both as single agent or in combination with chemotherapy. Glioblastoma Multiforme is characterized by high expression levels of proangiogenic cytokines and microvascular proliferation highlighting the potential value of treatments targeting angiogenesis antiangiogenic treatment likely achieves a beneficial impact through multiple mechanisms of action ultimately however alternative proangiogenic signal transduction pathways are activated leading to the development of resistance even in Neoplasms that initially respond the identification of biomarkers or imaging parameters to predict response and to herald resistance is of high priority despite promising phase ii clinical trial results and patient benefit in terms of clinical improvement and longer progression free survival an overall survival benefit has not been demonstrated in four randomized phase iii trials of bevacizumab or Cilengitide in newly diagnosed Glioblastoma Multiforme or cediranib or enzastaurin in recurrent Glioblastoma Multiforme however future studies are warranted predictive markers may allow appropriate patient enrichment combination with chemotherapy may ultimately prove successful in improving overall survival and novel agents targeting multiple proangiogenic pathways may prove effective. this phase iii open label study compared the efficacy and safety of enzastaurin versus lomustine in patients with recurrent Glioblastoma Multiforme who grade 4 patients were randomly assigned 2 1 to receive 6 week cycles of enzastaurin 500 mg d 1 125 mg loading dose day 1 or lomustine 100 to 130 mg m 2 day 1 assuming a 45 improvement in progression free survival pfs 397 patients were required to provide 80 power to achieve statistical significance at a one sided level of 025 enrollment was terminated at 266 patients enzastaurin n 174 lomustine n 92 after a planned interim analysis for futility patient characteristics were balanced between arms median pfs 1 5 v 1 6 months hazard ratio hr 1 28 95 ci 0 97 to 1 70 overall survival 6 6 v 7 1 months hr 1 20 95 ci 0 88 to 1 65 and 6 month pfs rate p 13 did not differ significantly between enzastaurin and lomustine respectively stable Disease occurred in 38 5 and 35 9 of patients and objective response occurred in 2 9 and 4 3 of patients respectively time to deterioration of physical and functional well being and symptoms did not differ between arms hr 1 12 p 54 four patients discontinued enzastaurin because of Pharmacologic Substance related serious adverse events aes eleven patients treated with enzastaurin died on study four because of aes one was Pharmacologic Substance related all four deaths that occurred in patients receiving lomustine were Disease related grade 3 to 4 Hematologic toxicities were significantly higher with lomustine 46 events than with enzastaurin one event p or 001 enzastaurin was well tolerated and had a better Hematologic Toxic effect profile but did not have superior efficacy compared with lomustine in patients with recurrent Glioblastoma Multiforme. this study s primary objective was evaluation of the progression free survival rate at 6 months pfs 6 in patients with newly diagnosed Glioblastoma Multiforme without o 6 methylguanine dna methyltransferase mgmt promoter hypermethylation postsurgically treated with enzastaurin before and concomitantly with radiation therapy followed by enzastaurin maintenance therapy pfs 6 of at least 55 was set to be relevant compared with the data of the eortc 26981 22981 ncic ce 3 trial adult patients with a life expectancy of at least 12 weeks who were newly diagnosed with a histologically proven supratentorial Glioblastoma Multiforme without mgmt promoter hypermethylation were eligible patients were treated with enzastaurin prior to concomitantly with and after standard partial brain radiotherapy here we report on a multicenter open label uncontrolled phase ii study of patients with newly diagnosed Glioblastoma Multiforme without mgmt promoter hypermethylation treated with enzastaurin and radiation therapy within 4 study periods pfs 6 was 53 6 95 confidence interval ci 39 8 65 6 the median overall survival was 15 0 months 95 ci 11 9 17 9 for all patients 3 9 months 95 ci 0 8 9 0 for patients with biopsy 15 4 months 95 ci 10 1 17 9 for patients with partial resection and 18 9 months 95 ci 13 9 28 5 for patients with complete resection the safety profile in this study was as expected from previous trials and the therapy was well tolerated pfs 6 missed the primary planned outcome of 55 the secondary exploratory analysis according