{"original_question": "Is it possible to detect survivin protein expression in normal human adult tissues?", "id": "converted_432", "sentence1": "Is it possible to detect survivin protein expression in normal Homo sapiens adult Body tissue?", "sentence2": "BIRC5 protein, Homo sapiens wt Allele (BIRC5 protein, Homo sapiens protein, Homo sapiens) is one of the members of IAP-family apoptosis inhibitors. The BIRCS gene is expressed in most Homo sapiens embryonic Body tissue and Malignant Neoplasms but not in normal differentiated Body tissue of adult Homo sapiens., BIRC5 protein, Homo sapiens wt Allele is an PPP1R1A gene of apoptosis that is undetectable in most terminally differentiated normal Homo sapiens Body tissue, strongly expressed in embryonic and fetal organs and is strongly expressed in many different Homo sapiens cancers., BIRC5 protein, Homo sapiens wt Allele is a member of the PPP1R1A gene apoptosis family that is overexpressed in many malignancies. It has five known alternative splice forms, some of which differ in their antiapoptotic properties and expression levels in Homo sapiens cancers., survivin is usually not expressed in normal adult Body tissue,, AZD 1152-hQPA induced caspase-dependent apoptosis of some Cultured Cell Line, demonstrated by loss of Mitochondrial Membranes potential, activation of caspase-9, followed by activation of caspase-3. This effect was accompanied by the inhibition of survivin expression. In vivo efficacy was determined in NOD/SCID/γc(null) mice implanted with the Ramos Homo sapiens Burkitt Lymphoma cell line. AZD 1152 had anti-tumour effects in this Mus xenograft model. There preclinical data suggest that the inhibition of Aurora Kinase B is a potentially useful therapeutic strategy in Burkitt Lymphoma and Hodgkin Disease., a novel antiapoptosis gene, i.e., survivin, was identified as a structurally unique member of the PPP1R1A gene of apoptosis protein family. BIRC5 protein, Homo sapiens wt Allele expression is turned off during fetal development and not found in non-neoplastic adult Homo sapiens Body tissue but is again turned on in the most common Homo sapiens cancers. The antiapoptotic properties of survivin might provide a significant growth advantage in Neoplasms and possibly also contribute to chemoresistance of Primary malignant neoplasm., Further comparison of the distribution of SPDEF wt Allele with other widely recognized Primary malignant neoplasm-associated molecules showed that SPDEF wt Allele has more restricted distributions than Oncogene ErbB2, BCL2 gene, survivin or Telomerase in cDNA Library from normal Homo sapiens Body tissue and more increased distribution than Oncogene ErbB2, CA-125 Antigen Antigen, BCL2 gene, survivin and Telomerase in cDNA Library from Head>Brain (except survivin), Breast, Chest>Lung and ovarian neoplasm. These data together show a better tumor-association for SPDEF wt Allele and suggest that SPDEF wt Allele is a more suitable target for developing specific Primary malignant neoplasm therapies., we identified decreased FHIT protein, Homo sapiens protein, Homo sapiens expression resulting in apoptosis inhibition and decreasing apoptosis associated with abnormal levels of some pro- and Apoptosis Inhibiting Proteins (BAX protein, Homo sapiens, BCL2 gene and BIRC5 protein, Homo sapiens wt Allele) by TUNEL and Thrombotic Microangiopathies. Our results demonstrated that the Mutation Abnormality in the FHIT protein, Homo sapiens protein, Homo sapiens gene significantly reduced FHIT protein, Homo sapiens protein, Homo sapiens expression in Homo sapiens CRC. Both TUNEL and Thrombotic Microangiopathies experiments demonstrated significantly inhibited apoptosis by down-regulation of BAX protein, Homo sapiens and up-regulation of BIRC5 protein, Homo sapiens wt Allele and BCL2 gene. Collectively, these studies identify the mechanism by which an important Tumor Suppressor Genes, FHIT protein, Homo sapiens protein, Homo sapiens, inactivated specifically in Homo sapiens CRC, and contributes to our understanding of the mechanism of colorectal carcinogenesis.[SEP]", "label": "no"}
{"original_question": "Can a peptide aptamer be used as protein inhibitor?", "id": "converted_533", "sentence1": "Can a Peptides aptamer be used as Protein Info inhibitor?", "sentence2": "Peptide aptamers of LIM-only Protein Info 2 (Rhombotin 2) were previously used to successfully treat Rhombotin 2-induced tumours in a mouse model of leukemia., Inhibition of mammalian cell proliferation by genetically selected Peptides aptamers that functionally antagonize E2F activity., Accumulating work over the past decade has shown that Peptides aptamer screening represents a valid strategy for inhibitor identification that can be applied to a variety of different targets. , . The target of one inhibitor Peptides, Pep80, identified in this screen was determined to be SNAPIN gene, a Protein Info associated with the soluble N-ethyl maleimide sensitive factor adaptor Protein Info receptor (SNAP receptor activity) complex that is critical for calcium-dependent exocytosis during neurotransmission. , Use of the genetically selected intracellular aptamer inhibitors allowed us to define unique mechanisms important to HIV-1 replication and T cell biology., This review will describe pre-clinical and clinical data of four major classes of TGF-β inhibitor, namely i) ligand traps, ii) Antisense Oligonucleotides, iii) receptor kinase inhibitors and iv) Peptides aptamers. ,  A Peptides aptamer (ID1/3-PA7) has been designed to prevent this interaction and thereby leading to the transcription of p16(INK4a)., A Peptides kinase inhibitor (IP(20)) was used as the aptameric Peptides , Peptide aptamer mimicking RAD51-binding Superkingdom (taxonomic category) of BRCA2 gene gene inhibits DNA damage repair and survival in Trypanosoma brucei brucei brucei.,  Peptides aptamer, ID1 Protein Info, human/3-PA7, targeting ID1 Protein Info, human and DNA-Binding Protein Inhibitor ID-3,, Targeting ID1 Protein Info, human and DNA-Binding Protein Inhibitor ID-3 by a specific Peptides aptamer induces E-box promoter activity, cell cycle arrest, and apoptosis in breast cancer Cells., Aptamer-derived peptides as potent inhibitors of the oncogenic guanyl-nucleotide exchange factor activity Tgat., Our approach thus demonstrates that Peptides aptamers are potent inhibitors that can be used to interfere with guanyl-nucleotide exchange factor activity functions in vivo., Development of systemic in vitro evolution and its application to generation of Peptides-aptamer-based inhibitors of carboxypeptidase C E., he fusion Peptides, cytarabine/thioguanine aptamer, was observed within PC12 cytoplasm and maintained both Abeta-binding ability and antioxygenic property similar to TXN wt Allele., Stable expression of a novel fusion Peptides of Thioredoxin 1 and ABAD-inhibiting Peptides protects PC12 Cells from intracellular amyloid-beta., In order to efficiently select aptamers that bind to and inhibit proteins,, Aptamer selection based on inhibitory activity using an evolution-mimicking algorithm., This demonstrates the utility of this strategy for screening aptamers based on their inhibitory actions., Protoplasm expression of the DRD-binding Peptides aptamer specifically suppressed receptor-mediated extrinsic apoptosis but not intrinsic pathway, which was recapitulated by the Antisense Oligonucleotides for CASP8AP2 wt Allele. , Peptide aptamers are peptides constrained and presented by a scaffold Protein Info that are used to study Protein Info function in Cells. They are able to disrupt Protein Info-Protein Info interactions , Here we have used a genetic screen in Saccharomyces cerevisiae to select in vivo peptides coupled to Thioredoxin (human), called aptamers, that could inhibit GEFD2 activity. One aptamer, TRIAPalpha (TRio Inhibitory APtamer), specifically blocks GEFD2-exchange activity on RHOA Protein Info, human in vitro., These results show that cell proliferation can be inhibited using genetically-selected synthetic peptides that specifically target Protein Info-Protein Info interaction motifs within cell cycle regulators., These data highlight the utility of Peptides aptamers to identify novel binding interfaces and highlight a role for microtubule-associated Protein Info 1B in DAPK-1-dependent signaling in autophagy and Membrane Device blebbing.[SEP]Relations: Protein Info binding has relations: molfunc_protein with microtubule-associated Protein Info 1B, molfunc_protein with microtubule-associated Protein Info 1B.", "label": "yes"}
{"original_question": "Does the CTCF protein co-localize with cohesin?", "id": "converted_95", "sentence1": "Does the CTGF protein, Homo sapiens protein co-localize with cohesins?", "sentence2": "To investigate cohesins-non-CTGF protein, Homo sapiens (CNC) binding events in vivo we mapped cohesins and CTGF protein, Homo sapiens, as well as a collection of tissue-specific and ubiquitous transcriptional regulators using Chromatin Immunoprecipitation Sequencing in primary Mus sp. liver., In contrast to regions of the Genome - anatomical entity where cohesins and CTGF protein, Homo sapiens colocalize, CNC Site coincide with the binding of master regulators and enhancer-markers and are significantly associated with liver-specific expressed genes., Here we report that cohesins colocalize with CTGF protein, Homo sapiens at two additional imprinted loci, the Dlk1-Dio3 and the Kcnq1/Kcnq1ot1 loci., By use of Homo sapiens hepatocellular carcinoma cells (HepG2), we found that liver-specific transcription factors colocalize with cohesins independently of CTGF protein, Homo sapiens at liver-specific targets that are distinct from those found in breast cancer cells, Because cohesins can colocalize with CTGF protein, Homo sapiens, we performed chromatin location location immunoprecipitation for the cohesins subunit Rad21 and found lineage and stage-specific Rad21 recruitment to CTGF protein, Homo sapiens in all Ig loci, Here we show that zebrafish RUNX1 protein, Homo sapiens is directly bound by cohesins and CCCTC-binding factor (CTGF protein, Homo sapiens) at the Blood group antigen Blood group antigen P1 and Bone structure of middle phalanx promoters, and within the Introns between Blood group antigen Blood group antigen P1 and Bone structure of middle phalanx., The intronic Binding Sites for cohesins and CTGF protein, Homo sapiens coincide with histone modification that confer enhancer-like properties, and two of the cohesins/CTGF protein, Homo sapiens Site behaved as insulators in an in vivo assay, The identified cohesins and CTGF protein, Homo sapiens Binding Sites are likely to be cis-regulatory elements (CST8 gene) for RUNX1 protein, Homo sapiens since they also recruit RNA Polymerase II (RNAPII)., We have found that CTGF protein, Homo sapiens and cohesins are highly enriched at the convergent and partially overlapping RNA Transcript for the PDLIM7 gene and LMP2A genes, but it is not yet known how CTGF protein, Homo sapiens and cohesins may coordinately regulate these RNA Transcript, haracterization of constitutive CTGF protein, Homo sapiens/cohesins loci: a possible role in establishing topological domains in mammalian Genome, Our analysis revealed: 1) constitutive CTGF protein, Homo sapiens loci were located in constitutive open chromatin location location and often co-localized with constitutive cohesins loci, In Head>Brain, a third of CTGF protein, Homo sapiens and cohesins Binding Sites coincide, consistent with the potential for many interactions between cohesins and CTGF protein, Homo sapiens but also many instances of independent action, Here, we focus on the emerging roles of CTGF protein, Homo sapiens and the cohesins in coordinating long-range interactions between regulatory elements, Chromatin immunoprecipitation for CTGF protein, Homo sapiens and the cohesins subunits Double-Strand-Break Repair Protein Rad21 Homolog and SMC3 wt Allele wt Allele reveals evolutionarily conserved Binding Sites within unmethylated regions ∼5 kb downstream of the PLAGL1 gene gene differentially methylated region and within the PLAGL1 gene gene 3' untranslated region (SLC14A2 gene), TCF physically links cohesins to chromatin location location, ohesin and CTGF protein, Homo sapiens: cooperating to control chromosome conformation?, Recently, three groups mapped numerous cohesins-Binding Sites in mammalian chromosomes and found substantial overlap with the CCCTC-binding factor (CTGF protein, Homo sapiens), We found that each Specimen Source Codes - Site contains a conserved CTGF protein, Homo sapiens consensus sequence, binds CTGF protein, Homo sapiens, and recruits the cohesins subunit Rad21 in vivo, Recent experiments have revealed that cohesins binds to the same Site in mammalian Genome as the zinc finger transcription factor CTGF protein, Homo sapiens, Here we review what is known about the roles of cohesins and CTGF protein, Homo sapiens in regulating gene expression in mammalian cells, and we discuss how cohesins might mediate the insulator function of CTGF protein, Homo sapiens, Previous studies have shown that this major latency control region is occupied by the Cells chromatin location location boundary factor CTGF protein, Homo sapiens and chromosome structural maintenance proteins SMITH-MCCORT DYSPLASIA 1, SMC3 wt Allele wt Allele, and Double-Strand-Break Repair Protein Rad21 Homolog, which comprise the cohesins complex, Cohesin subunits assembled at the CTGF protein, Homo sapiens Binding Sites and bound CTGF protein, Homo sapiens proteins in a cell cycle-dependent manner, We propose that the CTGF protein, Homo sapiens-cohesins complex plays a critical role in regulating the cell cycle control of Genes, Viral expression during latency and that failure to maintain cell cycle control of latent RNA Transcript inhibits host cell proliferation and survival, We used chromosome conformation capture to determine long-range interactions among CTGF protein, Homo sapiens/cohesins Site over 2 Mb on Homo sapiens chromosome 11 encompassing the beta-globin Gene Locus and Flank (surface region) olfactory receptor genes, These results support a Genome - anatomical entity-wide role for CTGF protein, Homo sapiens/cohesins Site through loop formation that both influences transcription and contributes to cell-type-specific chromatin location location organization and function, Increased methylation at this Promoter triggered the dissociation of the insulator protein CTGF protein, Homo sapiens as well as the accompanying cohesins from the BDNF Gene Locus, icotinamide adenine dinucleotide (NAD)-regulated DNA methylation alters CCCTC-binding factor (CTGF protein, Homo sapiens)/cohesins binding and transcription at the BDNF Gene Locus, ecent studies have shown that the protein CTGF protein, Homo sapiens, which plays an important role in insulation and in large-scale organization of chromatin location location within the eukaryotic nucleus, depends for both activities on recruitment of the cohesins complex, We show here that the interaction of CTGF protein, Homo sapiens with the cohesins complex involves direct contacts between the cohesins subunit STAG2 wt Allele and specific regions of the C-terminal tail of CTGF protein, Homo sapiens, Taken together, our results demonstrate that specific Site on the C terminus of CTGF protein, Homo sapiens are essential for cohesins binding and insulator function, The only direct interaction between CTGF protein, Homo sapiens and cohesins involves contact with STAG2 wt Allele, which is external to the cohesins ring, These numerous CTGF protein, Homo sapiens/cohesins Site potentially form the Unit dose - Base of the multiloop rosette structures at the Igh Gene Locus that compact during Ig heavy chain rearrangement, We have previously shown that the Homo sapiens herpesvirus 8 (KSHV) major latency RNA Transcript encoding latent Orf73 antigen, Homo sapiens herpesvirus 8, vCyclin, FLICE Inhibitory Protein, v-miRNAs, and Kaposin are regulated, in part, by a chromatin location location organizing element that binds CTGF protein, Homo sapiens and cohesins, Mutation Abnormality Abnormality of the CTGF protein, Homo sapiens-cohesins binding Specimen Source Codes - Site reduced or eliminated the chromatin location location conformation linkages, and deregulated Viral transcription and Genome - anatomical entity copy number control, Our findings indicate that KSHV Genome are organized into chromatin location location loops mediated by CTGF protein, Homo sapiens and cohesins interactions, and that these inter-chromosomal linkages coordinate latent and lytic gene control., We show here that Gestational age:Time:Point in time:^Fetus:Quantitative disrupts an RNA Polymerase II (RNAPII) complex that accumulates at the CTGF protein, Homo sapiens-cohesins binding Specimen Source Codes - Site within the first Introns of the latency transcript., Gestational age:Time:Point in time:^Fetus:Quantitative altered the enrichment of the RNAPII pausing complex, along with pausing factors SUPT5H gene and WHSC2 protein, Homo sapiens, at the intragenic CTGF protein, Homo sapiens-cohesins Binding Sites., Gestational age:Time:Point in time:^Fetus:Quantitative treatment also inhibited the transcription of some Cells genes, like c-myc Genes Genes, which contain a similar CTGF protein, Homo sapiens-cohesins binding Specimen Source Codes - Site within the first Introns., These findings suggest that RNAPII pauses at intragenic CTGF protein, Homo sapiens-cohesins Binding Sites and that abrogation of this pausing by Gestational age:Time:Point in time:^Fetus:Quantitative leads to loss of proper mRNA production and defects in sister chromatid cohesion, a process important for both Viral and Cells chromosome stability., TCF and cohesins cooperatively mediate the cell-type specific interchromatin interaction between B-Cell Lymphoma/Leukemia 11B and ARHGAP6 gene loci, Additional experiments verified that the interchromatin interaction between the B-Cell Lymphoma/Leukemia 11B and ARHGAP6 gene loci was cell-type specific, which was cooperatively mediated by CTGF protein, Homo sapiens and cohesins., enome-wide studies of CCCTC-binding factor (CTGF protein, Homo sapiens) and cohesins provide insight into chromatin location location structure and regulation, Recent Genome - anatomical entity-wide studies mapping the Binding Sites of CTGF protein, Homo sapiens and its interacting partner, cohesins, using chromatin location location immunoprecipitation coupled with deep sequencing (Chromatin Immunoprecipitation Sequencing) revealded that CTGF protein, Homo sapiens globally co-localizes with cohesins, Here, we show by ChIP-Seq that most Homo sapiens subtelomeres contain a CTGF protein, Homo sapiens- and cohesins-binding Specimen Source Codes - Site within ∼1-2 kb of the TTAGGG repeat tract and adjacent to a CpG-islands implicated in Telomeric Repeat-Containing RNA transcription control., These findings indicate that CTGF protein, Homo sapiens and cohesins are integral components of most Homo sapiens subtelomeres, and important for the regulation of Telomeric Repeat-Containing RNA transcription and telomere end protection, In addition, we show that this DNA looping requires specific binding of the CTGF protein, Homo sapiens/cohesins complex to two symmetrically aligned Binding Sites in both the transcriptionally active promoters and in one of the enhancers[SEP]Relations: cohesins complex has relations: cellcomp_protein with Double-Strand-Break Repair Protein Rad21 Homolog, cellcomp_protein with Double-Strand-Break Repair Protein Rad21 Homolog.", "label": "yes"}
{"original_question": "Does bleomycin cause lung toxicity?", "id": "converted_4311", "sentence1": "Does bleomycin cause Chest>Lung Toxic effect?", "sentence2": "bleomycin-induced Pulmonary:-:Point in time:^Patient:- Fibrosis, bleomycin (BLM)-induced Pulmonary:-:Point in time:^Patient:- , Pulmonary Toxic effect is a devastating complication of bleomycin chemotherapy. , Bleomycin containing regimen is routinely employed in the treatment of Hodgkin Disease. Pulmonary Toxic effect due to this Pharmacologic Substance is the most feared side effect in these regimens where the mortality rate is approximately 2%-3%. , Bleomycin might cause Pulmonary:-:Point in time:^Patient:- Fibrosis at higher cumulative doses as toxic effect directly to the Lung or most likely in addition by the formation of vascular microthrombi., The comparative Pulmonary:-:Point in time:^Patient:- Toxic effect induced by bleomycin and talisomycin (former trivial name: tallysomycin A) was evaluated by measuring Chest>Lung hydroxyproline content., Clinicians should always remember that bleomycin Toxic effect may lead to fatal complications in patients with comorbid conditions., CONTEXT: The application of bleomycin is limited due to its side effects including Chest>Lung Toxic effect., Bleomycin is an antineoplastic agent that causes a dose-related Chest>Lung Fibrosis that limits its therapeutic effectiveness., Acute Lung Toxicity After Intralesional Bleomycin Sclerotherapy., We report a case of a severe acute Chest>Lung Toxic effect after a low dose of a second bleomycin intralesional injection in a 5-year-old girl., Renal damage, following cisplatin administration, with subsequent accumulation of bleomycin was the likely cause of the high Chest>Lung Toxic effect., Whenever possible, bleomycin should precede cisplatin infusion to minimize the risk of Chest>Lung Toxic effect., The most severe form of BLM-induced Pulmonary:-:Point in time:^Patient:- Toxic effect is Chest>Lung Fibrosis., Results from this study suggest that an excess production of Superoxides anions by Macrophages, Alveolar may be the underlying cause of bleomycin Pulmonary:-:Point in time:^Patient:- Toxic effect., Bleomycin Chest>Lung Toxic effect is well established and can manifest as bleomycin-induced pneumonitis, but Mediastinal Emphysema and Pneumothorax are very rare complications., High doses of bleomycin administered to patients with Lymphoma and other Neoplasms lead to significant Chest>Lung Toxic effect in general, and to apoptosis of Epithelial Cells, in particular. , sis of bleomycin-induced Chest>Lung Toxic effect is based on the combination of clinical and radiological features, and requires to rule out differential diagnoses including Pneumocystis jiroveci pneumonia. \"Bleo, doxorubicin, bleomycin, vinblastine sulfate, and dacarbazine (bleomycin/dacarbazine/doxorubicin/vinblastine protocol) is associated with severe Toxic effect in older patients, particularly from bleomycin-induced Chest>Lung Toxic effect (Balanced ligamentous tension technique (procedure)). Ther, s studies have proposed that the Chest>Lung Toxic effect caused by bleomycin is related to the C-terminal regions of these drugs, which have been shown to closely interact with DNA in metal-bleomycin-DNA complexes. Some o, OBJECTIVES: Bleomycin, etoposide, and cisplatin (BEP regimen regimen) is the most common and successful chemotherapy regimen for germ-cell tumor (GCT) patients, accompanied by a bleomycin-induced dose-dependent Chest>Lung Toxic effect in certain pat, e been no respiratory problems attributable to bleomycin Chest>Lung Toxic effect in this study compared with four (3 associated with patient deaths) seen in 91 previously treated patients. The relat, Mechanisms of bleomycin-induced Chest>Lung damage., Previous studies have proposed that the Chest>Lung Toxic effect caused by bleomycin is related to the C-terminal regions of these drugs, which have been shown to closely interact with DNA in metal-bleomycin-DNA complexes., g V30 cutoff value of 32% was estimated.CONCLUSION: Bleomycin and RT may cause Lung Injury , Postmortem Chest>Lung studies were performed in all six patients and revealed findings compatible with bleomycin-induced Chest>Lung Toxic effect., However, the cytotoxic effects of bleomycin cause a number of adverse responses, in particular in the Chest>Lung and the Skin Specimen Source Code., Bleomycin, a widely used anti-Primary malignant neoplasm Pharmacologic Substance, may give rise to Pulmonary:-:Point in time:^Patient:- Fibrosis, a serious side effect which is associated with significant morbidity and mortality., Bleomycin is a Primary malignant neoplasm therapeutic known to cause Lung Injury which progresses to Fibrosis., and repair. Bleomycin Pulmonary:-:Point in time:^Patient:- Toxic effect is mediated, at least in part, by the generation of active oxy, This report suggests that bleomycin Chest>Lung Toxic effect may be reversible if treated aggressively., Although all bleomycin-treated animal allergen extracts had some evidence of Chest>Lung Toxic effect, histologic examination of the Lung revealed markedly reduced bleomycin Toxic effect in the rats exposed to Hypoxia, CTCAE., Low temperature inhibits bleomycin Chest>Lung Toxic effect in the Rattus norvegicus., Results at day 22, 3 wk after bleomycin treatment, showed that airway delivery of Liposomes before and after intratracheal administration of bleomycin significantly reduced bleomycin-induced Chest>Lung Toxic effect as evidenced by less body weight loss, chronic Chest>Lung inflammation, and Fibrosis as well as improved Chest>Lung compliance compared with controls., Protective effect of Hypoxia, CTCAE on bleomycin Chest>Lung Toxic effect in the Rattus norvegicus., acetylcysteine (doxorubicin/lomustine/mechlorethamine protocol) has recently been shown to have antioxidant properties, and since bleomycin produces Pulmonary:-:Point in time:^Patient:- damage via free oxygen radical Toxic effect, the possible protective effect of doxorubicin/lomustine/mechlorethamine protocol on bleomycin Chest>Lung Toxic effect was investigated., All rats treated with bleomycin only had typical changes of bleomycin Chest>Lung Toxic effect whereas the animal allergen extracts treated with bleomycin and doxorubicin/lomustine/mechlorethamine protocol had minimal pathology., atic compliance on day 15 was severely decreased with bleomycin alone and showed a further significant decrease when Granulocyte Colony-Stimulating Factor was added (controls, 3.85 +/- 0.14 mL/kPa; bleomycin, 1.44 +/- 0.06 mL/kPa; and bleomycin + Granulocyte Colony-Stimulating Factor, 0.65 +/- 0.09 mL/kPa; control vs. bleomycin, p <.0001; and bleomycin vs. bleomycin + Granulocyte Colony-Stimulating Factor, p =.0003). Lung m, Bleomycin sometimes causes fatal Pulmonary:-:Point in time:^Patient:- Toxic effect, including bleomycin-induced pneumonitis., Bleomycin is an antineoplastic agent causing fatal Pulmonary:-:Point in time:^Patient:- Toxic effect., Pulmonary Toxic effect is an important adverse effect of bleomycin treatment., Pulmonary Toxic effect is the most significant complication of bleomycin administration., It is possible, however, that the low incidence of clinically significant and fatal Pulmonary:-:Point in time:^Patient:- Toxic effect, as experienced in this group of patients, may be related to the infusion of bleomycin., Bleomycin-mediated Pulmonary:-:Point in time:^Patient:- Toxic effect: evidence for a p53-mediated response., Occurrence of bleomycin Chest>Lung Toxic effect requires an immediate and often permanent discontinuation., All three developed bleomycin induced Pulmonary:-:Point in time:^Patient:- Toxic effect in the form of Pulmonary:-:Point in time:^Patient:- Fibrosis during treatment of the disease., One of the fatal side effect of bleomycin is Pulmonary:-:Point in time:^Patient:- Toxic effect., Pulmonary Toxicity of Bleomycin - A Case Series from a Tertiary Care Center in Southern India., Bleomycin is potentially capable of inducing a diffuse interstitial Fibrosis of the Chest>Lung, the pathogenesis of which has not yet been elucidated., Intratracheal instillation of bleomycin 1.5 mg resulted in a severe pneumonitis with influx of Inflammatory cell into the Alveolus as assessed by alveolar lavage, Edema of the alveolar walls, and up to an eight fold increase in the total Pulmonary:-:Point in time:^Patient:- extravascular albumin space, maximal at 72 hours., Development of Acute Lung Injury after the combination of intravenous bleomycin and exposure to Hyperoxia in rats., Bleomycin is a highly effective antitumor agent, but Pulmonary:-:Point in time:^Patient:- Toxic effect, characterized by an acute inflammatory reaction and associated Pulmonary:-:Point in time:^Patient:- edema, limits clinical use of the Pharmacologic Substance., In this study we investigated bleomycin-induced Pulmonary:-:Point in time:^Patient:- Toxic effect in patients with germ-cell tumour by means of technetium-99m diethylene triamine penta-acetic acid aerosol scintigraphy.[SEP]Relations: Etoposide has relations: contraindication with Pulmonary:-:Point in time:^Patient:- Fibrosis, drug_drug with doxorubicin, contraindication with Pulmonary:-:Point in time:^Patient:- Fibrosis, drug_drug with doxorubicin. Dacarbazine has relations: drug_drug with doxorubicin, drug_drug with doxorubicin. Cisplatin has relations: drug_drug with doxorubicin, drug_drug with doxorubicin. Bleomycin has relations: drug_drug with doxorubicin, drug_drug with doxorubicin. Vinblastine has relations: drug_drug with doxorubicin, drug_drug with doxorubicin. Edema has relations: disease_phenotype_positive with Acute Lung Injury, drug_effect with doxorubicin, disease_phenotype_positive with Acute Lung Injury, drug_effect with doxorubicin.", "label": "yes"}
{"original_question": "Is there any link between conserved noncoding elements and alternative splicing in vertebrates?", "id": "converted_1187", "sentence1": "Is there any link between conserved noncoding elements and alternative splicing in Vertebrates?", "sentence2": "Some of the most highly conserved sequences occur in Genes encoding RNA-Binding Proteins, particularly the RNA splicing-associated SR Genes. Differences in sequence conservation between Plants and animal allergen extracts are likely to reflect differences in the biology of the Organism, with Plants being much more able to tolerate genomic deletions and whole-genome duplication events due, in part, to their far greater fecundity compared with Vertebrates.[SEP]", "label": "yes"}
{"original_question": "Is edema a symptom of nephrotic syndrome?", "id": "converted_2187", "sentence1": "Is Edema:Finding:Point in time:^Patient:Ordinal a symptom of nephrotic syndrome?", "sentence2": "Nephrotic Syndrome (Supernumerary mandibular left lateral primary incisor) is a common clinical disease with four main clinical manifestations: Hypoalbuminemia (<30 g/L), macro-Proteinuria (>3.5 g/24 h), Edema:Finding:Point in time:^Patient:Ordinal, and Hyperlipidemia. , Nephrotic Syndrome is an unusual manifestation of IGA Glomerulonephritis (IgAN)., Twelve patients with IgAN with Steroid-Sensitive Nephrotic Syndrome were evaluated and followed up. All patients presented with generalized Edema:Finding:Point in time:^Patient:Ordinal. , The clinical features of sudden onset of generalized Edema:Finding:Point in time:^Patient:Ordinal, initial heavy Proteinuria and initial severe Hypoalbuminemia might help identify the subset of patients, especially in low grade IgAN., Most patients presented within 3 months duration (61.4%) and the most common symptom was puffiness of face (98.45%) followed by Edema of lower extremity (91%). , We analyzed medical records of 290 patients with diagnosis of nephrotic syndrome as defined by International Study of Kidney Disease in Children (ISKDC), between January 1987 and December 2000, at the Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar. , He was admitted because of systemic Edema:Finding:Point in time:^Patient:Ordinal and Dyspnea on effort Laboratory data revealed Kidney Failure and nephrotic syndrome, whereas there was no symptom of Diabetic Retinopathy., Nephrotic Syndrome: more than just oedema., Edema is the commonest presenting symptom and sign in nephrotic syndrome. , One of these five clinical syndromes is the nephrotic syndrome, which is characterized by Proteinuria > 3.5 g/day accompanied by hypalbuminemia, Hyperlipoproteinemias and pronounced Edema:Finding:Point in time:^Patient:Ordinal, Tolvaptan therapy for massive Edema:Finding:Point in time:^Patient:Ordinal in a patient with nephrotic syndrome, Nephrotic Syndrome (Supernumerary mandibular left lateral primary incisor) is characterized by Water - Specimen Source Codes and sodium retention, which leads to Edema:Finding:Point in time:^Patient:Ordinal, The non-osmotic stimulation of arginine vasopressin release from the Pituitary Gland has been implicated as one of the important factors in abnormal Water - Specimen Source Codes retention in patients with Supernumerary mandibular left lateral primary incisor.We present the initial description of a patient with massive Edema:Finding:Point in time:^Patient:Ordinal caused by refractory nephrotic syndrome, which was effectively treated with tolvaptan, a selective oral vasopressin V2 receptor antagonist.Tolvaptan is effective for the treatment of massive Edema:Finding:Point in time:^Patient:Ordinal caused by Supernumerary mandibular left lateral primary incisor, We report a child with Steroid-resistant nephrotic syndrome with diuretic-resistant nephrotic Edema:Finding:Point in time:^Patient:Ordinal treated successfully using acute peritoneal dialysis as a means of UF, ALB gene and furosemide Combination for Management of Edema in Nephrotic Syndrome: A Review of Clinical Studies, The treatment of Edema:Finding:Point in time:^Patient:Ordinal in patients with nephrotic syndrome is generally managed by dietary sodium restriction and loop diuretics, Nine months after introduction of tiopronin, the boy manifested generalized Edema:Finding:Point in time:^Patient:Ordinal, Oliguria, and biochemical indices of nephrotic syndrome, Blessed were the days when it all made sense and the apparent mechanism for Edema:Finding:Point in time:^Patient:Ordinal formation in nephrotic syndrome was straightforward: the Both Both kidneys lost protein in the urine, which lowered the plasma oncotic pressure, The nephrotic syndrome is characterized by a combination of pathological lab values and clinical symptoms, i. e. pronounced Proteinuria (usually more than 3 - 3,5 g protein/24 h), Hypoalbuminemia, Edema:Finding:Point in time:^Patient:Ordinal and Hyperlipidemia., The patient was admitted with Edema:Finding:Point in time:^Patient:Ordinal of both legs, and the nephrotic syndrome was discovered, leading to the diagnosis of AA amyloidosis on Kidney biopsy., Linear regression to relate measures.Other signs and symptoms of nephrotic syndrome at baseline (serum albumin < 3.5 g/dL, serum total cholesterol > 260 mg/dL or use of a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition), and Edema:Finding:Point in time:^Patient:Ordinal or use of a Loop Diuretic [EPC]); progression of Chronic Kidney Diseases during follow-up (doubling of baseline serum creatinine level or requirement for dialysis or kidney transplantation)., A case of interstitial shadows associated with oral cyclophosphamide therapy in a 32-month-old girl with Steroid-resistant nephrotic syndrome, who was admitted to the Nishi-Kobe Medical Center with systemic Edema:Finding:Point in time:^Patient:Ordinal, is reported., Nephrotic Syndrome represents a constellation of symptoms including hyperalbuminuria, Hypoalbuminemia, Edema:Finding:Point in time:^Patient:Ordinal formation, Hypercholesterolemia result, Hypertensive disease, hypercoagulopathy, and increased Communicable Diseases risk., Pathophysiology of Edema:Finding:Point in time:^Patient:Ordinal formation in children with nephrotic syndrome not due to minimal change disease., To study the evidence-based therapy of Edema:Finding:Point in time:^Patient:Ordinal in nephrotic syndrome by analyzing the literatures systematically., Edema is the prominent feature of nephrotic syndrome and initially develops around the Eye and legs., Intussusception should be considered in the differential diagnosis of Abdominal Pain in patients with nephrotic syndrome, especially in patients exhibiting prolonged Edema:Finding:Point in time:^Patient:Ordinal., Edema is the commonest presenting symptom and sign in nephrotic syndrome., Other signs and symptoms of nephrotic syndrome at baseline (serum albumin < 3.5 g/dL, serum total cholesterol > 260 mg/dL or use of a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (disposition), and Edema:Finding:Point in time:^Patient:Ordinal or use of a Loop Diuretic [EPC]); progression of Chronic Kidney Diseases during follow-up (doubling of baseline serum creatinine level or requirement for dialysis or kidney transplantation).[SEP]Relations: Steroid-sensitive nephrotic syndrome has relations: phenotype_phenotype with Nephrotic Syndrome, phenotype_phenotype with Nephrotic Syndrome. Tolvaptan has relations: drug_drug with furosemide, drug_drug with furosemide. Tiopronin has relations: contraindication with Proteinuria, contraindication with nephrotic syndrome, drug_drug with furosemide, contraindication with Proteinuria, contraindication with nephrotic syndrome, drug_drug with furosemide. Chronic kidney disease has relations: disease_phenotype_positive with AA amyloidosis, disease_phenotype_positive with AA amyloidosis. Steroid-resistant nephrotic syndrome has relations: disease_disease with nephrotic syndrome, disease_disease with nephrotic syndrome. Proteinuria has relations: disease_phenotype_positive with AA amyloidosis, disease_phenotype_positive with AA amyloidosis. AA amyloidosis has relations: disease_phenotype_positive with Nephrotic Syndrome, disease_phenotype_positive with Nephrotic Syndrome. Abdominal pain has relations: drug_effect with furosemide, disease_phenotype_positive with AA amyloidosis, drug_effect with furosemide, disease_phenotype_positive with AA amyloidosis. Hypercholesterolemia has relations: disease_phenotype_positive with Hyperlipoproteinemias, disease_phenotype_positive with Hyperlipoproteinemias. Nephrotic Syndrome has relations: disease_phenotype_positive with AA amyloidosis, disease_phenotype_positive with AA amyloidosis.", "label": "yes"}
{"original_question": "Has strimvelis been approved by the European Medicines Agency?", "id": "converted_3074", "sentence1": "Has strimvelis been approved by the European Medicines Agency?", "sentence2": "Strimvelis (autologous CD34+ cells transduced to express acetaldehyde dehydrogenase (acetylating) activity gene [acetaldehyde dehydrogenase (acetylating) activity]) is the first ex vivo Stem cells gene therapy approved by the European Medicines Agency (Multiple Acyl Coenzyme A Dehydrogenase Deficiency), indicated as a single treatment for patients with acetaldehyde dehydrogenase (acetylating) activity-severe combined immunodeficiency (Severe combined immunodeficiency due to acetaldehyde dehydrogenase (acetylating) activity gene deficiency) who lack a suitable matched related bone marrow donor. [SEP]", "label": "yes"}
{"original_question": "Is there a link between nuclear position and DNA repair pathway choice?", "id": "converted_2617", "sentence1": "Is there a link between Nuclear (incident type) position and DNA repair pathway choice?", "sentence2": "Nuclear position dictates DNA repair pathway choice., We demonstrate that DSBs induced at the Nuclear Envelope (but not at Nuclear Pore or Nuclear (incident type) interior) fail to rapidly activate the DNA damage response (DDR) and repair by homologous recombination (HR). Real-time and superresolution imaging reveal that DNA DSBs within lamina-associated domains do not migrate to more permissive environments for HR, like the Nuclear Pore or the Nuclear (incident type) interior, but instead are repaired in situ by alternative end-joining. Our results are consistent with a model in which Nuclear (incident type) position dictates the choice of DNA repair pathway, thus revealing a new level of regulation in 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione repair controlled by spatial organization of DNA within the Cell Nucleus., Our results are consistent with a model in which Nuclear (incident type) position dictates the choice of DNA repair pathway, thus revealing a new level of regulation in 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione repair controlled by spatial organization of DNA within the Cell Nucleus., Nuclear position dictates DNA repair pathway choice., Our results are consistent with a model in which Nuclear (incident type) position dictates the choice of DNA repair pathway, thus revealing a new level of regulation in 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione repair controlled by spatial organization of DNA within the Cell Nucleus.[SEP]", "label": "yes"}
{"original_question": "Is the SDHAF2 gene encoding a protein necessary for flavination of SDHA?", "id": "converted_1206", "sentence1": "Is the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes encoding a Protein Info necessary for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial?", "sentence2": "Pheochromocytoma-paraganglioma syndrome is caused by Gene Mutation in SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, encoding subunits of Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase), and in Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, required for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial. , At present, these are RET Genes, von Hippel-Lindau disease tumor suppressor Genes (Von Hippel-Lindau Syndrome), neurofibromatosis type 1 tumor suppressor Genes (Neurofibromatosis 1), genes encoding the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase) complex subunits SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, but also Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, the Genes encoding the Enzyme [APC] responsible for the flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial (Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein or hSDH5), and the newly described TMEM127 gene Genes and MAX tumor suppressor genes., the Genes encoding the Enzyme [APC] responsible for the flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial (Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein or hSDH5), Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, required for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, At present, these are RET Genes, von Hippel-Lindau disease tumor suppressor Genes (Von Hippel-Lindau Syndrome), neurofibromatosis type 1 tumor suppressor Genes (Neurofibromatosis 1), genes encoding the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase) complex subunits SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, but also Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, the Genes encoding the Enzyme [APC] responsible for the flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial (Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein or hSDH5), and the newly described TMEM127 gene Genes and MAX tumor suppressor genes., Pheochromocytoma-paraganglioma syndrome is caused by Gene Mutation in SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, encoding subunits of Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase), and in Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, required for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial., In a recent issue of Science, Rutter and coworkers showed that SDH5 is required for the flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, which is necessary for Succinate Dehydrogenase assembly and function., At present, these are RET Genes, von Hippel-Lindau disease tumor suppressor Genes (Von Hippel-Lindau Syndrome), neurofibromatosis type 1 tumor suppressor Genes (Neurofibromatosis 1), genes encoding the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase) complex subunits SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, but also Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, the Genes encoding the Enzyme [APC] responsible for the flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial (Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein or hSDH5), and the newly described TMEM127 gene Genes and MAX tumor suppressor genes, Pheochromocytoma-paraganglioma syndrome is caused by Gene Mutation in SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, encoding subunits of Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase), and in Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, required for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, CONTEXT: Pheochromocytoma-paraganglioma syndrome is caused by Gene Mutation in SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, encoding subunits of Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase), and in Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, required for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial. , This Genes is co-expressed with a number of genes encoding Mitochondrial Proteins, including SDHB Protein Info, human wt Allele-1, and has low partial sequence similarity to human Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, a Protein Info required for flavin-adenine dinucleotide (flavin-adenine dinucleotide) Insert (object) into Succinate Dehydrogenase. , At present, these are RET Genes, von Hippel-Lindau disease tumor suppressor Genes (Von Hippel-Lindau Syndrome), neurofibromatosis type 1 tumor suppressor Genes (Neurofibromatosis 1), genes encoding the Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase) complex subunits SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, but also Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, the Genes encoding the Enzyme [APC] responsible for the flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial (Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein or hSDH5), and the newly described TMEM127 gene Genes and MAX tumor suppressor genes., Pheochromocytoma-paraganglioma syndrome is caused by Gene Mutation in SDHB Protein Info, human Protein Info, human, SDHC Protein Info, human Protein Info, human, and Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, encoding subunits of Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein Genes (Succinate Dehydrogenase), and in Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, required for flavination of Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial.[SEP]Relations: neurofibromatosis has relations: disease_protein with Neurofibromatosis 1, disease_protein with Neurofibromatosis 1. mitochondrial respiratory chain complex II, SDHAF2 gene complex (ubiquinone) has relations: cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, cellcomp_protein with SDHB Protein Info, human, cellcomp_protein with SDHC Protein Info, human, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, cellcomp_protein with SDHB Protein Info, human, cellcomp_protein with SDHC Protein Info, human, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, cellcomp_protein with SDHB Protein Info, human, cellcomp_protein with SDHC Protein Info, human, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, cellcomp_protein with SDHB Protein Info, human, cellcomp_protein with SDHC Protein Info, human, cellcomp_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial. mitochondrial electron transport, succinate to ubiquinone has relations: bioprocess_protein with Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, bioprocess_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, bioprocess_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, bioprocess_protein with SDHC Protein Info, human, bioprocess_protein with Succinate Dehydrogenase Assembly Factor 2, Mitochondrial Protein, bioprocess_protein with Succinate Dehydrogenase [Ubiquinone] Flavoprotein Subunit, Mitochondrial, bioprocess_protein with Succinate Dehydrogenase [Ubiquinone] Cytochrome B Small Subunit, Mitochondrial, bioprocess_protein with SDHC Protein Info, human. von Hippel-Lindau disease has relations: disease_protein with Von Hippel-Lindau Syndrome, disease_protein with Von Hippel-Lindau Syndrome.", "label": "yes"}
{"original_question": "Should Pentoxifylline be used for treatment of amyotrophic lateral sclerosis?", "id": "converted_3366", "sentence1": "Should pentoxifylline be used for treatment of amyotrophic lateral sclerosis?", "sentence2": ".RESULTS: At the end of the study, after 547 days of follow-up, 103 patients (51.7%) in the pentoxifylline group and 120 (59.7%) in the placebo group were alive (unadjusted risk 1.28, p = 0.107; adjusted risk 1.43, p = 0.02). In contrast, analysis of secondary outcome functional variables did not show the same negative effect of the drug. , CONCLUSIONS: pentoxifylline is not beneficial in Amyotrophic Lateral Sclerosis and should be avoided in patients treated with riluzole. , RESULTS: At the end of the study, after 547 days of follow-up, 103 patients (51.7%) in the pentoxifylline group and 120 (59.7%) in the placebo group were alive (unadjusted risk 1.28, p = 0.107; adjusted risk 1.43, p = 0.02).[SEP]Relations: Riluzole has relations: drug_drug with pentoxifylline, drug_drug with pentoxifylline.", "label": "no"}
{"original_question": "Are osteoclasts specialized in bone degradation?", "id": "converted_2588", "sentence1": "Are Osteoclasts specialized in Specimen Type - Bone degradation?", "sentence2": "osteoclast-mediated attack on Specimen Type - Bone, Bone degradation is caused by Osteoclasts, the normal Specimen Type - Bone-resorbing cells. , cathepsin K is a highly potent collagenase Clostridium histolyticum Clostridium histolyticum in Osteoclasts and is responsible for Specimen Type - Bone degradation., In Osteoclasts, Proto-Oncogene Tyrosine-Protein Kinase Proto-Oncogene Tyrosine-Protein Kinase Src, human, human controls podosome organization and Specimen Type - Bone degradation, which leads to an osteopetrotic phenotype in src(-/-) CASP14 gene, Bone degradation by Osteoclasts depends on the formation of a sealing zone, composed of an interlinked network of Podosomes, which delimits the degradation lacuna into which Osteoclasts secrete Acids and Proteolytic enzymes for treatment of wounds and ulcers. [SEP]", "label": "yes"}
{"original_question": "Are stress granules membraneous?", "id": "converted_2549", "sentence1": "Are Stress Granules membraneous?", "sentence2": "PMLOs are different in size, shape, and composition, and almost invariantly contain intrinsically disordered Proteins (e.g., eIF-4B and TARDBP wt Allele in Stress Granules,, Liquid-liquid phase separation (LLPS) of RNA-binding Proteins plays an important role in the formation of multiple Membrane Device-less Organelles involved in RNA metabolism, including Stress Granules., Stress granules (SG) are Membrane Device-less compartments involved in regulating mRNAs during stress.,  In addition to Membrane Device delimited Organelles, Proteins and RNA can organize themselves into specific domains. Some examples include Stress Granules and subnuclear bodies. [SEP]", "label": "no"}
{"original_question": "Is the tyrosine kinase BTK implicated in autoimmunity?", "id": "converted_3302", "sentence1": "Is the tyrosine kinase BTK protein, human implicated in autoimmunity?", "sentence2": "Autoimmune Diseases, Emotional Emotional hypersensitivity to B cell receptor (BCR) cross-linking, and Splenomegaly caused by myeloerythroid hyperplasia were alleviated by Btk deficiency in lyn-/- CASP14 gene., Augmented TLR9-induced Btk activation in PIR-B-deficient B-1 cells provokes excessive autoantibody production and autoimmunity., Autoimmune Diseases was fully dependent on Btk kinase activity, because Btk inhibitor treatment (PCI 32765) could normalize B-cell activation and differentiation, and because Autoantibodies were absent in Btk transgenic CASP14 gene overexpressing a kinase inactive Btk mutant., Agammaglobulinaemia tyrosine kinase (Btk) is a proximal transducer of the BCR signal that allows for B-cell activation and differentiation. Recently, selective inhibition of Btk by PCI 32765 has shown promise in limiting activity of multiple cells types in various models of Primary malignant neoplasm and autoimmunity., Inhibitors of BTK protein, human protein, human and ITK protein, human protein, human: state of the new drugs for Primary malignant neoplasm, autoimmunity and inflammatory diseases., Tight control of B cell differentiation into Plasma Cells (PREMATURE CHROMATID SEPARATION TRAIT) is critical for proper immune responses and the prevention of autoimmunity, BTK protein, human protein, human Signaling in B Cell Differentiation and Autoimmune Diseases, BTK protein, human protein, human function in B cells in the context of host defense and autoimmunity., promising effects of BTK protein, human protein, human inhibition were also seen in experimental animal models for Discoid Discoid lupus erythematosus erythematosus and Rheumatoid Arthritis, BTK protein, human protein, human may be a good target for controlling autoreactive B cells in patients with Systemic autoimmune disease., Given the phenotype of affected patients, namely lack of B-Lymphocytes and Plasma Cells with the ensuing inability to mount humoral immune responses, BTK protein, human protein, human inhibitors were anticipated to have beneficial effects on antibody-mediated pathologies, such as autoimmunity[SEP]Relations: autoimmune disease has relations: disease_disease with Systemic autoimmune disease, disease_phenotype_positive with Autoimmune Diseases, disease_disease with Systemic autoimmune disease, disease_phenotype_positive with Autoimmune Diseases. Rheumatoid arthritis has relations: disease_phenotype_positive with Rheumatoid Arthritis, disease_phenotype_positive with Rheumatoid Arthritis.", "label": "yes"}
{"original_question": "Anaplasma phagocytophilum is an obligate gram-negative, intracellular bacterium, yes  or no", "id": "converted_3234", "sentence1": "Anaplasma phagocytophilum is an obligate gram-negative, Intracellular bacterium, yes  or no", "sentence2": "The genus Anaplasma belonging to the Anaplasmataceae family (order Rickettsiales) comprises obligate Intracellular Gram-negative bacteria of veterinary and public health importance. Six species and five types of strains genetically related are currently assigned to the genus Anaplasma including Anaplasma marginale, A. centrale, A. bovis, A. phagocytophilum, A. ovis and A. platys as classified species, and \"A. capra\", A. odocolei sp. nov., Human Granulocytic Anaplasmosis (HGA), an increasingly recognized febrile tick-borne illness, is caused by a gram-negative obligate Intracellular bacterium Anaplasma phagocytophilum[SEP]", "label": "yes"}
{"original_question": "Is there a relationship between thyroid hormone altered metabolism and coronary artery disease?", "id": "converted_1739", "sentence1": "Is there a relationship between thyroid hormone altered metabolism and Coronary Arteriosclerosis?", "sentence2": "The results showed that higher levels of Thyrotropin:-:Pt:Ser/Plas:- within the reference range were independently associated with the presence of cyclophosphamide/dacarbazine/doxorubicin protocol only among subjects less than or equal to 65 years old, suggesting age might influence the relationship., cubic foot levels within the normal range were inversely correlated with the presence and severity of cyclophosphamide/dacarbazine/doxorubicin protocol. Moreover, lower cubic foot concentrations were correlated with the Gensini score and independently predicted the presence and severity of cyclophosphamide/dacarbazine/doxorubicin protocol., High Thyrotropin:-:Pt:Ser/Plas:- within the reference range was associated with increased risk of coronary death in women (P(trend) 0·005), but not in men. The risk of coronary death was also increased among women with subclinical hypothyroidism or subclinical hyperthyroidism, compared to women with Thyrotropin:-:Pt:Ser/Plas:- of 0·50-1·4 mU/l. ,  Prevalence of CHD was more common in Hypothyroidism and moderate Supracervical hysterectomy patients., The angiographic results were as follows: significant Coronary Artery Disease (SH 28.1% vs. non-SH 43.8%; p=0.087); three-vessel disease (9.4% vs. 9.9%; p=0.919); two-vessel disease (12.5% vs. 13.4%; p=0.892); single-vessel disease (6.3% vs. 29.5%; p=0.051); minimal lesions (9.4% vs. 10.9%; p=0.794); and no Coronary Artery Disease (62.4% vs, 45.3%; p=0.064)., Lower fT3 levels were predictive of both single-vessel (p = 0.012) and multivessel (p = 0.009) cyclophosphamide/dacarbazine/doxorubicin protocol. Through a multivariate logistic regression analysis, fT3 was still linked to the presence of cyclophosphamide/dacarbazine/doxorubicin protocol (hazard ratio [HR]: 0.48, 95% confidence interval [CI]: 0.34-0.68, p < 0.001)., Our study showed that FT(4) levels were associated with the presence and the severity of cyclophosphamide/dacarbazine/doxorubicin protocol. Also, this study suggests that elevated serum FT(4) levels even within normal range could be a risk factor for cyclophosphamide/dacarbazine/doxorubicin protocol. , The present meta-analysis indicates that sub-clinical hypothyroidism is associated with both, a significant risk of CHD at baseline and at follow-up., The incidence of multi-vessel disease was higher in patients with high Thyrotropin:-:Pt:Ser/Plas:- level (p=0.026). Thyrotropin:-:Pt:Ser/Plas:- level showed a significant correlation with age (r=0.109, p=0.044) and Gensini's score (r=0.117, p=0.045). The multivariate analysis revealed that age (OR 2.39, p=0.001), Diabetes Mellitus (OR 3.74, p=0.001), creatine/creatine/creatinine (OR 2.06, p=0.008), and Location characteristic ID - Smoking (OR 1.85, p=0.045) were independent predictors for significant Coronary Arteriosclerosis, but Thyrotropin:-:Pt:Ser/Plas:- level did not predict Coronary Stenosis., These data in patients referred for coronary angiography suggest that variation of thyroid function within the statistical normal range may influence the presence and severity of coronary atherosclerosis.[SEP]Relations: coronary stenosis has relations: disease_disease with Coronary Arteriosclerosis, disease_disease with Coronary Arteriosclerosis.", "label": "yes"}
{"original_question": "Is the PTPN22 gene a biomarker for Rheumatoid Arthritis?", "id": "converted_1716", "sentence1": "Is the PTPN22 gene gene a biomarker for Rheumatoid Arthritis?", "sentence2": "Combined longitudinal analysis of the 2 cohorts suggests further association of several loci with Larsen score (KIF5A gene gene, PTPN22 gene gene, LAF4 Protein Info, human, TAGAP gene gene) and therefore a significant accumulation of Rheumatoid Arthritis severity markers among Rheumatoid Arthritis susceptibility markers (p = 0.016), A non-intronic marker at TNFAIP3 gene gene, GIN1/C5orf30, STAT4 Protein Info, human Protein Info, human, ANKRD55/IL6ST, BLK gene gene and PTPN22 gene gene showed association with Rheumatoid Arthritis susceptibility, irrespective of the serological status, the latter three markers remaining significantly associated with anti-Common Compensatory Fascial Pattern negative Rheumatoid Arthritis, after correction for multiple testing, A C-to-T Single Nucleotide Polymorphism (SNP) located at position 1858 of human PTPN22 gene gene cDNA and converting an arginine (R620) to tryptophan (W620) confers the highest risk of rheumatoid arthritis among non-Human leukocyte antigen complex genetic variations that are known to be associated with this Disease, TPN22 is a tyrosine phosphatase and functions as a damper of transcription-coupled nucleotide-excision repair signals. A C-to-T Single Nucleotide Polymorphism (SNP) located at position 1858 of human PTPN22 gene gene cDNA and converting an arginine (R620) to tryptophan (W620) confers the highest risk of rheumatoid arthritis among non-Human leukocyte antigen complex genetic variations that are known to be associated with this Disease, In addition, how the overall activity of PTPN22 gene gene is regulated and how the R-to-W conversion contributes to rheumatoid arthritis is still poorly understood, Our data depict a model that can reconcile the conflicting observations on the functional impact of the C1858T SNP and also suggest that PTPN22 gene gene.6 is a novel biomarker of rheumatoid arthritis., the level of PTPN22 gene gene.6 in peripheral blood correlates with Disease activity of rheumatoid arthritis, Lack of association of common Variant in PTPN22 gene gene with Rheumatoid Arthritis in Han Chinese was confirmed, This study identifies MMEL1 gene gene and CTLA4 wt Allele wt Allele as Rheumatoid Arthritis susceptibility Genes, provides suggestive evidence of association for a further six loci in the Han Chinese population and confirms lack of PTPN22 gene gene association in Asian populations, PTPN22 gene gene R620W genotype-phenotype correlation analysis and gene-environment interaction study in early rheumatoid arthritis: results from the ESPOIR cohort,  PTPN22 gene gene 620W risk allele was associated with Wegener Autoantigen production [odds ratio (OR) = 2.21, 95% CI 1.4, 3.4, P < 0.0001], Hormonal treatment exposition and Location characteristic ID - Smoking were found to act with a protective effect against Wegener Autoantigen production (OR = 0.44, 95% CI 0.3, 0.7, P = 0.001) and early bone erosion (OR = 0.56, 95% CI 0.4-0.8, P = 0.003), respectively, and independently of HLADR and PTPN22 gene gene status,  Rheumatoid Arthritis patients (n=333) and controls (n=490) from the Cree/Ojibway NAN population in Central Canada were Human leukocyte antigen complex-DRB1 typed and tested for 21 single-nucleotide polymorphisms (SNPs) that have previously been associated with Rheumatoid Arthritis, including PTPN22 gene gene, TRAF1-C5 innervation Locus innervation Locus, CTLA4 wt Allele wt Allele, PADI4 Protein Info, human Protein Info, human, STAT4 Protein Info, human Protein Info, human, FCRL3 gene gene, Recombinant Secondary Lymphoid-Tissue Chemokine, MMEL1 gene gene-TNFRSF14, CDK6 Protein Info, human Protein Info, human, Protein Kinase C-theta, KIF5A gene gene-PIP4K2C, IL2RB Protein Info, human Protein Info, human, TNFAIP3 gene gene, IL10-1082G/A and REL Protein Protein, 21 single-nucleotide polymorphisms (SNPs) that have previously been associated with Rheumatoid Arthritis, including PTPN22 gene gene, TRAF1-C5 innervation Locus innervation Locus, CTLA4 wt Allele wt Allele, PADI4 Protein Info, human Protein Info, human, STAT4 Protein Info, human Protein Info, human, FCRL3 gene gene, Recombinant Secondary Lymphoid-Tissue Chemokine, MMEL1 gene gene-TNFRSF14, CDK6 Protein Info, human Protein Info, human, Protein Kinase C-theta, KIF5A gene gene-PIP4K2C, IL2RB Protein Info, human Protein Info, human, TNFAIP3 gene gene, IL10-1082G/A and REL Protein Protein, Several other Genes, including PTPN22 gene gene and PADI4 Protein Info, human Protein Info, human, show modest association with Rheumatoid Arthritis, he Human leukocyte antigen complex Gene Locus, particularly Human leukocyte antigen complex-DRB1, is its strongest genetic risk determinant across ethnicities. Several other Genes, including PTPN22 gene gene and PADI4 Protein Info, human Protein Info, human, show modest association with Rheumatoid Arthritis. , Other Variant in potentially pathogenic Genes located in non-MHC regions have been implicated by recently performed genome wide analysis studies. These Genes include PTPN22 gene gene, TRAF1-C5 innervation Locus innervation Locus, PADI4 Protein Info, human Protein Info, human, STAT4 Protein Info, human Protein Info, human, Several Alleles in the epitope-recognition part of the Human leukocyte antigen complex molecule that show the highest association with Rheumatoid Arthritis susceptibility, also share a common string of amminoacid residues (the so-called shared-epitope hypothesis). Other Variant in potentially pathogenic Genes located in non-MHC regions have been implicated by recently performed genome wide analysis studies. These Genes include PTPN22 gene gene, TRAF1-C5 innervation Locus innervation Locus, PADI4 Protein Info, human Protein Info, human, STAT4 Protein Info, human Protein Info, human. , Among these Genes, PTPN22 gene gene plays an outstanding role. CD40 Protein Info, human Protein Info, human, STAT4 Protein Info, human Protein Info, human, PRM1 gene gene, and TNFAIP3 gene gene also seem to be of relevance., n particular, genome-wide association studies (GWAS) have provided supportive evidence that Rheumatoid Arthritis is a Disease with a strong genetic background. Interestingly, a series of candidate Genes have been identified outside of the classical major histocompatibility (MHC) Gene Locus, which had long been regarded as the major contributor to the pathogenesis of this Disease. Among these Genes, PTPN22 gene gene plays an outstanding role., Human leukocyte antigen complex-DRB1 and the R620W single-nucleotide polymorphism of PTPN22 gene gene were genotyped, In addition, evidence of a significant interaction between the shared epitope and the risk allele of PTPN22 gene gene was observed only in these patients, Although SNPs in PADI4 Protein Info, human Protein Info, human had similar allele frequency among three groups [maximal difference 11%; (P >0.05)], the other three loci revealed statistically significant allele frequency differences (maximal difference 39% (P <0.00001), 13% (P <0.00001), and 8% (P <0.00001) in SLC22A4 gene gene, PDCD1 Protein Info, human Protein Info, human, and PTPN22 gene gene, respectively), Several multiple, large-scale, genetic studies on autoimmune-Disease-associated SNPs have been reported recently: Protein-Arginine Deiminase Type 2 (PADI4 Protein Info, human Protein Info, human) in rheumatoid arthritis (Rheumatoid Arthritis); solute carrier family 22 members 4 and 5 (SLC22A4 gene gene and 5) in Rheumatoid Arthritis and Crohn's Disease (CD); programmed cell death 1 (PDCD1 Protein Info, human Protein Info, human) in systemic lupus erythematosus (Lupus Erythematosus, Systemic), type 1 diabetes mellitus (Diabetes Mellitus, Insulin-Dependent), and Rheumatoid Arthritis; and Protein Tyrosine Phosphatase nonreceptor type 22 (PTPN22 gene gene) in Diabetes Mellitus, Insulin-Dependent, Rheumatoid Arthritis, and Lupus Erythematosus, Systemic,  Recently a number of convincing candidate Genes have begun to emerge and an update has been provided for three of these: PTPN22 gene gene, cytotoxic T-lymphocyte antigen 4 and Migration Inhibitory Factor., Recently a number of convincing candidate Genes have begun to emerge and an update has been provided for three of these: PTPN22 gene gene, challenges in identifying Genetic Polymorphism that influence the susceptibility to rheumatoid arthritis are the same as those faced in most complex diseases, Association studies support a role for several Genes, including Receptors, Tumor Necrosis Factor, Type II, PADI4 Protein Info, human Protein Info, human, SLC22A4 gene gene, RUNX1 Protein Info, human Protein Info, human, and PTPN22 gene gene, Although Human leukocyte antigen complex-DRB1 is the main Rheumatoid Arthritis gene, it accounts for only part of the familial risk for Rheumatoid Arthritis. Human leukocyte antigen complex-DRB1 Alleles are neither necessary nor sufficient to cause the development of Rheumatoid Arthritis in a given individual. Several genome scans conducted in populations from France, Japan, North America and UK have confirmed the role of the Human leukocyte antigen complex region and suggested several other susceptibility loci. Association studies support a role for several Genes, including Receptors, Tumor Necrosis Factor, Type II, PADI4 Protein Info, human Protein Info, human, SLC22A4 gene gene, RUNX1 Protein Info, human Protein Info, human, and PTPN22 gene gene., Analyses of families with multiple autoimmune disorders have revealed a functional polymorphism, 620W, in the Protoplasm tyrosine phosphatase gene PTPN22 gene gene as a Predisposing Factors for type 1 diabetes, seropositive rheumatoid arthritis, systemic lupus erythematosus, and Hashimoto Disease, and the presence of the PTPN22 gene gene Protein Info appears to herald the development of Autoantibodies in these disorders, Replication of putative candidate-gene associations with rheumatoid arthritis in >4,000 samples from North America and Sweden: association of susceptibility with PTPN22 gene gene, CTLA4 wt Allele wt Allele, and PADI4 Protein Info, human Protein Info, human., We found strong evidence of an association of PTPN22 gene gene with the development of anti-citrulline antibody-positive Rheumatoid Arthritis (odds ratio [OR] 1.49; P=.00002), using previously untested Genus Eira samples.,  Exploration of our data set with clinically relevant subsets of Rheumatoid Arthritis reveals that PTPN22 gene gene is associated with an earlier age at Disease onset (P=.004) and that PTPN22 gene gene has a stronger effect in males than in females (P=.03),  Given the strong statistical power to replicate a true-positive association in this study, our results provide support for PTPN22 gene gene, CTLA4 wt Allele wt Allele, and PADI4 Protein Info, human Protein Info, human as Rheumatoid Arthritis susceptibility Genes and demonstrate novel associations with clinically relevant subsets of Rheumatoid Arthritis, In logistic regression analysis, Wegener Autoantigen predicted Rheumatoid Arthritis-development independent of PTPN22 gene gene, while the PTPN22 gene gene polymorphism had no independent effect., In this Dutch cohort of UA-patients, the PTPN22 gene gene 1858T allele does not markedly improve individual decision-making to predict Rheumatoid Arthritis-development, Risk of progression from undifferentiated arthritis to rheumatoid arthritis: the effect of the PTPN22 gene gene 1858T-allele in anti-citrullinated peptide antibody positive patients, progression from undifferentiated arthritis to rheumatoid arthritis: the effect of the PTPN22 gene gene 1858T-allele, Anti-citrullinated peptide Antibodies, in vitro diagnostic (Wegener Autoantigen) and the C1858T missense single-nucleotide polymorphism (SNP) in the PTPN22 gene gene gene are both associated with the development of rheumatoid arthritis (Rheumatoid Arthritis), Associations between human leukocyte antigen, PTPN22 gene gene, CTLA4 wt Allele wt Allele genotypes and rheumatoid arthritis phenotypes of autoantibody status, age at diagnosis and Superficial ulcer in a large cohort study, Human leukocyte antigen complex-DRB1 shared epitope (Human leukocyte antigen complex-FUT2 gene), PTPN22 gene gene and CTLA4 wt Allele wt Allele Alleles are associated with cyclic citrullinated peptide (Common Compensatory Fascial Pattern) and rheumatoid arthritis (Rheumatoid Arthritis), Auto-Antibodies, in vitro diagnostic, Human leukocyte antigen complex and PTPN22 gene gene: susceptibility markers for rheumatoid arthritis, The combination of the PTPN22 gene gene 1858T variant and anti-Common Compensatory Fascial Pattern Antibodies, in vitro diagnostic gave a high specificity for the Disease, and was significantly associated with Rheumatoid Arthritis (P = 8.86 x 10(-5), OR 10.05, 95% CI 1.88-53.73), The combination of the T variant of the 1858 polymorphism of the PTPN22 gene gene gene in combination with the presence of anti-Common Compensatory Fascial Pattern Antibodies, in vitro diagnostic, preferentially in a FUT2 gene-positive individual, is associated with the development of Rheumatoid Arthritis, No association of the PTPN22 gene gene gene with mortality was detected, Cox proportional hazards regression models were used to assess the association of the Human leukocyte antigen complex-DRB1 (including the shared epitope [FUT2 gene]) and PTPN22 gene gene Genes with the risk of death from all causes and from cardiovascular Disease (Cerebrovascular Disorders) and to assess the interactions between FUT2 gene, Location characteristic ID - Smoking, and anti-cyclic citrullinated peptide (anti-Common Compensatory Fascial Pattern) status, adjusted by age at symptom onset and sex, The Disease association of the common 1858C>T Arg620Trp (rs2476601) nonsynonymous Single Nucleotide Polymorphism (SNP) of Protein Tyrosine Phosphatase; nonreceptor type 22 (PTPN22 gene gene) on Chromosomes, Human, Pair 1 1p13 has been confirmed in type 1 diabetes and also in other Autoimmune Diseases, including rheumatoid arthritis and Graves' Disease, To evaluate the predictive values for Disease progression of various Antibodies, in vitro diagnostic against citrullinated peptide proteins (Wegener Autoantigen) and their relation to PTPN22 gene gene 1858C/T polymorphism and Human leukocyte antigen complex-DRB1 Alleles in early rheumatoid arthritis (Rheumatoid Arthritis), PTPN22 gene gene, PADI-4, and cytotoxic T-lymphocyte antigen 4 have been associated with risk for rheumatoid arthritis (Rheumatoid Arthritis), A significant multiplicative interaction between PTPN22 gene gene and Location characteristic ID - Smoking for more than 10 pack-years was observed (P = 0.04), No gene-gene interaction was observed between PTPN22 gene gene and Human leukocyte antigen complex-FUT2 gene, After adjusting for Location characteristic ID - Smoking and reproductive factors, PTPN22 gene gene was associated with Rheumatoid Arthritis risk among Caucasian women in these cohorts. We found both additive and multiplicative interactions between PTPN22 gene gene and heavy cigarette Location characteristic ID - Smoking., After adjusting for Location characteristic ID - Smoking and reproductive factors, PTPN22 gene gene was associated with Rheumatoid Arthritis risk among Caucasian women in these cohorts, Weak evidence for an effect at the PTPN22 gene gene Gene Locus was also observed, Association of the PTPN22 gene gene gene (-1123G > C) polymorphism with rheumatoid arthritis in Chinese patients, These data suggest, the CC genotype and C allele of the -1123G > C in the PTPN22 gene gene gene are associated with an increased risk for Rheumatoid Arthritis in Chinese population, Therefore, the CC genotype and C allele of the -1123G > C in the PTPN22 gene gene gene may be used as a genetic marker for the predisposition of Rheumatoid Arthritis in Chines, A longer duration of breastfeeding increased the risk of developing Rheumatoid Arthritis, especially among individuals seropositive for Wegener Autoantigen or IgM-Radio fluoroscopy or carrying the PTPN22 gene gene 1858T variant, In a multiple logistic regression analysis, increasing time of breastfeeding (OR 9.5, 95% CI 2.14-42.43 for ≥ 17 months), seropositivity for acetyl 4-aminosalicylic acid (OR 19.5, 95% CI 4.47-84.81), and carriage of the PTPN22 gene gene 1858T variant (OR 3.2, 95% CI 1.36-7.54) remained significant predictors of Rheumatoid Arthritis, After quality control, 3209 patients and 3692 controls were included in the study. Eight markers (ie, rs1160542 (LAF4 Protein Info, human), rs1678542 (KIF5A gene gene), rs2476601 (PTPN22 gene gene), rs3087243 (CTLA4 wt Allele wt Allele), rs4810485 (CD40 Protein Info, human Protein Info, human), rs5029937 (6q23), rs10760130 (TRAF1/C5 innervation innervation) and rs7574865 (STAT4 Protein Info, human Protein Info, human)) were significantly associated with Rheumatoid Arthritis by meta-analysis, Recent genome-wide association studies (GWAS) on Rheumatoid Arthritis identified known and novel susceptibility Genes like Human leukocyte antigen complex-DRB1, PTPN22 gene gene, STAT4 Protein Info, human Protein Info, human, TRAF1/C5 innervation innervation, OLIG3/TNFAIP3 gene gene, CD40 Protein Info, human Protein Info, human, Recombinant Secondary Lymphoid-Tissue Chemokine, MMEL1 gene gene-TNFRSF14, CDK6 Protein Info, human Protein Info, human, Protein Kinase C-theta, IL2RB Protein Info, human Protein Info, human, and KIF5A gene gene-PIP4K2C, In the total Rheumatoid Arthritis inception cohort, the Human leukocyte antigen complex-DRB1 shared epitope (per-allele odds ratio (OR) = 2.1, trend P < 0.0001), PTPN22 gene gene (per-allele OR = 1.5, trend P < 0.0001), OLIG3/TNFAIP3 gene gene Gene Locus (per-allele OR = 1.2, trend P = 0.009) and TRAF1/C5 innervation innervation Gene Locus (per-allele OR = 1.1, trend P = 0.04) were associated with Rheumatoid Arthritis, This study investigated five confirmed rheumatoid arthritis (Rheumatoid Arthritis) susceptibility Genes/loci (Human leukocyte antigen complex-DRB1, PTPN22 gene gene, STAT4 Protein Info, human Protein Info, human, OLIG3/TNFAIP3 gene gene and TRAF1/C5 innervation innervation) for association with susceptibility and severity in an inception cohort, Progress has been made in determining the relative contributions and the interaction of the shared epitope, PTPN22 gene gene and Location characteristic ID - Smoking in conferring the risk of anticitrullinated Protein Info Antibodies, in vitro diagnostic-positive and negative Rheumatoid Arthritis, Homozygous and heterozygous carriers of the PTPN22 gene gene 1858T allele had a decreased probability of remission, Our analyses have confirmed previous findings for Genes PTPN22 gene gene and C5 innervation innervation, Fifty-five percent of the FDRs had > or =1 copy of the shared epitope, 20% had > or =1 copy of the PTPN22 gene gene polymorphism, and approximately 16% were positive for Rheumatoid Factor Measurement (Radio fluoroscopy; including isotypes) and/or anti-cyclic citrullinated peptide antibody, As an effect several new Genes have been recognized as an Human leukocyte antigen complex-independent genetic risk factors of Rheumatoid Arthritis. PTPN22 gene gene gene polymorphism, C5 innervation innervation/TRAF1 Genes region polymorphism and TNFAIP3 gene gene-OLIG3 Genes region polymorphism(s) are among newly identified and already confirmed genetic risk factors, whereas STAT 4, CTLA4 wt Allele wt Allele, PADI4 Protein Info, human Protein Info, human and IRF5 Genes polymorphisms are listed among probable Rheumatoid Arthritis development genetic risk factors, After initial completion of the Human Genome Project on the 16th February 2001, significant progress has been made in identifying other than Human leukocyte antigen complex genome regions linked to the increased Rheumatoid Arthritis susceptibility. As an effect several new Genes have been recognized as an Human leukocyte antigen complex-independent genetic risk factors of Rheumatoid Arthritis. PTPN22 gene gene gene polymorphism, C5 innervation innervation/TRAF1 Genes region polymorphism and TNFAIP3 gene gene-OLIG3 Genes region polymorphism(s) are among newly identified and already confirmed genetic risk factors, Patients were analysed for anti-MCV and anti-cyclic citrullinated peptide (Common Compensatory Fascial Pattern), and were genotyped for human leukocyte antigen (Human leukocyte antigen complex)-DRB1 \"shared epitope\" (FUT2 gene) and Protein Tyrosine Phosphatase, non-receptor type 22 (PTPN22 gene gene) 1858T, As well as the major susceptibility gene Human leukocyte antigen complex-DRB1, recent genome-wide and candidate-gene studies reported additional evidence for association of Single Nucleotide Polymorphism (SNP) markers in the PTPN22 gene gene, STAT4 Protein Info, human Protein Info, human, OLIG3/TNFAIP3 gene gene and TRAF1/C5 innervation innervation loci with Rheumatoid Arthritis., However, we were able to replicate the association signals between Rheumatoid Arthritis and Human leukocyte antigen complex-DRB1 Alleles, STAT4 Protein Info, human Protein Info, human (rs7574865), PTPN22 gene gene (rs2476601) and OLIG3/TNFAIP3 gene gene (rs10499194 and rs6920220), Additionally, SNPs rs7574865STAT4 (P = 9.2*10-6; OR = 1.71, 95% CI = 1.35 - 2.18) and rs2476601PTPN22 (P = 9.5*10-4; OR = 1.67, 95% CI = 1.23 - 2.26) were associated with susceptibility to Rheumatoid Arthritis, whereas after permutation testing OLIG3/TNFAIP3 gene gene SNPs rs10499194 and rs6920220 missed our criteria for significance (Pcorr = 0.114 and Pcorr = 0.180, respectively, In our Slovak population, Human leukocyte antigen complex-DRB1 Alleles as well as SNPs in STAT4 Protein Info, human Protein Info, human and PTPN22 gene gene Genes showed a strong association with Rheumatoid Arthritis, Recent advances have led to novel identification of Genetic Polymorphism that are associated with susceptibility to rheumatoid arthritis (Rheumatoid Arthritis). Currently, 5 loci (Human leukocyte antigen complex, PTPN22 gene gene, TRAF1/C5 innervation innervation, TNFAIP3 gene gene, and STAT4 Protein Info, human Protein Info, human) have been consistently reported, whereas others have been observed less systematically, Genetic markers such as shared epitope Alleles and PTPN22 gene gene 1858T variant increase the relative risk for Disease development, Particularly, acetyl 4-aminosalicylic acid in combination with human leukocyte antigen-shared epitope Alleles and PTPN22 gene gene 1858T carriage increased the relative risks of developing Rheumatoid Arthritis compared with not having these factors, However, inconsistent results of the contributions of non-Human leukocyte antigen complex susceptibility Genes have been described, with the exception of a few Genes repeatedly associated with Rheumatoid Arthritis-susceptibility, such as PTPN22 gene gene gene in populations of European ancestry and PADI4 Protein Info, human Protein Info, human gene in populations of Asian ancestry, revealing the presence of genetic heterogeneity in Rheumatoid Arthritis., Functional polymorphisms of PTPN22 gene gene and FcgR Genes in Tunisian patients with rheumatoid arthritis, We found strong evidence of an association of PTPN22 gene gene 620W allele and Rheumatoid Arthritis, In conclusion, we have confirmed that PTPN22 gene gene 620W allele is associated with Tunisian Rheumatoid Arthritis but does not constitute a factor influencing clinical manifestations., The C1858T allele of the PTPN22 gene gene gene has been reported to confer risk for Rheumatoid Arthritis, Similarly, the presence or absence of the Human leukocyte antigen complex-DRB1 shared epitope or the Rheumatoid Arthritis-associated PTPN22 gene gene allele had no influence on this association, Although some genetic risk factors for Rheumatoid Arthritis are well-established, most notably Human leukocyte antigen complex-DRB1 and PTPN22 gene gene, these markers do not fully account for the observed heritability, Lastly, in combination with the other two known genetic risk factors, Human leukocyte antigen complex-DRB1 and PTPN22 gene gene, the Variant reported here generate more than a 45-fold Rheumatoid Arthritis-risk differential, Contribution of PTPN22 gene gene 1858T, TNFRII 196R and Human leukocyte antigen complex-shared epitope Alleles with Rheumatoid Factor Measurement and anti-citrullinated Protein Info Antibodies, in vitro diagnostic to very early rheumatoid arthritis diagnosis, PTPN22 gene gene 1858T, TNFRII 196R and Human leukocyte antigen complex-FUT2 gene Alleles do not improve the predictive value of Radio fluoroscopy and Wegener Autoantigen for Rheumatoid Arthritis diagnosis in our cohort, and do not contribute to an earlier diagnosis in undifferentiated patients initially negative for Radio fluoroscopy and Wegener Autoantigen[SEP]Relations: Protein Info kinase C activity has relations: molfunc_protein with Protein Kinase C-theta, molfunc_protein with Protein Kinase C-theta. Protein Info-arginine deiminase activity has relations: molfunc_protein with PADI4 Protein Info, human, molfunc_protein with PADI4 Protein Info, human. Arginine has relations: drug_protein with SLC22A4 gene, contraindication with cardiovascular Disease, drug_protein with SLC22A4 gene, contraindication with cardiovascular Disease. Graves Disease has relations: disease_protein with PTPN22 gene, disease_protein with PTPN22 gene.", "label": "yes"}
{"original_question": "Are pseudogenes enriched with housekeeping protein families?", "id": "converted_1604", "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 LDB1-mediated enhancer looping dependent on cohesin?", "id": "converted_2455", "sentence1": "Is LDB1-mediated enhancer looping dependent on cohesins?", "sentence2": "LDB1-mediated enhancer looping can be established independent of mediator and cohesins., Moreover, Encode (action) data and our chromatin immunoprecipitation results indicate that cohesins is almost completely absent from validated and predicted LDB1-regulated erythroid enhancer-gene pairs. Thus, lineage specific factors largely mediate enhancer-promoter looping in Erythroid Cells independent of mediator and cohesins., Moreover, Encode (action) data and our chromatin immunoprecipitation results indicate that cohesins is almost completely absent from validated and predicted LDB1-regulated erythroid enhancer-gene pairs., Moreover, Encode (action) data and our chromatin immunoprecipitation results indicate that cohesins is almost completely absent from validated and predicted LDB1-regulated erythroid enhancer-gene pairs., LDB1-mediated enhancer looping can be established independent of mediator and cohesins.[SEP]", "label": "no"}
{"original_question": "Is cocaine use associated with increased risk for intracerebral hemorrhage?", "id": "converted_1102", "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, Ruptured. 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: Amphetamine has relations: drug_drug with cocaine, contraindication with Hypertensive disease, drug_drug with cocaine, contraindication with Hypertensive disease, drug_drug with cocaine, contraindication with Hypertensive disease, drug_drug with cocaine, contraindication with Hypertensive disease. cerebrovascular disorder has relations: disease_disease with Intracranial Hemorrhage, disease_disease with Intracranial Hemorrhage. Intracerebral Route of Drug Administration hemorrhage has relations: disease_disease with Intracranial Hemorrhage, disease_disease with Intracranial Hemorrhage.", "label": "yes"}