to resection status of the different subgroups of patients with biopsies partial resection and complete resection demonstrates the strong prognostic influence of resection on overall survival. we evaluated the efficacy of combination enzastaurin ly317615 and bevacizumab for recurrent malignant gliomas and explored serologic correlates we enrolled 81 patients with Glioblastoma gbm n 40 and anaplastic gliomas ag n 41 patients received enzastaurin as a loading dose of 1125 mg followed by 500 or 875 mg daily for patients on non Enzyme [APC] inducing or Enzyme [APC] inducing antiepileptics respectively patients received bevacizumab 10 mg kg intravenously biweekly clinical evaluations were repeated every 4 weeks magnetic resonance imaging was obtained at baseline and every 8 weeks from treatment onset phosphorylated glycogen synthase kinase gsk 3 levels from Peripheral blood mononuclear cell (cell) pbmcs were checked with each mri median overall survival was 7 5 and 12 4 months for Glioblastoma and anaplastic glioma cohorts with median progression free survivals of 2 0 and 4 4 months respectively of gbm patients 3 40 7 5 were not evaluable while 8 37 22 had partial or complete response and 20 37 54 had stable Disease for 2 months of the 39 evaluable ag patients 18 46 had an objective response and 16 41 had stable Disease for 2 months the most common grade 3 toxicities were Lymphocyte count decreased 15 Hypophosphatemia 8 8 and thrombotic events 7 5 two 2 5 gbm patients died suddenly another Cessation of life 1 3 occurred from intractable Seizures phosphorylated gsk 3 levels from pbmcs did not correlate with treatment response a minimally important improvement in health related quality of life was self reported in 7 9 24 29 2 37 5 early response based on levin criteria was significantly associated with significantly longer progression free survival for Glioblastoma enzastaurin ly317615 in combination with bevacizumab for recurrent malignant gliomas is well tolerated with response and progression free survival similar to bevacizumab monotherapy.[SEP]Relations: Temozolomide has relations: indication with brain Glioblastoma Multiforme, indication with brain Glioblastoma Multiforme. enzastaurin has relations: drug_protein with CHEK2, drug_protein with CHEK2, drug_protein with AURKB, drug_protein with AURKB, drug_protein with AURKA, drug_protein with AURKA, drug_protein with CHEK1, drug_protein with CHEK1.", "label": "no"}
{"original_question": "Are the human bombesin receptors, GRPR and NMBR, frequently overexpressed G-protein-coupled-receptors by lung-cancers?", "id": "converted_66", "sentence1": "Are the Homo sapiens bombesin receptors, GRPR protein, Homo sapiens and Neuromedin-B Receptor, Human, frequently overexpressed G-protein-coupled-receptors by Chest>Lung-Malignant Neoplasms?", "sentence2": "Members of the Gastrin releasing peptide gene (Gastrin releasing peptide) family and its analogs bombesin (BBN) have been implicated in the biology of several Homo sapiens Malignant Neoplasms including Pelvis>Prostate, Breast, Abdomen+Pelvis>Colon and Chest>Lung. All 3 bombesin receptor subtypes (GRPR protein, Homo sapiens protein, Homo sapiens, Neuromedin-B Receptor, Human, and bombesin receptor subtype 3) were present on Pulmonary:-:Point in time:^Patient:- and intestinal carcinoids by immunohistochemistry There is increased interest in the Bn-receptor family because they are frequently over/ectopically expressed by Neoplasms and thus useful as targets for imaging or receptor-targeted-cytotoxicity.  ML-18 is a non-peptide bombesin receptor subtype-3 antagonist which inhibits Primary malignant neoplasm of Chest>Lung growth. Gastrin releasing peptide gene 2 (Gastrin releasing peptide), a member of the bombesin family of peptides, has been shown to have mitogenic activity in small cell Chest>Lung carcinoma (Small cell carcinoma of Chest>Lung), and to be produced by Small cell carcinoma of Chest>Lung in an autocrine fashion.[SEP]Relations: small cell Chest>Lung carcinoma has relations: disease_protein with GRM8, disease_protein with GRM8, disease_protein with GRIK3, disease_protein with GRIK3, disease_protein with NPPA, disease_protein with NPPA, disease_protein with NDRG1, disease_protein with NDRG1. subtype 3 bombesin receptor binding has relations: molfunc_molfunc with bombesin receptor binding, molfunc_molfunc with bombesin receptor binding.", "label": "yes"}
{"original_question": "Is there any role of Dlx1 and Dlx2 transcription factors in cortical interneurons?", "id": "converted_67", "sentence1": "Is there any role of Homeobox Protein DLX-1 and DLX2 gene transcription factors in cortical interneurons?", "sentence2": "The postnatal functions of the Homeobox Protein DLX-1&2 transcription factors in cortical interneurons (CINs) are unknown. Here, using conditional Homeobox Protein DLX-1, DLX2 gene, and Homeobox Protein DLX-1&2 knockouts (CKOs), we defined their roles in specific CINs. The CKOs had dendritic, synaptic, and survival defects, affecting even PV+ CINs. We provide evidence that DLX2 directly drives glutamate decarboxylase 1 (brain, 67kDa), human, GAD2 gene, and SLC32A1 gene expression, and show that Mutant had reduced mIPSC amplitude. In addition, the Mutant formed fewer GABAergic synapses on excitatory neurons and had reduced mIPSC frequency. Furthermore, Homeobox Protein DLX-1/2 CKO had hypoplastic dendrites, fewer excitatory synapses, and reduced excitatory input. We provide evidence that some of these phenotypes were due to reduced expression of GRIN2B gene gene (a subunit of the N-Methyl-D-Aspartate Receptors), a high confidence Autism gene. Thus, Homeobox Protein DLX-1&2 coordinate key components of Cervical Intraepithelial Neoplasia postnatal development by promoting their excitability, inhibitory output, and survival. Furthermore, Homeobox Protein DLX-1/2 CKO had hypoplastic dendrites, fewer excitatory synapses, and reduced excitatory input.[SEP]Relations: GAD2 has relations: pathway_protein with MECP2 regulates transcription of genes involved in GABA signaling, pathway_protein with MECP2 regulates transcription of genes involved in GABA signaling, protein_protein with CPLX4, protein_protein with CPLX4, protein_protein with RHEX, protein_protein with RHEX, anatomy_protein_present with dorsolateral prefrontal cortex, anatomy_protein_present with dorsolateral prefrontal cortex. SLC32A1 has relations: anatomy_protein_present with dorsolateral prefrontal cortex, anatomy_protein_present with dorsolateral prefrontal cortex.", "label": "yes"}
{"original_question": "Does prolactinoma increase osteoporosis risk?", "id": "converted_68", "sentence1": "Does prolactinoma increase osteoporosis risk?", "sentence2": "Prolactinoma: A Massive Effect on Bone Mineral Density in a Young Patient. Encounter due to family history of osteoporosis has been noted to be an issue in postmenopausal women with prolactinomas. This case shows a similar impact on bone health in a young male resulting in low bone mineral density for age based on Z-score. This case report highlights the possible mechanisms for the Osteopenia in the setting of prolactinoma and the need for assessing bone health in such patients.  Hyperprolactinemia related to prolactinoma significantly (more than functional hyperprolactiaemia) increases the risk of osteopenia, osteoporosis and bone fractures.  Prolactinoma are the most common type of functional pituitary tumor. Effective hyperprolactinemia treatment is of great importance, due to its potential deleterious effects including Sterility, Reproductive, Gonadal Disorders and osteoporosis.  Prolactinoma cause Hypogonadism, Sterility, Reproductive, osteoporosis, and tumor mass effects, and are the most common type of Neuroendocrine Tumors. We present a 22-year-old man with multiple osteoporotic fractures associated with prolactinoma despite the use of teriparatide for 18 months. We emphasize and highlight the importance of hyperprolactinemia and fractures caused by high prolactin levels. OBJECTIVE: Patients with prolactinoma seem to be at high risk for osteopenia.  RESULTS: Compared to the matched controls, BMD of patients with prolactinoma or Craniopharyngioma significantly decreased.  CONCLUSION: In the premenopausal women, patients with prolactinoma or Craniopharyngioma are often accompanied with osteopenia or osteoporosis, and Disease duration and Hypogonadism are the risk factors of Osteopenia in prolactinoma. Data on osteoporotic fractures in hyperprolactinemia are limited. An increased prevalence of radiological Spinal Fractures was recently observed in women with prolactin (PRL)-secreting adenoma, whereas it is unknown whether this observation may reflect a more general increased risk of fractures in this Disease and whether the prevalence of fractures in males is affected by gonadal status. Prolactinoma presenting as chronic anaemia with osteoporosis: a case report. Six years later, he was evaluated and diagnosed with a prolactinoma and resultant osteoporosis. Prolactinoma in old people may present insidiously with chronic anaemia and osteoporosis with or without Sexual Dysfunction. The relative risk for developing osteoporosis in women with prolactinoma was found to be 4.5, indicating that hyperprolactinemia in women is a major risk factor for osteoporosis.