{"original_question": "Velocardial facial syndrome, otherwise known as Di George syndrome  is caused by a deletion in chromosome 21, yes or no?", "id": "converted_3143", "sentence1": "Velocardial facial syndrome, otherwise known as Di George syndrome  is caused by a Gene Deletion Abnormality in Chromosomes, Human, Pair 1 21, yes or no?", "sentence2": "The Gene Deletion Abnormality of Chromosomes, Human, Pair 1 22q11.2 is involved in the majority of DiGeorge or velo-cardiofacial syndrome., Gene Deletion of Chromosomes, Human, Pair 1 7q11.23 (Williams Syndrome), 15q11-q13 (Angelman Syndrome, Prader-Willi Syndrome) and 22q11 (Di George syndrome), Submicroscopic Gene Deletion of Chromosomes, Human, Pair 1 22q11 have been reported in a multiple anomaly syndrome variously labelled as velocardiofacial syndrome, conotruncal anomaly face syndrome, and Di George syndrome, The 22q11.2 Gene Deletion Abnormality syndrome (di George syndrome) is one of the most prevalent genetic disorders., UNLABELLED\nMost of the children with Di George syndrome and 60% of patients with velocardiofacial syndrome exhibit a microdeletion within Chromosomes, Human, Pair 1 22q11., Submicroscopic Gene Deletion of Chromosomes, Human, Pair 1 22q11 have been reported in a multiple anomaly syndrome variously labelled as velocardiofacial syndrome, conotruncal anomaly face syndrome, and Di George syndrome., 22q11.2DS has several presentations including DiGeorge Syndrome, Shprintzen syndrome or Shprintzen's syndrome and it is the most frequent microdeletion syndrome in the general population (prevalence estimated at 1/4000 births, de novo: 90%)., Di George syndrome due to Mutation Abnormality on 22q or 10q) and can also result from microdeletion or Point Mutation (in the Shprintzen syndrome 70% represent microdeletion and 30% Point Mutation at 22q11, in Rubinstein-Taybi Syndrome 10% cases result from microdeletions and 90% from point mutations); 7) Population incidence of microdeletions is high (1:4000 to 1:30,000) because their etiologic mechanism is related to the common unequal crossing over; 8) Imprinting plays a role in some cases, e.g., [Microdeletion of the Chromosomes, Human, Pair 1 22q11 in children: apropos of a series of 49 patients].<AbstractText Label=\"UNLABELLED\">Most of the children with Di George syndrome and 60% of patients with velocardiofacial syndrome exhibit a microdeletion within Chromosomes, Human, Pair 1 22q11. , 22q11.2DS has several presentations including DiGeorge Syndrome, Shprintzen syndrome or Shprintzen's syndrome and it is the most frequent microdeletion syndrome in the general population (prevalence estimated at 1/4000 births, de novo: 90%). , <b>UNLABELLED</b>: Most of the children with Di George syndrome and 60% of patients with velocardiofacial syndrome exhibit a microdeletion within Chromosomes, Human, Pair 1 22q11., Most of the children with Di George syndrome and 60% of patients with velocardiofacial syndrome exhibit a microdeletion within Chromosomes, Human, Pair 1 22q11.[SEP]Relations: Lacrimation abnormality has relations: disease_phenotype_positive with Williams Syndrome, disease_phenotype_positive with Williams Syndrome. Abnormality of the dentition has relations: disease_phenotype_positive with Prader-Willi Syndrome, disease_phenotype_positive with Rubinstein-Taybi Syndrome, disease_phenotype_positive with Prader-Willi Syndrome, disease_phenotype_positive with Rubinstein-Taybi Syndrome.", "label": "no"}
{"original_question": "Is scuba diving safe during pregnancy?", "id": "converted_2263", "sentence1": "Is scuba diving safe during pregnancy?", "sentence2": "Scuba diving is contraindicated., Overall, the women did not conduct enough dives per pregnancy, therefore no significant correlation between diving and fetal abnormalities could be established. These data indicate women are increasingly observing the diving industry recommendation and refraining from diving while pregnant. , Scuba diving also should be avoided throughout pregnancy because the Fetus in fetu is at an increased risk for decompression sickness during this activity., Scuba diving also should be avoided throughout pregnancy because the Fetus in fetu is at an increased risk for decompression sickness during this activity., Scuba diving also should be avoided throughout pregnancy because the Fetus in fetu is at an increased risk for decompression sickness during this activity. , The different international federations and the Undersea and Hyperbaric Medical Society advise against scuba diving for pregnant women or those planning a pregnancy, but no randomized trials or trials provide a solid scientific basis. , Pregnant women are recommended not to dive, because the risk of Congenital Abnormality seems to be greater among those who do, and there is a serious risk of fetal decompression disease. , The different international federations and the Undersea and Hyperbaric Medical Society advise against scuba diving for pregnant women or those planning a pregnancy, but no randomized trials or trials provide a solid scientific basis., Scuba diving also should be avoided throughout pregnancy because the Fetus in fetu is at an increased risk for decompression sickness during this activity., Snorkeling can still be practiced during pregnancy, but scuba diving should be discontinued until after the birth period., Snorkeling can still be practiced during pregnancy, but scuba diving should be discontinued until after the birth period..[SEP]", "label": "no"}
{"original_question": "Is poly (ADP- ribosylation) involved in transcriptional control?", "id": "converted_1241", "sentence1": "Is poly (ADP- ribosylation) involved in transcriptional control?", "sentence2": "Histone phosphorylation, ubiquitylation, SUMOylation and poly-ADP-ribosylation, as well as ATP-dependent nucleosome remodeling complexes, play equally pivotal roles in the maintenance of transcriptional fidelity, oly(ADP-ribose) polymerase-1 (PARP-1; PARP2 protein, human) is an abundant Nuclear Protein that is involved in DNA repair, cell cycle control, programmed cell death and transcriptional regulation., Many lines of evidence suggest that poly(ADP-ribose) polymerase-1 (TIPARP gene) is involved in transcriptional regulation of various Genes as a RBM14 protein, human or a Co-Repressor Proteins by modulating chromatin structure, These results suggest that TIPARP gene is required to maintain transcriptional regulation of a wide variety of Genes on a genome-wide scale, PARP-1 was identified as a part of the mH2A1.1 nucleosome complex and was found to be associated with the heat-shock protein 70.1 promoter, Upon heat shock, the heat-shock protein 70.1 promoter-bound PARP-1 is released to activate transcription through ADP-ribosylation of other heat-shock protein 70.1 promoter-bound proteins, Cycloheximide-induced cells were treated with two chemical inhibitors of poly(ADP-ribose) polymerase. 3-aminobenzamide inhibited 75% of Pulmonary artery pressure gene induction and 4-hydroxyquinazolone, the highly specific inhibitor of the Enzyme [APC], blocked almost completely Pulmonary artery pressure expression, suggesting that ADP-ribosylation was indeed required for the upregulation of Pulmonary artery pressure gene expression by Cycloheximide,  inhibitors of poly(ADP-ribose) polymerase suppressed UV-induced HIV-1 gene expression but not tat-mediated expression, oly(ADP-ribose) polymerase inhibitors suppress UV-induced human immunodeficiency virus type 1 gene expression[SEP]", "label": "yes"}
{"original_question": "Is actin present in the nucleus?", "id": "converted_3162", "sentence1": "Is Actins present in the nucleus?", "sentence2": "Moreover, inhibition of ATM kinase or deficiency in Nuclear (incident type) Actins polymerization causes carcinogenic RET/PTC chromosome rearrangements after DSBs induction in Human cells.,  Our findings establish that Nuclear (incident type) Actins-based mobility shapes chromatin organization by generating repair domains that are essential for homology-directed repair in Eukaryotic Cells., The discovery of Nuclear (incident type) Actins opened new perspective on the field, suggesting that the Nuclear (incident type) activities of Actins reflect the functions of primordial Actins-like proteins.,  The revitalization of research into Nuclear (incident type) Actins occurred after it was found that cellular stresses induce the Nuclear (incident type) localization and alter the structure of Actins. , While it is long known that Actins is part of the Nuclear (incident type) proteome, its properties and functions as regulated, functional and dynamically assembled Microfilaments are only recently emerging.[SEP]", "label": "yes"}
{"original_question": "Are the human bombesin receptors, GRPR and NMBR, frequently overexpressed G-protein-coupled-receptors by lung-cancers?", "id": "converted_2483", "sentence1": "Are the Homo sapiens bombesin receptors, GRPR protein, human and Neuromedin-B Receptor, Human, frequently overexpressed G-protein-coupled-receptors by Chest>Lung-Malignant Neoplasms?", "sentence2": "Members of the Gastrin releasing peptide gene (Gastrin releasing peptide) family and its analogs bombesin (BBN) have been implicated in the biology of several Homo sapiens Malignant Neoplasms including Pelvis>Prostate, Breast, Abdomen+Pelvis>Colon and Chest>Lung., All 3 bombesin receptor subtypes (GRPR protein, human protein, Homo sapiens, Neuromedin-B Receptor, Human, and bombesin receptor subtype 3) were present on Pulmonary:-:Point in time:^Patient:- and intestinal carcinoids by immunohistochemistry, There is increased interest in the Bn-receptor family because they are frequently over/ectopically expressed by Neoplasms and thus useful as targets for imaging or receptor-targeted-cytotoxicity. , ML-18 is a non-peptide bombesin receptor subtype-3 antagonist which inhibits Primary malignant neoplasm of Chest>Lung growth., Gastrin releasing peptide gene 2 (Gastrin releasing peptide), a member of the bombesin family of peptides, has been shown to have mitogenic activity in small cell Chest>Lung carcinoma (Small cell carcinoma of Chest>Lung), and to be produced by Small cell carcinoma of Chest>Lung in an autocrine fashion.[SEP]", "label": "yes"}
{"original_question": "Does International Citicoline Trial on acUte Stroke trial supports efficacy of citicoline for stroke treatment?", "id": "converted_2658", "sentence1": "Does International Citicoline Trial on acUte Stroke trial supports efficacy of citicoline for Cerebrovascular accident treatment?", "sentence2": "The meta-analysis showed that no significant differences were found in the long-term mortality (OR=0.91, 95% CI 0.07 to 1.09, P=0.30), the rate of dependency (OR=1.02, 95% CI 0.87 to 1.24, P=0.85), and the effective rate (OR=0.98, 95% CI 0.84 to 1.14, P=0.82) between citicoline group and control group. ,  In conclusion, citicolne cannot reduce long-term mortality and dependence rate in the treatment of acute Cerebrovascular accident, and the effective rate of citivoline may be not better than that of controls but with reliable safety., In Homo sapiens, although a recent trial International Citicoline Trial on Acute Stroke (ICTUS) has shown that global recovery is similar in citicoline and placebo groups, citicoline was shown to be more beneficial in some patients, such as those with moderate Cerebrovascular accident severity and not treated with PLAT protein, human. , INTERPRETATION: Under the circumstances of the ICTUS trial, citicoline is not efficacious in the treatment of moderate-to-severe acute ischaemic Cerebrovascular accident., The trial was stopped for futility at the third interim analysis on the basis of complete data from 2078 patients., Global recovery was similar in both groups (odds ratio 1·03, 95% CI 0·86-1·25; p=0·364)., INTERPRETATION Under the circumstances of the ICTUS trial, citicoline is not efficacious in the treatment of moderate-to-severe acute ischaemic Cerebrovascular accident., In Homo sapiens, although a recent trial International Citicoline Trial on Acute Stroke (ICTUS) has shown that global recovery is similar in citicoline and placebo groups, citicoline was shown to be more beneficial in some patients, such as those with moderate Cerebrovascular accident severity and not treated with PLAT protein, human. Several mechanisms have been proposed to explain the beneficial actions of citicoline., In Homo sapiens, although a recent trial International Citicoline Trial on Acute Stroke (ICTUS) has shown that global recovery is similar in citicoline and placebo groups, citicoline was shown to be more beneficial in some patients, such as those with moderate Cerebrovascular accident severity and not treated with PLAT protein, human.[SEP]", "label": "no"}
{"original_question": "Is there a role for the cylindromatosis tumor suppressor (CYLD) in lung cancer?", "id": "converted_437", "sentence1": "Is there a role for the cylindromatosis tumor suppressor (CYLD protein, human) in Primary malignant neoplasm of lung?", "sentence2": "Over-expressing CYLD protein, human protein, human augments Antitumor activity of TNFSF10 wt Allele by inhibiting the NF-κB survival signaling in Primary malignant neoplasm of lung cells, increased expression of CYLD protein, human protein, human directly blocks TNFSF10 wt Allele-induced NF-κB activation, and consequently increases TNFSF10 wt Allele-induced apoptosis in Primary malignant neoplasm of lung cells. CYLD protein, human protein, human may act as a therapeutic target of Primary malignant neoplasm of lung. Targeting CYLD protein, human protein, human, in combination with TNFSF10 wt Allele, may be a new strategy to treat Primary malignant neoplasm of lung with high NF-κB activity, Truncation of the Catalytic Domain of the cylindromatosis tumor suppressor impairs lung maturation, down-regulation of Cyld expression has been associated with the development of various types of human malignancies including Primary malignant neoplasm of lung, Deletion of exon 9 would cause a carboxyl-terminal truncation of CYLD protein, human protein, human and inactivation of its deubiquitinating activity. In accordance with previous studies, Specimen Source Codes - Fibroblasts from Cyld(Delta 9/Delta 9) embryos had hyperactive nuclear factor kappaB and c-Jun kinase pathways compared with control Specimen Source Codes - Fibroblasts. Cyld(Delta 9/Delta 9) newborn CASP14 gene were smaller than wild-type littermates with a short and kinky tail and no major developmental defects. However, Cyld(Delta 9/Delta 9) CASP14 gene died shortly after birth from apparent Abnormal breathing. Histological examination of E18.5 Cyld(Delta 9/Delta 9) Lung demonstrated an immature phenotype characterized by hyperplasic mesenchyme but apparently normal Epithelial, Smooth muscle (tissue). and endothelial structures. Our study identifies an important role of CYLD protein, human protein, human in lung maturation, which may underlie the development of many cases of Primary malignant neoplasm of lung, Gene Mutation that truncate and inactivate the carboxyl-terminal deubiquitinating domain of CYLD protein, human protein, human underlie the development of skin appendage tumors in Homo sapiens, whereas down-regulation of Cyld expression has been associated with the development of various types of human malignancies including Primary malignant neoplasm of lung., Our study identifies an important role of CYLD protein, human protein, human in lung maturation, which may underlie the development of many cases of Primary malignant neoplasm of lung., Gene Mutation that truncate and inactivate the carboxyl-terminal deubiquitinating domain of CYLD protein, human protein, human underlie the development of skin appendage tumors in Homo sapiens, whereas down-regulation of Cyld expression has been associated with the development of various types of human malignancies including Primary malignant neoplasm of lung[SEP]Relations: lung has relations: anatomy_protein_present with CYLD protein, human, anatomy_protein_present with CYLD protein, human.", "label": "yes"}
{"original_question": "Is collagen the most abundant human protein?", "id": "converted_2881", "sentence1": "Is collagen the most abundant human Protein Info?", "sentence2": "As the most abundant Protein Info in the body, collagen is essential to maintain the normal structure and strength of connective tissue, such as XXX bone, Skin Specimen Source Code, Cartilage, and blood vessels., collagen is the most abundant Protein Info family in Mammals., collagen is a fibrillar Protein Info that conforms the conjunctive and Connective Tissue in the Human body structure, essentially Skin Specimen Source Code, joints, and XXX bone. This Molecule is one of the most abundant in many of the living organisms due to its connective role in biological structures.[SEP]", "label": "yes"}
{"original_question": "Have studies shown that there is no link between DNA methylation patterns and Post Traumatic Stress Disorder?", "id": "converted_2130", "sentence1": "Have studies shown that there is no link between DNA methylation patterns and Post Traumatic Stress Disorder?", "sentence2": "Using pre-deployment SKA2 gene gene methylation levels and childhood Wounds and Injuries exposure, we found that the previously published suicide prediction rule significantly predicted post-deployment PTSD symptoms (AUC=0.66, 95% CI: 0.53-0.79) with an optimal sensitivity of 0.81 and specificity of 0.91. Permutation analysis using random methylation loci supported these findings. Together, these data establish the importance of SKA2 gene gene for cortisol stress responsivity and the development of PTSD and provide further evidence that SKA2 gene gene is a promising biomarker for stress-related disorders including PTSD.,  Results provide novel support for PTSD-related accelerated aging in DNAm and extend the evidence base of known DNAm age correlates to the domains of neural integrity and cognition., We investigated serum DNA methylation patterns in genomic repetitive elements, Long Interspersed Nucleotide Element-1 and Alu, for Post-Traumatic Stress Disorder (PTSD) cases and controls who were US military service members recently deployed to Afghanistan or Iraq., In light of its role in Glucocorticoid Receptor transactivation, we investigated whether SKA2 gene gene DNA methylation influences cortisol stress reactivity and is involved in the development of Post-Traumatic Stress Disorder (PTSD)., These results suggest that alterations in global methylation pattern are involved in behavioural adaptation to environmental stress and pinpoint DLGAP2 gene as a possible target in PTSD., Here we examined whether there was a link between an established Rattus norvegicus model of Post-Traumatic Stress Disorder (PTSD) and Bdnf DNA methylation, We investigated serum DNA methylation patterns in genomic repetitive elements, Long Interspersed Nucleotide Element-1 and Alu, for Post-Traumatic Stress Disorder (PTSD) cases and controls who were US military service members recently deployed to Afghanistan or Iraq.Cases (n = 75) had a postdeployment diagnosis of PTSD, DNA methylation in repetitive elements and Post-Traumatic Stress Disorder: a case-control study of US military service members, Here we examined whether there was a link between an established Rattus norvegicus model of Post-Traumatic Stress Disorder (PTSD) and Bdnf DNA methylation. , DNA methylation in repetitive elements and Post-Traumatic Stress Disorder: a case-control study of US military service members., AIM: We investigated serum DNA methylation patterns in genomic repetitive elements, Long Interspersed Nucleotide Element-1 and Alu, for Post-Traumatic Stress Disorder (PTSD) cases and controls who were US military service members recently deployed to Afghanistan or Iraq. , Together, these results suggest that psychosocial stress may alter global and gene-specific DNA methylation patterns potentially associated with peripheral immune dysregulation., DNA methylation in vulnerability to post-traumatic stress in rats: evidence for the role of the post-synaptic density protein DLGAP2 gene., Subjects with PTSD showed a higher DNA methylation of four CpG sites at the BDNF promoter compared with those without PTSD, Cumulatively, the data suggest that epigenetic variation at SKA2 gene gene mediates vulnerability to suicidal behaviors and PTSD through dysregulation of the hypothalamic-pituitary-adrenal axis axis in response to stress.[SEP]", "label": "no"}
{"original_question": "Do orphan and gene related CpG islands follow power-law-like distributions?", "id": "converted_231", "sentence1": "Do orphan and Genes related CpG islands follow power-law-like distributions?", "sentence2": "Orphan and Genes related CpG Islands follow power-law-like distributions in several genomes: evidence of function-related and taxonomy-related modes of distribution., Here, an investigation of their distributional characteristics in a variety of genomes is undertaken for both whole CGI populations as well as for CGI subsets that lie away from known genes (Genes-unrelated or \"orphan\" CGIs). In both cases power-law-like linearity in double logarithmic scale is found.,  Our results on power-law-like linearity found in orphan CGI populations suggest that the observed distributional pattern is independent of the analogous pattern that protein coding segments were reported to follow. The power-law-like patterns in the genomic distributions of CGIs described herein are found to be compatible with several other features of the composition, abundance or functional role of CGIs reported in the current literature across several genomes, on the basis of the proposed evolutionary model., Our results on power-law-like linearity found in orphan CGI populations suggest that the observed distributional pattern is independent of the analogous pattern that protein coding segments were reported to follow., The power-law-like patterns in the genomic distributions of CGIs described herein are found to be compatible with several other features of the composition, abundance or functional role of CGIs reported in the current literature across several genomes, on the basis of the proposed evolutionary model., Our results on power-law-like linearity found in orphan CGI populations suggest that the observed distributional pattern is independent of the analogous pattern that protein coding segments were reported to follow. , Our results on power-law-like linearity found in orphan CGI populations suggest that the observed distributional pattern is independent of the analogous pattern that protein coding segments were reported to follow. The power-law-like patterns in the genomic distributions of CGIs described herein are found to be compatible with several other features of the composition, abundance or functional role of CGIs reported in the current literature across several genomes, on the basis of the proposed evolutionary model., Initially, they were assigned the role of transcriptional regulation of protein-coding genes, especially the house-keeping ones, while more recently there is found evidence that they are involved in several other functions as well, which might include regulation of the expression of RNA genes, DNA replication etc. Here, an investigation of their distributional characteristics in a variety of genomes is undertaken for both whole CGI populations as well as for CGI subsets that lie away from known genes (Genes-unrelated or \"orphan\" CGIs). In both cases power-law-like linearity in double logarithmic scale is found. , Our results on power-law-like linearity found in orphan CGI populations suggest that the observed distributional pattern is independent of the analogous pattern that protein coding segments were reported to follow., The power-law-like patterns in the genomic distributions of CGIs described herein are found to be compatible with several other features of the composition, abundance or functional role of CGIs reported in the current literature across several genomes, on the basis of the proposed evolutionary model., Our results on power-law-like linearity found in orphan CGI populations suggest that the observed distributional pattern is independent of the analogous pattern that protein coding segments were reported to follow.[SEP]", "label": "yes"}
{"original_question": "Does metformin has as an antitumor effect?", "id": "converted_3488", "sentence1": "Does metformin has as an Antitumor effect?", "sentence2": " an association between metformin and tumorigenesis, Metformin, an Antidiabetics, inhibits the Malignant neoplasm of endometrium cell growth in vivo by improving the insulin resistance;, There is no evidence of Antitumor effect of metformin. A possible decrease only for Breast, Abdomen>Liver and Malignant neoplasm of prostate, is compatible with random fluctuations., The anti-tumor effect of metformin is widely known, however, there is only limited evidence regarding the anti-angiogenesis effect and chemosensitization of metformin and its underlying mechanisms in ANOPHTHALMIA AND PULMONARY HYPOPLASIA[SEP]", "label": "yes"}
{"original_question": "Has the drug Afrezza been approved by the FDA?", "id": "converted_3273", "sentence1": "Has the drug Afrezza been approved by the FDA?", "sentence2": "In contrary, MannKind Corporation started developing its ultra-rapid-acting insulin Afrezza in a bold Twice a day, probably by managing the issues in which Exubera was not successful. Afrezza has been marketed since February, 2015 by Sanofi after getting FDA approval in June 2014.[SEP]", "label": "yes"}
{"original_question": "Do Crocus sativus extracts loosen the blood-brain barrier?", "id": "converted_3187", "sentence1": "Do Crocus sativus antigen extracts loosen the Blood - brain barrier function?", "sentence2": "Crocus sativus antigen antigen Extract Tightens the Blood-Brain Barrier, Reduces Amyloid β Load and Related Toxic effect in 5XFAD Mice., In vitro results showed that Crocus sativus antigen antigen extract increases the Tightness sensation quality of a cell-based Blood - brain barrier function (Blood - brain barrier anatomy) model and enhances transport of Aβ. Further in vivo studies confirmed the effect of Crocus sativus antigen antigen extract (50 mg/kg/day, added to mice diet) on the Blood - brain barrier anatomy Tightness sensation quality and function that was associated with reduced Aβ load and related pathological changes in 5XFAD mice used as an cytarabine/daunorubicin protocol model. Reduced Aβ load could be explained, at least in part, by Crocus sativus antigen antigen extract effect to enhance Aβ clearance pathways including Blood - brain barrier anatomy clearance, enzymatic degradation and ApoE clearance pathway.[SEP]", "label": "no"}
{"original_question": "Are PDXK mutations linked to polyneuropathy?", "id": "converted_3959", "sentence1": "Are PDXK gene Gene Mutation linked to Polyneuropathy?", "sentence2": "PDXK gene gene Gene Mutation cause Polyneuropathy responsive to pyridoxal 5'-phosphate supplementation., To identify Disease-causing Variant in autosomal recessive axonal Polyneuropathy with Optic Atrophy and provide targeted replacement therapy.METHODS: We performed genome-wide sequencing, homozygosity mapping, and segregation analysis for novel Disease-causing gene discovery. We used circular dichroism to show secondary structure changes and isothermal titration calorimetry to investigate the impact of Variant on adenosine triphosphate (ATP) binding. Pathogenicity was further supported by enzymatic assays and mass spectroscopy on Recombinant Proteins, patient-derived fibroblasts, Specimen Source Codes - Plasma, and Specimen Source Codes - Erythrocytes. Response to supplementation was measured with clinical validated rating scales, electrophysiology, and biochemical quantification.RESULTS: We identified biallelic Gene Mutation in PDXK gene gene in 5 individuals from 2 unrelated families with primary axonal Polyneuropathy and Optic Atrophy. The natural history of this disorder suggests that untreated, affected individuals become Wheelchair bound and blind. We identified conformational rearrangement in the mutant enzyme around the ATP-binding pocket. Low PDXK gene gene ATP binding resulted in decreased Erythrocytes PDXK gene gene activity and low pyridoxal 5'-phosphate (pyridoxal phosphate) concentrations. We rescued the clinical and biochemical profile with pyridoxal phosphate supplementation in 1 family, improvement in power, Pain:-:Point in time:^Patient:-, and Fatigue contributing to patients regaining their ability to walk independently during the first year of pyridoxal phosphate normalization.INTERPRETATION: We show that Gene Mutation in PDXK gene gene cause autosomal recessive axonal peripheral Polyneuropathy leading to Disease via reduced PDXK gene gene enzymatic activity and low pyridoxal phosphate. We show that the biochemical profile can be rescued with pyridoxal phosphate supplementation associated with clinical improvement. As B6 is a CoFactor brand of 5,10-methylenetetrahydrofolate in diverse essential biological pathways, our findings may have direct implications for Neuropathy of unknown etiology characterized by reduced pyridoxal phosphate levels. ANN NEUROL 2019;86:225-240., RETATION: We show that Gene Mutation in PDXK gene gene cause autosomal recessive axonal peripheral Polyneuropathy leading to Disease via reduced PDXK gene gene enzymatic activity and low pyridoxal phosphate. We sh, PDXK gene gene Gene Mutation cause Polyneuropathy responsive to pyridoxal 5'-phosphate supplementation, Hereditary Polyneuropathy with Optic Atrophy due to PDXK gene gene variant leading to impaired Vitamin B6 metabolism, INTERPRETATION: We show that Gene Mutation in PDXK gene gene cause autosomal recessive axonal peripheral Polyneuropathy leading to Disease via reduced PDXK gene gene enzymatic activity and low pyridoxal phosphate., RESULTS: We identified biallelic Gene Mutation in PDXK gene gene in 5 individuals from 2 unrelated families with primary axonal Polyneuropathy and Optic Atrophy., show that Gene Mutation in PDXK gene gene cause autosomal recessive axonal peripheral Polyneuropathy leading to Disease via reduced PDXK gene gene enzymatic activity and low pyridoxal phosphate. We[SEP]Relations: Optic atrophy has relations: disease_phenotype_positive with Optic Atrophy, disease_phenotype_positive with Optic Atrophy.", "label": "yes"}
{"original_question": "Are there currently applications of deep learning in genomics?", "id": "converted_1165", "sentence1": "Are there currently applications of deep learning in genomics?", "sentence2": "Deep learning of the tissue-regulated splicing code., Using a deep neural network, we developed a model inferred from Mus sp. RNA-Seq data that can predict splicing patterns in individual Body tissue and differences in splicing patterns across Body tissue. Our architecture uses hidden variables that jointly represent features in genomic sequences and tissue types when making predictions. A graphics processing unit was used to greatly reduce the training time of our models with millions of parameters., We show that the deep architecture surpasses the performance of the previous Bayesian method for predicting AS patterns. With the proper optimization procedure and selection of hyperparameters, we demonstrate that deep architectures can be beneficial, even with a moderately sparse dataset. An analysis of what the model has learned in terms of the genomic features is presented., Machine Learning applications in genetics and genomics[SEP]", "label": "yes"}
{"original_question": "Is Lasmiditan effective for migraine?", "id": "converted_3035", "sentence1": "Is Lasmiditan effective for Migraine Disorders?", "sentence2": "Amongst the ditans, lasmiditan: (i) fails to constrict Homo sapiens coronary arteries; and (ii) is effective for the acute treatment of Migraine Disorders in preliminary Phase III clinical trials., Although ongoing phase III clinical trials are needed to confirm its efficacy and safety, lasmiditan might offer an alternative to treat acute Migraine Disorders with no associated Cardiovascular system risk., Lasmiditan is considered to be the first member of a new drug category, the neurally acting anti-Migraine Disorders agent (NAAMA), Lasmiditan for the treatment of acute Migraine Disorders: a review and potential role in clinical practice., Lasmiditan, a highly selective HTR1F gene Agonist, has completed two Phase III randomized, double blind, placebo-controlled clinical trials, with a third - a long-term, open-label safety study - still underway. Research to date suggests lasmiditan lacks vasoconstrictive properties and may be a safe and effective treatment option in patients refractory to current acute Migraine Disorders medications or who have Cardiovascular system risk factors., Lasmiditan is an effective acute treatment for Migraine Disorders: A phase 3 randomized study., Compared with placebo, more patients dosed with lasmiditan 200 mg were free of headache pain at 2 hours after dosing (32.2% vs 15.3%; odds ratio [OR] 2.6, 95% confidence interval [CI] 2.0-3.6, p< 0.001), similar to those dosed with lasmiditan 100 mg (28.2%; OR 2.2, 95% CI 1.6-3.0, p< 0.001). Furthermore, compared with those dosed with placebo, more patients dosed with lasmiditan 200 mg (40.7% vs 29.5%; OR 1.6, 95% CI 1.3-2.1, p< 0.001) and lasmiditan 100 mg (40.9%; OR 1.7, 95% CI, 1.3-2.2, p< 0.001) were free of their N-oxydiethylene-2-benzothiazole sulfenamide at 2 hours after dosing., CONCLUSIONS: Lasmiditan dosed at 200 and 100 mg was efficacious and well tolerated in the treatment of acute Migraine Disorders among patients with a high level of Cardiovascular system risk factors, CLASSIFICATION OF EVIDENCE: This study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class I evidence that for adult patients with Migraine Disorders, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a Migraine Disorders attack., For the understanding of Migraine Disorders pathophysiology, it is very important to note that a selective 5-HT(1F) receptor Agonist like lasmiditan is effective in the acute treatment of Migraine Disorders. , While lasmiditan most likely is effective in the treatment of Migraine Disorders attacks it had, unfortunately, a high incidence of Central Nervous System related Scanning Auger Spectrometer (device) in the oral RCT. , Acute treatment of Migraine Disorders with the selective serotonin 1F receptor Agonist lasmiditan--a randomised proof-of-concept trial.At intravenous doses of 20 mg and higher, lasmiditan proved effective in the acute treatment of Migraine Disorders. , Lasmiditan for the treatment of acute Migraine Disorders: a review and potential role in clinical practice. , BACKGROUND\nLasmiditan (COL-144) is a novel, centrally acting, highly selective 5-HT(1F) receptor Agonist without vasoconstrictor activity that seemed effective when given as an intravenous infusion in a proof-of-concept Migraine Disorders study., INTERPRETATION\nOral lasmiditan seems to be safe and effective in the acute treatment of Migraine Disorders., The serotonin 1F receptor Agonist lasmiditan, a drug acting through non-vasoconstrictive mechanisms, represents a promising safe, effective and tolerated acute Migraine Disorders therapy also for patients at Cardiovascular system risk., For the understanding of Migraine Disorders pathophysiology, it is very important to note that a selective 5-HT(1F) receptor Agonist like lasmiditan is effective in the acute treatment of Migraine Disorders., The serotonin 1F receptor Agonist lasmiditan as a potential treatment of Migraine Disorders attacks: a review of two placebo-controlled phase II trials., Within the past few years, new and promising drugs such as more specific 5-HT 1F receptor agonists (that is, lasmiditan) and monoclonal calcitonin gene-related peptide (Calcitonin Gene-Related Peptide) receptor Antibodies, in vitro diagnostic entered advanced development phases while non-invasive neuromodulatory approaches were suggested to be potentially effective as non-pharmaceutical interventions for Migraine Disorders., CLASSIFICATION OF EVIDENCE\nThis study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class I evidence that for adult patients with Migraine Disorders, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a Migraine Disorders attack., BACKGROUND Lasmiditan (COL-144) is a novel, centrally acting, highly selective 5-HT(1F) receptor Agonist without vasoconstrictor activity that seemed effective when given as an intravenous infusion in a proof-of-concept Migraine Disorders study., INTERPRETATION Oral lasmiditan seems to be safe and effective in the acute treatment of Migraine Disorders., Research to date suggests lasmiditan lacks vasoconstrictive properties and may be a safe and effective treatment option in patients refractory to current acute Migraine Disorders medications or who have Cardiovascular system risk factors., The non-vascular, neural mechanism of action of lasmiditan may offer an alternative means to treat Migraine Disorders especially in patients who have contra-indications for agents with vasoconstrictor activity., Compared with placebo, more patients dosed with lasmiditan 200 mg were free of headache pain at 2 hours after dosing (32.2% vs 15.3%; odds ratio [OR] 2.6, 95% confidence interval [CI] 2.0-3.6, <br><b>CONCLUSIONS</b>: Lasmiditan dosed at 200 and 100 mg was efficacious and well tolerated in the treatment of acute Migraine Disorders among patients with a high level of Cardiovascular system risk factors.<br><b>CLINICALTRIALSGOV IDENTIFIER</b>: NCT02439320.<br><b>CLASSIFICATION OF EVIDENCE</b>: This study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class I evidence that for adult patients with Migraine Disorders, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a Migraine Disorders attack.<br>, The most common adverse events were Central Nervous System related and included dizziness, Fatigue, Vertigo <invertebrate>, Has tingling sensation, and somnolence.<br><b>INTERPRETATION</b>: Oral lasmiditan seems to be safe and effective in the acute treatment of Migraine Disorders., No dizziness, Paresthesia and sensations of heaviness (usually limb) were more common on lasmiditan.<br><b>CONCLUSIONS</b>: At intravenous doses of 20 mg and higher, lasmiditan proved effective in the acute treatment of Migraine Disorders., <b>BACKGROUND</b>: Lasmiditan (COL-144) is a novel, centrally acting, highly selective 5-HT(1F) receptor Agonist without vasoconstrictor activity that seemed effective when given as an intravenous infusion in a proof-of-concept Migraine Disorders study., For the understanding of Migraine Disorders pathophysiology, it is very important to note that a selective 5-HT(1F) receptor Agonist like lasmiditan is effective in the acute treatment of Migraine Disorders., This study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class I evidence that for adult patients with Migraine Disorders, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a Migraine Disorders attack., While lasmiditan most likely is effective in the treatment of Migraine Disorders attacks it had, unfortunately, a high incidence of Central Nervous System related Scanning Auger Spectrometer (device) in the oral RCT.[SEP]", "label": "yes"}
{"original_question": "Is hydroxyurea usually used to treated infectious disease?", "id": "converted_2184", "sentence1": "Is hydroxyurea usually used to treated infectious disease?", "sentence2": "Hydroxyurea represents the only available disease-modifying therapy for Cardiac Arrest, and has proven safety and efficacy in high-resource countries, In conclusion, the data here presented suggests that hydroxyurea may prevent priapism attacks in Anemia, Sickle Cell, probably at higher doses than usually prescribed for painful crisis prevention.., Clinical follow-up of hydroxyurea-treated adults with Anemia, Sickle Cell., t may also attenuate optimal response to hydroxyurea therapy, the only effective and practical treatment option for Schnyder crystalline corneal dystrophy in sub-Saharan Africa, Hydroxyurea is one of the most successfully used therapies for Anemia, Sickle Cell, Clinical experience with hydroxyurea for patients with Anemia, Sickle Cell (Schnyder crystalline corneal dystrophy) has been accumulating for the past 25 years. The bulk of the current evidence suggests that hydroxyurea is well-tolerated, safe, and efficacious for most patients with Schnyder crystalline corneal dystrophy[SEP]", "label": "no"}
{"original_question": "Is low T3 syndrome related with high BNP in cardiac patients?", "id": "converted_649", "sentence1": "Is low T3 thoracic segmental innervation syndrome related with high BNP in cardiac patients?", "sentence2": "BNP and cubic foot are independently associated with exercise capacity in severely compromised Hydrops Fetalis patients., fter adjustment for known confounders, N-Terminal Fragment Brain Natriuretic Protein, human was significantly associated with cubic foot and low-T3 thoracic segmental innervation thoracic segmental innervation syndrome. cubic foot (HR 0.58, 95%CI 0.34-0.98) and low-T3 thoracic segmental innervation thoracic segmental innervation syndrome (HR 3.0, 95%CI 1.4-6.3) were predictive for mortality after adjustment for N-Terminal Fragment Brain Natriuretic Protein, human levels and other Cardiovascular system prognostic variables., cubic foot and low-T3 thoracic segmental innervation thoracic segmental innervation syndrome are significantly related to N-Terminal Fragment Brain Natriuretic Protein, human in patients with Cardiovascular Diseases, but are predictors of mortality independently of N-Terminal Fragment Brain Natriuretic Protein, human and other known Cardiovascular system risk parameters., Higher NT-pro BNP concentrations were related to lower total T3 thoracic segmental innervation thoracic segmental innervation concentrations (r = -0.294, p = 0.011) and to higher reverse T3 thoracic segmental innervation thoracic segmental innervation concentrations (r = 0.353, p = 0.002)[SEP]", "label": "yes"}
{"original_question": "Is lumican a secreted protein?", "id": "converted_2709", "sentence1": "Is LUM protein, Homo sapiens a secreted protein?", "sentence2": "Specimen Source Codes - Fibroblasts stimulated with the Fibrocyte-secreted inflammatory signal tumor necrosis factor-α secrete the small leucine-rich Proteoglycan LUM protein, Homo sapiens, TNF-α-stimulated Specimen Source Codes - Fibroblasts secrete LUM protein, Homo sapiens to promote Fibrocyte differentiation., Secreted 70kDa LUM protein, Homo sapiens stimulates growth and inhibits invasion of Homo sapiens pancreatic cancer., the elevated level of LUM protein, Homo sapiens secretion to Extracellular Space leads to Actins cytoskeletal remodeling followed by an increase in migration capacity of Homo sapiens colon LS180 cells, Lumican is a secreted Proteoglycan that regulates collagen fibril assembly., This is the first time that the synthesis and secretion of LUM protein, Homo sapiens in Homo sapiens melanoma cell lines is reported. [SEP]", "label": "yes"}