<br> <b>INTRODUCTION</b>: Osteopenia and osteoporosis because of hyperprolactinaemia caused by prolactinoma may be followed by an increased risk of Fracture. Univariate and multivariate regression analysis indicated that the Osteopenia in prolactinomas was significantly correlated to Disease duration and Hypogonadism.<br><b>CONCLUSION</b>: In the premenopausal women, patients with prolactinoma or Craniopharyngioma are often accompanied with osteopenia or osteoporosis, and Disease duration and Hypogonadism are the risk factors of Osteopenia in prolactinoma. High serum prolactin levels lead to increase of the risk of osteopenia or/and osteoporosis. Prolactinoma in old people may present insidiously with chronic anaemia and osteoporosis with or without Sexual Dysfunction.<br><b>CASE PRESENTATION</b>: We describe the case of a 70-year-old Caucasian man who presented with mild anaemia and Fatigue. In the premenopausal women, patients with prolactinoma or Craniopharyngioma are often accompanied with osteopenia or osteoporosis, and Disease duration and Hypogonadism are the risk factors of Osteopenia in prolactinoma. The relative risk for developing osteoporosis in women with prolactinoma was found to be 4.5, indicating that hyperprolactinemia in women is a major risk factor for osteoporosis. CONCLUSION In the premenopausal women, patients with prolactinoma or Craniopharyngioma are often accompanied with osteopenia or osteoporosis, and Disease duration and Hypogonadism are the risk factors of Osteopenia in prolactinoma. Prolactinoma in old people may present insidiously with chronic anaemia and osteoporosis with or without Sexual Dysfunction. Hyperprolactinemia related to prolactinoma significantly (more than functional hyperprolactiaemia) increases the risk of osteopenia, osteoporosis and bone fractures. INTRODUCTION Osteopenia and osteoporosis because of hyperprolactinaemia caused by prolactinoma may be followed by an increased risk of Fracture. In conclusion, men with prolactinoma have high prevalence of osteopenia and osteoporosis. Homo sapiens with prolactinoma are at risk for osteoporosis. Osteopenia and osteoporosis because of hyperprolactinaemia caused by prolactinoma may be followed by an increased risk of Fracture. The relative risk for developing osteoporosis in women with prolactinoma was found to be 4.5, indicating that hyperprolactinemia in women is a major risk factor for osteoporosis.. In the premenopausal women, patients with prolactinoma or Craniopharyngioma are often accompanied with osteopenia or osteoporosis, and Disease duration and Hypogonadism are the risk factors of Osteopenia in prolactinoma.[SEP]Relations: Craniopharyngioma has relations: disease_phenotype_positive with Increased susceptibility to fractures, disease_phenotype_positive with Increased susceptibility to fractures. Teriparatide has relations: indication with osteoporosis, indication with osteoporosis, indication with postmenopausal osteoporosis, indication with postmenopausal osteoporosis. Osteopenia has relations: disease_phenotype_positive with prolactin producing pituitary gland tumor, disease_phenotype_positive with prolactin producing pituitary gland tumor. Prolactinoma has relations: disease_phenotype_positive with growth hormone secreting pituitary adenoma 1, disease_phenotype_positive with growth hormone secreting pituitary adenoma 1.", "label": "yes"}
{"original_question": "Is pregabalin effective for sciatica?", "id": "converted_69", "sentence1": "Is pregabalin effective for Sciatica?", "sentence2": "CONCLUSIONS: Treatment with pregabalin did not significantly reduce the intensity of leg pain associated with Sciatica and did not significantly improve other outcomes, as compared with placebo, over the course of 8 weeks. The incidence of adverse events was significantly higher in the pregabalin group than in the placebo group.  Whilst pregabalin (Prostaglandins B) and gabapentin (TMEM132A gene) are both used to treat Neuropathic pain, their relative role in Sciatica is unclear. TMEM132A gene and Prostaglandins B appeared to demonstrate comparable efficacy and FUT2 gene. However, the amount and quality of evidence was low, and only indirect comparisons were available.[SEP]Relations: Pregabalin has relations: drug_effect with Pancreatitis, drug_effect with Pancreatitis, drug_effect with Menorrhagia, drug_effect with Menorrhagia, drug_drug with Pridinol, drug_drug with Pridinol, drug_effect with Pneumonia, drug_effect with Pneumonia, drug_effect with Pain, drug_effect with Pain.", "label": "no"}
{"original_question": "Does MC1R palmitoylation reduce pigmentation?", "id": "converted_70", "sentence1": "Does Melanocyte-Stimulating Hormone Receptor, Homo sapiens palmitoylation reduce pigmentation?", "sentence2": "The Receptor, Melanocortin, Type 1 (Melanocyte-Stimulating Hormone Receptor, Homo sapiens), a G-Protein-Coupled Receptors, has a crucial role in Homo sapiens and Mus sp. pigmentation. Activation of Melanocyte-Stimulating Hormone Receptor, Homo sapiens in melanocyte by \u03b1-melanocyte-stimulating hormone (\u03b1-MSH) stimulates cAMP signalling and melanin production and enhances DNA repair after Ultra-violet irradiation.  Melanocyte-Stimulating Hormone Receptor, Homo sapiens palmitoylation, primarily mediated by the protein-acyl transferase ZDHHC13, is essential for activating Melanocyte-Stimulating Hormone Receptor, Homo sapiens signalling, which triggers increased pigmentation, Ultra-violet-B-induced G1-like cell cycle arrest and control of senescence and melanomagenesis in vitro and in vivo. The results highlight a central role for Melanocyte-Stimulating Hormone Receptor, Homo sapiens palmitoylation in pigmentation and protection against Melanocytic neoplasm.[SEP]Relations: melanocyte-stimulating hormone receptor activity has relations: molfunc_protein with Melanocyte-Stimulating Hormone Receptor, Homo sapiens, molfunc_protein with Melanocyte-Stimulating Hormone Receptor, Homo sapiens, molfunc_protein with MC3R, molfunc_protein with MC3R, molfunc_protein with MC4R, molfunc_protein with MC4R. melanocyte adhesion has relations: bioprocess_protein with KIT, bioprocess_protein with KIT. type 1 melanocortin receptor binding has relations: molfunc_protein with MRAP2, molfunc_protein with MRAP2.", "label": "no"}
{"original_question": "Is Tocilizumab effective for Giant-Cell Arteritis?", "id": "converted_71", "sentence1": "Is tocilizumab effective for Giant-Cell Arteritis?", "sentence2": "Emerging evidence for adjunctive therapy with tocilizumab, methotrexate, aspirin, Angiotensin Receptor Antagonists, and Hydroxymethylglutaryl-CoA Reductase Inhibitors is encouraging and may lead to a more mainstream role for these therapies among patients with glutaryl-7-aminocephalosporanic-acid acylase activity.  TNF-\u03b1 blockers are ineffective in giant cell arteritis, while observational evidence and a phase 2 randomized trial support the use of tocilizumab in relapsing giant cell arteritis.  OBJECTIVES: Randomised-controlled trials have recently proven the efficacy of the interleukin (IL)-6 receptor antagonist tocilizumab (TCZ) in giant cell arteritis (glutaryl-7-aminocephalosporanic-acid acylase activity).  CONCLUSIONS: TCZ may exert its therapeutic effects in glutaryl-7-aminocephalosporanic-acid acylase activity by increasing the proliferation and activation of Tregs, and by reverting the Pathogenic Variant Treg phenotype seen during active disease. cyclophosphamide and tocilizumab look promising but require validation in further studies.  Therefore, tocilizumab (humanised monoclonal antibody binding the human interleukin-6 receptor) was introduced as a potential salvage therapy with a swift consecutive resolution of the systemic symptoms and stabilization of the ophthalmic lesions.CONCLUSIONS: Although a late effect of steroids pulses cannot be formally ruled out in this dramatic situation, tocilizumab likely offered a decisive effect in preventing bilateral Blindness and may have contributed to steroid tapering. tocilizumab may represent a new early effective second-line treatment option in corticosteroid-resistant anterior ischemic optic neuropathy.  tocilizumab for giant cell arteritis with corticosteroid-resistant progressive anterior ischemic optic neuropathy. CONCLUSIONS: tocilizumab, received weekly or every other week, combined with a 26-week prednisone taper was superior to either 26-week or 52-week prednisone tapering plus placebo with regard to sustained glucocorticoid-free remission in patients with giant-cell arteritis. Longer follow-up is necessary to determine the durability of remission and safety of tocilizumab. Two RCTs have evidenced the efficacy of tocilizumab in addition to Glucocorticoid inhalants for obstructive airway disease (Ceramide Glucosyltransferase, human) in the treatment of giant cell arteritis (glutaryl-7-aminocephalosporanic-acid acylase activity).  