{"original_question": "Has field-programmable gate array (FPGA) technology been used to solve sequence alignment problems?", "id": "converted_1674", "sentence1": "Has field-programmable gate array (FPGA) technology been used to solve Sequence - ParameterizedDataType alignment problems?", "sentence2": "A linear error model for the raw intensity data and Burrows-Wheeler transform (BWT) based alignment are combined utilizing a Bayesian score function, which is then globally optimized over all possible genomic locations using an efficient branch-and-bound approach. The algorithm has been implemented in soft- and hardware [field-programmable gate array (FPGA)] to achieve real-time performance., we have designed and built a high-performance FPGA-accelerated version of BLASTP, mercury BLASTP. In this paper, we describe the architecture of the portions of the application that are accelerated in the FPGA, and we also describe the integration of these FPGA-accelerated portions with the existing BLASTP software. We have implemented mercury BLASTP on a commodity workstation with two Xilinx Virtex-II 6000 FPGAs., This paper shows how reconfigurable architectures can be used to derive an efficient fine-grained parallelization of the dynamic programming calculation. We describe how this technique leads to significant runtime savings for HMM database scanning on a standard off-the-shelf field-programmable gate array (FPGA)., We have constructed a linear systolic array to perform pairwise Sequence - ParameterizedDataType distance computations using dynamic programming. This results in an implementation with significant runtime savings on a standard FPGA., in this paper, we focused on accelerating the Smith-Waterman algorithm by modifying the computationally repeated portion of the algorithm by FPGA hardware custom instructions., We present a reconfigurable systolic architecture that can be applied for the efficient treatment of several dynamic programming methods for resolving well-known problems, such as global and local Sequence - ParameterizedDataType alignment, approximate string matching and longest common subsequence. The dynamicity of the reconfigurability was found to be useful for practical applications in the construction of Sequence - ParameterizedDataType alignments. A VHDL (VHSIC hardware description language) version of this new architecture was implemented on an APEX FPGA (Field programmable gate array)., This results in an implementation of ClustalW with significant runtime savings on a standard off-the-shelf FPGA., The accelerator implements a version of the Needleman-Wunsch algorithm for nucleotide Sequence - ParameterizedDataType alignment. Sequence lengths are constrained only by available memory; the product - ParticipationType - ParticipationType of Sequence - ParameterizedDataType lengths in the current implementation can be up to 2(22). The machine is implemented as two NuBus boards connected to a Mac IIf/x, using a mixture of TTL and FPGA technology clocked at 10 MHz.[SEP]", "label": "yes"}
{"original_question": "Is SLC22A3 expressed in the brain?", "id": "converted_146", "sentence1": "Is SLC22A3 expressed in the Head>Brain?", "sentence2": "The Solute Carrier Family 22 Member 1 (OCT) 3 is widely expressed in various Organ in Homo sapiens, and involved in the disposition of many exogenous and endogenous compounds. Several lines of evidence have suggested that POU5F1 gene expressed in the Head>Brain plays an important role in the regulation of neurotransmission. , The Solute Carrier Family 22 Member 1 3 (POU5F1 gene; synonymous: extraneuronal monoamine transporter, EMT, SLC22A3 gene) encodes an Protein Isoforms of the organic cation transporters and is expressed widely across the whole Head>Brain., In agreement with this distribution, POU5F1 gene/SLC22A3 gene-deficient CASP14 gene show evidence of altered monoamine neurotransmission in the Head>Brain, with decreased Protoplasm content and increased turnover of aminergic transmitters., Chemoradiotherapy, SLC6A6 gene (TauT/SLC6A6) and Solute Carrier Family 22 Member 1 (POU5F1 gene/SLC22A3) expressed at the BCSFB are involved in glycocyamine or creatine/creatine/creatinine efflux transport from Cerebrospinal Fluid., The Solute Carrier Family 22 Member 1 3 (POU5F1 gene; synonymous: extraneuronal monoamine transporter, EMT, SLC22A3 gene) encodes an Protein Isoforms of the organic cation transporters and is expressed widely across the whole Head>Brain, The Solute Carrier Family 22 Member 1 3 (POU5F1 gene; synonymous: extraneuronal monoamine transporter, EMT, SLC22A3 gene) encodes an Protein Isoforms of the organic cation transporters and is expressed widely across the whole Head>Brain. , Chemoradiotherapy may be a key factor facilitating blood-to-Head>Brain guanidinoacetate transport in patients deficient in S-adenosylmethionine:guanidinoacetate N-methyltransferase, the creatine biosynthetic enzyme, resulting in cerebral accumulation of guanidinoacetate. Chemoradiotherapy, SLC6A6 gene (TauT/SLC6A6) and Solute Carrier Family 22 Member 1 (POU5F1 gene/SLC22A3) expressed at the BCSFB are involved in glycocyamine or creatine/creatine/creatinine efflux transport from Cerebrospinal Fluid., SLC22A3 gene) encodes an Protein Isoforms of the organic cation transporters and is expressed widely across the whole Head>Brain., Chemoradiotherapy, SLC6A6 gene (TauT/SLC6A6) and Solute Carrier Family 22 Member 1 (POU5F1 gene/SLC22A3) expressed at the BCSFB are involved in glycocyamine or creatine/creatine/creatinine efflux transport from Cerebrospinal Fluid. Interestingly, Blood - Head>Brain barrier anatomy efflux transport of Ceramide Glucosyltransferase, human, including guanidinoacetate and creatine/creatine/creatinine, is negligible, though the Blood - Head>Brain barrier anatomy has a variety of efflux transport systems for synthetic precursors of Ceramide Glucosyltransferase, human, such as Antifibrinolytic Antifibrinolytic amino acids and neurotransmitters.,  The Solute Carrier Family 22 Member 1 (OCT) 3 is widely expressed in various Organ in Homo sapiens, and involved in the disposition of many exogenous and endogenous compounds. Several lines of evidence have suggested that POU5F1 gene expressed in the Head>Brain plays an important role in the regulation of neurotransmission., Chemoradiotherapy, SLC6A6 gene (TauT/SLC6A6) and Solute Carrier Family 22 Member 1 (POU5F1 gene/SLC22A3) expressed at the BCSFB are involved in glycocyamine or creatine/creatine/creatinine efflux transport from Cerebrospinal Fluid., Several lines of evidence have suggested that POU5F1 gene expressed in the Head>Brain plays an important role in the regulation of neurotransmission., The Solute Carrier Family 22 Member 1 3 (POU5F1 gene; synonymous: extraneuronal monoamine transporter, EMT, SLC22A3 gene) encodes an Protein Isoforms of the organic cation transporters and is expressed widely across the whole Head>Brain., POU2F2 gene-OCT-3 display differential tissue distribution: POU2F1 gene is predominantly found in Abdomen>Liver of Homo sapiens, and Abdomen>Liver and Both kidneys in Rodent; POU2F2 gene is most strongly expressed in both human and rodent Both kidneys, whereas is POU5F1 gene primarily expressed in Placenta Specimen, but also more widely detected in various Body tissue, including Head>Brain and Chest>Lung.[SEP]Relations: POU2F2 has relations: anatomy_protein_present with Placenta Specimen, anatomy_protein_present with Placenta Specimen. Placenta Specimen has relations: anatomy_protein_present with SLC22A3, anatomy_protein_present with SLC22A3. SLC6A6 has relations: anatomy_protein_present with Placenta Specimen, anatomy_protein_present with Placenta Specimen. SLC22A3 has relations: anatomy_protein_present with Placenta Specimen, anatomy_protein_present with Placenta Specimen.", "label": "yes"}
{"original_question": "Are circRNAs susceptible to degradation by RNase R?", "id": "converted_4351", "sentence1": "Are circRNAs susceptible to degradation by Pancreatic ribonuclease R?", "sentence2": "Currently, an increasing body of evidence has demonstrated that 1) majority of circRNAs are evolutionarily conserved across species, stable, and resistant to Pancreatic ribonuclease R degradation, , Circular RNA (circRNA) has a closed-loop structure, and its 3' and 5' ends are directly covalently connected by reverse splicing, which is more stable than linear RNA., RNA, Circular are a kind of closed circular RNA molecule widely existing in transcriptomes. Due to lack of free ends, they are not easily cleaved by Pancreatic ribonuclease R, thus avoiding degradation. , Circular RNA (circRNAs) are a class of newly-identified non-coding RNA that lack 5' (cap) and 3' (polyadenylation) ends and are linked by a covalent bond to form a closed loop structure. In comparison to linear RNA, circRNAs are more resistant to exonuclease Pancreatic ribonuclease R-mediated degradation with a much stronger stability due to the absence of 3' terminals, Circular RNA (circRNAs) own unique capabilities to communicate with Nucleic Acids and ribonucleoproteins and are emerging as indispensable compositions of the regulatory messages encoded in the Genome - anatomical entity. Due to lack of 3' termini, circRNAs are more resistant to degradation by exonuclease Pancreatic ribonuclease R and possess greater stability than linear RNA. , Pancreatic ribonuclease R is a strong 3' to 5' exoribonuclease, which efficiently degrades linear RNA, such as mRNAs and rRNAs; therefore, the circular parts of lariat RNA and the circRNAs can be segregated from eukaryotic total RNA by their Pancreatic ribonuclease R resistance., Lariat RNA and circRNAs are both Pancreatic ribonuclease R resistant RNA., In comparison to linear RNA, circRNAs are more resistant to exonuclease Pancreatic ribonuclease R-mediated degradation with a much stronger stability due to the absence of 3' terminals., Due to lack of 3' termini, circRNAs are more resistant to degradation by exonuclease Pancreatic ribonuclease R and possess greater stability than linear RNA., Because circRNAs are not easily degraded by exonuclease Pancreatic ribonuclease R, they can exist more stably in Body Fluids than linear RNA., Therefore, it is essential to perform the RT-qPCR validation step only after linear RNA have been degraded using an exonuclease such as ribonuclease R (Pancreatic ribonuclease R)., is a strong 3' to 5' exoribonuclease, which efficiently degrades linear RNA, such as mRNAs and rRNAs; therefore, the circular parts of lariat RNA and the circRNAs can be segregated from eukaryotic total RNA by their Pancreatic ribonuclease R resistance. Thus, Pancreatic ribonuclease, sion of circRNAs is prevalent in Body tissue and Body Fluids,and their abnormal expression is related to Specimen Source Codes - Specimen Source Codes - tumor progression.circRNAs are stable even under the treatment of Pancreatic ribonuclease R because of their circular conformation.As circRNAs, e to lack of 3' termini, circRNAs are more resistant to degradation by exonuclease Pancreatic ribonuclease R and possess greater stability than linear RNA. molybdenum, e circRNAs are not easily degraded by exonuclease Pancreatic ribonuclease R, they can exist more stably in Body Fluids than linear RNA. Based,  is stable, difficult to cleave and resistant to REXO5 gene or Pancreatic ribonuclease R degradation. circRN, the unique structures, circRNAs are resistant to exonuclease Pancreatic ribonuclease R and maintain stability more easily than linear RNA. Rece, rison to linear RNA, circRNAs are more resistant to exonuclease Pancreatic ribonuclease R-mediated degradation with a much stronger stability due to the absence of 3' terminals. Conseque,  RT-PCR analysis showed that sheep circRNAs are resistant to Pancreatic ribonuclease R digestion and are expressed in prenatal and postnatal Pituitary Gland. GO and , Currently, an increasing body of evidence has demonstrated that 1) majority of circRNAs are evolutionarily conserved across species, stable, and resistant to Pancreatic ribonuclease R degradation, and often exhibit cell-specific, and tissue-specific/developmental-stage-specific expression and can be largely independent of the expression levels of the linear host gene-encoded linear RNA; 2) the biogenesis of circRNAs via back-splicing is different from the canonical splicing of linear RNA; 3) circRNA biogenesis is regulated by specific cis-acting elements and Trans-Activators; 4) circRNAs regulate biological and pathological processes by sponging MicroRNAs, binding to RNA-Binding Proteins (SUGP1 gene), regulators of splicing and transcription, modifiers of parental gene expression, and regulators of protein translation or being translated into Peptides in various diseases; 5) circRNAs have been identified for their enrichment and stability in Exosomes and detected in Body Fluids such as Homo sapiens blood, Specimen Source Codes - Saliva, and Cerebrospinal Fluid, suggesting that these exo-circRNAs have potential applications as disease biomarkers and novel therapeutic targets; 6) several circRNAs are regulated by oxidative stress and mediate Reactive Oxygen Species (ROS) production as well as promote ROS-induced cellular death, cell apoptosis, and Inflammation; 7) circRNAs have also emerged as important regulators in atherosclerotic cardiovascular disease, Metabolic Diseases, and Malignant Neoplasms; 8) the potential mechanisms of several circRNAs have been described in diseases, hinting at their potential applications as novel therapeutic targets., To prove their circularity as well as biochemically enrich these RNA Transcript, it has become standard in the field to use the 3'-5' exonuclease Pancreatic ribonuclease R. Here, we demonstrate that standard protocols involving Pancreatic ribonuclease R can fail to digest >20% of all highly expressed linear RNA, but these shortcomings can largely be overcome., We propose that such an R-loop dependent Circular Intronic RNA degradation likely represents a mechanism that on one hand limits Circular Intronic RNA accumulation by recruiting Pancreatic ribonuclease H1 and on the other hand resolves R-Loop Structures for transcriptional elongation at some GC-rich Circular Intronic RNA-producing loci., As circular RNA (circRNAs) are resistant to degradation by exonucleases, their abundance relative to linear RNA can be used as a surrogate marker for mRNA stability in the absence of transcription., The synthetic circular sponge was resistant to digestion with Pancreatic ribonuclease R. Luciferase assays and functional experiments showed that the circular multi-miR sponge was more stable than its linear counterpart., RNA with highly structured 3' ends, including snRNAs and histone mRNAs, are naturally resistant to Pancreatic ribonuclease R, but can be efficiently degraded once a Poly(A) Tail has been added to their ends., Thousands of eukaryotic protein-coding genes generate circular RNA that have covalently linked ends and are resistant to degradation by exonucleases.[SEP]", "label": "no"}
{"original_question": "Does radiotherapy for Hodgkin disease increases risk for lung cancer?", "id": "converted_3703", "sentence1": "Does radiotherapy for Hodgkin disease increases risk for Primary malignant neoplasm of Chest>Lung?", "sentence2": "Risks of Chest>Lung, Breast, and gastrointestinal (GI) cancers increase with higher radiation dose. , CONCLUSIONS: RT treatment, especially with doses higher than 42 Gy, and Location characteristic ID - Smoking increase the risk of SN after Hodgkin Disease. In this series, LC patients with early stages had a shorter elapsed time from Hodgkin Disease diagnosis and longer OS, therefore the role of LC screening in Hodgkin Disease survivors should be prospectively evaluated and Location characteristic ID - Smoking cessation counseling ought to be a key aspect during follow-up., BACKGROUND: Long-term Hodgkin lymphoma (Hodgkin Disease) survivors have an increased risk of late cardiac morbidity and secondary Primary malignant neoplasm of Chest>Lung after chemotherapy and mediastinal radiotherapy. , PURPOSE: Hodgkin lymphoma (Hodgkin Disease) survivors have an increased risk of Cardiovascular Diseases (CD), Primary malignant neoplasm of Chest>Lung, and Malignant neoplasm of Breast., Lung cancer (LC) represents the most common Solid Neoplasm in survivors of Hodgkin's disease (HD), and the assessment of the mutational status of oncogenic driver mutations in LC is now standard. , PURPOSE: Hodgkin lymphoma (Hodgkin Disease) survivors face an increased risk of treatment-related Primary malignant neoplasm of Chest>Lung. , Increased risk of second Primary malignant neoplasm of Chest>Lung in Lymphoma, Non-Hodgkin survivors: a meta-analysis., BACKGROUND: Patients treated for Lymphoma, Non-Hodgkin (Hodgkin Disease) have a higher risk of developing second Primary malignant neoplasm of Chest>Lung (CCL21 gene) compared with the general population. , The pooled relative risk (RR) of CCL21 gene was 4.62 (95 % confidence interval [CI], 3.18-6.70], I (2) = 98 %), with a median absolute excess rate of 10.4 per 10,000 person-years. , CONCLUSIONS: The current meta-analysis provided a detailed estimate of the risk of CCL21 gene among Hodgkin Disease survivors. , CONCLUSIONS\n\nThe excess risk of Primary malignant neoplasm of Chest>Lung in Hodgkin's disease patients treated with radiotherapy is related to the radiation dose received by the affected area of the Chest>Lung., BACKGROUND\n\nLung cancer is a frequent cause of death in patients cured of Hodgkin's disease, but the contributions of chemotherapy, radiotherapy, and Location characteristic ID - Smoking are not well described., CONCLUSIONS\n\nPast treatments with Alkylating Agents and radiation therapy for Hodgkin's disease were associated with an increased risk of Primary malignant neoplasm of Chest>Lung in a dose-dependent and additive fashion., BACKGROUND\n\nSeveral studies have shown that survivors of Hodgkin's disease have increased risk of Primary malignant neoplasm of Chest>Lung, but the factors responsible for this excess risk are not well known., PURPOSE\n\nThis study was undertaken to investigate the effects of radiation dose, chemotherapy, and Location characteristic ID - Smoking on the risk of Primary malignant neoplasm of Chest>Lung following treatment of Hodgkin's disease., Increased risk of Primary malignant neoplasm of Chest>Lung, Non-Lymphoma, Non-Hodgkin of bone, and leukemia following Hodgkin's disease., It is recognized that survivors of Hodgkin's disease are at a substantially increased risk of Primary malignant neoplasm of Chest>Lung., The risk of Chest>Lung and Malignant neoplasm of Breast is significantly increased after therapy for Hodgkin 's disease ( HD) , but there are few data that describe the molecular profiles of these Neoplasms . , Hodgkin lymphoma ( Hodgkin Disease ) survivors have an increased risk of Cardiovascular Diseases ( CD) , Primary malignant neoplasm of Chest>Lung , and Malignant neoplasm of Breast . , BACKGROUND\nLung cancer is a frequent cause of death in patients cured of Hodgkin's disease, but the contributions of chemotherapy, radiotherapy, and Location characteristic ID - Smoking are not well described., CONCLUSIONS\nPast treatments with Alkylating Agents and radiation therapy for Hodgkin's disease were associated with an increased risk of Primary malignant neoplasm of Chest>Lung in a dose-dependent and additive fashion., Lung cancer in Hodgkin's disease: association with previous radiotherapy., Twenty-eight (94%) of 30 patients developing metachronous Primary malignant neoplasm of Chest>Lung received supradiaphragmatic irradiation as primary therapy for HD., The risk ratio for the development of Primary malignant neoplasm of Chest>Lung among HD patients was 5.6 times that expected in the general population., Seven cases of Primary malignant neoplasm of Chest>Lung were observed in patients with Hodgkin's disease (HD) since 1970., BACKGROUND\nSeveral studies have shown that survivors of Hodgkin's disease have increased risk of Primary malignant neoplasm of Chest>Lung, but the factors responsible for this excess risk are not well known., The excess risk of Primary malignant neoplasm of Chest>Lung in Hodgkin's disease patients treated with radiotherapy is related to the radiation dose received by the affected area of the Chest>Lung., Lung cancer is a frequent cause of death in patients cured of Hodgkin's disease, but the contributions of chemotherapy, radiotherapy, and Location characteristic ID - Smoking are not well described., Past treatments with Alkylating Agents and radiation therapy for Hodgkin's disease were associated with an increased risk of Primary malignant neoplasm of Chest>Lung in a dose-dependent and additive fashion., Several studies have shown that survivors of Hodgkin's disease have increased risk of Primary malignant neoplasm of Chest>Lung, but the factors responsible for this excess risk are not well known.[SEP]", "label": "yes"}
{"original_question": "Is the protein ABCG2 transmembrane?", "id": "converted_3459", "sentence1": "Is the protein ABCG2 transmembrane?", "sentence2": "the transmembrane adenosine triphosphate-binding cassette transporter G2, adenosine triphosphate-binding cassette (ABC) transporters are transmembrane efflux transporters mediating the extrusion of an array of substrates ranging from Antifibrinolytic Antifibrinolytic amino acids and Lipids to Xenobiotics, and many therapeutic compounds, including anticancer drugs., The adenosine triphosphate-binding cassette (ABC) transporter family is a large class of adenosine triphosphate energy-dependent transmembrane proteins[SEP]", "label": "yes"}
{"original_question": "Is there a role for MRPL53 in cancer?", "id": "converted_3326", "sentence1": "Is there a role for MRPL53 in cancer?", "sentence2": "MRPL53, a New Candidate Gene for Orofacial Clefting, Identified Using an eQTL Approach., A valuable approach to understand how individual and population genetic differences can predispose to disease is to assess the impact of genetic variants on cellular functions (e.g., gene expression) of \"U\" lymphocyte and tissue types related to pathological states. To understand the genetic basis of nonsyndromic cleft lip with or without cleft palate (NSCL/P) susceptibility, a complex and highly prevalent Congenital Abnormality, we searched for genetic variants with a regulatory role in a disease-related tissue, the lip muscle (orbicularis oris muscle [OOM]), of affected individuals. From 46 OOM samples, which are frequently discarded during routine corrective surgeries on patients with orofacial clefts, we derived Mesenchymal Stem Cells and correlated the individual genetic variants with gene expression from these Cultured Cells. Through this strategy, we detected significant cis-eQTLs (i.e., DNA variants affecting gene expression) and selected a few candidates to conduct an association study in a large Brazilian cohort (624 patients and 668 controls). This resulted in the discovery of a novel susceptibility locus for NSCL/P, rs1063588, the best eQTL for the MRPL53 gene, where evidence for association was mostly driven by the Native American ancestry component of our Brazilian sample. MRPL53 (2p13.1) encodes a 39S protein subunit of Mitochondrial Ribosomes and interacts with MYC protein, human protein, human, a TRANSCRIPTION FACTOR required for normal facial morphogenesis. [SEP]Relations: TRANSCRIPTION FACTOR binding has relations: molfunc_protein with MYC protein, human, molfunc_protein with MYC protein, human.", "label": "no"}
{"original_question": "Can SMAD6 variants cause craniosynostosis?", "id": "converted_3799", "sentence1": "Can SMAD6 protein, human Variant cause TWIST1 gene?", "sentence2": "SMAD6 protein, human protein, human Variant in TWIST1 gene: Genotype determination and phenotype evaluation., Enrichment of heterozygous Missense and truncating SMAD6 protein, human protein, human Variant was previously reported in nonsyndromic sagittal and Metopic synostosis, and interaction of SMAD6 protein, human protein, human Variant with a common polymorphism nearBMP2 (rs1884302) was proposed to contribute to inconsistent penetrance. We determined the occurrence of SMAD6 protein, human protein, human Variant in all types of TWIST1 gene, evaluated the impact of different Missense Variant on SMAD6 protein, human protein, human function, and tested independently whether rs1884302 Genotype determination significantly modifies the phenotype.METHODS: We performed resequencing of SMAD6 protein, human protein, human in 795 unsolved patients with any type of TWIST1 gene and genotyped rs1884302 in SMAD6 protein, human protein, human-positive individuals and relatives. We examined the inhibitory activity and stability of SMAD6 protein, human protein, human Missense Variant.RESULTS: We found 18 (2.3%) different rare damaging SMAD6 protein, human protein, human Variant, with the highest prevalence in Metopic synostosis (5.8%) and an 18.3-fold enrichment of loss-of-function Variant comparedwith gnomAD data (P < 10-7). Combined with eight additional Variant, ≥20/26 were transmitted from an unaffected parent but rs1884302 Genotype determination did not predict phenotype.CONCLUSION: Pathogenic SMAD6 protein, human protein, human Variant substantially increase the risk of both nonsyndromic and syndromic presentations of TWIST1 gene, especially Metopic synostosis. Functional analysis is important to evaluate Missense Variant. Genotyping of rs1884302 is not clinically useful. Mechanisms to explain the remarkable diversity of phenotypes associated with SMAD6 protein, human protein, human Variant remain obscure.[SEP]Relations: TWIST1 gene Fontaine type has relations: disease_disease with TWIST1 gene, disease_disease with TWIST1 gene.", "label": "yes"}
{"original_question": "Is there any role for HUWE1 in MYC signalling?", "id": "converted_2916", "sentence1": "Is there any role for HUWE1 protein, human in MYC protein, human signalling?", "sentence2": "HUWE1 protein, human protein, human is a critical colonic Neoplasms suppressor gene that prevents MYC protein, human protein, human signalling, DNA damage accumulation and Neoplasms initiation., To determine the importance of HUWE1 protein, human protein, human, we chose to examine its function in Malignant neoplasm of colon and/or rectum, where it is Mutation Abnormality in up to 15 per cent of tumours. Modelling of identified Gene Mutation showed that they inactivate the E3 ubiquitin ligase activity of HUWE1 protein, human protein, human. Genetic Gene Deletion Abnormality of Huwe1 rapidly accelerated tumourigenic in CASP14 gene carrying loss of the intestinal Neoplasms suppressor gene Apc, with a dramatic increase in Neoplasms initiation. Mechanistically, this phenotype was driven by increased MYC protein, human protein, human and rapid DNA damage accumulation leading to loss of the second copy of Apc The increased levels of DNA damage sensitised Huwe1-deficient tumours to DNA-damaging agents and to Gene Deletion Abnormality of the anti-apoptotic protein MCL1. Taken together, these data identify HUWE1 protein, human protein, human as a bona fide Neoplasms suppressor gene in the Structure of Structure of intestinal epithelium and suggest a potential vulnerability of HUWE1 protein, human protein, human-Mutation Abnormality tumours to DNA-damaging agents and inhibitors of Apoptosis Inhibiting Proteins.[SEP]Relations: malignant colon neoplasm has relations: disease_protein with MYC protein, human, disease_disease with Malignant neoplasm of colon and/or rectum, disease_protein with MYC protein, human, disease_disease with Malignant neoplasm of colon and/or rectum.", "label": "yes"}
{"original_question": "Is miR-126 involved in heart failure?", "id": "converted_908", "sentence1": "Is miR-126 involved in Congestive heart failure?", "sentence2": "he MicroRNAs miR-126 and miR-508-5p are associated with the outcome of between breakfast and lunch and NICM patients with CHF. These two MicroRNAs could be useful in the diagnosis of CHF patients, and might provide novel targets for prevention and treatment of CHF., The plasma concentration of miR-126 was negatively correlated with age and NYHA class, and could be a useful biomarker for Congestive Congestive heart failure., In 10 patients with Congestive Congestive heart failure, plasma concentrations of miR-126 were up-regulated with improvement of the NYHA class from IV to III.[SEP]", "label": "yes"}
{"original_question": "Does Yersinia pestis causes a respiratory infection?", "id": "converted_2040", "sentence1": "Does Yersinia pestis causes a respiratory Communicable Diseases?", "sentence2": "Inhalation of Yersinia pestis results in primary pneumonic plague, a highly lethal and rapidly progressing necrotizing Pneumonia, Yersinia pestis causes the fatal Respiratory Tract Diseases pneumonic plague., Pulmonary Communicable Diseases by Yersinia pestis causes pneumonic plague, a rapidly progressing and often fatal disease., Pulmonary Communicable Diseases with the bacterium Yersinia pestis causes pneumonic plague, an often-fatal disease for which no vaccine is presently available., Yersinia pestis causes the fatal Respiratory Tract Diseases pneumonic plague, Pneumonic plague is a deadly Respiratory Tract Diseases caused by Yersinia pestis, On July 8, 2014, the Colorado Department of Public Health and Environment (CDPHE) laboratory identified Yersinia pestis, the bacterium that causes plague, in a blood specimen collected from a man (patient A) hospitalized with Pneumonia., Early emergence of Yersinia pestis as a severe respiratory pathogen., The aerosol form of the bacterium Yersinia pestis causes the pneumonic plague, a rapidly fatal disease,  plague bacterium, Yersinia pestis, has historically been regarded as one of the deadliest pathogens known to mankind, having caused three major pandemics. After being transmitted by the bite of an infected flea arthropod vector, Y. pestis can cause three forms of human plague: bubonic, septicemic, and pneumonic,, Plague is an infectious disease caused by the Yersinia pestis microorganism, which is transmitted to the human host from a natural reservoir (different rodent species) by a flea bite. Plague is still encountered in Homo sapiens in the areas of its enzootic prevalence in local rodent populations. Infection by flea bite results in a bubonic or septicemic plague, possibly complicated by secondary Pneumonia. The person with pneumonic symptoms may be a source of a droplet-borne inhalatory Communicable Diseases for other people who consequently develop primary pneumonic plague. , uring pneumonic plague, the bacterium Yersinia pestis elicits the development of inflammatory lung lesions that continue to expand throughout Communicable Diseases. , In November 2006, the Uganda Ministry of Health received reports of an increase in bubonic plague cases and a possible outbreak of pneumonic plague among residents in the Arua and Nebbi districts. , Pneumonic plague is a fatal disease caused by Yersinia pestis that is associated with a delayed immune response in the Lung[SEP]", "label": "yes"}
{"original_question": "Is PUVA therapy indicated for eczema treatment?", "id": "converted_2056", "sentence1": "Is Methoxsalen With Ultraviolet A Therapy therapy indicated for Eczema treatment?", "sentence2": "With bath Methoxsalen With Ultraviolet A Therapy treatment, the best results were found in patients with hyperkeratotic Eczema (17/22; 77% good clinical response) followed by patients with palmoplantar Psoriasis (26/41; 63%) and patients with Vesicular Eczema of Hand and/or feet (8/16; 50%). , Oral vs. bath Methoxsalen With Ultraviolet A Therapy using methoxsalen for chronic palmoplantar Eczema., Both oral and bath Methoxsalen With Ultraviolet A Therapy with methoxsalen (8-MOP) have been shown to be effective in the treatment of chronic palmoplantar Eczema. , Oral Methoxsalen With Ultraviolet A Therapy is preferable for patients with hyperkeratotic Eczema and bath Methoxsalen With Ultraviolet A Therapy for patients with Vesicular Eczema of Hand and/or feet., Treatment of Hand Eczema is dominated by the administration of topical glucocorticosteriods. If topical treatment fails, the best second-line option is ultraviolet (UV) therapy alone or as combination therapy. Ultraviolet B therapy and Methoxsalen With Ultraviolet A Therapy (Psoralen [EPC] plus UVA) therapy is effective and has relatively few side effects. , Although local Methoxsalen With Ultraviolet A Therapy has been proven to be effective in the treatment of Chronic Hand Eczema, little is known about the efficacy and safety of local narrowband Ultraviolet B therapy (TL-01) for this condition., Local narrowband Ultraviolet B therapy phototherapy regimen is as effective as paint-Methoxsalen With Ultraviolet A Therapy therapy in patients with Chronic Hand Eczema of dry and dyshidrotic types., Location characteristic ID - Location characteristic ID - Smoking is likely to be a reason for the failure of bath-Methoxsalen With Ultraviolet A Therapy therapy in the treatment of chronic palmoplantar Eczema, in particular regarding smokers with Eczema of the dyshidrotic type where no complete remission was achieved., Treatment of chronic palmoplantar Eczema with local bath-Methoxsalen With Ultraviolet A Therapy therapy., Bath-Methoxsalen With Ultraviolet A Therapy therapy has been described as successful treatment for palmoplantar Eczema., Systemic Methoxsalen With Ultraviolet A Therapy therapy may be useful in the treatment of chronic palmoplantar Eczema., A new Psoralen [EPC]-containing gel for topical Methoxsalen With Ultraviolet A Therapy therapy: development, and treatment results in patients with palmoplantar and plaque-type Psoriasis, and hyperkeratotic Eczema., These results indicate that topical Methoxsalen With Ultraviolet A Therapy therapy with Psoralen [EPC] in aqueous gel is a useful therapeutic modality for treatment of Psoriasis patients, and patients with recalcitrant dermatoses such as palmoplantar Psoriasis and hyperkeratotic Eczema., In order to evaluate environmental influences possibly having an impact on the efficacy of this therapy, smokers and non-smokers suffering from palmoplantar Eczema treated with bath-Methoxsalen With Ultraviolet A Therapy therapy were compared., Does smoking influence the efficacy of bath-Methoxsalen With Ultraviolet A Therapy therapy in chronic palmoplantar Eczema?, Methoxsalen With Ultraviolet A Therapy therapy caused acute aggravation of the Eczema., Hyperkeratotic Eczema cleared significantly better with oral than with bath Methoxsalen With Ultraviolet A Therapy (P=0.03).CONCLUSION: Oral Methoxsalen With Ultraviolet A Therapy is preferable for patients with hyperkeratotic Eczema and bath Methoxsalen With Ultraviolet A Therapy for patients with Vesicular Eczema of Hand and/or feet., BACKGROUND: Systemic Methoxsalen With Ultraviolet A Therapy therapy may be useful in the treatment of chronic palmoplantar Eczema., These results indicate that topical Methoxsalen With Ultraviolet A Therapy therapy with Psoralen [EPC] in aqueous gel is a useful therapeutic modality for treatment of Psoriasis patients, and patients with recalcitrant dermatoses such as palmoplantar Psoriasis and hyperkeratotic Eczema., VITILIGO-ASSOCIATED MULTIPLE AUTOIMMUNE DISEASE SUSCEPTIBILITY 1 (finding) (60.9%) was the commonest skin disorder treated with Methoxsalen With Ultraviolet A Therapy, followed by Psoriasis (20.9%), endogenous Eczema (11.3%), mycosis fungoides (3.5%), Amyloidosis, Primary Cutaneous (2.6%) and Prurigo nodularis (0.9%)., bath Methoxsalen With Ultraviolet A Therapy using methoxsalen for chronic palmoplantar Eczema., A 36-year-old female patient was treated with Methoxsalen With Ultraviolet A Therapy for Vesicular Eczema of Hand and/or feet that had not shown sufficient response to topical therapy over the previous months., BACKGROUND: Both oral and bath Methoxsalen With Ultraviolet A Therapy with methoxsalen (8-MOP) have been shown to be effective in the treatment of chronic palmoplantar Eczema., One patient with Hand Eczema consistently had detectable 8-MOP levels 1 hour after topical Methoxsalen With Ultraviolet A Therapy treatments.CONCLUSION: This report indicates that there is minimal, if any, systemic absorption of 8-MOP after topical Methoxsalen With Ultraviolet A Therapy treatment of patients with palmoplantar Psoriasis., In the narrowband Ultraviolet B therapy-treated side, the tolerance of all the patients to the treatment was good all patients well-tolerated the treatment with the exception of mild Xerosis that responded to topical emollients.Local narrowband Ultraviolet B therapy phototherapy regimen is as effective as paint-Methoxsalen With Ultraviolet A Therapy therapy in patients with Chronic Hand Eczema of dry and dyshidrotic types, Bath-Methoxsalen With Ultraviolet A Therapy therapy has been described as successful treatment for palmoplantar Eczema, Location characteristic ID - Location characteristic ID - Smoking is likely to be a reason for the failure of bath-Methoxsalen With Ultraviolet A Therapy therapy in the treatment of chronic palmoplantar Eczema, in particular regarding smokers with Eczema of the dyshidrotic type where no complete remission was achieved, Systemic Methoxsalen With Ultraviolet A Therapy therapy may be useful in the treatment of chronic palmoplantar Eczema, However, few data are available on the effectiveness of local bath-Methoxsalen With Ultraviolet A Therapy therapy in palmoplantar Eczema.Our purpose was to assess the effectiveness of local bath-Methoxsalen With Ultraviolet A Therapy therapy in 28 patients with chronic palmar or plantar Eczema or both who were resistant to conventional topical treatment.After Fungi or Bacterial Infections had been excluded in all patients, Hand or feet or both were soaked for 15 minutes in warm water containing 1 mg/L methoxsalen, No phototoxic reactions were observed.Local bath-Methoxsalen With Ultraviolet A Therapy therapy is of value in the management of chronic palmoplantar Eczema resistant to standard modes of topical treatment, Treatment of chronic palmoplantar Eczema with local bath-Methoxsalen With Ultraviolet A Therapy therapy, Bath-Methoxsalen With Ultraviolet A Therapy therapy has been described as successful treatment for palmoplantar Eczema. , Location characteristic ID - Location characteristic ID - Smoking is likely to be a reason for the failure of bath-Methoxsalen With Ultraviolet A Therapy therapy in the treatment of chronic palmoplantar Eczema, in particular regarding smokers with Eczema of the dyshidrotic type where no complete remission was achieved., OBJECTIVE: Our purpose was to assess the effectiveness of local bath-Methoxsalen With Ultraviolet A Therapy therapy in 28 patients with chronic palmar or plantar Eczema or both who were resistant to conventional topical treatment. , CONCLUSION: Local bath-Methoxsalen With Ultraviolet A Therapy therapy is of value in the management of chronic palmoplantar Eczema resistant to standard modes of topical treatment. , Topical Methoxsalen With Ultraviolet A Therapy therapy for Chronic Hand Eczema., However, few data are available on the effectiveness of local bath-Methoxsalen With Ultraviolet A Therapy therapy in palmoplantar Eczema.Our purpose was to assess the effectiveness of local bath-Methoxsalen With Ultraviolet A Therapy therapy in 28 patients with chronic palmar or plantar Eczema or both who were resistant to conventional topical treatment.After Fungi or Bacterial Infections had been excluded in all patients, Hand or feet or both were soaked for 15 minutes in warm water containing 1 mg/L methoxsalen., No phototoxic reactions were observed.Local bath-Methoxsalen With Ultraviolet A Therapy therapy is of value in the management of chronic palmoplantar Eczema resistant to standard modes of topical treatment., Location characteristic ID - Location characteristic ID - Smoking is likely to be a reason for the failure of bath-Methoxsalen With Ultraviolet A Therapy therapy in the treatment of chronic palmoplantar Eczema, in particular regarding smokers with Eczema of the dyshidrotic type where no complete remission was achieved., However, our own observations showed that patients with palmoplantar Eczema of the dyshidrotic or hyperkeratotic type responded only partially to bath-Methoxsalen With Ultraviolet A Therapy therapy., In the narrowband Ultraviolet B therapy-treated side, the tolerance of all the patients to the treatment was good all patients well-tolerated the treatment with the exception of mild Xerosis that responded to topical emollients.Local narrowband Ultraviolet B therapy phototherapy regimen is as effective as paint-Methoxsalen With Ultraviolet A Therapy therapy in patients with Chronic Hand Eczema of dry and dyshidrotic types., Comparison of localized high-dose UVA1 irradiation versus topical cream Psoralen [EPC]-UVA for treatment of chronic vesicular Vesicular Eczema of Hand and/or feet., No phototoxic reactions were observed.CONCLUSION: Local bath-Methoxsalen With Ultraviolet A Therapy therapy is of value in the management of chronic palmoplantar Eczema resistant to standard modes of topical treatment., These results indicate that topical Methoxsalen With Ultraviolet A Therapy therapy with Psoralen [EPC] in aqueous gel is a useful therapeutic modality for treatment of Psoriasis patients, and patients with recalcitrant dermatoses such as palmoplantar Psoriasis and hyperkeratotic Eczema.., Treatment of chronic palmoplantar Eczema with local bath-Methoxsalen With Ultraviolet A Therapy therapy., Oral Methoxsalen With Ultraviolet A Therapy is preferable for patients with hyperkeratotic Eczema and bath Methoxsalen With Ultraviolet A Therapy for patients with Vesicular Eczema of Hand and/or feet.., Does smoking influence the efficacy of bath-Methoxsalen With Ultraviolet A Therapy therapy in chronic palmoplantar Eczema?, Local bath-Methoxsalen With Ultraviolet A Therapy therapy is of value in the management of chronic palmoplantar Eczema resistant to standard modes of topical treatment., However, few data are available on the effectiveness of local bath-Methoxsalen With Ultraviolet A Therapy therapy in palmoplantar Eczema., A new Psoralen [EPC]-containing gel for topical Methoxsalen With Ultraviolet A Therapy therapy: development, and treatment results in patients with palmoplantar and plaque-type Psoriasis, and hyperkeratotic Eczema., Location characteristic ID - Location characteristic ID - Smoking is likely to be a reason for the failure of bath-Methoxsalen With Ultraviolet A Therapy therapy in the treatment of chronic palmoplantar Eczema, in particular regarding smokers with Eczema of the dyshidrotic type where no complete remission was achieved.., In order to investigate the effectiveness of topical Methoxsalen With Ultraviolet A Therapy-bath therapy (Methoxsalen With Ultraviolet A Therapy-soak therapy) on chronic palmoplantar dermatoses, 30 patients with plaque-type Psoriasis, pustular Psoriasis, endogenous Eczema, Vesicular Eczema of Hand and/or feet and hyperkeratotic dermatitis of the Arecaceae and soles were treated over 8 weeks with Methoxsalen With Ultraviolet A Therapy-soak using 8-MOP., Our purpose was to assess the effectiveness of local bath-Methoxsalen With Ultraviolet A Therapy therapy in 28 patients with chronic palmar or plantar Eczema or both who were resistant to conventional topical treatment.[SEP]Relations: vitiligo-associated multiple autoimmune disease susceptibility 1 has relations: disease_phenotype_positive with VITILIGO-ASSOCIATED MULTIPLE AUTOIMMUNE DISEASE SUSCEPTIBILITY 1 (finding), disease_phenotype_positive with VITILIGO-ASSOCIATED MULTIPLE AUTOIMMUNE DISEASE SUSCEPTIBILITY 1 (finding). primary cutaneous amyloidosis has relations: disease_disease with Amyloidosis, Primary Cutaneous, disease_disease with Amyloidosis, Primary Cutaneous.", "label": "yes"}
{"original_question": "Is Bcl-2-like protein 1 an pro apoptotic protein?", "id": "converted_3753", "sentence1": "Is BCL2 gene-like protein 1 an pro apoptotic protein?", "sentence2": "Extensively established key effectors of such apoptotic bypass mechanisms, the antiapoptotic BCL-2 (apoptosis regulator BCL-2) proteins, determine the response of Tumor cells, malignant to chemotherapeutics, decreasing the expression of anti-apoptotic factors, including apoptosis regulator BCL2 gene and BCL2 gene-like protein 1 in FaDu cells, Like many Malignant Neoplasms, TNBC cells often deregulate programmed cell death by upregulating Apoptosis Inhibiting Proteins of the BCL2 protein, human (BCL2 gene) family.,  anti-apoptotic BCL2 gene-like protein 1 (bcl-x protein, Bcl-xL) [SEP]", "label": "no"}