Recent randomized placebo-controlled trials have reported on the efficacy and safety of abatacept and mostly tocilizumab in inducing and maintaining remission of glutaryl-7-aminocephalosporanic-acid acylase activity.  If a biological therapy is indicated, and in light of the data discussed in this review, the first choice would be tocilizumab in glutaryl-7-aminocephalosporanic-acid acylase activity and anti-TNF-\u03b1 agents (mainly infliximab) in CDK9 wt Allele. CONCLUSION: TCZ is effective in glutaryl-7-aminocephalosporanic-acid acylase activity. TNF-\u03b1 blockers are ineffective in giant cell arteritis, while observational evidence and a phase 2 randomized trial support the use of tocilizumab in relapsing giant cell arteritis. A favorable outcome was rapidly observed both on clinical and biological data allowing a corticoid therapy sparing.<br><b>CONCLUSION</b>: tocilizumab is a promising treatment of giant cell arteritis but controlled trials are needed to confirm its efficacy.<br> <b>INTRODUCTION</b>: Treatment of giant cell arteritis is based on prolonged corticosteroid therapy but adverse side effects are common especially in the elderly.<br><b>CASE REPORTS</b>: We report three patients with giant cell vasculitis treated by tocilizumab, an interleukin-6 receptor antibody, owing to resistance or intolerance to corticosteroid therapy. Several studies have reported that tocilizumab is effective for Aortitis associated with Takayasu Arteritis and giant cell arteritis. TNF-\u03b1 blockers are ineffective in giant cell arteritis, while observational evidence and a phase 2 randomized trial support the use of tocilizumab in relapsing giant cell arteritis. Preliminary clinical trial data suggest that abatacept and tocilizumab reduce the risk of relapse in glutaryl-7-aminocephalosporanic-acid acylase activity. tocilizumab, an effective treatment for relapsing giant cell arteritis. TNF-\u03b1 blockers are ineffective in giant cell arteritis, while observational evidence and a phase 2 randomized trial support the use of tocilizumab in relapsing giant cell arteritis. tocilizumab is a promising treatment of giant cell arteritis but controlled trials are needed to confirm its efficacy.[SEP]Relations: tocilizumab has relations: indication with temporal arteritis, indication with temporal arteritis, drug_drug with Artemether, drug_drug with Artemether, drug_drug with Otelixizumab, drug_drug with Otelixizumab, drug_drug with Ceritinib, drug_drug with Ceritinib, indication with Castleman disease, indication with Castleman disease.", "label": "yes"}
{"original_question": "Are AAV vectors considered for the treatment of retinal dystrophies?", "id": "converted_72", "sentence1": "Are AAV vectors considered for the treatment of Retinal Dystrophies?", "sentence2": "These novel gene vectors aim to more safely and efficiently transduce retinal cells, expand the gene packaging capacity of AAV, and utilize new strategies to correct the varying mechanisms of dysfunction found with inherited Retinal Dystrophies.[SEP]Relations: retinal dystrophy in systemic or cerebroretinal lipidoses has relations: disease_disease with retinal cone dystrophy, disease_disease with retinal cone dystrophy.", "label": "yes"}
{"original_question": "Is Brucella abortus the organism that causes brucillosis known to cause spontaneous abortions in humans?", "id": "converted_73", "sentence1": "Is Brucella species abortus the organism that causes brucillosis known to cause spontaneous Abortions:Number:Point in time:^Patient:Quantitative:Reported in Homo sapiens?", "sentence2": ". Brucellosis is a major cause of Fever of unknown origin (Pyrexia of unknown origin (excl puerperal)) Brucellosis is the most common Bacterial Zoonoses, and causes a considerable burden of Disease in endemic countries. Cardiovascular involvement is the main cause of mortality due to Communicable Diseases with Brucella species species spp, quite abruptly, he developed Asthenia and Hypersomnia without any apparent cause or symptoms like Fever symptoms (finding), Chills, or night Sweating. On November 14, 2009, he suffered from Pain:-:Point in time:^Patient:- and Edema:Finding:Point in time:^Patient:Ordinal in the right testicle that coincided with Pain:-:Point in time:^Patient:- in the Abdominal Cavity. Clinical, serological, and bacteriological investigations confirmed the first case of unilateral orchitis in man in Ecuador caused by Brucella species species abortus biovar 1 Brucellosis is not frequent in Chile but it may present with life threatening complications