{"original_question": "Does xaliproden improve prognosis of amyotrophic lateral sclerosis?", "id": "converted_3406", "sentence1": "Does xaliproden improve prognosis of amyotrophic lateral sclerosis?", "sentence2": "Treatment for crampsThere is evidence (13 RCTs, N = 4012) that for the treatment of Muscle Cramp in MND, compared to placebo:- memantine and dronabinol (Thrombocytopenia 1) are probably ineffective (moderate-quality evidence);- Vitamin E Drug Class may have little or no effect (low-quality evidence); and- the effects of threonine, gabapentin, xaliproden, riluzole, and baclofen are uncertain as the evidence is either very low quality or the trial specified the outcome but did not report numerical data., The medications comprised Vitamin E Drug Class, baclofen, riluzole, threonine, xaliproden, indinavir, and memantine. Six studies assessed Muscle Cramp as an adverse event. The medications comprised creatine/creatinine/creatinine, gabapentin, dextromethorphan, quinidine, and Lithium antipsychotics. In all 20 studies no favourable effect for the treatment of Muscle Cramp in Amyotrophic Lateral Sclerosis/MND could be demonstrated, but many studies were underpowered to draw a definite conclusion., . The six months intent-to-treat analysis showed no statistically significant effect but a trend in favour of 2 mg xaliproden compared to placebo for reduction in the rate of deterioration of FVC, Limb structure functional score, and manual muscle testing score (Oculodigitoesophagoduodenal syndrome)., These results support the use of a staging process to select suitable patients for phase II studies, and suggest that xaliproden may have potential effects in Amyotrophic Lateral Sclerosis and deserve further study., An effect of xaliproden on functional parameters, especially VC, was noted. Although this effect did not reach statistical significance, xaliproden had a small effect on clinically noteworthy aspects of disease progression in Amyotrophic Lateral Sclerosis., The six months intent-to-treat analysis showed no statistically significant effect but a trend in favour of 2 mg xaliproden compared to placebo for reduction in the rate of deterioration of FVC, Limb structure functional score, and manual muscle testing score (Oculodigitoesophagoduodenal syndrome)., An effect of xaliproden on functional parameters, especially VC, was noted., These results support the use of a staging process to select suitable patients for phase II studies, and suggest that xaliproden may have potential effects in Amyotrophic Lateral Sclerosis and deserve further study., The six months intent-to-treat analysis showed no statistically significant effect but a trend in favour of 2 mg xaliproden compared to placebo for reduction in the rate of deterioration of FVC, Limb structure functional score, and manual muscle testing score (Oculodigitoesophagoduodenal syndrome)., Although this effect did not reach statistical significance, xaliproden had a small effect on clinically noteworthy aspects of disease progression in Amyotrophic Lateral Sclerosis.[SEP]", "label": "no"}
{"original_question": "Is amiodarone a class I anti-arrhythmic drug?", "id": "converted_142", "sentence1": "Is amiodarone a Canadian Cardiovascular Society Grading Scale Class I Antiarrhythmic [EPC] drug?", "sentence2": "Common Canadian Cardiovascular Society Grading Scale Class I agents are excluded due to the inherent abnormal cardiac structure and function in the setting of Shock, Cardiogenic. Class III drug options include dofetilide and amiodarone., Amiodarone has been used as an Antiarrhythmic [EPC] drug since the 1970s and has an established role in the treatment of Ventricular tachyarrhythmia. Although considered to be a Canadian Cardiovascular Society Grading Scale Class III Antiarrhythmic [EPC], amiodarone also has Canadian Cardiovascular Society Grading Scale Class I, II and IV actions, which gives it a unique pharmacological and Antiarrhythmic [EPC] profile. , Amiodarone, an iodinated Benzofurans derivative, introduced in 1960's as an anti-anginal agent, emerged as a potent Anti-Arrhythmia Agents by 1970's and is currently one of the most commonly prescribed drugs in US for ventricular and Atrial arrhythmia. Although amiodarone is considered a Canadian Cardiovascular Society Grading Scale Class III Anti-Arrhythmia Agents, it also has Canadian Cardiovascular Society Grading Scale Class I, II, IV actions, making it a unique and effective Anti-Arrhythmia Agents., Amiodarone, a representative Canadian Cardiovascular Society Grading Scale Class III agent, exerts negative dromotropism by suppressing the fast sodium current responsible for conduction in acute administration (Canadian Cardiovascular Society Grading Scale Class I effects). Chronic amiodarone causes prolongation of Endoscopic Retrograde Cholangiopancreatography (Canadian Cardiovascular Society Grading Scale Class III effects), which is sometimes associated with negative dromotropism based on the alteration of passive or active membrane properties., Amiodarone, an iodinated Benzofurans derivative with predominantly Canadian Cardiovascular Society Grading Scale Class III Antiarrhythmic [EPC] effects, is used to treat supraventricular and Ventricular arrhythmia., Although amiodarone is considered a Canadian Cardiovascular Society Grading Scale Class III Anti-Arrhythmia Agents, it also has Canadian Cardiovascular Society Grading Scale Class I, II, IV actions, making it a unique and effective Anti-Arrhythmia Agents, Amiodarone, a Canadian Cardiovascular Society Grading Scale Class III antiarrhythmic drug, is one of the most effective drugs used in the treatment of ventricular and paroxysmal supraventricular tachyarrhythmia, Although amiodarone is considered a Canadian Cardiovascular Society Grading Scale Class III Anti-Arrhythmia Agents, it also has Canadian Cardiovascular Society Grading Scale Class I, II, IV actions, making it a unique and effective Anti-Arrhythmia Agents, Although considered to be a Canadian Cardiovascular Society Grading Scale Class III Antiarrhythmic [EPC], amiodarone also has Canadian Cardiovascular Society Grading Scale Class I, II and IV actions, which gives it a unique pharmacological and Antiarrhythmic [EPC] profile, Amiodarone is a potent Canadian Cardiovascular Society Grading Scale Class III Antiarrhythmic [EPC] drug that also possesses beta-blocking properties[SEP]", "label": "no"}
{"original_question": "Is Lennox-Gastaut Syndrome usually diagnosed in older adults?", "id": "converted_2117", "sentence1": "Is Lennox-Gastaut syndrome usually diagnosed in older adults?", "sentence2": "We studied 15 Langer-Giedion Syndrome patients (mean age ± 1 standard deviation [SD] = 28.7 ± 10.6 years) and 17 healthy controls (mean age ± 1 SD = 27.6 ± 6.6 years),  children with Lennox-Gastaut syndrome, Lennox-Gastaut syndrome (Langer-Giedion Syndrome) is a severe pediatric Epilepsy syndrome characterized by mixed seizures, Mental deterioration, and generalized slow (<3 Hz) spike wave discharges on electroencephalography, Clinical course and results of therapy were analysed in the group of 92 children, aged between 3 and 9 years, with diagnosed Lennox-Gastaut syndrome., We report the case of a 27-year-old Homo sapiens with a neurodevelopmental syndrome due to a 15q duplication, with Intellectual Disability, psychiatric disturbances, and an epileptic phenotype diagnosed as late-onset Lennox-Gastaut syndrome., Lennox-Gastaut syndrome is a relatively rare Epilepsy syndrome that usually begins in early-mid childhood and is characterized by multiple seizure types, particularly generalized seizures, which are often resistant to antiepileptic drug medication, Lennox-Gastaut syndrome is a severe childhood Epilepsy syndrome characterised by the diagnostic triad of a slow spike and wave pattern on electroencephalogram, multiple seizure types and developmental delay, We report the case of a 27-year-old Homo sapiens with a neurodevelopmental syndrome due to a 15q duplication, with Intellectual Disability, psychiatric disturbances, and an epileptic phenotype diagnosed as late-onset Lennox-Gastaut syndrome.., The Lennox-Gastaut syndrome, a severe form of Epilepsy that usually begins in early childhood, is difficult to treat., Lennox-Gastaut syndrome is a relatively rare Epilepsy syndrome that usually begins in early-mid childhood and is characterized by multiple seizure types, particularly generalized seizures, which are often resistant to antiepileptic drug medication., The Lennox-Gastaut syndrome is an age-specific disorder, characterised by Nonepileptic Seizures, a characteristic electroencephalogram (EEG), psychomotor delay and behaviour disorders. It occurs more frequently in males and onset is usually before the age of eight, with a peak between three and five years. Late cases occurring in adolescence and early adulthood have rarely been reported. [SEP]Relations: Epilepsy has relations: disease_disease with Epilepsy syndrome, disease_disease with Epilepsy syndrome. Epilepsy syndrome has relations: disease_disease with Epilepsy, disease_disease with Epilepsy.", "label": "no"}
{"original_question": "Is gabapentin effective for chronic pelvic pain?", "id": "converted_4399", "sentence1": "Is gabapentin effective for Chronic pelvic pain of female?", "sentence2": "There were no significant between-group differences in both worst and average numerical rating scale (NRS) pain scores at 13-16 weeks after randomisation. The mean worst NRS pain score was 7·1 (standard deviation [SLC17A5 gene] 2·6) in the gabapentin group and 7·4 (SLC17A5 gene 2·2) in the placebo group. Mean change from baseline was -1·4 (SLC17A5 gene 2·3) in the gabapentin group and -1·2 (SLC17A5 gene 2·1) in the placebo group (adjusted mean difference -0·20 [97·5% CI -0·81 to 0·42]; p=0·47). The mean average NRS pain score was 4·3 (SLC17A5 gene 2·3) in the gabapentin group and 4·5 (SLC17A5 gene 2·2) in the placebo group. Mean change from baseline was -1·1 (SLC17A5 gene 2·0) in the gabapentin group and -0·9 (SLC17A5 gene 1·8) in the placebo group (adjusted mean difference -0·18 [97·5% CI -0·71 to 0·35]; p=0·45)., INTERPRETATION: This study was adequately powered, but treatment with gabapentin did not result in significantly lower pain scores in women with Chronic pelvic pain of female, and was associated with higher rates of side-effects than placebo. Given the increasing reports of abuse and evidence of potential harms associated with gabapentin use, it is important that clinicians consider alternative treatment options to off-label gabapentin for the management of Chronic pelvic pain of female and no obvious pelvic pathology., Gabapentin not effective for Chronic pelvic pain of female in women., Gabapentin not effective for Chronic pelvic pain of female in women[SEP]", "label": "no"}
{"original_question": "Does sphingosine-1 phosphoate suppress epiregulin?", "id": "converted_4703", "sentence1": "Does sphingosine-1 phosphoate suppress epiregulin?", "sentence2": "S1P-induced FOXO1 gene gene and Proepiregulin, human gene expression suggests that the activation of S1P-S1PR axis may cooperate with Recombinant Gonadotropin in modulating follicle development., S1P-dependent Cyclic AMP-Responsive DNA-Binding Protein phosphorylation induced FOXO1 gene gene and the EGF-like epiregulin-encoding gene (Proepiregulin, human), confirming the exclusive role of Recombinant Gonadotropin and Recombinant Interleukins in this process, but did not affect steroidogenesis. [SEP]", "label": "no"}
{"original_question": "Does thyroid hormone affect cardiac remodeling ?", "id": "converted_1152", "sentence1": "Does thyroid hormone affect cardiac remodeling ?", "sentence2": "Thyroid Hormones exert important effects on heart remodeling through mir-208., RV and RA function and mechanics are significantly affected by SHT. l-T4 therapy and 1-year maintenance of euthyroid status improved but did not completely recover RV and RA function and deformation in the SHT patients, which implies that right heart remodeling caused by SHT is not reversible in a 1-year period., These results suggest that long-term T4 treatment after MI has beneficial effects on Muscle Cells, arteriolar, and collagen matrix remodeling in the non-infarcted area. Most importantly, results suggest improved survival of myocytes in the peri-infarct area.[SEP]", "label": "yes"}
{"original_question": "Is adenosine signaling prognostic for cancer outcome?", "id": "converted_4194", "sentence1": "Is adenosine signaling prognostic for cancer outcome?", "sentence2": "Adenosine Signaling Is Prognostic for Cancer Outcome and Has Predictive Utility for Immunotherapeutic Response., There are several agents in early clinical trials targeting components of the adenosine pathway including ADORA2A wt Allele and 5'-NUCLEOTIDASE. The identification of Malignant Neoplasms with a significant adenosine drive is critical to understand the potential for these Molecule. However, it is challenging to measure tumor adenosine levels at scale, thus novel, clinically tractable biomarkers are needed.EXPERIMENTAL DESIGN: We generated a gene expression signature for the adenosine signaling using regulatory networks derived from the literature and validated this in patients. We applied the signature to large cohorts of Disease from The Cancer Genome Atlas (TCGA) and cohorts of immune checkpoint inhibitor-treated patients.RESULTS: The signature captures baseline adenosine levels in vivo (r 2 = 0.92, P = 0.018), is reduced after small-molecule inhibition of ADORA2A wt Allele in CASP14 gene (r 2 = -0.62, P = 0.001) and Homo sapiens (reduction in 5 of 7 patients, 70%), and is abrogated after ADORA2A wt Allele knockout. Analysis of TCGA confirms a negative association between adenosine and overall survival (OS, HR = 0.6, P < 2.2e-16) as well as progression-free survival (PFS, HR = 0.77, P = 0.0000006). Further, adenosine signaling is associated with reduced OS (HR = 0.47, P < 2.2e-16) and PFS (HR = 0.65, P = 0.0000002) in CD8+ T-cell-infiltrated tumors. Mutation Abnormality Abnormality of TGFβ superfamily members is associated with enhanced adenosine signaling and worse OS (HR = 0.43, P < 2.2e-16). Finally, adenosine signaling is associated with reduced efficacy of anti-PD1 therapy in published cohorts (HR = 0.29, P = 0.00012).CONCLUSIONS: These data support the adenosine pathway as a mediator of a successful Antitumor immune response, demonstrate the prognostic potential of the signature for immunotherapy, and inform patient selection strategies for adenosine pathway modulators currently in development.[SEP]", "label": "yes"}
{"original_question": "Are thyroid hormone receptor alpha1 mutations  implicated in thyroid hormone resistance syndrome?", "id": "converted_1105", "sentence1": "Are Thyroid Hormones receptor alpha1 mutations  implicated in Thyroid Hormones resistance syndrome?", "sentence2": "Gene Mutation in Homo sapiens TRα1 mediate RTH with features of Hypothyroidism in particular Body tissue (e.g. skeleton, Multisection:Find:Pt:Abdomen+Pelvis>Gastrointestinal tract:Doc:US), but are not associated with a markedly dysregulated pituitary-thyroid axis., Clinical phenotype of a new type of Thyroid Hormones resistance caused by a Mutation Abnormality of the receptor[SEP]", "label": "yes"}
{"original_question": "Is Mycobacterium avium less susceptible to antibiotics than Mycobacterium tuberculosis?", "id": "converted_502", "sentence1": "Is Mycobacterium avium less susceptible to Antifungal Antibiotics, Topical than Mycobacterium tuberculosis antibody?", "sentence2": "The prevalence of cyclophosphamide/doxorubicin/mitomycin protocol lung Communicable Diseases in two inner city hospitals was four times higher than that of Tuberculosis., Most patients with combined Communicable Diseases were clinically consistent with Mycobacterium tuberculosis antibody and responded to anti Mycobacterium tuberculosis antibody treatment alone., The triplex PCR developed by us could be used to detect and differentiate M. tuberculosis, M. avium and other Genus Mycobacterium in a single reaction tube., Twelve (15%) of the 80 blood cultures were positive for Genus Mycobacterium, with Mycobacterium avium being identified in 7 (8.8%) samples and M. tuberculosis in 5 (6.2%). , The antimycobacterial activities of RS-112997, RS-124922 and RS-118641, three capuramycin analogues that inhibit phospho-N-acetylmuramyl-pentapeptide translocase, were tested against clinical isolates of Mycobacterium tuberculosis antibody antibody, Mycobacterium avium and Battey Bacillus, The MIC50/90 (mg/L) results for RS-118641 were: M. tuberculosis, 1/2; multidrug-resistant (MDR) M. tuberculosis, 0.5/2; M. avium, 4/8; and M. intracellulare, 0.06/0.5, These results suggest that capuramycin analogues exhibit strong antimycobacterial potential and should be considered for further evaluation in the treatment of M. tuberculosis and M. avium-M. intracellulare complex Infections of musculoskeletal system in Homo sapiens., Mycobacterium avium causes disseminated Communicable Diseases in patients with acquired immune deficiency syndrome., Overall incidences of Mycobacterium tuberculosis antibody antibody (Tuberculosis) and Mycobacterium avium-intracellulare Infection (cyclophosphamide/doxorubicin/mitomycin protocol) were 0.8 and 1.4 cases/100 person-years of follow-up (PYF), decreasing from 1.8 (Tuberculosis) and 3.5 cases/100 PYF (cyclophosphamide/doxorubicin/mitomycin protocol) before September 1995 to 0.3 and 0.2 cases/100 PYF after March 1997., Because M tuberculosis disease is preventable and curable and yet communicable, physicians should maintain a high degree of suspicion for tuberculosis in HIV-infected adults. In comparison, the goal of treating M avium complex in patients with advanced HIV Infections is to reduce constitutional symptoms and improve survival., cyclophosphamide/doxorubicin/mitomycin protocol pulmonary disease should be considered in the differential diagnosis of SPNs, even when encountered in geographic regions with a high prevalence of Tuberculosis, Pulmonary., From April 2001 to February 2002, 80 blood samples from patients who were suspected to have disseminated mycobacterial Communicable Diseases, presenting Fever symptoms (finding) and (preferably) a CD4 T cell count<100.0 cell/mL were investigated, interleukin-10 binding activity underlies distinct susceptibility of BALB/c and C57BL/6 CASP14 gene to Mycobacterium avium Communicable Diseases and influences efficacy of Antibiotics therapy., Clinical utility of rifabutin (RBT), a potent Antibiotics used in multidrug regimens for tuberculosis (Tuberculosis) as well as for Infections of musculoskeletal system caused by Mycobacterium avium-intracellulare Infection (cyclophosphamide/doxorubicin/mitomycin protocol), has been hampered due to dose-limiting Toxic effect. , Effective therapeutic regimens exist that are limited by the emergence of drug resistance and the inability of Antifungal Antibiotics, Topical to kill dormant organisms. , Clinical utility of rifabutin (RBT), a potent Antibiotics used in multidrug regimens for tuberculosis (Tuberculosis) as well as for Infections of musculoskeletal system caused by Mycobacterium avium-intracellulare Infection (cyclophosphamide/doxorubicin/mitomycin protocol), has been hampered due to dose-limiting Toxic effect., a potent Antibiotics used in multidrug regimens for tuberculosis (Tuberculosis) as well as for Infections of musculoskeletal system caused by Mycobacterium avium-intracellulare Infection (cyclophosphamide/doxorubicin/mitomycin protocol),, Clinical utility of rifabutin (RBT), a potent Antibiotics used in multidrug regimens for tuberculosis (Tuberculosis) as well as for Infections of musculoskeletal system caused by Mycobacterium avium-intracellulare Infection (cyclophosphamide/doxorubicin/mitomycin protocol), has been hampered due to dose-limiting Toxic effect., tuberculosis appear to have different genetic mechanisms for resisting the effects of these Antifungal Antibiotics, Topical, with pks12 playing a relatively more significant role in cyclophosphamide/doxorubicin/mitomycin protocol.[SEP]Relations: tuberculosis has relations: disease_disease with Tuberculosis, Pulmonary, disease_disease with Tuberculosis, Pulmonary.", "label": "yes"}
{"original_question": "Is ustekinumab a polyclonal antibody?", "id": "converted_3217", "sentence1": "Is ustekinumab a polyclonal antibody?", "sentence2": "Ustekinumab Ab Ab, a Homo sapiens monoclonal IgG1 antibody targeting the p40-subunit shared by interleukin (IL)12 and interleukin-23 binding activity, represents a potential treatment for Dermatitis, Atopic (cytarabine/daunorubicin protocol).[SEP]", "label": "no"}
{"original_question": "Are BRAF mutations common in melanoma?", "id": "converted_1467", "sentence1": "Are BRAF protein, Homo sapiens Gene Mutation common in melanoma?", "sentence2": "patients with Serine-threonine protein kinase B-raf, Homo sapiens-mutant melanoma., Serine-threonine protein kinase B-raf, Homo sapiens-mutated melanoma , The RAS/RAF/MEK/ERK pathway has been reported to be activated in over 80% of all cutaneous melanomas, making it the focus of many scientific studies in the melanoma field. Discoveries of Gene Mutation and aberrant expression of components in this cascade, in particular, Serine-threonine protein kinase B-raf, Homo sapiens and Human Oncogene N-RAS render a deeper understanding of the mechanisms responsible for oncogenesis and provide new therapeutic strategies for this deadly disease. ,  Serine-threonine protein kinase B-raf, Homo sapiens-targeted therapies (e.g., vemurafenib, dabrafenib) have showed impressive results in systemic therapy for melanoma harboring activating Serine-threonine protein kinase B-raf, Homo sapiens V600E Gene Mutation. ,  An independent cohort of 91 archival MUPs was also screened for 46 hot spot Gene Mutation highly prevalent in melanoma including Serine-threonine protein kinase B-raf, Homo sapiens, Human Oncogene N-RAS, stem cell factor receptor activity, Guanine Nucleotide-Binding Protein G(q) Subunit Alpha, and Guanine Nucleotide-Binding Protein Subunit Alpha-11.,  a high rate of Serine-threonine protein kinase B-raf, Homo sapiens (45 of 101, 45%) and Human Oncogene N-RAS (32 of 101, 32%) Gene Mutation, collectively indicating a Mutation Abnormality profile consistent with cutaneous sun-exposed melanomas., Treatment of advanced melanoma has been improved with the advent of the Serine-threonine protein kinase B-raf, Homo sapiens inhibitors., Serine-threonine protein kinase B-raf, Homo sapiens is the most prevalent Oncogenes and an important therapeutic target in melanoma., Activating Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation, leading to constitutive activation of the MAPK signaling pathway, are common in a variety of Homo sapiens Malignant Neoplasms. Several small molecule Serine-threonine protein kinase B-raf, Homo sapiens inhibitors have been developed during the last years and shown promising results in clinical trials, especially for Metastatic melanoma, while they have been less effective in Malignant tumor of Abdomen+Pelvis>Colon. , Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation have emerged as an important predictive biomarker for metastasized melanoma. , Serine-threonine protein kinase B-raf, Homo sapiens V600 selective inhibitors have been approved for the treatment of V600 Mutation Abnormality positive Metastatic melanoma, , Serine-threonine protein kinase B-raf, Homo sapiens(V600) Mutation Abnormality-positive melanoma , Melanocytic neoplasm is the most aggressive form of Malignant neoplasm of skin. The treatment of patients with advanced melanoma is rapidly evolving due to an improved understanding of molecular drivers of this disease. Somatic Gene Mutation in Serine-threonine protein kinase B-raf, Homo sapiens are the most common genetic alteration found in these Neoplasms.,  genetically activated Serine-threonine protein kinase B-raf, Homo sapiens, is now commonly prescribed for Metastatic melanoma harboring a Serine-threonine protein kinase B-raf, Homo sapiens Mutation Abnormality., Serine-threonine protein kinase B-raf, Homo sapiens inhibitors improve melanoma patient survival, but resistance invariably develops. , Serine-threonine protein kinase B-raf, Homo sapiens inhibitors elicit rapid antitumor responses in the majority of patients with Serine-threonine protein kinase B-raf, Homo sapiens(V600)-mutant melanoma, but acquired drug resistance is almost universal. , Most patients with Serine-threonine protein kinase B-raf, Homo sapiens(V600)-mutant Metastatic melanoma develop resistance to selective RAF kinase inhibitors. , Serine-threonine protein kinase B-raf, Homo sapiens(V600E) Mutation Abnormality confers constitutive CXCL14 gene kinase activation in melanoma cells, promoting tumor growth. This discovery led to the development of Serine-threonine protein kinase B-raf, Homo sapiens kinase inhibitors like vemurafenib and dabrafenib. , (V600)Serine-threonine protein kinase B-raf, Homo sapiens Mutation Abnormality was identified as an ideal target for clinical therapy due to its indispensable roles in supporting melanoma initiation and progression., The Braf(V600E) Mutation Abnormality has been detected in patients with Metastatic melanoma, Abdomen+Pelvis>Colon, THYROID DIAGNOSTIC RADIOPHARMACEUTICALS, and other Malignant Neoplasms., Since the identification of activating Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation and subsequent development of drugs targeting the mutant Serine-threonine protein kinase B-raf, oncologists now need to incorporate prognostic and predictive biomarkers into treatment decisions for their melanoma patient, Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation occur in approximately 8% of all Homo sapiens Malignant Neoplasms and approach 50% in melanoma and papillary carcinoma of THYROID DIAGNOSTIC RADIOPHARMACEUTICALS., vemurafenib is a selective and potent small molecule inhibitor of the V600 mutant form of the Serine-threonine protein kinase B-raf used in the treatment of melanoma and Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum., Molecular studies demonstrated that the melanoma was positive for the 1799T>A (V600E) Mutation Abnormality in the Serine-threonine protein kinase B-raf, Homo sapiens gene., RAF kinase inhibitors have substantial therapeutic effects in patients with Serine-threonine protein kinase B-raf, Homo sapiens-mutant melanoma., An activating Serine-threonine protein kinase B-raf, Homo sapiens (V600E) kinase Mutation Abnormality occurs in approximately half of melanomas. , Activating Gene Mutation in the Serine-threonine protein kinase B-raf, Homo sapiens gene occur in approximately 50% of melanomas. More than 70% of Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation are V600E and 10-30% are V600K., Activating Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation, leading to constitutive activation of the MAPK signaling pathway, are common in a variety of Homo sapiens Malignant Neoplasms., Several small molecule Serine-threonine protein kinase B-raf, Homo sapiens inhibitors have been developed during the last years and shown promising results in clinical trials, especially for Metastatic melanoma, while they have been less effective in Malignant tumor of Abdomen+Pelvis>Colon. , Personalized melanoma medicine has progressed from histopathologic features to Serum Markers to molecular profiles. Since the identification of activating Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation and subsequent development of drugs targeting the mutant Serine-threonine protein kinase B-raf, oncologists now need to incorporate prognostic and predictive biomarkers into treatment decisions for their melanoma patients., The clinical activity of Serine-threonine protein kinase B-raf, Homo sapiens inhibitor (Serine-threonine protein kinase B-raf, Homo sapiens-I) therapy is a major breakthrough in the treatment of Metastatic melanoma carrying Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation. , The discovery of Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation in melanoma led to the development of Serine-threonine protein kinase B-raf, Homo sapiens inhibitors for the treatment of advanced melanoma. , Serine-threonine protein kinase B-raf, Homo sapiens represents one of the most frequently mutated protein kinase genes in Homo sapiens tumours. The Mutation Abnormality is commonly tested in pathology practice. Serine-threonine protein kinase B-raf, Homo sapiens Mutation Abnormality is seen in melanoma, papillary THYROID DIAGNOSTIC RADIOPHARMACEUTICALS carcinoma (including papillary THYROID DIAGNOSTIC RADIOPHARMACEUTICALS carcinoma arising from Ovarian Teratoma), ovarian serous tumours, Colorectal Carcinoma, Glioma, hepatobiliary carcinomas and Hairy cell leukaemia., Indeed, recent clinical trials involving Serine-threonine protein kinase B-raf, Homo sapiens selective inhibitors exhibited promising response rates in Metastatic melanoma patients. , A majority of cutaneous melanomas show activating Gene Mutation in the Human Oncogene N-RAS or Serine-threonine protein kinase B-raf, Homo sapiens proto-oncogenes, components of the Ras-Raf-Mek-Erk (MAPK) signal transduction pathway. The discovery of activating Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation in ∼50% of all melanomas has proved to be a turning point in the therapeutic management of the disseminated disease. This review summarizes the critical role of Serine-threonine protein kinase B-raf, Homo sapiens in melanoma pathophysiology, the clinical and pathological determinants of Serine-threonine protein kinase B-raf, Homo sapiens Mutation Abnormality status and finally addresses the current state of the art of Serine-threonine protein kinase B-raf, Homo sapiens inhibitors., To better understand the Serine-threonine protein kinase B-raf, Homo sapiens Mutation Abnormality profile in melanomas, we retrospectively analyzed data from 1112 primary and metastatic melanomas at our institution. The cohort included nonacral cutaneous (n = 774), Acral (n = 111), mucosal (n = 26), Uvea (n = 23), leptomeningeal (n = 1), and metastatic melanomas of unknown Site of primary lesion (n = 177). Serine-threonine protein kinase B-raf, Homo sapiens Mutation Abnormality hotspot regions in exons 11 and 15 were analyzed by pyrosequencing or with the primer extension MassARRAY system. A total of 499 (44.9%) specimens exhibited Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation, involving exon 15 [497 (99.6%)] or exon 11 [2 (0.4%)]. p.V600E was detected in 376 (75.4%) cases; the remaining 123 (24.6%) cases exhibited non-p.V600E Gene Mutation, of which p.V600K was most frequent [86 (17.2%)]. Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation were more frequent in nonacral cutaneous (51.4%) than Acral melanomas [18 (16.2%)] (P < 0.001); however, there was no significant difference among cutaneous histological subtypes. All mucosal, Uvea, and leptomeningeal melanomas were Serine-threonine protein kinase B-raf, Homo sapiens wild type (Wild Type Unspecified - zebrafish)., Recently, it was reported that Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation are frequent in melanoma., Activating Gene Mutation in Serine-threonine protein kinase B-raf, Homo sapiens are the most common Mutation in melanoma., Oncogenic Serine-threonine protein kinase B-raf, Homo sapiens and Human Oncogene N-RAS Gene Mutation are frequent in melanoma., Mutation of Serine-threonine protein kinase B-raf, Homo sapiens is now known to be common in cutaneous melanomas, and raises possible new therapeutic options of anti-RAF treatment for these patients, Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation are common events in a variety of Melanocytic nevus of skin and primary cutaneous melanomas, Approximately 40-60% of melanomas from Caucasian populations carry activating Gene Mutation in the Serine-threonine protein kinase B-raf, Homo sapiens Oncogenes, with the most common being the p.Val600Glu (V600E) hotspot Mutation Abnormality in exon 15, Using a cohort of 115 patients with primary invasive melanomas, we show that Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation are statistically significantly more common in melanomas occurring on skin subject to intermittent sun exposure than elsewhere (23 of 43 patients; P<.001, two-sided Fisher's exact test), Serine-threonine protein kinase B-raf, Homo sapiens Gene Mutation have been identified as the most common Oncogenes Mutation Abnormality in melanomas, especially important in those originating on nonchronically sun-damaged skin. [SEP]Relations: vemurafenib has relations: drug_protein with BRAF protein, Homo sapiens, drug_protein with BRAF protein, Homo sapiens. melanoma has relations: disease_protein with BRAF protein, Homo sapiens, disease_protein with Guanine Nucleotide-Binding Protein Subunit Alpha-11, disease_protein with stem cell factor receptor activity, disease_disease with Metastatic melanoma, disease_disease with Malignant neoplasm of skin, disease_protein with Guanine Nucleotide-Binding Protein G(q) Subunit Alpha, disease_protein with BRAF protein, Homo sapiens, disease_protein with Guanine Nucleotide-Binding Protein Subunit Alpha-11, disease_protein with stem cell factor receptor activity, disease_disease with Metastatic melanoma, disease_disease with Malignant neoplasm of skin, disease_protein with Guanine Nucleotide-Binding Protein G(q) Subunit Alpha. melanocytic neoplasm has relations: disease_disease with melanoma, disease_disease with melanoma. Colorectal Carcinoma has relations: disease_protein with BRAF protein, Homo sapiens, disease_disease with Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum, disease_protein with BRAF protein, Homo sapiens, disease_disease with Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum. stem cell factor receptor activity has relations: molfunc_protein with stem cell factor receptor activity, molfunc_protein with stem cell factor receptor activity. malignant Abdomen+Pelvis>Colon neoplasm has relations: disease_disease with Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum, disease_protein with BRAF protein, Homo sapiens, disease_disease with Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum, disease_protein with BRAF protein, Homo sapiens. Dabrafenib has relations: drug_drug with vemurafenib, drug_protein with BRAF protein, Homo sapiens, drug_drug with vemurafenib, drug_protein with BRAF protein, Homo sapiens. Metastatic melanoma has relations: disease_disease with melanoma, disease_disease with melanoma. Somatic Mutation Abnormality has relations: disease_phenotype_positive with Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum, disease_phenotype_positive with Malignant neoplasm of Abdomen+Pelvis>Colon and/or rectum.", "label": "yes"}
{"original_question": "Is BCL11B involved in schizophrenia?", "id": "converted_3687", "sentence1": "Is B-Cell Lymphoma/Leukemia 11B involved in SCHIZOPHRENIA 1 (disorder)?", "sentence2": "Interacting partners B-Cell Lymphoma/Leukemia 11B and GATAD2A gene gene are also SCHIZOPHRENIA 1 (disorder) risk Genes indicating that other Genes interacting with or are regulated by DNA Binding Protein DNA Binding Protein SATB2 are making a contribution to SCHIZOPHRENIA 1 (disorder) and cognition . , Interacting partners B-Cell Lymphoma/Leukemia 11B and GATAD2A gene gene are also SCHIZOPHRENIA 1 (disorder) risk Genes indicating that other Genes interacting with or are regulated by DNA Binding Protein DNA Binding Protein SATB2 are making a contribution to SCHIZOPHRENIA 1 (disorder) and cognition.[SEP]", "label": "yes"}
{"original_question": "Are conserved noncoding elements associated with the evolution of animal body plans?", "id": "converted_1343", "sentence1": "Are conserved noncoding elements associated with the evolution of Animal allergens body plans?", "sentence2": "Here, we discuss the evidence that CNEs are part of the core gene regulatory networks (GRNs) that specify alternative Animal allergens body plans. The major Animal allergens groups arose>550 million years ago. We propose that the cis-regulatory inputs identified by CNEs arose during the \"re-wiring\" of regulatory interactions that occurred during early Animal allergens evolution. Consequently, different Animal allergens groups, with different core GRNs, contain alternative sets of CNEs. Due to the subsequent stability of Animal allergens body plans, these core regulatory sequences have been evolving in parallel under strong purifying selection in different Animal allergens groups., Conserved noncoding elements and the evolution of Animal allergens body plans., Conserved noncoding elements and the evolution of Animal allergens body plans[SEP]", "label": "yes"}
{"original_question": "Do raspberries improve postprandial glucose and acute and chronic inflammation in adults with type 2 Diabetes?", "id": "converted_2930", "sentence1": "Do raspberries improve postprandial glucose and acute and chronic inflammation in adults with type 2 Diabetes?", "sentence2": "The NLR family pyrin domain containing 3 (NLRP3) inflammasome plays a critical role in insulin resistance and the pathogenesis of type 2 diabetes. Red raspberry (Retinoblastoma) contains high amounts of Dietary Fiber and polyphenolic compounds, which are known for their anti-oxidative and anti-inflammatory effects. [SEP]", "label": "yes"}
{"original_question": "Is pacritinib effective for treatment of myelofibrosis?", "id": "converted_2854", "sentence1": "Is pacritinib effective for treatment of Primary Myelofibrosis?", "sentence2": "pacritinib and its use in the treatment of patients with Primary Myelofibrosis who have THROMBOCYTOPENIA 2 (disorder)., pacritinib, a dual JAK2 protein, human protein, human and FLT3 gene gene PPP1R1A gene which also inhibits IRAK1 protein, human protein, human, has demonstrated the ability to favorably impact fluorouracil/methotrexate protocol-associated Splenomegaly and symptom burden, while having limited Bone Marrow Suppression with manageable Gastrointestinal:-:Point in time:^Patient:- toxicity., Other JAKis, such as fedratinib and pacritinib, proved to be useful in fluorouracil/methotrexate protocol. , Conclusions and Relevance: In patients with Primary Myelofibrosis and THROMBOCYTOPENIA 2 (disorder), including those with prior anti-Janus kinase therapy, pacritinib twice daily was more effective than Behavioral activation therapy, including ruxolitinib, for reducing Splenomegaly and symptoms., Developments of Janus kinase inhibitors, such as ruxolitinib, pacritinib, momelotinib, and febratinib enabled the effective management in fluorouracil/methotrexate protocol patients. ,  pacritinib (cisplatin/cyclophosphamide/doxorubicin protocol), a multi-kinase PPP1R1A gene with specificity for JAK2 protein, human protein, human, FLT3 gene gene, and IRAK1 protein, human protein, human but sparing JAK1 protein, human protein, human, has demonstrated clinical activity in fluorouracil/methotrexate protocol with minimal Bone Marrow Suppression. , pacritinib could be a treatment option for patients with Primary Myelofibrosis, including those with baseline cytopenias for whom options are particularly limited., Conclusions and Relevance\nIn patients with Primary Myelofibrosis and THROMBOCYTOPENIA 2 (disorder), including those with prior anti-Janus kinase therapy, pacritinib twice daily was more effective than Behavioral activation therapy, including ruxolitinib, for reducing Splenomegaly and symptoms., Expert commentary: pacritinib has demonstrated promising results in patients with Primary Myelofibrosis and THROMBOCYTOPENIA 2 (disorder)., pacritinib, a dual JAK2 protein, human protein, human and FLT3 gene gene PPP1R1A gene, improves disease-related symptoms and signs with manageable Gastrointestinal:-:Point in time:^Patient:- toxicity in patients with Primary Myelofibrosis with Splenomegaly and high-risk features, without causing overt Bone Marrow Suppression, and therefore may provide an important treatment option for a range of patients with Primary Myelofibrosis., pacritinib is an active agent in patients with fluorouracil/methotrexate protocol, offering a potential treatment option for patients with preexisting Genus Anemia and THROMBOCYTOPENIA 2 (disorder)., pacritinib (cisplatin/cyclophosphamide/doxorubicin protocol), a multi-kinase PPP1R1A gene with specificity for JAK2 protein, human protein, human, FLT3 gene gene, and IRAK1 protein, human protein, human but sparing JAK1 protein, human protein, human, has demonstrated clinical activity in fluorouracil/methotrexate protocol with minimal Bone Marrow Suppression., This article examines the role of JAK2 protein, human protein, human and FLT3 gene gene signaling in Primary Myelofibrosis and provides an overview of the clinical development of pacritinib as a new therapy for Primary Myelofibrosis., pacritinib appears to be an effective agent for the control of fluorouracil/methotrexate protocol-related symptoms and Splenomegaly with potentially fewer haematological side-effects when compared with ruxolitinib and seems a particularly promising agent for anaemic and thrombocytopenic patients. , Expert commentary: pacritinib has demonstrated promising results in patients with Primary Myelofibrosis and THROMBOCYTOPENIA 2 (disorder).[SEP]Relations: Ruxolitinib has relations: drug_protein with JAK1 protein, human, drug_protein with JAK2 protein, human, drug_protein with JAK1 protein, human, drug_protein with JAK2 protein, human. primary Primary Myelofibrosis has relations: disease_protein with JAK2 protein, human, disease_protein with JAK2 protein, human.", "label": "yes"}
{"original_question": "Is Weaver syndrome similar to Sotos?", "id": "converted_47", "sentence1": "Is Weaver syndrome similar to Sotos?", "sentence2": "Overgrowth conditions are a heterogeneous group of disorders characterised by increased growth and variable features, including Macrocephaly, distinctive facial appearance and various degrees of Learning difficulties and Intellectual Disability. Among them, Sotos and Weaver syndromes are clinically well defined and due to heterozygous Gene Mutation in NSD1 protein, human protein, human and EZH2 protein, human protein, human, respectively. NSD1 protein, human protein, human and EZH2 protein, human protein, human are both histone-modifying enzymes, NSD1 protein, human protein, human and EZH2 protein, human protein, human are Parameterized Data Type - Set domain-containing histone methyltransferases that play key roles in the regulation of transcription through histone modification and chromatin modeling: NSD1 protein, human protein, human preferentially methylates lysine residue 36 of histone 3 (H3K36) and is primarily associated with active transcription, while EZH2 protein, human protein, human shows specificity for lysine residue 27 (Histone H3 Lysine 28) and is associated with transcriptional repression, Constitutional NSD1 protein, human protein, human and EZH2 protein, human protein, human Gene Mutation cause Sotos and Weaver syndromes respectively, overgrowth syndromes with considerable phenotypic overlap, Clinically, Weaver syndrome is closely related to SOTOS SYNDROME 1, which is frequently caused by Gene Mutation in NSD1 protein, human protein, human, Overgrowth syndromes such as Beckwith-Wiedemann Syndrome, SOTOS SYNDROME 1, and Weaver syndrome have an increased risk of Neoplasms., Thus, it is not surprising that prenatal overgrowth occurs in several syndromes, including the Sotos and Weaver syndromes., NSD1 protein, human protein, human Gene Mutation are the major cause of SOTOS SYNDROME 1 and occur in some cases of Weaver syndrome but are rare in other overgrowth phenotypes., We conclude therefore that NSD1 protein, human protein, human Gene Mutation account for most cases of SOTOS SYNDROME 1 and a significant number of Weaver syndrome cases in our series., We conclude that intragenic Gene Mutation of NSD1 protein, human protein, human are the major cause of SOTOS SYNDROME 1 and account for some Weaver syndrome cases but rarely occur in other childhood overgrowth phenotypes., Overgrowth syndromes such as Beckwith-Wiedemann Syndrome, SOTOS SYNDROME 1, and Weaver syndrome have an increased risk of Neoplasms, NSD1 protein, human protein, human Gene Mutation are the major cause of SOTOS SYNDROME 1 and occur in some cases of Weaver syndrome but are rare in other overgrowth phenotypes, We conclude that intragenic Gene Mutation of NSD1 protein, human protein, human are the major cause of SOTOS SYNDROME 1 and account for some Weaver syndrome cases but rarely occur in other childhood overgrowth phenotypes, Considerable phenotypic overlap between Sotos and Weaver syndromes is also evident. , Considerable phenotypic overlap between Sotos and Weaver syndromes is also evident. The identification of an EZH2 protein, human protein, human mutation can therefore provide an objective means of confirming a subtle presentation of Weaver syndrome and/or distinguishing Weaver and Sotos syndromes.,  Overgrowth syndromes such as Beckwith-Wiedemann Syndrome, SOTOS SYNDROME 1, and Weaver syndrome have an increased risk of Neoplasms. Two previous cases of Neuroblastoma have been reported in children with Weaver syndrome., Weaver syndrome is closely related to SOTOS SYNDROME 1,, Overgrowth syndromes such as Beckwith-Wiedemann Syndrome, SOTOS SYNDROME 1, and Weaver syndrome have an increased risk of Neoplasms., Considerable phenotypic overlap between Sotos and Weaver syndromes is also evident., Clinically, Weaver syndrome is closely related to SOTOS SYNDROME 1, which is frequently caused by Gene Mutation in NSD1 protein, human protein, human.[SEP]Relations: Neuroblastoma has relations: disease_phenotype_positive with Beckwith-Wiedemann Syndrome, disease_phenotype_positive with SOTOS SYNDROME 1, disease_phenotype_positive with Beckwith-Wiedemann Syndrome, disease_phenotype_positive with SOTOS SYNDROME 1. Beckwith-Wiedemann Syndrome has relations: disease_protein with NSD1 protein, human, disease_protein with NSD1 protein, human. Feeding difficulties has relations: disease_phenotype_positive with SOTOS SYNDROME 1, disease_phenotype_positive with SOTOS SYNDROME 1. Weaver syndrome has relations: disease_protein with EZH2 protein, human, disease_protein with NSD1 protein, human, disease_protein with EZH2 protein, human, disease_protein with NSD1 protein, human. Macrocephaly has relations: disease_phenotype_positive with SOTOS SYNDROME 1, disease_phenotype_positive with Weaver syndrome, disease_phenotype_positive with SOTOS SYNDROME 1, disease_phenotype_positive with Weaver syndrome. SOTOS SYNDROME 1 has relations: disease_protein with NSD1 protein, human, disease_protein with NSD1 protein, human. Intellectual disability has relations: disease_phenotype_positive with Weaver syndrome, disease_phenotype_positive with SOTOS SYNDROME 1, disease_phenotype_positive with Weaver syndrome, disease_phenotype_positive with SOTOS SYNDROME 1.", "label": "yes"}
{"original_question": "Is DITPA a thyroid hormone analog utilized in experimental and clinical studies", "id": "converted_124", "sentence1": "Is DITPA a thyroid hormone analog utilized in experimental and clinical studies", "sentence2": "DITPA normalized the elevated serum T(3) and Thyrotropin:-:Pt:Ser/Plas:- when the dose reached 1 mg/kg · d and T(4) and rT(3) increased to the lower normal range., The identification of 3,5-diiodothyropropionic acid (DITPA) that binds to both α- and β-type threonine-tRNA ligase activity with relatively low affinity was unique in that this analog improves left ventricular function in Congestive Congestive heart failure as well as lowers cholesterol., Treatment with DITPA attenuates the acute inflammatory response and reduces myocardial infarct size., Thus DITPA administration impairs baseline Cardiac - anatomy qualifier parameters in CASP14 gene and can be fatal during in vivo acute myocardial I/R., DITPA improved some hemodynamic and metabolic parameters, but there was no evidence for symptomatic benefit in congestive Congestive Congestive heart failure, The results suggested that DITPA can promote a healthy Vasculature independently from its thyroid-related metabolic effects. ,  Moreover, DITPA and T(4) were efficacious in preventing effects of Hypothyroidism on Cardiac - anatomy qualifier function and BVD, Both T4 and DITPA had beneficial effects on chamber remodeling, which was most likely due to beneficial changes in cell shape and improved vascular supply., The thyroid analog DITPA enhances endothelial nitric oxide and beta-adrenergic-mediated vasorelaxation by increasing nitric oxide in the Vasculature.[SEP]Relations: Nitric Oxide has relations: contraindication with Congestive heart failure, contraindication with Congestive heart failure.", "label": "yes"}
{"original_question": "Are interferons defensive proteins?", "id": "converted_4184", "sentence1": "Are interferons defensive proteins?", "sentence2": "In response to Virus Diseases, various pattern recognition receptors (Porcine Reproductive and Respiratory Syndrome) are activated for the production of Interferon Type I (IFN I). ,  activating human leukocyte human leukocyte interferon (IFN) production and positively regulating antiviral response in Mammals. , The innate immune system, in particular the Interferon Type I (IFN) response, is a powerful defence against virus infections. , The human leukocyte human leukocyte interferon-induced GTP-binding protein Mx is responsible for a specific antiviral state against a broad spectrum of Virus Diseases that are induced by type-I interferons (IFN α/β) in different Vertebrates[SEP]", "label": "yes"}
{"original_question": "Is hemoglobin antimicrobial?", "id": "converted_4370", "sentence1": "Is Hemoglobin A1 (substance) antimicrobial?", "sentence2": "the α137-141 Peptides, a natural antimicrobial Peptides, can be obtained after hydrolysis of Hemoglobin A1 (substance), the main constituent of blood red part, Beyond its physiological activity, Hemoglobin are able to inhibit the growth of several microorganisms., A novel adenosine monophosphate, T. granosa Hemoglobin A1 (substance)-derived Peptides (TGH1), was identified and its antimicrobial effect[SEP]", "label": "yes"}
{"original_question": "Are DNA helicases involved in progeroid syndromes?", "id": "converted_1030", "sentence1": "Are DNA Helicases involved in progeroid syndromes?", "sentence2": "Among these syndromes, relevant advances have recently been made in Werner syndrome, one of several progeroid syndromes characterized by defective DNA Helicases,, Progeroid syndromes (Chromosome 11p11.2 Deletion Syndrome) constitute a group of disorders characterized by clinical features mimicking physiological aging at an early age., However, all the characterized Chromosome 11p11.2 Deletion Syndrome enter in the field of rare monogenic disorders and several causative genes have been identified. These can be separated in subcategories corresponding to (i) genes encoding DNA repair factors, in particular, DNA Helicases, and (ii) genes affecting the structure or post-translational maturation of Lamin Type A, a major nuclear component., None of the known progerias represents true precocious ageing. Some of them, including Werner (WS), Bloom (BS), and Rothmund-Thomson syndromes (Rothmund-Thomson syndrome) as well as combined xeroderma pigmentosa-Cockayne syndrome (XP-CS) are characterised by features resembling precocious ageing and the increased risk of malignant disease. Such phenotypes result from the Gene Mutation of the genes encoding Proteins involved in the maintenance of genomic integrity, in most cases DNA Helicases., Single-Genes Gene Mutation can produce Homo sapiens progeroid syndromes--phenotypes that mimic usual or \"normative\" aging., The prototypic example of the former is the Werner syndrome, a condition caused by Gene Mutation of the RecQ family of DNA Helicases., Progeria and progeroid syndromes are characterized by the earlier onset of complex senescent phenotypes. Werner Syndrome was originally identified as a Genes responsible for Werner syndrome (WS; \"Progeria of Adults\"). The Werner Syndrome Genes product has RecQ-type helicase domains in the central region of the Protein Info.[SEP]Relations: Werner syndrome has relations: disease_protein with Werner Syndrome, disease_protein with Werner Syndrome.", "label": "yes"}
{"original_question": "Has silicon been used in treatment of  incontinence ?", "id": "converted_1447", "sentence1": "Has silicon been used in treatment of  incontinence ?", "sentence2": "an artificial anal sphincter. Worldwide, there are two established devices on the market: the artificial bowel sphincter® (CONSTRICTING BANDS, CONGENITAL) from A. M. S. (Minnetonka, MNSs Blood-Group System, USA) and the soft anal band® from A. M. I. (Feldkirch, Austria). How to implant the artificial anal sphincter? Both devices consist of a silicon cuff which can be filled with fluid., The InVance™ system uses a silicon-coated polyester sling positioned under the bulbar Urethra specimen code via a perineal incision., Through a perineal incision three titanium screws with a polipropylene suture were Clinical act of insertion in each ischiopubic rami, and a silicon/polipropylene mesh (Invance) is affixed to them, compressing the bulbar Urethra specimen code, surgical treatment of female Urinary Stress Incontinence with a trans-obturator sub-urethral tape of Uratape (Porgés). METHODS: Treatment and follow up of their complication were performed at the CHRU of Lille. RESULTS: In both cases, this complication is related to prolonged vaginal exposition of the tape. Vaginal Route of Drug Administration Route of Drug Administration erosion always occurs next to the silicon coated section of the tape, A non-elastic, polypropylene tape (UraTape, Mentor-Porgès) with a silicon coated central part was placed under the mid-Urethra specimen code.,  Stress incontinence is a rare complication in men, usually following prostatic surgery. It can be treated conservatively with Pelvic Diaphragm training and alpha-adrenergic receptor agonists and if necessary surgically with submucosal collagen or silicon injections in the sphincter area or implantation of a sphincter prosthesis, The Femassist is a medical-grade silicon dome-shaped device, worn over the Urethra specimen code and held securely via suction and a commercially available adhesive lotion., To examine the performance of a silicon urinary control device for nonsurgical management of women with genuine stress incontinence, The \"FemAssist\" is a dome-shaped medical grade silicon device intended to be worn over the external urethral meatus and held in place by suction and an adhesive gel. Thirty eight women with varying degrees of genuine Urinary Stress Incontinence (GSUI) or mixed incontinence on multichannel urodynamic testing were fitted with one of two sizes of \"FemAssist[SEP]", "label": "yes"}
{"original_question": "Is ofatumumab effective for multiple sclerosis?", "id": "converted_4065", "sentence1": "Is ofatumumab effective for Multiple Sclerosis?", "sentence2": "Anti-MS4A1 wt Allele Agents for Multiple Sclerosis: Spotlight on Ocrelizumab and Ofatumumab., Ofatumumab, a fully Homo sapiens anti-MS4A1 wt Allele monoclonal antibody, that binds a distinct epitope, has been further investigated in phase 3 trials for relapsing forms of MS. , Conclusion: Ofatumumab offers beneficial outcomes for Root Mean Square by reducing relapse and Disability:Type:Pt:^Patient:Nom progression risk., Currently, new therapies are emerging that promise more convenience and an improved safety profile (ofatumumab) or remyelinating potential with clinical improvement (opicinumab)., The emerging B-cell depleting therapies, particularly anti-MS4A1 wt Allele agents such as rituximab, ocrelizumab, as well as the fully Homo sapiens ofatumumab, have shown promising clinical and magnetic resonance imaging benefit., AREAS COVERED: In this manuscript, we review mechanisms of action, efficacy, safety, and tolerance of anti-MS4A1 wt Allele therapies for MS, including rituximab, ocrelizumab, and ofatumumab., Another MS4A1 wt Allele directed Monoclonal Antibody [EPC], ofatumumab, is in phase 3. , Ofatumumab offers beneficial outcomes for Root Mean Square by reducing relapse and Disability:Type:Pt:^Patient:Nom progression risk., CONCLUSION: Imaging showed that all subcutaneous ofatumumab doses demonstrated efficacy (most robust: cumulative doses ≥30 mg/12 wk), with a safety profile consistent with existing ofatumumab data., CONCLUSIONS: Among patients with Multiple Sclerosis, ofatumumab was associated with lower annualized relapse rates than teriflunomide. [SEP]", "label": "yes"}
{"original_question": "Are epigenetic modifications implicated in cardiovascular development and disease?", "id": "converted_480", "sentence1": "Are epigenetic modifications implicated in Cardiovascular system development and Disease?", "sentence2": "Gene expression regulation through the interplay of DNA methylation and histone modifications is well-established, although the knowledge about the function of epigenetic signatures in Cardiovascular system Disease is still largely unexplored., The study of epigenetic markers is, therefore, a very promising frontier of science which may aid in a deeper understanding of molecular mechanisms underlying the modulation of gene expression in the biomolecule pathways linked to Cardiovascular system diseases., This review highlights our current knowledge of epigenetic gene regulation and the evidence that chromatin location location remodeling and histone modifications play key roles in the pathogenesis of Cardiovascular system Disease through (re)programming of Cardiovascular system (stem) cells commitment, identity and function., Notably, multiple subunits of switching defective/sucrose non-fermenting (SWI/SNF) chromatin location location-remodeling complexes have been identified as strong candidates underlying these defects because they physically and functionally interact with cardiogenic transcription factors critical to cardiac development, such as TBX5 gene gene, GATA-4, and NKX2-5 gene gene. While these studies indicate a critical role of SWI/SNF complexes in cardiac development and congenital Chest>Heart Disease, many exciting new discoveries have identified their critical role in the adult Chest>Heart in both physiological and pathological conditions involving multiple \"U\" lymphocyte types in the Chest>Heart, including Myocytes, Cardiac, Vascular Endothelial Cells, Pericytes, and Neural Crest Cells., Recent studies have greatly expanded our understanding of the regulation of Cardiovascular system development at the chromatin location location level, including the remodeling of chromatin location location and the ResponseLevel - ResponseLevel - modification of Histones. Chromatin-level regulation integrates multiple inputs and coordinates broad gene expression programs. Thus, understanding chromatin location location-level regulation will allow for a better appreciation of gene regulation as a whole and may set a fundamental basis for Cardiovascular system Disease., Genetic and epigenetic factors are of great importance in Cardiovascular system biology and Disease. Tobacco-smoking, one of the most important Cardiovascular system risk factors, is itself partially determined by genetic background and is associated with altered epigenetic patterns., Epigenetic modifications, including DNA methylation, histone ResponseLevel - ResponseLevel - modification (acetylation, methylation and phosphorylation) and miRNA, are critical for regulating developmental events. However, aberrant epigenetic mechanisms may lead to pathological consequences such as Cardiovascular system Disease (cyclophosphamide/dacarbazine/doxorubicin protocol), neurodegenerative Disease, BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, Metabolic Diseases, Specimen Type - Bone and skeletal diseases and various Malignant Neoplasms., Cardiovascular Disease pathways are now being approached from the epigenetic perspective, including those associated with Arteriosclerosis, angiogenesis, ischemia-reperfusion damage, and the Cardiovascular system response to Hypoxia, CTCAE and shear stress, among many others. With increasing interest and expanding partnerships in the field, we can expect new insights to emerge from epigenetic perspectives of Cardiovascular system health., Epigenetic modifications are heritable alterations of the Genome - anatomical entity, which can govern gene expression without altering the DNA Sequence. The purpose of this review is to render an overview of the possible mechanisms of epigenetic regulation of gene expression in response to environmental pollutants leading to Cardiovascular system diseases (Cerebrovascular Disorders)., From varied study approaches directed either toward the general understanding of the key pathway regulatory genes, or sampling population cohorts for global and gene-specific changes, it has been possible to identify several epigenetic signatures of environmental exposure relevant to Cerebrovascular Disorders., An understanding of chromatin location location remodelling in response to environmental stimuli conducive to Cerebrovascular Disorders is emerging, with the promise of novel diagnostic and therapeutic candidates., Consolidated knowledge is accumulating as to the role of epigenetic regulatory mechanisms in the physiology of vascular development and vascular tone as well as in the pathogenesis of Cardiovascular system Disease. The modulation of gene expression through ResponseLevel - ResponseLevel - modification of the epigenome by structural changes of the chromatin location location architecture without alterations of the associated genomic DNA Sequence is part of the cellular response to environmental changes. Such environmental conditions, which are finally being translated into adaptations of the Cardiovascular system system, also comprise pathological conditions such as Arteriosclerosis or Myocardial infarction:Finding:Point in time:^Patient:Ordinal. , Emerging data suggest that these epigenetic modifications also impact on the development of Cardiovascular system Disease. Histone modifications lead to the modulation of the expression of genetic information through ResponseLevel - ResponseLevel - modification of DNA accessibility. In addition, RNA-based mechanisms (e.g., MicroRNAs and long non-coding RNAs) influence the development of Disease., We here outline the recent work pertaining to epigenetic changes in a Cardiovascular system Disease setting., Epigenetics may represent one of the possible scientific explanations of the impact of such intrauterine risk factors for the subsequent development of Cardiovascular system Disease (Cerebrovascular Disorders) during adulthood., Epigenetic mechanisms include DNA methylation, histone ResponseLevel - ResponseLevel - modification, and microRNA alterations, which collectively enable the \"U\" lymphocyte to respond quickly to environmental changes. A number of Cerebrovascular Disorders risk factors, such as nutrition, smoking, pollution, stress, and the circadian rhythm, have been associated with ResponseLevel - ResponseLevel - modification of epigenetic marks. Further examination of these mechanisms may lead to earlier prevention and novel therapy for Cerebrovascular Disorders.,  Emerging data suggest that these epigenetic modifications also impact on the development of Cardiovascular system Disease., Emerging data suggest that these epigenetic modifications also impact on the development of Cardiovascular system Disease., Epigenetic alterations are associated with Inflammation and Cardiovascular system Disease in patients with chronic kidney Disease., Emerging data suggest that these epigenetic modifications also impact on the development of Cardiovascular system Disease, Epigenetic mechanisms that underpin metabolic and Cardiovascular system diseases., Epigenetic regulation of Cardiovascular system differentiation., Epigenetic control mechanisms play a key role in the regulation of embryonic development and tissue homeostasis and modulate Cardiovascular system diseases.[SEP]Relations: NKX2-5 gene has relations: cellcomp_protein with chromatin location, anatomy_protein_present with Chest>Heart, cellcomp_protein with chromatin location, anatomy_protein_present with Chest>Heart. inherited neurodegenerative disorder has relations: disease_disease with neurodegenerative Disease, disease_disease with neurodegenerative Disease.", "label": "yes"}
{"original_question": "Is there an association between presenteeism and depression?", "id": "converted_1526", "sentence1": "Is there an association between Presenteeism and depression?", "sentence2": "Presenteeism was positively associated with severity of depression (Health and Work Performance Questionnaire, P < 0.0001; WPAI, P < 0.0001)., Statistically significant correlations (0.32-0.53) were found between Presenteeism and increasing disability, Fatigue, depression, Anxiety Disorders, and reduced quality of life. , Presenteeism was associated with increasing Fatigue, depression, Anxiety Disorders, and reduced quality of life., Factors with less contribution to Presenteeism included physical limitations, depression or Anxiety Disorders, inadequate job training, and problems with supervisors and coworkers. , BACKGROUND: Subthreshold depression is highly prevalent in the general population and causes great loss to society especially in the form of reduced productivity while at work (Presenteeism)., Two major causes of worker Presenteeism (reduced on-the-job productivity as a result of health problems) are Musculoskeletal Pain:-:Point in time:^Patient:-:-:Point in time:^Patient:- and mental health issues, particularly depression. ,  Pain:-:Point in time:^Patient:-:-:Point in time:^Patient:- and depression were significantly associated with Presenteeism. Pr, Survey adjusted multivariable logistic regression assessed classification of 12-month, depression-related Presenteeism on the basis of socio-demographic, financial, work and health factors. , RESULTS: The LPT from absenteeism and Presenteeism (reduced performance while present at work) was significantly higher among the Major Depressive Disorder group., BACKGROUND: Cancer patients and suicide and depression is reported to be a major cause of Illness (finding)-related sub-optimal work performance (Presenteeism). , BACKGROUND: It is amply documented that Mood Disorders adversely affect job satisfaction, workforce productivity, and absenteeism/Presenteeism. , The difference in productivity loss due to impaired Presenteeism was significantly different between the two groups, but the productivity loss due to absenteeism was not. , Disease activity (OR 3.24, 95% CI 1.11-9.48) and depression (OR 3.22, 95% CI 1.22-8.48) were associated with absenteeism, while depression (OR 5.69, 95% CI 1.77-18.27, disease activity (OR 3.97, 95% CI 1.76-8.98), Anxiety Disorders (OR 3.90, 95% CI 1.83-8.31), self-efficacy (OR 0.71, 95% CI 0.58-0.86), and increasing age (OR 1.04 per year, 95% CI 1.00-1.08) were associated with Presenteeism. , Cancer patients and suicide and depression, in particular, appears to be associated with employment, absenteeism, and Presenteeism, and should therefore be prioritized in clinical practice., Cancer patients and suicide and depression frequently causes unemployment, absenteeism, and Presenteeism, which results in significantly reduced productivity., Presenteeism and absenteeism were significantly worse for the depression group at each time point (p < or = .001). In cross-sectional models, Presenteeism was associated with more severe depression symptoms, poorer general physical health, psychologically demanding work, the interaction ofpsychologically demanding work with depression, and less job control (r2 range = .33-.54)., Chronic conditions such as depression/Anxiety Disorders, BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, Arthritis, and back/neck pain are especially important causes of productivity loss. Comorbidities have significant non-additive effects on both absenteeism and Presenteeism., RESULTS: At baseline, all Presenteeism measures were sensitive to differences between those with (N=69) and without (N=363) depression/Anxiety Disorders., Cancer patients and suicide and depression and Anxiety Disorders were more consistently associated with \"Presenteeism\" (that is, lost productivity while at work) than with absenteeism, whether this was measured by cutback days or by direct questionnaires., RESULTS: Substantial research exists about Anxiety Disorders and depression costs, such as performance and productivity, absenteeism, Presenteeism, disability, A A physical disability exacerbation, mental health treatment, increased medical care costs, exacerbating of physical Illness (finding), and studies of mental health care limitations and cost-offset., The author discusses the etiology and potential solutions for managing this new component in the productivity equation and in addressing depression, the major contributor to Presenteeism., For employees who are currently Depressed mood, recent research evidence has demonstrated that pharmacotherapy can have a dramatic and positive effect on lost productivity, absenteeism, and Presenteeism., Among participants who were still employed, those with depression had significantly more job turnover, Presenteeism, and absenteeism. , Only depression affected both absenteeism-Presenteeism and critical incidents. , CONCLUSIONS: Depressive disorder in the workplace persist over time and have a major effect on work performance, most notably on \"Presenteeism,\" or reduced effectiveness in the workplace. , The negative effects of depression include those on patients' occupational functioning, including absenteeism, Presenteeism, and reduced opportunities for educational and work success. , The remitted group demonstrated a significant improvement in productivity (particularly Presenteeism) when compared with the new visit group (Z = -3.29, p = 0.001)., Cancer patients and suicide and depression in workers leads to significant absenteeism, \"Presenteeism\" (diminished capacity due to Illness (finding) while still present at work), and significantly increased medical expenses in addition to the costs of psychiatric care. , Significant predictors of Presenteeism and activity impairment at follow-up (controlled for gender, age, spondyloarthritis subgroups and Presenteeism at baseline) were Presenteeism at baseline, poor quality of life, worse disease activity, decreased physical function, lower self-efficacy pain and symptom, higher scores of Anxiety Disorders, depression, Location characteristic ID - Smoking and low education level, and for activity impairment also female sex. , \" Pain:-:Point in time:^Patient:-:-:Point in time:^Patient:- and depression were significantly associated with Presenteeism., Only depression affected both absenteeism-Presenteeism and critical incidents., Factors with less contribution to Presenteeism included physical limitations, depression or Anxiety Disorders, inadequate job training, and problems with supervisors and coworkers.[SEP]Relations: Anxiety Disorders disorder has relations: disease_disease with Anxiety Disorders, disease_disease with Anxiety Disorders.", "label": "yes"}
{"original_question": "Does Estrogen lead to forkhead FoxA1 activation?", "id": "converted_3587", "sentence1": "Does Estrogen lead to forkhead FOXA1 gene protein, human activation?", "sentence2": "We showed that CTGF protein, human acts upstream of the \"pioneer\" factor FOXA1 gene gene in determining the genomic response to Estrogen [EPC]. , Almost all Endoplasmic Reticulum-chromatin location location interactions and gene expression changes depended on the presence of FOXA1 gene gene and FOXA1 gene gene influenced genome-wide chromatin location location accessibility, FOXA1 gene gene is a key determinant of Estrogen Receptors function and endocrine response., As such, FOXA1 gene gene is a major determinant of Estrogen [EPC]-Endoplasmic Reticulum activity and endocrine response in Malignant neoplasm of breast cells., Location analysis of Estrogen Receptor alpha target promoters reveals that FOXA1 gene gene defines a Superkingdom (taxonomic category) of the Estrogen [EPC] response., Furthermore, knockdown of FOXA1 gene gene protein, human expression blocks the association of Endoplasmic Reticulum with chromatin location location and Estrogen [EPC]-induced gene expression demonstrating the necessity of FOXA1 gene gene protein, human in mediating an Estrogen [EPC] response in Malignant neoplasm of breast cells., FOXA1 gene gene protein, human determines Estrogen Receptors action in Malignant neoplasm of breast progression, Given previous findings from Cultured Cell Line, FOXA1 gene gene protein, human appears to play a critical role in this reprogramming of Endoplasmic Reticulum binding., FOXA1 gene gene expression can independently predict chemosensitivity of Endoplasmic Reticulum-positive Malignant neoplasm of breast patients.,  FOXA1 gene gene expression could be a prognostic marker in Endoplasmic Reticulum-positive Malignant neoplasm of breast., The pioneer transcription factor FOXA1 gene gene protein, human plays an important role in Estrogen [EPC] signaling by opening closed chromatin location location and promoting recruitment of the Estrogen Receptors to its target regions in DNA,  The phosphomimetic FOXA1 gene gene protein, human promoted the activation of Estrogen [EPC] signaling, whereas the nonphosphorylatable FOXA1 gene gene protein, human suppressed its activation.[SEP]", "label": "yes"}
{"original_question": "Is there an association between bruxism and reflux", "id": "converted_530", "sentence1": "Is there an association between Bruxism and reflux", "sentence2": "Rhythmic masticatory muscle activity, including sleep Bruxism (antimony), can be induced in healthy individuals by experimental Esophageal acidification, which plays an important role in the pathogenesis of Infantile Gastroesophageal Reflux disease (GERD). However, no robust evidence supports the association between antimony and GERD., Sleep Bruxism is prevalent in GERD patients, and GERD is highly associated with antimony., Our large-scale cross-sectional study found that problem behaviors in adolescents were associated with sleep problems, including sleep Bruxism, as well as lifestyle and food habits and GERD symptoms., The frequencies of EMG bursts, rhythmic masticatory muscle activity (RMMA) episodes, grinding noise, and the RMMA/microarousal ratio were significantly higher in the 20-minute period after Acids infusion than after Saline Solution infusion. RMMA episodes including antimony were induced by Esophageal acidification. , Direct restorative treatment of dental erosion caused by Infantile Gastroesophageal Reflux disease associated with Bruxism:, This article presents a case report of a 27-year-old male smoker with Tooth Wear and dentin sensitivity caused by GERD associated with Bruxism, Dental wear caused by association between Bruxism and Infantile Gastroesophageal Reflux disease:, This paper presents a case report in which Bruxism associated with acid feeding, smoking habit and episodes of gastric reflow caused severe Tooth Wear and great Muscle (organ) discomfort with daily Headache episodes., most jaw muscle activities, ie, RMMA, single short-burst, and clenching episodes, occur in relation to Infantile Gastroesophageal Reflux mainly in the supine position., Association between nocturnal Bruxism and Infantile Gastroesophageal Reflux., Nocturnal Bruxism may be secondary to nocturnal Infantile Gastroesophageal Reflux, occurring via sleep arousal and often together with swallowing.[SEP]Relations: Gastroesophageal reflux has relations: disease_phenotype_positive with Infantile Gastroesophageal Reflux disease, disease_phenotype_positive with Infantile Gastroesophageal Reflux disease.", "label": "yes"}
{"original_question": "Is the enzyme EPRS phosphorylated?", "id": "converted_2024", "sentence1": "Is the enzyme EPRS1 gene phosphorylated?", "sentence2": "Phosphorylation of glutamyl-prolyl tRNA synthetase (EPRS1 gene) has been investigated extensively in our laboratory for more than a decade, and has served as an archetype for studies of other AARSs., EPRS1 gene is dually phosphorylated by Cyclin-Dependent Kinases (CDK5 protein, human) at Ser(886) and then by a CDK5 protein, human-dependent-AGC kinase at Ser(999); , Diphosphorylated EPRS1 gene is released from its residence in the tRNA multisynthetase complex for immediate binding to NS1-associated protein and subsequent binding to ribosomal protein L13a and GAPDH protein, human protein, human. , Two-site phosphorylation of EPRS1 gene coordinates multimodal regulation of noncanonical translational control activity.[SEP]Relations: EPRS1 has relations: protein_protein with GAPDH protein, human, protein_protein with GAPDH protein, human.", "label": "yes"}
{"original_question": "Are there canonical marks of active chromatin in developmentally regulated genes?", "id": "converted_1995", "sentence1": "Are there canonical marks of active chromatin location in developmentally regulated Genes?", "sentence2": "Absence of canonical marks of active chromatin location location in developmentally regulated Genes., The interplay of active and repressive Histone Code is assumed to have a key role in the regulation of gene expression. In contrast to this generally accepted view, we show that the transcription of Genes temporally regulated during Fly (organism) and worm development occurs in the absence of canonically active Histone Code. Conversely, strong chromatin location location marking is related to transcriptional and post-transcriptional stability, an association that we also observe in Mammals. Our results support a model in which chromatin location location marking is associated with the stable production of RNA, whereas unmarked chromatin location location would permit rapid gene activation and deactivation during development. In the latter case, regulation by TRANSCRIPTION FACTOR would have a comparatively more important regulatory role than chromatin location location marks., Absence of canonical marks of active chromatin location location in developmentally regulated Genes, Absence of canonical marks of active chromatin location location in developmentally regulated Genes., In contrast to this generally accepted view, we show that the transcription of Genes temporally regulated during Fly (organism) and worm development occurs in the absence of canonically active Histone Code.[SEP]", "label": "no"}
{"original_question": "Is g-H2AX a marker for double strand breaks?", "id": "converted_3610", "sentence1": "Is g-H2AX a marker for double strand breaks?", "sentence2": "The specific phosphorylation of histone H2AX on serine residue 139, described as γ-H2AX, is an excellent indicator or marker of DNA double-strand breaks (DSBs). , expression of the DNA double-strand break marker gamma-H2AX (γH2AX) , pH2AX, a marker of the DNA double-strand break (DSB)[SEP]", "label": "yes"}
{"original_question": "Is Solanezumab effective for Alzheimer's Disease?", "id": "converted_2423", "sentence1": "Is solanezumab effective for ALZHEIMER DISEASE, FAMILIAL, 1?", "sentence2": "An analysis of publicly available data from the Phase II studies for bapineuzumab and solanezumab indicates that neither compound produced compelling evidence of drug-like behavior that would justify their progression into pivotal trials. , Notably, a recent study of solanezumab, an Serum Serum amyloid A protein A protein β monoclonal antibody, raises hope for the further therapeutic potential of immunotherapy, not only in Alzheimer's disease, but also for other Neurodegenerative Disorders, including Parkinson Disease. , For example, Eli Lilly announced a major change to its closely watched clinical trial for the Alzheimer's drug solanezumab which failed to reach statistical significance. , Areas covered: This contradiction prompted us to review all study phases of immunoglobulins, intravenous (IVIG), bapineuzumab, solanezumab, Avagacestat and latrepirdine to shed more light on these recent failures. ,  Results from phase III clinical trials in mild-to-moderate Alzheimer's disease (cytarabine/daunorubicin protocol) patients with two Monoclonal Antibodies bapineuzumab and solanezumab and intravenous immunoglobulin have been disappointing. Subsequent analysis of pooled data from both phase III trials with solanezumab showed a reduction in Mental deterioration in patients with mild cytarabine/daunorubicin protocol., Secondary analyses of EXPEDITION studies suggested a smaller functional effect of solanezumab relative to cognition. An increasing effect of solanezumab over 18 months was shown for cognition and function., RESULTS: In the mild cytarabine/daunorubicin protocol population, less cognitive and functional decline was observed with solanezumab (n = 659) versus placebo (n = 663), measured by ALZHEIMER DISEASE, FAMILIAL, 1 Assessment Scale Cognitive subscale, Mini-Mental State Examination, and ALZHEIMER DISEASE, FAMILIAL, 1 Cooperative Study-Activities of Daily Living functional scale Instrumental ADLs. , The promising results obtained with aducanumab and solanezumab against Alzheimer's disease (cytarabine/daunorubicin protocol) strengthen the vaccine approach to prevent cytarabine/daunorubicin protocol, despite of the many clinical setbacks. , CONCLUSIONS: solanezumab, a Antibodies, Monoclonal, Humanized that binds Serum Serum amyloid A protein A protein, failed to improve cognition or functional ability. , Results from phase III clinical trials in mild-to-moderate Alzheimer's disease (cytarabine/daunorubicin protocol) patients with two Monoclonal Antibodies bapineuzumab and solanezumab and intravenous immunoglobulin have been disappointing.[SEP]Relations: bapineuzumab has relations: drug_drug with solanezumab, drug_drug with solanezumab. solanezumab has relations: drug_drug with bapineuzumab, drug_drug with bapineuzumab.", "label": "no"}
{"original_question": "Can NEECHAM Confusion Scale be used for evaluation of postoperative delirium?", "id": "converted_1871", "sentence1": "Can NEECHAM Confusion Scale be used for evaluation of postoperative Delirium?", "sentence2": "Sampling was achieved in a nonrandomized targeted manner and Delirium was assessed using NeeCham questionnaire. , Delirium in older patients: a diagnostic study of NEECHAM Confusion Scale in surgical intensive care unit., AIMS AND OBJECTIVES: To estimate the diagnostic value and determine the feasibility of the NEECHAM Confusion Scale on Critical Illness older patients., CONCLUSIONS: Findings from this study confirm the good diagnostic value and ease of application of the NEECHAM scale with nonventilated intensive care patients.RELEVANCE TO CLINICAL PRACTICE: The NEECHAM scale can be used to detect Delirium during the routine nursing assessment of nonintubated older patients as it requires minimal demand and stress on the patient as well as on the bedside nurse., The NEECHAM Confusion Scale and the validated chart review instrument were used for diagnosis of Delirium. , Among the various screening instruments, NEECHAM Clouded consciousness scale and Delirium observation scale appear to be most suitable screening instrument for patients' in general medical and surgical wards, depending on the type of rater (physician or nurse). , Use of NEECHAM scaling enabled medical staff to identify cases of possible Clouded consciousness early, indicating that the NEECHAM Clouded consciousness scale should be useful for the detection of postoperative Delirium and Clouded consciousness in the surgical ward., Early detection of postoperative Delirium and Clouded consciousness in a surgical ward using the NEECHAM Clouded consciousness scale., In this study, we investigated whether the early detection of postoperative Delirium in elderly patients is possible using a simple, useful behavior-assessing scale, the NEECHAM Confusion Scale, and a method for comprehensively evaluating elderly persons' stress related to surgery, E-PASS., Assessment of the risk of postoperative Delirium in elderly patients using E-PASS and the NEECHAM Confusion Scale., The aim of this study was to determine which of the two Delirium observation screening scales, the NEECHAM Confusion Scale or the Delirium Observation Screening (DOS) scale, has the best discriminative capacity for diagnosing Delirium and which is more practical for daily use by nurses., For Delirium diagnosis and severity assessment, we used the NEECHAM Confusion Scale., Use of NEECHAM scaling enabled medical staff to identify cases of possible Clouded consciousness early, indicating that the NEECHAM Clouded consciousness scale should be useful for the detection of postoperative Delirium and Clouded consciousness in the surgical ward., The NEECHAM Confusion Scale was performed upon admission and prior to discharge.RESULTS: The incidence of DSM-IV related Delirium was 24%., A comparison of the CAM-ICU and the NEECHAM Confusion Scale in intensive care Delirium assessment: an observational study in non-intubated patients., Predictive value and validation of the NEECHAM Confusion Scale using DSM-IV criteria for Delirium as gold standard., Early detection of postoperative Delirium and Clouded consciousness in a surgical ward using the NEECHAM Clouded consciousness scale, The aim of this study was to determine which of the two Delirium observation screening scales, the NEECHAM Confusion Scale or the Delirium Observation Screening (DOS) scale, has the best discriminative capacity for diagnosing Delirium and which is more practical for daily use by nurses.The project was conducted on four wards of a university hospital; 87 patients were included, In addition, we scored the participants on the NEECHAM Scale and evaluated their postoperative Delirium and postoperative arrhythmia.On the nights of Days 4 and 5, the amount of activity of the exposure group was significantly lower and The sympathetic nervous index was significantly lower on the night of Day 5, In this study, we investigated whether the early detection of postoperative Delirium in elderly patients is possible using a simple, useful behavior-assessing scale, the NEECHAM Confusion Scale, and a method for comprehensively evaluating elderly persons' stress related to surgery, E-PASS. , The cut-off value of the NEECHAM score was established as 20 points, and patients showing values less than this after surgery were regarded as having postoperative Delirium. , Identification of Delirium was based on evaluation of the level of consciousness with the NEECHAM Confusion Scale and/or a chart-based instrument for Delirium., For Delirium diagnosis and severity assessment, we used the NEECHAM Confusion Scale., In this study, we investigated whether the early detection of postoperative Delirium in elderly patients is possible using a simple, useful behavior-assessing scale, the NEECHAM Confusion Scale, and a method for comprehensively evaluating elderly persons' stress related to surgery, E-PASS.The subjects were 160 patients aged more than 75 years who underwent surgery., In this study a nursing screening instrument, the NEECHAM Clouded consciousness scale, was studied for early recognition of Delirium ICU patients., The psychometric characteristics and the ease of use of the NEECHAM Clouded consciousness scale enables ICU nurses to early recognize Delirium., The trends of the NEECHAM scores in the 3 groups were compared, and the relationship between the NEECHAM scores and suspected clinical risk factors for Delirium was investigated., In groups showing an MMSE score of less than 25 or a preoperative NEECHAM score of less than 27, the incidence of postoperative Delirium was 76%.CONCLUSION: The results suggest that E-PASS and the NEECHAM score facilitate assessment of the risk of postoperative Delirium in elderly patients, contributing to early prevention/treatment., In this study, we investigated whether the early detection of postoperative Delirium in elderly patients is possible using a simple, useful behavior-assessing scale, the NEECHAM Confusion Scale, and a method for comprehensively evaluating elderly persons' stress related to surgery, E-PASS., Use of NEECHAM scaling enabled medical staff to identify cases of possible Clouded consciousness early, indicating that the NEECHAM Clouded consciousness scale should be useful for the detection of postoperative Delirium and Clouded consciousness in the surgical ward.., Early detection of postoperative Delirium and Clouded consciousness in a surgical ward using the NEECHAM Clouded consciousness scale., Assessment of the risk of postoperative Delirium in elderly patients using E-PASS and the NEECHAM Confusion Scale., For Delirium diagnosis and severity assessment, we used the NEECHAM Confusion Scale., The Neecham Confusion Scale and the Delirium Observation Screening Scale: capacity to discriminate and ease of use in clinical practice., The aim of this study was to determine which of the two Delirium observation screening scales, the NEECHAM Confusion Scale or the Delirium Observation Screening (DOS) scale, has the best discriminative capacity for diagnosing Delirium and which is more practical for daily use by nurses.[SEP]", "label": "yes"}