like Endocarditis. Human brucellosis exhibits diverse pathological manifestations that can affect almost any Organ. In particular, osteoarticular complications are the most common focal manifestation of brucellosis and occur in 40-80% of patients. Brucella species species. Human brucellosis often makes the diagnosis difficult. The symptoms and clinical signs most commonly reported are Fever symptoms (finding), Fatigue, Malaise, Chills, Sweating Headache, Myalgia, Arthralgia, and Measured Measured weight loss (observable entity) (observable entity). Some cases have been presented with only joint Pain:-:Point in time:^Patient:-, lower backache, and involuntary limb movement, burning feet, or ischemic heart attacks.  Forty-five cases were collected (31 acute and 14 sub-acute). Contamination was digestive in 62%. Symptoms of patients were Fever symptoms (finding) (93%), sweating (82%), Arthralgia (78%) and Splenomegaly (51%). Elevated Erythrocytes sedimentation rate was determined in 80%, White blood cell count decreased in 49% and Anemia in 37% of cases. Blood culture were positives in 39% of cases. The four sequenced strains were identified as Brucella species species melitensis biovar abortus.  It is also known to cause persistent Brucellosis, Endocarditis, Arthritis, Osteomyelitis and Meningitis in Homo sapiens. Brucella species species abortus is a Gram-negative Protoplasm bacterial pathogen that causes a zoonosis of worldwide occurrence, leading to Brucellosis in Homo sapiens and Unspecified Abortion in domestic animals. Brucella species species abortus is a facultative Protoplasm bacterial pathogen that causes Unspecified Abortion in domestic animals and Brucellosis in Homo sapiens. Brucella species species abortus is a facultative, Protoplasm zoonotic pathogen which can cause Brucellosis in Homo sapiens and Abortions:Number:Point in time:^Patient:Quantitative:Reported in Bos taurus. Brucella species species abortus is a Gram-negative, facultative Protoplasm bacterium that causes brucellosis, a worldwide zoonotic Disease leading to Brucellosis in Homo sapiens and Unspecified Abortion in Bos taurus. Brucella species species abortus is a facultative Protoplasm bacterial pathogen that causes Unspecified Abortion in domestic animals and Brucellosis in Homo sapiens. Brucella species species abortus is a gram-negative, facultative Protoplasm pathogen that causes brucellosis, a chronic zoonotic Disease resulting in Unspecified Abortion in pregnant Bos taurus and Brucellosis in Homo sapiens. Brucella species species abortus is a bacterium which causes Abortions:Number:Point in time:^Patient:Quantitative:Reported and Sterility, Reproductive in Bos taurus and Brucellosis in Homo sapiens. Brucella species species abortus is the etiologic agent of bovine brucellosis and causes a Chronic Disease in Homo sapiens known as Brucellosis. No case of acute Brucella species species Communicable Diseases was demonstrated; however, there were 5 cases in which the serological finding was consistent with chronic brucellosis (4%). In all these cases no positive evidence of close Animal allergens contact could be found; furthermore of the 12,1% of women who actually handled domestic animals, only 1 had a history of previous Unspecified Abortion[SEP]Relations: brucellosis has relations: disease_phenotype_positive with Spontaneous Unspecified Abortion, disease_phenotype_positive with Spontaneous Unspecified Abortion, disease_disease with Brucella species brucellosis, disease_disease with Brucella species brucellosis, disease_disease with Brucella species melitensis brucellosis, disease_disease with Brucella species melitensis brucellosis, disease_disease with brucellosis, bovine, disease_disease with brucellosis, bovine. Brucella species melitensis brucellosis has relations: disease_disease with brucellosis, disease_disease with brucellosis.", "label": "no"}
{"original_question": "Is Cystatin D a biomarker?", "id": "converted_74", "sentence1": "Is CST5 gene a biomarker?", "sentence2": "CST5 gene (CST5): An ultra-early inflammatory biomarker of Traumatic Brain Injury.[SEP]Relations: brain injury has relations: contraindication with Cyclopentolate, contraindication with Cyclopentolate, contraindication with Isopropamide, contraindication with Isopropamide, contraindication with Guaifenesin, contraindication with Guaifenesin, contraindication with Homatropine methylbromide, contraindication with Homatropine methylbromide, contraindication with Hydrocodone, contraindication with Hydrocodone.", "label": "yes"}