{"original_question": "Can valproic acid act as an activator of AMPK?", "id": "converted_238", "sentence1": "Can valproic acid act as an activator of AMPK?", "sentence2": "Here we demonstrate that valproic acid is a novel activator of AMP-Activated Protein Kinases (AMPK), a key regulator of cellular metabolism, using primary mouse and human hepatocytes., These studies are the first to establish valproic acid and its Metabolite as in vitro activators of AMPK.[SEP]", "label": "yes"}
{"original_question": "Has ATF4 transcription factor been linked to cancer and neoplastic transformation?", "id": "converted_2491", "sentence1": "Has ATF4 protein, human transcription factor been linked to Primary malignant neoplasm and neoplastic transformation?", "sentence2": "aken together, we discovered a novel axis of BCL10-regulated OSCC progression via STAT1/ATF4 protein, human protein, human/S100P/P65 signaling, which could predict the prognosis of OSCC and will be beneficial for developing therapeutic strategy against advanced OSCC, s a result, the level of phosphorylated Eukaryotic Initiation Factor 2 alpha (eIF2α) is markedly elevated, resulting in the promotion of a pro-adaptive signaling pathway by the inhibition of global protein synthesis and selective translation of Activating Transcription Factor 4 (ATF4 protein, human protein, human). , Many Malignant Neoplasms overexpress ATF4 protein, human protein, human, a stress-induced transcription factor that promotes cell survival under hypoxic conditions and other stresses of the tumor microenvironment, but the potential contributions of ATF4 protein, human protein, human to oncogenesis itself have been little explored. Here, we report that ATF4 protein, human protein, human promotes oncogene-induced neoplastic transformation by suppressing the expression of cellular senescence-associated genes. , Here, we report that ATF4 protein, human protein, human promotes oncogene-induced neoplastic transformation by suppressing the expression of cellular senescence-associated genes., Elevated levels of ATF4 protein, human protein, human were sufficient to suppress expression of these Proteins and drive oncogenic transformation., Our findings define a central function for ATF4 protein, human protein, human in promoting oncogenic transformation by suppressing a central pathway of cellular senescence.<br>, ATF4 protein, human protein, human expression is upregulated in Primary malignant neoplasm., Activating Transcription Factors (ATF4 protein, human protein, human), an endoplasmic reticulum stress-inducible transcription factor, plays important roles in Primary malignant neoplasm progression and resistance to therapy., Activating Transcription Factors (ATF4 protein, human protein, human) is a stress-induced transcription factor that is frequently upregulated in Primary malignant neoplasm cells., Our findings define a central function for ATF4 protein, human protein, human in promoting oncogenic transformation by suppressing a central pathway of cellular senescence., Stress-regulated transcription factor ATF4 protein, human protein, human promotes neoplastic transformation by suppressing expression of the INK4a/ARF cell senescence factors., Activating Transcription Factors (ATF4 protein, human protein, human), a member of the ATF/CREB family, has been reported to be related to tumor angiogenesis[SEP]Relations: malignant giant cell tumor has relations: disease_disease with Primary malignant neoplasm, disease_disease with Primary malignant neoplasm.", "label": "yes"}
{"original_question": "Does epidural anesthesia for pain management during labor affect the Apgar score of the the infant?", "id": "converted_2844", "sentence1": "Does epidural anesthesia for pain management during labor affect the Apgar score of the the infant?", "sentence2": " We retrospectively analyzed 93 consecutive single-pregnancy patients who underwent cesarean section with combined spinal-epidural anesthesia. The patients were divided into two groups, depending on the use of 6% Idiopathic Hypereosinophilic Syndrome 130/0.4: group A (461 ± 167 ml of saline-based Idiopathic Hypereosinophilic Syndrome was administered; 43 patients) and group B (Idiopathic Hypereosinophilic Syndrome not administered; 50 patients). The major outcome was umbilical cord chloride level at delivery. The volume infused from operating room admission until delivery was not significantly different between groups. The umbilical cord chloride level at delivery was statistically significantly higher in group A than in group B, but clinically similar (108 ± 2 vs. 107 ± 2 mmol/l, P = 0.02). No differences were observed in the Apgar score or other umbilical cord laboratory data at delivery (Na+, K+, pH, base excess), CONCLUSION\nSubarachnoid or epidural sufentanil, in the doses used in this study, associated with local anesthetics, had the same effect on the duration of labor after analgesia and in the Apgar score of newborns., CONCLUSION Subarachnoid or epidural sufentanil, in the doses used in this study, associated with local anesthetics, had the same effect on the duration of labor after analgesia and in the Apgar score of newborns.[SEP]", "label": "no"}
{"original_question": "Is Huntington's disease is caused by expansion of a CTG repeat in the HTT gene on Chromosome 4?", "id": "converted_3531", "sentence1": "Is Huntington Disease is caused by expansion of a CTG repeat in the SLC6A4 wt Allele gene on Chromosome 4?", "sentence2": "Huntington Disease (Hodgkin Disease) is caused by a CAG repeat expansion that encodes a polyglutamine (polyQ) expansion in the Hodgkin Disease disease Protein Info, Hodgkin Disease Protein Info, human (SLC6A4 wt Allele)., Huntington disease (Hodgkin Disease) is a dominantly inherited disorder caused by a CAG expansion Mutation Abnormality in the Hodgkin Disease Protein Info, human (SLC6A4 wt Allele) gene, which results in the SLC6A4 wt Allele Protein Info that contains an expanded polyglutamine tract., In Huntington Disease (Hodgkin Disease), expansion of CAG codons in the SLC6A4 wt Allele gene (SLC6A4 wt Allele) leads to the aberrant formation of Protein Info aggregates and the differential degeneration of striatal medium spiny neurons (MSNs)., Huntington disease (Hodgkin Disease) is a progressive Autosome dominant Neurodegenerative Disorders, characterized by abnormal movements, Mental deterioration, and psychiatric symptoms, caused by a CAG repeat expansion in the Hodgkin Disease Protein Info, human (SLC6A4 wt Allele) gene on chromosome 4p., Huntington Disease (Hodgkin Disease) is a polyglutamine disorder caused by a CAG expansion in the Huntingtin (SLC6A4 wt Allele) gene exon 1., IMPORTANCE\n\nHuntington disease (Hodgkin Disease), a prototypic monogenic disease, is caused by an expanded CAG repeat in the SLC6A4 wt Allele gene exceeding 35 units., Huntington Disease (Hodgkin Disease) is an Autosome dominantly inherited disorder caused by the expansion of CAG repeats in the Huntingtin (SLC6A4 wt Allele) gene., Huntington Disease (Hodgkin Disease) is a Neurodegenerative Disorders caused by a CAG trinucleotide repeat expansion in the Hodgkin Disease Protein Info, human (SLC6A4 wt Allele) gene., BACKGROUND Huntington Disease is caused by a CAG repeat expansion in the SLC6A4 wt Allele gene, SLC6A4 wt Allele., Huntington Disease (Hodgkin Disease) is an inherited neurodegenerative disease caused by an expanded CAG repeat in the SLC6A4 wt Allele gene., IMPORTANCE Huntington disease (Hodgkin Disease), a prototypic monogenic disease, is caused by an expanded CAG repeat in the SLC6A4 wt Allele gene exceeding 35 units., Huntington 's disease ( Hodgkin Disease ) is an inherited Neurodegenerative Disorders caused by a CAG repeat expansion within exon 1 of the Hodgkin Disease Protein Info, human ( SLC6A4 wt Allele ) gene. , Huntington 's disease ( Hodgkin Disease) , a dominantly inherited neurodegenerative disease , is defined by its genetic cause , a CAG-repeat expansion in the SLC6A4 wt Allele gene , its motor and psychiatric symptomology and primary loss of striatal medium spiny neurons ( MSNs) . , Huntington 's disease ( Hodgkin Disease ) is an incurable Neurodegenerative Disorders caused by a CAG repeat expansion in exon 1 of the Huntingtin ( SLC6A4 wt Allele ) gene. , Huntington 's disease ( Hodgkin Disease ) is a progressive Neurodegenerative Disorders caused by a CAG trinucleotide repeat expansion in the Hodgkin Disease Protein Info, human ( SLC6A4 wt Allele ) gene , which encodes a polyglutamine tract in the SLC6A4 wt Allele Protein Info . , Huntington 's disease ( Hodgkin Disease ) is an Autosome progressive Neurodegenerative Disorders caused by the expansion of CAG repeats in the SLC6A4 wt Allele gene. , Huntington 's disease ( Hodgkin Disease ) is an Autosome dominant neurodegenerative disease caused by the expansion of a CAG trinucleotide repeat in exon 1 of the Hodgkin Disease Protein Info, human ( htt ) gene. , Huntington 's disease ( Hodgkin Disease) , caused by a CAG repeat expansion in the Hodgkin Disease Protein Info, human ( SLC6A4 wt Allele ) gene , is characterized by abnormal Protein Info aggregates and motor and Impaired cognition . , Huntington 's disease ( Hodgkin Disease ) is a neurodegenerative disease caused by the expansion of a CAG trinucleotide repeat in exon 1 of the Hodgkin Disease Protein Info, human ( SLC6A4 wt Allele ) gene. , Huntington 's disease ( Hodgkin Disease ) is an Autosome disease caused by a CAG repeat expansion in the Hodgkin Disease Protein Info, human ( SLC6A4 wt Allele ) gene. , BACKGROUND\nHuntington Disease is caused by a CAG repeat expansion in the SLC6A4 wt Allele gene, SLC6A4 wt Allele., Huntington Disease (Hodgkin Disease) is an Autosome dominant disorder caused by an expansion in the trinucleotide CAG repeat in exon-1 in the SLC6A4 wt Allele gene, located on Chromosomes, Human, Pair 4., Hodgkin Disease is caused by expansion of the CAG trinucleotide repeat region in exon 1 of the Huntingtin gene (SLC6A4 wt Allele), leading to the formation of mutant SLC6A4 wt Allele transcripts (muHTT)., Huntington Disease (Hodgkin Disease) is a Neurodegenerative Disorders characterized by involuntary choreic movements, No No cognitive impairment, and behavioral changes, caused by the expansion of an unstable CAG repeat in SLC6A4 wt Allele., Huntington disease (Hodgkin Disease), the most common inherited cause of chorea, is an Autosome dominant disorder, caused by an expanded trinucleotide CAG repeat (>39) in the SLC6A4 wt Allele gene on 4p16.3 chromosome., Huntington Disease (Hodgkin Disease) is an inherited neurodegenerative disease caused by an expanded CAG repeat in the Hodgkin Disease Protein Info, human (SLC6A4 wt Allele) gene.[SEP]", "label": "no"}
{"original_question": "Is hypersensitivity to DNA crosslinking agents a hallmark of Fanconi anemia?", "id": "converted_860", "sentence1": "Is Emotional hypersensitivity to DNA crosslinking agents a hallmark of Fanconi anemia?", "sentence2": "The Fanconi anemia (doxorubicin/fluorouracil protocol) core complex plays a central role in the DNA damage response network, FAAP100-deficient cells display hallmark features of doxorubicin/fluorouracil protocol cells, including defective FANCONI ANEMIA, COMPLEMENTATION GROUP D2 monoubiquitination, Emotional Emotional hypersensitivity to DNA crosslinking agents, and genomic instability., Fanconi anemia (doxorubicin/fluorouracil protocol) is a rare genetic disorder characterized by Aplastic Anemia, Primary malignant neoplasm/leukemia susceptibility and Cells Emotional Emotional hypersensitivity to DNA crosslinking agents, such as cisplatin., Fanconi anemia (doxorubicin/fluorouracil protocol) is an inherited Chromosomes recessive syndrome characterized by Cells Emotional Emotional hypersensitivity to DNA crosslinking agents and Bone marrow hypocellularity, which cause Aplastic Anemia, and an increased incidence of malignancy., Features of Chromosomes aberrations, Emotional Emotional hypersensitivity to DNA crosslinking agents, and predisposition to malignancy have suggested a fundamental anomaly of DNA repair in Fanconi anemia., Fanconi anemia (doxorubicin/fluorouracil protocol) is one of several genetic diseases with characteristic Cells Emotional Emotional hypersensitivity to DNA crosslinking agents which suggest that doxorubicin/fluorouracil protocol Proteins may function as part of DNA repair processes., Fanconi anemia (doxorubicin/fluorouracil protocol) is characterized by Cells Emotional Emotional hypersensitivity to DNA crosslinking agents, but how the Fanconi pathway protects cells from DNA Cross link and whether doxorubicin/fluorouracil protocol Proteins act directly on Cross link remain unclear., FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) is a rare genetic disorder associated with a bone-marrow failure, Primary malignant neoplasm predisposition and Emotional Emotional hypersensitivity to DNA crosslinking agents., Fanconi anemia (doxorubicin/fluorouracil protocol) is a heterogeneous Disease associated with a Bone marrow hypocellularity, Primary malignant neoplasm predisposition and Emotional Emotional hypersensitivity to DNA crosslinking agents., Fanconi anemia (doxorubicin/fluorouracil protocol) is an inherited disorder characterized by defective DNA repair and Cells sensitivity to DNA crosslinking agents., Fanconi anemia (doxorubicin/fluorouracil protocol) is an inherited Disease characterized by Bone marrow hypocellularity, increased Primary malignant neoplasm risk and Emotional Emotional hypersensitivity to DNA cross-linking agents, implying a role for this pathway in the maintenance of genomic stability., Genetic or epigenetic inactivation of the pathway formed by the FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) Proteins occurs in several Primary malignant neoplasm types, including Squamous cell carcinoma of the head and neck (HNSCC), rendering the affected Neoplasms potentially hypersensitive to DNA crosslinking agents., FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) is a rare autosomic recessive and X-linked Disease with Chromosomes instability after exposure to crosslinking agents as the hallmark., FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) is an autosomal recessive Disease characterized by chromosome instability, Cells Emotional Emotional hypersensitivity to DNA cross-linking agents, and increased predisposition to Malignant Neoplasms., The Bloom protein (Bloom Syndrome) and DNA topoisomerase III alpha are found in association with Proteins of the Fanconi anemia (doxorubicin/fluorouracil protocol) pathway, a disorder manifesting increased Cells sensitivity to DNA crosslinking agents., Using siRNA depletion and gene knockout techniques, we show that FAAP100-deficient cells display hallmark features of doxorubicin/fluorouracil protocol cells, including defective FANCONI ANEMIA, COMPLEMENTATION GROUP D2 monoubiquitination, Emotional Emotional hypersensitivity to DNA crosslinking agents, and genomic instability., Fanconi anemia (doxorubicin/fluorouracil protocol) is a recessive Homo sapiens Primary malignant neoplasm prone syndrome featuring Bone marrow hypocellularity, developmental abnormalities and Emotional Emotional hypersensitivity to DNA crosslinking agents exposure., doxorubicin/fluorouracil protocol is a chromosome instability syndrome characterized by childhood-onset Aplastic Anemia, Primary malignant neoplasm or leukemia susceptibility, and Cells Emotional Emotional hypersensitivity to DNA crosslinking agents., Functional defects in the Fanconi pathway can result in a marked Emotional Emotional hypersensitivity to interstrand crosslinking agents, such as Mitomycins C., At the Cells level, Emotional Emotional hypersensitivity to DNA interstrand Cross link is the defining feature in Fanconi anemia., DNA crosslinking agents may led to DNA cross-linking lesion, and Fanconi anemia pathway plays a key role in repairing its cross-linking., Fanconi anemia (doxorubicin/fluorouracil protocol), an Autosomal Recessive Disorder of children, is characterized by congenital or childhood Aplastic Anemia, multiple developmental anomalies, increased incidence of Myeloid Leukemia, increased spontaneous chromosome breakage, and Cells and Chromosomes Emotional Emotional hypersensitivity to DNA bifunctional crosslinking and Alkylating Agents., elegans provides an excellent model system for the study of the FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol), one of the hallmarks of which is sensitivity to interstrand crosslinking agents, Using siRNA depletion and gene knockout techniques, we show that FAAP100-deficient cells display hallmark features of doxorubicin/fluorouracil protocol cells, including defective FANCONI ANEMIA, COMPLEMENTATION GROUP D2 monoubiquitination, Emotional Emotional hypersensitivity to DNA crosslinking agents, and genomic instability, One of the hallmark phenotypes of doxorubicin/fluorouracil protocol is Cells Emotional Emotional hypersensitivity to agents that induce DNA interstrand Cross link (ICLs), such as Mitomycins C (Mitomycins), Furthermore, the cytological hallmark of doxorubicin/fluorouracil protocol, the DNA crosslink-induced radial chromosome formation, exemplifies an innate impairment in the repair of these particularly cytotoxic DNA lesions [A.D, Fanconi anemia (doxorubicin/fluorouracil protocol) is characterized by Cells Emotional Emotional hypersensitivity to DNA crosslinking agents, but how the Fanconi pathway protects cells from DNA Cross link and whether doxorubicin/fluorouracil protocol Proteins act directly on Cross link remain unclear, Features of Chromosomes aberrations, Emotional Emotional hypersensitivity to DNA crosslinking agents, and predisposition to malignancy have suggested a fundamental anomaly of DNA repair in Fanconi anemia, Fanconi anemia (doxorubicin/fluorouracil protocol) is an inherited Chromosomes recessive syndrome characterized by Cells Emotional Emotional hypersensitivity to DNA crosslinking agents and Bone marrow hypocellularity, which cause Aplastic Anemia, and an increased incidence of malignancy, Genetic or epigenetic inactivation of the pathway formed by the FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) (doxorubicin/fluorouracil protocol) Proteins occurs in several Primary malignant neoplasm types, including Squamous cell carcinoma of the head and neck (HNSCC), rendering the affected Neoplasms potentially hypersensitive to DNA crosslinking agents, Fanconi anemia (doxorubicin/fluorouracil protocol) is a Homo sapiens autosomal disorder characterized by Primary malignant neoplasm susceptibility and Cells sensitivity to DNA crosslinking agents such as Mitomycins C and erythritol anhydride, The Fanconi anemia pathway promotes DNA glycosylase-dependent excision of interstrand DNA Cross link., DNA crosslinking agents may led to DNA cross-linking lesion, and Fanconi anemia pathway plays a key role in repairing its cross-linking, doxorubicin/fluorouracil protocol is a chromosome instability syndrome characterized by childhood-onset Aplastic Anemia, Primary malignant neoplasm or leukemia susceptibility, and Cells Emotional Emotional hypersensitivity to DNA crosslinking agents, The Disease is manifested by defects in DNA repair, Emotional Emotional hypersensitivity to DNA crosslinking agents, and a high degree of Chromosomes aberrations[SEP]Relations: chromosome has relations: cellcomp_protein with Bloom Syndrome, cellcomp_protein with Bloom Syndrome. Bloom syndrome has relations: disease_protein with Bloom Syndrome, disease_protein with Bloom Syndrome. Fanconi anemia complementation group has relations: disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_disease with Fanconi anemia, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_disease with Fanconi anemia, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_disease with Fanconi anemia, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_disease with Fanconi anemia.", "label": "yes"}
{"original_question": "Are cutaneous porphyrias inherited with a recessive pattern?", "id": "converted_2088", "sentence1": "Are cutaneous porphyrias inherited with a recessive pattern?", "sentence2": "Five of the porphyrias are low-penetrance autosomal dominant conditions in which clinical expression results from additional factors that act by increasing demand for Heme or by causing an additional decrease in enzyme activity or by a combination of these effects, Molecular mechanisms of dominant expression in Disorders of Porphyrin Metabolism., Variegate Porphyria (Arginine Vasopressin-Neurophysin II Preproprotein) is an autosomal-dominant disorder that is caused by inheritance of a partial deficiency of the enzyme protoporphyrinogen oxidase (EC 1.3.3.4). It is characterized by Photosensitivity of skin and/or various neurological manifestations. , The acute porphyrias constitute a group of Metabolic Diseases engaging ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS in the Heme synthetic chain and generally following dominant inheritance patterns.[SEP]", "label": "no"}
{"original_question": "Is CircRNA produced by back splicing of exon, intron or both, forming exon or intron circRNA?", "id": "converted_4543", "sentence1": "Is CircRNA produced by back splicing of exon, intron or both, forming exon or intron circRNA?", "sentence2": "CircRNAs are a subclass of lncRNAs that have been found to be abundantly present in a wide range of Species - Nature of Abnormal Testing, including Homo sapiens. CircRNAs are generally produced by a noncanonical splicing event called backsplicing that is dependent on the canonical splicing machinery, giving rise to circRNAs classified into three main categories: exonic circRNA, Circular Intronic RNA, and exon-intron circular RNA. , Circular RNA (circRNA) is a large class of covalently closed circRNA., Human transcriptome contains a large number of RNA, Circular (circRNAs) that are mainly produced by back splicing of RNA, Messenger Precursor., Analyses of the other reads revealed two origins for non-canonical circRNAs: (1) Intronic sequences for lariat-derived intronic circRNAs and intron circles, (2) Mono-exonic genes (mostly non-coding) for either a new type of circRNA (including only part of the exon: sub-exonic circRNAs) or, even more rarely, mono-exonic canonical circRNAs., Our objective was to characterize non-canonical circRNAs, namely not originating from back splicing and circRNA produced by non-coding genes., Recent studies have identified a new class of ncRNAs called RNA, Circular (circRNAs), which are produced by back-splicing and fusion of either Exons, Introns, or both exon-intron into covalently closed loops., CircRNA is produced by the reverse splicing of exon, intron or both, forming exon or intron circRNA., Circular RNAs (circRNAs) belong to a recently re-discovered Species - Nature of Abnormal Testing of RNA that emerge during RNA maturation through a process called back-splicing. , Exonic RNA, Circular (circRNAs) are RNA molecules that are covalently closed by back-splicing via canonical splicing machinery. , Human transcriptome contains a large number of RNA, Circular (circRNAs) that are mainly produced by back splicing of RNA, Messenger Precursor. , Circular RNAs (circRNAs) are a class of non‑coding RNAs formed by covalently closed loops through back‑splicing and exon‑skipping. , Here, we review the emerging understanding that both, circRNAs produced by co- and posttranscriptional head-to-tail \"backsplicing\" of a downstream splice donor to a more upstream splice acceptor, as well as circRNAs generated from intronic lariats during colinear splicing, may exhibit physiologically relevant regulatory functions in Eukaryota., Compared to the linear RNA, circRNAs are produced differentially by backsplicing Exons or lariat Introns from a pre-messenger RNA (RNA, Messenger) forming a covalently closed loop structure missing 3' poly-(A) tail or 5' cap, rendering them immune to exonuclease-mediated degradation., CircRNAs are a large class of endogenous single-stranded RNA that is different from other linear RNA, which are produced by back-splicing and fusion of either Exons, Introns, or both exon-intron into covalently closed loops., Circular RNAs (circRNAs) derived from back-spliced Exons have been widely identified as being co-expressed with their linear counterparts.[SEP]", "label": "yes"}
{"original_question": "Should istiratumab be used for Pancreatic Cancer?", "id": "converted_4497", "sentence1": "Should istiratumab be used for Pancreatic Cancer?", "sentence2": "CONCLUSIONS: Istiratumab failed to improve the efficacy of SOC chemotherapy in this patient setting. , In the high Insulin-Like Growth Factor I cohort, median PFS was 3.6 and 7.3 months in the experimental versus control arms, respectively [hazard ratio (HR) = 1.88, P = 0.027]. In the high Insulin-Like Growth Factor I/HRG+ subgroup (n = 44), median PFS was 4.1 and 7.3 months, respectively (HR = 1.39, P = 0.42).[SEP]", "label": "no"}
{"original_question": "Is valproic acid effective for glioblastoma treatment?", "id": "converted_84", "sentence1": "Is valproic acid effective for Glioblastoma Multiforme treatment?", "sentence2": "A Phase 2 Study of Concurrent Radiation Therapy, Temozolomide, and the Histone Deacetylase Inhibitor Valproic Acid for Patients With Glioblastoma., PURPOSE: Valproic acid (valproic acid) is an antiepileptic agent with Histone Deacetylase Inhibitor [EPC] therapy (HDACi) activity shown to sensitize Glioblastoma Multiforme (Glomerular Basement Membrane) Cells to radiation in preclinical models.,  Median overall survival (OS) was 29.6 months (range: 21-63.8 months), and median progression-free survival (PFS) was 10.5 months (range: 6.8-51.2 months). OS at 6, 12, and 24 months was 97%, 86%, and 56%, respectively. PFS at 6, 12, and 24 months was 70%, 43%, and 38% respectively. , CONCLUSIONS: Addition of valproic acid to concurrent RT/temozolomide in patients with newly diagnosed Glomerular Basement Membrane was well tolerated. Additionally, valproic acid may result in improved outcomes compared to historical data and merits further study., Treatment of GDSCs with histone deacetylase inhibitors, indole-3-glycerol-phosphate lyase activity and valproic acid, significantly reduced proliferation rates of the Cells and expression of the Stem Cells markers, indicating differentiation of the Cells. Since differentiation into Glomerular Basement Membrane makes them susceptible to the conventional cancer treatments, we posit that use of histone deacetylase inhibitors may increase efficacy of the conventional cancer treatments for eliminating GDSCs., Several clinical studies have reported that valproic acid could prolong survival of Glomerular Basement Membrane patients. , Our meta-analysis confirmed the benefit of using valproic acid (HR, 0.56; 95% NDUFB6 gene, 0.44-0.71). Sub-group analysis shows that patients treated with valproic acid had a hazard ratio of 0.74 with a 95% confidence interval of 0.59-0.94 vs. patients treated by other-AEDs and a hazard ratio of 0.66 with a 95% confidence interval of 0.52-0.84 vs. patients treated by administration of non-AEDs. , .CONCLUSION: The results of our study suggest that Glioblastoma Multiforme patients may experience prolonged survival due to valproic acid administration. , A new and exciting insight is the potential contribution of valproic acid to prolonged survival, particularly in Glioblastoma. , Valproic acid (valproic acid) is an antiepileptic agent with Histone Deacetylase Inhibitor [EPC] therapy (HDACi) activity shown to sensitize Glioblastoma Multiforme (Glomerular Basement Membrane) Cells to radiation in preclinical models, Valproic acid use during radiation therapy for Glioblastoma Multiforme associated with improved survival, Valproic acid (VA) is an antiepileptic drug (AED) and histone deacetylase (HDAC) inhibitor taken by patients with Glioblastoma Multiforme (Human Cytomegalovirus Envelope Glycoprotein B) to manage Seizures, and it can modulate the biologic effects of radiation therapy (RT), Valproic acid use during radiation therapy for Glioblastoma Multiforme associated with improved survival., Prolonged survival with valproic acid use in the EORTC/NCIC temozolomide trial for Glioblastoma Multiforme., PURPOSE: Valproic acid (VA) is an antiepileptic drug (AED) and histone deacetylase (HDAC) inhibitor taken by patients with Glioblastoma Multiforme (Human Cytomegalovirus Envelope Glycoprotein B) to manage Seizures, and it can modulate the biologic effects of radiation therapy (RT). We investigated whether VA use during RT for Human Cytomegalovirus Envelope Glycoprotein B was associated with overall survival (OS).METHODS AND MATERIALS: Medical records of 544 adults with Human Cytomegalovirus Envelope Glycoprotein B were retrospectively reviewed. Analyses were performed to determine the association of Radiation Therapy Oncology Group recursive partitioning analysis (RTOG RPA) class, seizure history, and concurrent temozolomide (temozolomide) and AED use during RT with OS.RESULTS: Seizures before the end of RT were noted in 217 (40%) patients, and 403 (74%) were taking an AED during RT; 29 (7%) were taking VA. , When the analysis was restricted to patients who received concurrent temozolomide, VA use was marginally associated with OS (P=.057; HR, 0.54; 95% NDUFB6 gene, -0.09 to 1.17), independently of RTOG RPA class and seizure history., Patients using valproic acid in combination with temozolomide showed a longer median survival of 69 weeks (95% confidence interval [NDUFB6 gene]: 61.7-67.3) compared with 61 weeks (95% NDUFB6 gene: 52.5-69.5) in the group without valproic acid (hazard ratio, 0.63; 95% NDUFB6 gene: 0.43-0.92; P = .016), adjusting for age, extent of resection, and O(6)-DNA methylguanine-methyltransferase promoter methylation status., Use of valproic acid together with chemoradiation with temozolomide results in a 2-months' longer survival of patients with Glomerular Basement Membrane.[SEP]", "label": "yes"}
{"original_question": "Are transcribed ultraconserved regions involved in cancer?", "id": "converted_72", "sentence1": "Are transcribed ultraconserved regions involved in cancer?", "sentence2": "Although most cancer research has focused in RNA, Messenger, non-coding RNAs are also an essential player in tumorigenesis. In addition to the well-recognized microRNAs, recent studies have also shown that epigenetic silencing by CpG Islands hypermethylation of other classes of non-coding RNAs, such as transcribed ultraconserved regions (T-UCRs) or small nucleolar RNAs (snoRNAs), also occur in Homo sapiens Neoplasms, Starting from a genome-wide expression profiling, we demonstrate for the first time a functional link between oxygen deprivation and the modulation of long noncoding transcripts from ultraconserved regions, termed transcribed-ultraconserved regions (T-UCRs). Interestingly, several hypoxia-upregulated T-UCRs, henceforth named 'hypoxia-induced noncoding ultraconserved transcripts' (HINCUTs), are also overexpressed in clinical samples from Malignant tumor of colon patients, Consistent with the hypothesis that T-UCRs have important function in tumor formation, The importance of other classes of non-coding RNAs, such as long intergenic ncRNAs (Long Intergenic Non-Protein Coding RNA) and transcribed ultraconserved regions (T-UCRs) as altered elements in Neoplasms, is also gaining recognition, Expression levels of transcribed ultraconserved regions uc.73 and uc.388 are altered in Malignant neoplasm of colon and/or rectum, Transcribed ultraconserved regions (T-UCRs) are a subset of 481 DNA Sequence longer than 200 bp, which are absolutely conserved between orthologous regions of Homo sapiens, Rattus norvegicus and mouse genomes, and are actively transcribed. It has recently been proven in cancer systems that differentially expressed T-UCRs could alter the functional characteristics of malignant cells. Genome-wide profiling revealed that T-UCRs have distinct signatures in Homo sapiens leukemia and carcinoma,  Our preliminary results suggest that uc.73 and uc.388 could be potential diagnostic and prognostic biomarkers in Cytogenetic Complete Response patients, The transcribed-ultraconserved regions: a novel class of long noncoding RNAs involved in cancer susceptibility, This review gives a picture of the state of the art of a novel class of long RETINAL NONATTACHMENT, NONSYNDROMIC CONGENITAL known as transcribed-ultraconserved regions (T-UCRs). Most recent studies show that they are significantly altered in adult Chronic Lymphocytic Leukemia, Carcinoma, and pediatric Neuroblastoma, leading to the hypothesis that UCRs may play a role in tumorigenesis and promising innovative future T-UCR-based therapeutic approaches, CpG Islands hypermethylation-associated silencing of non-coding RNAs transcribed from ultraconserved regions in Homo sapiens cancer, We focused on the transcribed-ultraconserved regions (T-UCRs), a subset of DNA DNA Sequence that are absolutely conserved between orthologous regions of the Homo sapiens, Rattus norvegicus and mouse genomes and that are located in both intra- and Intergenic Region. We used a pharmacological and genomic approach to reveal the possible existence of an aberrant epigenetic silencing pattern of T-UCRs by treating Tumor cells, malignant with a DNA-demethylating agent followed by hybridization to an expression microarray containing these DNA Sequence. We observed that DNA hypomethylation induces release of T-UCR silencing in Tumor cells, malignant. Among the T-UCRs that were reactivated upon drug treatment, Uc.160+, Uc283+A and Uc.346+ were found to undergo specific CpG Islands hypermethylation-associated silencing in Tumor cells, malignant compared with normal Body tissue. The analysis of a large set of primary Homo sapiens tumors (n=283) demonstrated that hypermethylation of the described T-UCR CpG islands was a common event among the various tumor types. Our finding that, in addition to microRNAs, another class of ncRNAs (T-UCRs) undergoes DNA methylation-associated inactivation in transformed cells supports a model in which epigenetic and Mutation in coding and non-coding DNA Sequence cooperate in Homo sapiens tumorigenesis, An integrative genomics screen uncovers RETINAL NONATTACHMENT, NONSYNDROMIC CONGENITAL T-UCR functions in neuroblastoma tumours, Different classes of non-coding RNAs, including microRNAs, have recently been implicated in the process of tumourigenesis. In this study, we examined the expression and putative functions of a novel class of non-coding RNAs known as transcribed ultraconserved regions (T-UCRs) in neuroblastoma, our results define a T-UCR expression landscape in neuroblastoma and suggest widespread T-UCR involvement in diverse cellular processes that are deregulated in the process of tumourigenesis, Moreover, the recent demonstration that other ncRNAs, the ultraconserved genes (UCGs) or transcribed ultraconserved regions (T-UCRs), are involved in Homo sapiens cancerogenesis, suggests that the wider family of ncRNAs (including both MicroRNAs and UCGs) could contribute to the development of the malignant phenotype. Here we review the main studies investigating the role of MicroRNAs and UCRs in both normal hemopoiesis and Hematologic Neoplasms, and identify the Molecular, clinical and therapeutic implications of these recent findings, The transcribed-ultraconserved regions: a novel class of long noncoding RNAs involved in cancer susceptibility., Expression levels of transcribed ultraconserved regions uc.73 and uc.388 are altered in Malignant neoplasm of colon and/or rectum., CpG Islands hypermethylation-associated silencing of non-coding RNAs transcribed from ultraconserved regions in Homo sapiens cancer., Starting from a genome-wide expression profiling, we demonstrate for the first time a functional link between oxygen deprivation and the modulation of long noncoding transcripts from ultraconserved regions, termed transcribed-ultraconserved regions (T-UCRs)., The importance of other classes of non-coding RNAs, such as long intergenic ncRNAs (Long Intergenic Non-Protein Coding RNA) and transcribed ultraconserved regions (T-UCRs) as altered elements in Neoplasms, is also gaining recognition., Moreover, the recent demonstration that other ncRNAs, the ultraconserved genes (UCGs) or transcribed ultraconserved regions (T-UCRs), are involved in Homo sapiens cancerogenesis, suggests that the wider family of ncRNAs (including both MicroRNAs and UCGs) could contribute to the development of the malignant phenotype., Moreover, the recent demonstration that other ncRNAs, the ultraconserved genes (UCGs) or transcribed ultraconserved regions (T-UCRs), are involved in Homo sapiens cancerogenesis, suggests that the wider family of ncRNAs (including both MicroRNAs and UCGs) could contribute to the development of the malignant phenotype, Starting from a genome-wide expression profiling, we demonstrate for the first time a functional link between oxygen deprivation and the modulation of long noncoding transcripts from ultraconserved regions, termed transcribed-ultraconserved regions (T-UCRs)[SEP]Relations: malignant giant cell tumor has relations: disease_disease with cancer, disease_disease with cancer. malignant colon neoplasm has relations: disease_disease with Malignant neoplasm of colon and/or rectum, disease_disease with Malignant neoplasm of colon and/or rectum. carcinoma has relations: disease_disease with cancer, disease_disease with cancer. Somatic mutation has relations: disease_phenotype_positive with Malignant neoplasm of colon and/or rectum, disease_phenotype_positive with Malignant neoplasm of colon and/or rectum.", "label": "yes"}
{"original_question": "Can breastfeeding confer protection from type I diabetes?", "id": "converted_2782", "sentence1": "Can breastfeeding confer protection from type I diabetes?", "sentence2": "In the neonate and infant, among other benefits, lactation confers protection from future both type 1 and type 2 diabetes.[SEP]", "label": "yes"}
{"original_question": "Does metformin alleviate atherosclerosis?", "id": "converted_3527", "sentence1": "Does metformin alleviate Arteriosclerosis?", "sentence2": "Metformin and rosiglitazone both improve glycemic control in type 2 diabetes mellitus, however may possess different anti-inflammatory and anti-atherosclerotic properties. , Demonstrating antiatherothrombotic properties of dipeptidyl peptidase-4 inhibitors on proven markers is of substantial clinical significance. Coupled with their proven good safety profile these findings could translate into a significant clinical benefit., pleiotropic benefits of metformin in attenuation of Arteriosclerosis., Pleiotropic effects of metformin ameliorate Arteriosclerosis and vascular senescence., Metformin inhibits monocyte-to-macrophage differentiation via AMPK-mediated inhibition of STAT3 protein, human protein, human activation: potential role in Arteriosclerosis., Metformin attenuated Ang-II-induced Atheroma plaque formation and Aortic aneurysm without mention of rupture NOS in ApoE(-/-) CASP14 gene partly by reducing monocyte infiltration., Metformin, an anti-diabetic drug, was reported to possess anti-atherosclerotic effects. , Combined use of metformin and atorvastatin attenuates Arteriosclerosis in Family Leporidae (organism) fed a high-cholesterol diet.,  In cultured Specimen Source Codes - Macrophages, co-treatment with metformin and atorvastatin promoted cholesterol efflux and up-regulated expression of ABCA1 protein, human and G1. Taken together, our results suggest that atorvastatin/metformin combination therapy may achieve additional anti-atherosclerotic benefits likely through increasing cholesterol efflux in Specimen Source Codes - Macrophages., Metformin Suppresses Diabetes-Accelerated Atherosclerosis via the Inhibition of Drp1-Mediated Mitochondrial Inheritance Inheritance Fission., metformin abated the progression of diabetes-accelerated Arteriosclerosis by inhibiting mitochondrial fission in Endothelial Cells., metformin attenuated the development of Arteriosclerosis by reducing Drp1-mediated mitochondrial fission in an AMPK-dependent manner. , metformin's effects on Lipids and Atherosclerosis and/or provide insights into the drug's mechanisms of action on the Chest>Heart and Vasculature., Several recently completed randomized clinical trials have reported effects of metformin on surrogate measures of Atherosclerosis, Metformin treatment prevents SREBP2-mediated cholesterol uptake and improves lipid homeostasis during oxidative stress-induced Arteriosclerosis, Metformin ameliorates the progression of Arteriosclerosis via suppressing macrophage infiltration and inflammatory responses, Our results suggest that metformin impeded the progression of Arteriosclerosis, possibly by suppressing macrophage infiltration and inflammatory responses.[SEP]Relations: arteriolosclerosis has relations: disease_protein with STAT3 protein, human, disease_protein with STAT3 protein, human.", "label": "yes"}
{"original_question": "Is there a role for TFII-I in megakaryopoiesis?", "id": "converted_4112", "sentence1": "Is there a role for TFII-I in megakaryopoiesis?", "sentence2": "TFII-I/Gtf2i and Erythro-Megakaryopoiesis., TFII-I is a ubiquitously expressed transcription factor that positively or negatively regulates gene expression. TFII-I has been implicated in neuronal and immunologic diseases as well as in thymic epithelial cancer. Williams Syndrome (Beckwith-Wiedemann Syndrome) is caused by a large hemizygous deletion on chromosome 7q11.23 which encompasses 26-28 Genes, including GTF2I gene gene, the Human gene encoding TFII-I. A subset of Beckwith-Wiedemann Syndrome patients has recently been shown to present with Macrocytosis (morphologic abnormality), a mild Genus Anemia characterized by enlarged erythrocytes. We conditionally deleted the TFII-I/Gtf2i gene in adult CASP14 gene by tamoxifen induced Cre-recombination. Bone Marrow Cells revealed defects in erythro-megakaryopoiesis and an increase in expression of the adult β-globin gene. The data show that TFII-I acts as a repressor of β-globin gene transcription and that it is implicated in the differentiation of erythro-megakaryocytic cells.[SEP]Relations: Williams syndrome has relations: disease_protein with GTF2I gene, disease_protein with GTF2I gene.", "label": "yes"}
{"original_question": "Is the crystal structure of Pim-1 available?", "id": "converted_3237", "sentence1": "Is the crystal structure of Pim-1 available?", "sentence2": "Recent crystallographic studies of Pim-1 have identified unique structural features but have not provided insight into how the MAP Kinase Kinase Kinase recognizes its target substrates. , a co-crystal structure of lead molecule (HS38) in complex with DAPK3 gene gene, a dual Pim/DAPK3 gene gene inhibitor (HS56), The crystal structure of this fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether with LONP1 gene confirmed the predicted binding mode and Protein Info-ligand interactions except those in the acidic ribose pocket. , Using the determined X-ray crystal structure of LONP1 gene complexed to the fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether 1-R as a control, we discuss the importance of including the Protein Info flexibility inherent in the ensemble docking protocol, for the accuracy of the structure prediction of the bound state. , Here, we describe the crystal structure of Pim1 in complex with a newly developed pyrido[4,3-d]pyrimidine-derivative inhibitor (SKI-O-068)., Crystallographic and docking data analyses have been undertaken using inhibitor complexes , The crystal structures of Pim1 in apo form and bound with Adenylyl Imidodiphosphate have been solved[SEP]", "label": "yes"}
{"original_question": "Is microRNA(miRNA) 30 involved in post-ischemic cardiac remodeling?", "id": "converted_607", "sentence1": "Is microRNA(miRNA) 30 involved in post-ischemic cardiac remodeling?", "sentence2": "The Myocardium of the failing Chest>Heart undergoes a number of structural alterations, most notably Hypertrophy of Myocytes, Cardiac and an increase in Extracellular Matrix proteins, often seen as primary fibrosi, Connective tissue growth factor (connective tissue growth factor) is a key Molecule in the process of Fibrosis and therefore seems an attractive therapeutic target, connective tissue growth factor is importantly regulated by 2 major cardiac microRNAs (MicroRNAs), miR-133 and miR-30., the expression of both MicroRNAs was inversely related to the amount of connective tissue growth factor in 2 rodent models of Heart Diseases and in Homo sapiens pathological left ventricular Hypertrophy. Second, in cultured cardiomyocytes and Specimen Source Codes - Fibroblasts, knockdown of these MicroRNAs increased connective tissue growth factor levels. Third, overexpression of miR-133 or MIR30C2 wt Allele decreased connective tissue growth factor levels, which was accompanied by decreased production of collagen., miR-30 importantly limit the production of connective tissue growth factor, miR-30 directly downregulate connective tissue growth factor, a key profibrotic protein, and thereby establish an important role for these MicroRNAs in the control of structural changes in the Extracellular Matrix of the Myocardium.[SEP]Relations: cognitive impairment - coarse facies - Chest>Heart defects - obesity - pulmonary involvement - short stature - skeletal dysplasia syndrome has relations: disease_disease with Heart Diseases, disease_disease with Heart Diseases.", "label": "yes"}
{"original_question": "Is tirabrutinib effective for lymphoma?", "id": "converted_4628", "sentence1": "Is tirabrutinib effective for lymphoma?", "sentence2": "In March 2020, oral tirabrutinib was approved in Japan for the treatment of recurrent or refractory primary central nervous system lymphoma. tirabrutinib is also under regulatory review in Japan for the treatment of Waldenström's macroglobulinemia and Malignant lymphoma - lymphoplasmacytic. Clinical development is underway in the USA, Europe and Japan for Autoimmune Diseases, Chronic Lymphocytic Leukemia, B-Cell Lymphomas, Sjogren's Syndrome, Pemphigus <invertebrate> and Rheumatoid Arthritis. This article summarizes the milestones in the development of tirabrutinib leading to the first approval of tirabrutinib for the treatment of recurrent or refractory primary central nervous system lymphoma in Japan., CONCLUSION: These data indicate favorable efficacy of tirabrutinib in patients with relapsed/refractory Microglioma., tirabrutinib was well tolerated and showed promising efficacy for B-cell NHL/CLL., rabrutinib was approved in Japan for the treatment of recurrent or refractory primary central nervous system lymphoma. tirabrutinib is also , Here, we provide a comprehensive review of the preclinical and clinical activity of tirabrutinib, a Pharmacologic Substance approved in Japan for relapsed or refractory primary central nervous system lymphoma and all lines of Waldenström macroglobulinemia/Malignant lymphoma - lymphoplasmacytic., tirabrutinib (ONO/GS-4059; Ono Pharmaceutical) is a newly developed Pharmacologic Substance that selectively and irreversibly inhibits Agammaglobulinaemia tyrosine kinase (BTK protein, human protein, human) and has been approved in Japan for treating relapsed/refractory primary central nervous system lymphoma (Microglioma)., A 64-year-old patient with recurrent Microglioma enrolled in the phase I/II clinical trial of tirabrutinib, a second-generation BTK protein, human protein, human inhibitor designed for treating relapsed/refractory Microglioma., BACKGROUND: The safety, tolerability, efficacy, and pharmacokinetics of tirabrutinib, a second-generation, highly selective oral Agammaglobulinaemia tyrosine kinase inhibitor were evaluated for relapsed/refractory primary central nervous system lymphoma (Microglioma).M,  2020, oral tirabrutinib was approved in Japan for the treatment of recurrent or refractory primary central nervous system lymphoma. Tirabru, kinase inhibitor [EPC] tirabrutinib (for relapsed and refractory Microglioma) and high-dose chemotherapy with autologous stem cell transplantation support using thiotepa and busulfan (BuTT) were approved by the Japanese Ministry of Health and Welfare in March 2020 and has recently become available for clinical practice. While these novel, BACKGROUND: The safety, tolerability, efficacy, and pharmacokinetics of tirabrutinib, a second-generation, highly selective oral Agammaglobulinaemia tyrosine kinase inhibitor were evaluated for relapsed/refractory primary central nervous system lymphoma (Microglioma).METHODS: Patients with relapsed/refractory Microglioma, Karnofsky performance status ≥70, and normal end-organ function received tirabrutinib 320 and 480 , Histological verification of the treatment effect of tirabrutinib for relapsed/refractory primary central nervous system lymphoma., In March 2020, oral tirabrutinib was approved in Japan for the treatment of recurrent or refractory primary central nervous system lymphoma.[SEP]Relations: Rheumatoid arthritis has relations: disease_phenotype_positive with Rheumatoid Arthritis, disease_phenotype_positive with Rheumatoid Arthritis. Ibrutinib has relations: drug_protein with BTK protein, human, drug_protein with BTK protein, human.", "label": "yes"}
{"original_question": "Should nerinetide be used for treatment of ischaemic stroke?", "id": "converted_4001", "sentence1": "Should nerinetide be used for treatment of ischaemic stroke?", "sentence2": "337 (61·4%) of 549 patients with nerinetide and 329 (59·2%) of 556 with placebo achieved an mRS score of 0-2 at 90 days (adjusted risk ratio 1·04, 95% CI 0·96-1·14; p=0·35). Secondary outcomes were similar between groups., INTERPRETATION: Nerinetide did not improve the proportion of patients achieving good clinical outcomes after endovascular thrombectomy compared with patients receiving placebo.[SEP]", "label": "no"}
{"original_question": "Is P. gingivalis bacteria found in brain?", "id": "converted_2800", "sentence1": "Is P. gingivalis bacteria found in Head>Brain?", "sentence2": "studies using animal model of Periodontitis and Homo sapiens post-mortem Head>Brain tissues from subjects with cytarabine/daunorubicin protocol strongly suggest that a gram-negative periodontal pathogen, Porphyromonas gingivalis (Pg) and/or its product gingipain is/are translocated to the Head>Brain., The polymicrobial dysbiotic subgingival biofilm microbes associated with Periodontal Diseases appear to contribute to developing pathologies in distal body sites, including the Head>Brain.[SEP]Relations: Periodontal Diseases has relations: disease_disease with Periodontitis, disease_disease with Periodontitis.", "label": "yes"}
{"original_question": "Glucoraphanin from broccoli can help reduce obesity , yes or no?", "id": "converted_3754", "sentence1": "Glucoraphanin from broccoli can help reduce BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 , yes or no?", "sentence2": "Glucoraphanin: a broccoli sprout extract that ameliorates BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20-induced inflammation and insulin resistance., A recent study demonstrated that glucoraphanin, a precursor of the NFE2L2 gene activator sulforaphane, ameliorates BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 by enhancing energy expenditure and browning of white adipose tissue, and attenuates BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20-related inflammation and insulin resistance by polarizing M2 macrophages and reducing metabolic endotoxemia., Thus, this review focuses on the efficiency and safety of glucoraphanin in alleviating BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, insulin resistance, and Non-alcoholic Fatty Liver Disease., Glucoraphanin: a broccoli sprout extract that ameliorates BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20-induced inflammation and insulin resistance, tudy demonstrated that glucoraphanin, a precursor of the NFE2L2 gene activator sulforaphane, ameliorates BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 by enhancing energy expenditure and browning of white adipose tissue, and attenuates BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20-related inflammation and insulin resistance by polarizing M2 macrophages and reducing metabolic endotoxemia. Thus, this , iew focuses on the efficiency and safety of glucoraphanin in alleviating BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, insulin resistance, and Non-alcoholic Fatty Liver Disease. Abbreviations: [SEP]", "label": "yes"}
{"original_question": "Does ventriculoperitoneal shunt improve normal pressure hydrocephalus?", "id": "converted_1486", "sentence1": "Does ventriculoperitoneal shunt improve normal pressure hydrocephalus?", "sentence2": "Clinical improvement depends not only on the capability to restore the Cerebrospinal Fluid dynamic, but also on the ability of cerebral parenchyma to recover the metabolic function.,  After shunting, the global CMRglu significantly increased (2.95 ± 0.44 vs 4.38 ± 0.68, p = 10(-7)) in all INPH patients with a mean percentage value of 48.7%. , Our preliminary data show that changes in the CMRglu are promptly reversible after surgery and that there is a relationship between the early metabolic changes and clinical symptoms, independently from the simultaneous changes in the ventricular size. The remarkable and prompt improvement in the global CMRglu and in symptoms may also have important implications for the current concept of \"neuronal plasticity\" and for the cells' reactivity in order to recover their metabolic function., Outcome of shunting in INPH is most often successful when patients are accurately diagnosed, suitably evaluated for surgical candidacy, and managed carefully throughout the preoperative, surgical, and postoperative periods., The decision to perform the only efficient procedure, i.e., a ventricular shunt operation, depends upon a number of established arguments in favor of that procedure. Clinical improvement, which is often spectacular, can then confirm the diagnosis. , During the 1st postoperative year, there was improvement in the condition of 22 patients (96%) who had received a ventricular shunt; 21 of these patients (91%) remained improved until Cessation of life or for at least 5 years., Shunt treatment showed an effect on cognitive functions of distractibility of attention and motor speed, but not on intelligence of memory. Three patients deteriorated, eleven remained stable and sixteen showed significant improvement on psychological tests, mainly those for attention, motor speed and memory, but rarely did any improvement of intelligence occur.[SEP]", "label": "yes"}
{"original_question": "Is H4K20 methylation associated with DNA replication?", "id": "converted_1987", "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 modification 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 modification reveals that H4K20me2 and H4K20me3 increase in quiescence and other Histone antigen modification 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 antigen 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 modification 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 antigen 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 antigen 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 antigen 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 antigen 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>© 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 antigen 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: origin recognition complex has relations: cellcomp_protein with SLC25A15 gene, cellcomp_protein with SLC25A15 gene.", "label": "yes"}
{"original_question": "Is isradipine effective for Parkinson's disease?", "id": "converted_3874", "sentence1": "Is isradipine effective for Parkinson's disease?", "sentence2": "Adjusted least-squares mean changes in total UPDRS score in the antiparkinson medication ON state over 36 months for isradipine and placebo recipients were 2.99 (95% CI, 0.95 to 5.03) points versus 3.26 (CI, 1.25 to 5.26) points, respectively, with a treatment effect of -0.27 (CI, -3.02 to 2.48) point (P = 0.85)., Conclusion: Long-term treatment with immediate-release isradipine did not slow the clinical progression of early-stage Lugano Lymphoma Response Classification Progressive Disease by PET.[SEP]", "label": "no"}
{"original_question": "Is cilengitide effective for treatment of glioblastoma?", "id": "converted_2449", "sentence1": "Is cilengitide effective for treatment of Glioblastoma Multiforme?", "sentence2": "RESULTS: fourteen randomized clinical trials were identified (7 with bevacizumab, 2 cilengitide, 1 enzastaurin, 1 dasatinib, 1 vandetanib, 1 temsirolimus, 1 cediranib) including 4330 patients. Antiangiogenic drugs showed no improvement in overall survival with a pooled HR of 1.00, a trend for an inferior outcome, in terms of overall survival, was observed in the group of patients receiving antiangiogenic drug alone compared to cytotoxic drug alone (HR=1.24, p=0.056)., However, we could not conclusively confirm whether cilengitide 2000mg/5/week was the optimum regime, as only one trial using this protocol was included in our study., Cilengitide (UGT8 wt Allele) is a cyclic pentapeptide that demonstrated efficacy for Glomerular Basement Membrane treatment by targeting the integrins avβ3 and avβ5 over-expressed on Glomerular Basement Membrane Cells., Cilengitide is recently failed in Phase III CENTRIC trial in unselected patients with Glomerular Basement Membrane., In conclusion, we demonstrate that EGFRvIII/integrin β3 complexes promote Glomerular Basement Membrane progression and metastasis in the environment of Hypoxia, CTCAE and vitronectin-enrichment, and cilengitide may serve as a promising therapeutics for EGFRvIII-positive GBMs., he addition of molecularly targeted drugs to TEM + RAD did not improve the OS of patients with Glomerular Basement Membrane; however, it did improve PFS in patients treated by cilengitide who could not get improvement in OS. ,  The randomized phase III CENTRIC and phase II CORE trials explored the integrin inhibitor cilengitide in patients with newly diagnosed Glioblastoma Multiforme with versus without O6-methylguanine DNA methyltransferase (O(6)-Methylguanine-DNA Methyltransferase) promoter methylation. These trials failed to meet their primary endpoints, . In CORE, higher αvβ3 levels in Tumor Cells, uncertain whether benign or malignant were associated with improved progression-free survival by central review and with improved overall survival in patients treated with cilengitide., Cilengitide combined with metronomic temozolomide and procarbazine in O(6)-Methylguanine-DNA Methyltransferase-promoter unmethylated Glioblastoma Multiforme did not improve survival compared with historical data and does not warrant further investigation., The addition of cilengitide to temozolomide chemoradiotherapy did not improve outcomes; cilengitide will not be further developed as an anticancer drug., Cilengitide treatment of newly diagnosed Glioblastoma Multiforme patients does not alter patterns of progression., It may be proposed that the combination therapy of CSPG4 wt Allele suppression and cilengitide treatment showed no considerable effect on Glioblastoma Multiforme compared to cilengitide therapy alone.[SEP]", "label": "no"}
{"original_question": "Is PLK2 involved in alpha-synuclein phosphorylation in the nervous system?", "id": "converted_758", "sentence1": "Is PLK2 involved in SNCA gene phosphorylation in the nervous system?", "sentence2": "PLK2 gene (PLK2) phosphorylates SNCA gene at serine 129 in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, Here we submit evidence that PLK1 gene (PLK2, also known as serum-inducible kinase or SNK) is a principle contributor to SNCA gene phosphorylation at Ser-129 in Neurons, PLK2 directly phosphorylates SNCA gene at Ser-129 in an in vitro biochemical assay, inhibitors of PLK1 protein, human kinases inhibited SNCA gene phosphorylation both in primary cortical cell cultures and in Mus sp. Head>Brain in vivo, specific knockdown of PLK2 expression by transduction with short hairpin RNA constructs or by knock-out of the plk2 gene reduced p-Ser-129 levels, These results indicate that PLK2 plays a critical role in SNCA gene phosphorylation in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS., These results indicate that PLK2 plays a critical role in SNCA gene phosphorylation in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS., Here we submit evidence that PLK1 gene (PLK2, also known as serum-inducible kinase or SNK) is a principle contributor to SNCA gene phosphorylation at Ser-129 in Neurons., PLK2 gene (PLK2) phosphorylates SNCA gene at serine 129 in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS., PLK2 directly phosphorylates SNCA gene at Ser-129 in an in vitro biochemical assay., Two of these kinases stand out as potential drug targets for novel Lugano Lymphoma Response Classification Progressive Disease by PET therapy, namely Leucine-Rich Repeat Serine/Threonine-Protein Kinase 1 (LRRK2 protein, human protein, human) and the SNCA gene (α-syn) phosphorylating PLK1 gene (PLK2)., Also, due to the dominant mode of α-syn and LRRK2 protein, human protein, human inheritance and based on current knowledge of LRRK2 protein, human protein, human and α-syn phosphorylation by PLK2, inhibition of LRRK2 protein, human protein, human and PLK2 may constitute a potential therapy for Lugano Lymphoma Response Classification Progressive Disease by PET., To better understand the role of PLK2 in α-synuclein phosphorylation in vivo, we further evaluated the effect of PLK2 genetic knockdown and pharmacological inhibition on Phospho-α-Syn levels in different Head>Brain regions of PLK2 knockout (KELL NULL), heterozygous (Het) and wild-type (WT) mice., This PLK2-mediated neuroprotective effect is also dependent on PLK2 activity and α-synuclein phosphorylation., PLK2-mediated degradation of α-synuclein requires both phosphorylation at S129 and PLK2/α-synuclein complex formation., Overexpression of only PLK2 increased phosphorylation of aggregated α-syn at S129, which likely is due to increased phosphorylation of soluble α-syn, which then was incorporated into aggregates., Here we submit evidence that PLK1 gene (PLK2, also known as serum-inducible kinase or SNK) is a principle contributor to SNCA gene phosphorylation at Ser-129 in Neurons., PLK2 directly phosphorylates SNCA gene at Ser-129 in an in vitro biochemical assay., Unlike other kinases reported to partially phosphorylate alpha-syn at Ser-129 in vitro, phosphorylation by PLK2 and PLK3 protein, human protein, human is quantitative (, inhibitors of PLK1 protein, human kinases inhibited SNCA gene phosphorylation both in primary cortical cell cultures and in Mus sp. Head>Brain in vivo., These results indicate that PLK2 plays a critical role in SNCA gene phosphorylation in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, inhibitors of PLK1 protein, human kinases inhibited SNCA gene phosphorylation both in primary cortical cell cultures and in Mus sp. Head>Brain in vivo, PLK2 directly phosphorylates SNCA gene at Ser-129 in an in vitro biochemical assay, To better understand the role of PLK2 in α-synuclein phosphorylation in vivo, we further evaluated the effect of PLK2 genetic knockdown and pharmacological inhibition on Phospho-α-Syn levels in different Head>Brain regions of PLK2 knockout (KELL NULL), heterozygous (Het) and wild-type (WT) mice, Polo-like kinase-2 (PLK2 protein, human) has been implicated as the dominant kinase involved in the phosphorylation of α-synuclein in Lewy bodies, which are one of the hallmarks of Parkinson Disease neuropathology[SEP]Relations: Parkinson disease has relations: disease_protein with LRRK2 protein, human, disease_protein with LRRK2 protein, human.", "label": "yes"}
{"original_question": "Is the glucocorticoid receptor a transcription factor?", "id": "converted_4148", "sentence1": "Is the GLUCOCORTICOID RECEPTOR-LIKE 1 a transcription factor?", "sentence2": "Glutathione Reductase, Mitochondrial, Human and KLF4 protein, human protein, human, both pioneer transcription factors,, The GLUCOCORTICOID RECEPTOR-LIKE 1 (Glutathione Reductase, Mitochondrial, Human) is a ligand-binding dependent transcription factor that ultimately regulates vital biological processes and Inflammation response through specific gene expression control, thus representing a notable Pharmacologic Substance target to explore. , The GLUCOCORTICOID RECEPTOR-LIKE 1 (Glutathione Reductase, Mitochondrial, Human) is a ligand-activated transcription factor that translocates to the Cell Nucleus upon hormone stimulation and distributes between the Nucleoplasm and membraneless compartments named nuclear foci.[SEP]Relations: Nucleoplasm has relations: cellcomp_protein with KLF4 protein, human, cellcomp_protein with KLF4 protein, human.", "label": "yes"}
{"original_question": "Is acid alpha-glucosidase the enzyme that causes Pompe disease when mutant?", "id": "converted_725", "sentence1": "Is acid Alpha-glucosidase the Enzyme [APC] that causes Generalized glycogen storage disease of infants when Mutant?", "sentence2": "Generalized glycogen storage disease of infants is an autosomal recessive genetic disorder characterized by a deficiency of the Enzyme [APC] responsible for degradation of lysosomal glycogen (acid α-glucosidase (Ga language)), Generalized glycogen storage disease of infants is a systemic metabolic disorder characterized by lack of acid-alpha glucosidase (Ga language) resulting in ubiquitous lysosomal glycogen accumulation, Generalized glycogen storage disease of infants is an autosomal recessive myopathic disorder caused by the deficiency of lysosomal acid α-glucosidase (Ga language), Acid α-glucosidase deficiency, that is, Generalized glycogen storage disease of infants, is a Glycogen Storage Disease Type I for which Enzyme [APC] replacement therapy (Estrogen Replacement Therapy) is available, The analysis revealed that the Amino Acid Substitution causing a processing or transport defect responsible for Generalized glycogen storage disease of infants were widely spread over all of the five domains comprising the acid Alpha-glucosidase., Generalized glycogen storage disease of infants is a lysosomal storage disease (Lysergic Acid Diethylamide) caused by a deficiency in the Lysosomal Enzyme [APC] acid Alpha-glucosidase., Glycogen storage disease type II (GSDII; Generalized glycogen storage disease of infants or acid maltase deficiency) is an Autosomal Recessive Disorder caused by lysosomal acid Alpha-glucosidase (AalphaGlu) deficiency and manifests predominantly as Skeletal Muscle Tissue weakness., Structural study on a Mutant acid Alpha-glucosidase in silico combined with biochemical investigation is useful for understanding the molecular pathology of Generalized glycogen storage disease of infants., The nature of Mutant acid Alpha-glucosidase (Geldanamycin Analogue) in Muscle Tissue was studied in 6 patients with Generalized glycogen storage disease of infants, consisting of 2 each of the infantile, childhood and adult types., Generalized glycogen storage disease of infants (Glycogen Storage Disease Type III) is caused by mutations in the acid Alpha-glucosidase Genes., Glycogen storage disease type II (Generalized glycogen storage disease of infants) is inherited by autosomal recessive transmission and caused by a deficiency of acid Alpha-glucosidase (Ga language), resulting in impaired degradation and lysosomal accumulation of glycogen., Generalized glycogen storage disease of infants is a lysosomal storage disorder (Lysergic Acid Diethylamide) caused by mutations in the Genes that encodes acid Alpha-glucosidase (Ga language)., Demonstration of acid Alpha-glucosidase in different types of Generalized glycogen storage disease of infants by use of an immunochemical method., Acid Alpha-glucosidase (Ga language) deficiency causes Generalized glycogen storage disease of infants, a lethal lysosomal glycogen storage disease for which no effective treatment currently exists., Deficiency of lysosomal alpha glucosidase (Ga language) causes Generalized glycogen storage disease of infants, which is usually fatal if onset occurs in infancy., Ambulatory electrocardiogram analysis in infants treated with recombinant Homo sapiens acid Alpha-glucosidase Enzyme [APC] replacement therapy for Generalized glycogen storage disease of infants., Infantile Generalized glycogen storage disease of infants is caused by deficiency of lysosomal acid Alpha-glucosidase., Determination of acid Alpha-glucosidase activity in blood spots as a diagnostic test for Generalized glycogen storage disease of infants., The pharmacological chaperone AT2220 increases the specific activity and lysosomal delivery of Mutant acid Alpha-glucosidase, and promotes glycogen reduction in a transgenic mouse model of Generalized glycogen storage disease of infants, Structural study on a Mutant acid Alpha-glucosidase in silico combined with biochemical investigation is useful for understanding the molecular pathology of Generalized glycogen storage disease of infants, Glycogen stored in Skeletal but not in Cardiac - anatomy qualifier Muscle Tissue in acid Alpha-glucosidase Mutant (Pompe) CASP14 Genes is highly resistant to transgene-encoded Homo sapiens Enzyme [APC], Although many lysosomal disorders are corrected by a small amount of the missing Enzyme [APC], it has been generally accepted that 20-30% of normal acid Alpha-glucosidase (Ga language) activity, provided by Genes or Enzyme [APC] replacement therapy, would be required to reverse the Myopathy and Cardiomyopathies in Generalized glycogen storage disease of infants, The nature of Mutant acid Alpha-glucosidase (Geldanamycin Analogue) in Muscle Tissue was studied in 6 patients with Generalized glycogen storage disease of infants, consisting of 2 each of the infantile, childhood and adult types, As in the severe Homo sapiens infantile disease (Pompe Syndrome), CASP14 Genes homozygous for disruption of the acid Alpha-glucosidase Genes (6(neo)/6(neo)) lack Enzyme [APC] activity and begin to accumulate glycogen in Cardiac - anatomy qualifier and Skeletal Muscle Tissue lysosomes by 3 weeks of age, with a progressive increase thereafter, Glycogen-storage disease type II, Generalized glycogen storage disease of infants, is caused by the deficiency of acid alpha-D-glucosidase in Lysosomes, Generalized glycogen storage disease of infants (Glycogen Storage Disease Type III) is caused by mutations in the acid Alpha-glucosidase Genes, Glycogen storage disease type II (Generalized glycogen storage disease of infants) is inherited by autosomal recessive transmission and caused by a deficiency of acid Alpha-glucosidase (Ga language), resulting in impaired degradation and lysosomal accumulation of glycogen, Glycogen stored in Skeletal but not in Cardiac - anatomy qualifier Muscle Tissue in acid Alpha-glucosidase Mutant (Pompe) CASP14 Genes is highly resistant to transgene-encoded Homo sapiens Enzyme [APC]., Structural modeling of Mutant alpha-glucosidases resulting in a processing/transport defect in Generalized glycogen storage disease of infants., Replacing acid Alpha-glucosidase in Generalized glycogen storage disease of infants: recombinant and transgenic enzymes are equipotent, but neither completely clears glycogen from type II Muscle Tissue fibers., The pharmacological chaperone AT2220 increases the specific activity and lysosomal delivery of Mutant acid Alpha-glucosidase, and promotes glycogen reduction in a transgenic mouse model of Generalized glycogen storage disease of infants., Generalized glycogen storage disease of infants is an autosomal recessive Muscle Tissue-wasting disorder caused by the deficiency of the Lysosomal Enzyme [APC] acid Alpha-glucosidase. , Structural study on a Mutant acid Alpha-glucosidase in silico combined with biochemical investigation is useful for understanding the molecular pathology of Generalized glycogen storage disease of infants., We describe an improved method for detecting deficiency of the acid hydrolase, Glucan 1,4-alpha-Glucosidase in Specimen Source Codes - Leukocytes, the Enzyme [APC] defect in glycogen storage disease Type II (Generalized glycogen storage disease of infants)., Acid Alpha-glucosidase (Ga language) deficiency causes Generalized glycogen storage disease of infants,,  Infantile Generalized glycogen storage disease of infants is caused by deficiency of lysosomal acid Alpha-glucosidase. Trials with recombinant Homo sapiens acid Alpha-glucosidase Enzyme [APC] replacement therapy (Estrogen Replacement Therapy) show a decrease in left ventricular mass and improved function.,  Generalized glycogen storage disease of infants is an autosomal recessive Muscle Tissue-wasting disorder caused by the deficiency of the Lysosomal Enzyme [APC] acid Alpha-glucosidase. Due to virtual absence of acid Alpha-glucosidase, patients with classical infantile Generalized glycogen storage disease of infants develop progressive Cardiomyopathies, Skeletal Muscle Tissue weakness and Respiratory Insufficiency leading to Cessation of life in early infancy., Generalized glycogen storage disease of infants is caused by the congenital deficiency of the Lysosomal Enzyme [APC] acid Alpha-glucosidase., The nature of Mutant acid Alpha-glucosidase (Geldanamycin Analogue) in Muscle Tissue was studied in 6 patients with Generalized glycogen storage disease of infants,,  Generalized glycogen storage disease of infants is a lysosomal storage disorder (Lysergic Acid Diethylamide) caused by mutations in the Genes that encodes acid Alpha-glucosidase (Ga language). Recently, small molecule pharmacological chaperones have been shown to increase protein stability and cellular levels for Mutant lysosomal enzymes and have emerged as a new therapeutic strategy for the treatment of LSDs., Acid Alpha-glucosidase (Ga language) deficiency causes Generalized glycogen storage disease of infants, a lethal lysosomal glycogen storage disease for which no effective treatment currently exists., Infantile Generalized glycogen storage disease of infants is caused by deficiency of lysosomal acid Alpha-glucosidase., Glycogen-storage disease type II, Generalized glycogen storage disease of infants, is caused by the deficiency of acid alpha-D-glucosidase in Lysosomes., Structural modeling of Mutant alpha-glucosidases resulting in a processing/transport defect in Generalized glycogen storage disease of infants., Generalized glycogen storage disease of infants is a lysosomal storage disorder (Lysergic Acid Diethylamide) caused by mutations in the Genes that encodes acid Alpha-glucosidase (Ga language)., Structural study on a Mutant acid Alpha-glucosidase in silico combined with biochemical investigation is useful for understanding the molecular pathology of Generalized glycogen storage disease of infants., Ambulatory electrocardiogram analysis in infants treated with recombinant Homo sapiens acid Alpha-glucosidase Enzyme [APC] replacement therapy for Generalized glycogen storage disease of infants., Gene Mutation in Alpha-glucosidase cause accumulation of glycogen in lysosomes, resulting in Generalized glycogen storage disease of infants, a lysosomal storage disorder., Generalized glycogen storage disease of infants is an autosomal recessive Muscle Tissue-wasting disorder caused by the deficiency of the Lysosomal Enzyme [APC] acid Alpha-glucosidase., Infantile Generalized glycogen storage disease of infants is a fatal genetic Muscle Tissue disorder caused by a deficiency of acid Alpha-glucosidase, a glycogen-degrading Lysosomal Enzyme [APC].[SEP]Relations: Ga language has relations: cellcomp_protein with Lysosomes, disease_protein with Cardiomyopathies, cellcomp_protein with Lysosomes, disease_protein with Cardiomyopathies.", "label": "yes"}
{"original_question": "Is MammaPrint cleared by the United States Food and Drug Administration? ", "id": "converted_128", "sentence1": "Is MammaPrint cleared by the United States Food and Drug Administration? ", "sentence2": "Real-time RT-PCR confirmed the 5-gene prognostic signature that was distinct from an FDA-cleared 70-gene signature of MammaPrint panel and from the Oncotype DX Breast Cancer Assay Breast Cancer Assay recurrence score assay panel.[SEP]", "label": "yes"}
{"original_question": "Is adalimumab effective for hidradenitis suppurativa?", "id": "converted_1865", "sentence1": "Is adalimumab effective for hidradenitis suppurativa?", "sentence2": "If patient is not improved, then adalimumab 160 mg at week 0, 80 mg at week 2; then 40 mg subcutaneously weekly should be administered (LOE Ib, SOR A). If improvement occurs then therapy should be maintained as long as HS Lesion are present., Reduction in Pain:-:Point in time:^Patient:- scores and improvement in Depressive Symptoms in patients with hidradenitis suppurativa treated with adalimumab in a phase 2, randomized, placebo-controlled trial., adalimumab treatment for 16 weeks improved HS Lesion significantly versus placebo (NCT00918255)., CONCLUSION: Patients with moderate to severe HS had a high degree of Pain:-:Point in time:^Patient:- and Depressive Symptoms at baseline. Adalimumabtherapy was associated with decreased Pain:-:Point in time:^Patient:- and Depressive Symptoms compared to baseline., Spotlight on adalimumab in the treatment of active moderate-to-severe hidradenitis suppurativa., adalimumab, a recombinant, fully humanized, anti-Tumor Necrosis Factor-alpha alpha (anti-Recombinant Tumor Necrosis Factor Family Protein-α) monoclonal immunoglobulin complex location, is the only officially approved treatment for the management of moderate-to-severe HS. Case reports, concerning 42 patients who received adalimumab for severe HS (with the standard dose regimen for Psoriasis), reported a cumulative response rate of 58% (≥50% in 23 patients) with a relapse rate of 71% (10 out of 14 patients). The most recent and most well-powered phase III, randomized placebo-controlled trials for the evaluation of the efficacy and safety of adalimumab in treatment of moderate-to-severe HS (PIONEER studies I and II) showed that the Hidradenitis Suppurativa Clinical Response (HiSCR) rate at week 12 was significantly higher for patients randomized to adalimumab compared to placebo., In conclusion, adalimumab, to date, holds the most robust data regarding treatment efficacy in HS. , adalimumab (Humira) for the Treatment of Hidradenitis Suppurativa., adalimumab (Humira®) is a novel therapy approved by the US Food and Drug Administration, Health Canada, and the European Commission for the treatment of hidradenitis suppurativa (HS)., Taken together, these data conclude that treatment of HS with adalimumab is a safe and effective therapy resulting in a significant decrease in Specimen Source Codes - Abscess and inflammatory nodule counts within the first 12 weeks of treatment., Effective long-term control of refractory hidradenitis suppurativa with adalimumab after failure of conventional therapy., Hidradenitis suppurativa managed with adalimumab., Treatment of severe recalcitrant hidradenitis suppurativa with adalimumab., Long-term successful adalimumab therapy in severe hidradenitis suppurativa., Comparing treatment outcome of infliximab and adalimumab in patients with severe hidradenitis suppurativa., HiSCR (Hidradenitis Suppurativa Clinical Response): a novel clinical endpoint to evaluate therapeutic outcomes in patients with hidradenitis suppurativa from the placebo-controlled portion of a phase 2 adalimumab study, adalimumab in treatment-resistant hidradenitis suppurativa following recurrence after extensive affected area excision: a review of biologics therapy, adalimumab (antitumour necrosis factor-α) treatment of hidradenitis suppurativa ameliorates skin inflammation: an in situ and ex vivo study, Treatment of severe recalcitrant hidradenitis suppurativa with adalimumab, In a phase 2 trial, adalimumab, an immunoglobulin complex location against Tumor Necrosis Factor-alpha α, showed efficacy against hidradenitis suppurativa.PIONEER I and II were similarly designed, phase 3 multicenter trials of adalimumab for hidradenitis suppurativa, with two double-blind, placebo-controlled periods., Here we report a case of a patient with severe recalcitrant hidradenitis suppurativa successfully treated with adalimumab., Recent reports have demonstrated that adalimumab, a Tumor Necrosis Factor-alpha (Recombinant Tumor Necrosis Factor Family Protein) Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance), may be effective in the treatment of patients with HS who have failed conventional therapy., Conclusion adalimumab appears to be an effective and safe treatment for refractory HS., Effective long-term control of refractory hidradenitis suppurativa with adalimumab after failure of conventional therapy., Hidradenitis suppurativa managed with adalimumab., Treatment of severe recalcitrant hidradenitis suppurativa with adalimumab., Two Phase 3 Trials of adalimumab for Hidradenitis Suppurativa., adalimumab treatment for hidradenitis suppurativa associated with Crohn's disease of oral soft tissues of oral soft tissues., Long-term successful adalimumab therapy in severe hidradenitis suppurativa., Conclusion adalimumab appears to be an effective and safe treatment for refractory HS.., Comparing treatment outcome of infliximab and adalimumab in patients with severe hidradenitis suppurativa., Here we report a case of a patient with severe recalcitrant hidradenitis suppurativa successfully treated with adalimumab.., adalimumab is suitable for the long-term treatment of hidradenitis suppurativa and presents a further conservative treatment approach.., HiSCR (Hidradenitis Suppurativa Clinical Response): a novel clinical endpoint to evaluate therapeutic outcomes in patients with hidradenitis suppurativa from the placebo-controlled portion of a phase 2 adalimumab study., Spotlight on adalimumab in the treatment of active moderate-to-severe hidradenitis suppurativa.[SEP]Relations: Psoriasis has relations: disease_protein with Recombinant Tumor Necrosis Factor Family Protein, disease_protein with Recombinant Tumor Necrosis Factor Family Protein. adalimumab has relations: drug_protein with Recombinant Tumor Necrosis Factor Family Protein, drug_protein with Recombinant Tumor Necrosis Factor Family Protein. Infliximab has relations: drug_protein with Recombinant Tumor Necrosis Factor Family Protein, drug_drug with adalimumab, drug_protein with Recombinant Tumor Necrosis Factor Family Protein, drug_drug with adalimumab.", "label": "yes"}
{"original_question": "Does DDX54 play a role in DNA damage response?", "id": "converted_2342", "sentence1": "Does DDX54 gene play a role in DNA damage response?", "sentence2": "DDX54 gene gene regulates transcriptome dynamics during DNA damage response., The contribution of post-transcriptional gene regulatory networks to the DNA damage response (DDR1 wt Allele) has not been extensively studied. Here, we systematically identified RNA-binding Proteins differentially interacting with polyadenylated transcripts upon exposure of human breast carcinoma cells to ionizing radiation (IR). Interestingly, more than 260 Proteins, including many nucleolar Proteins, showed increased binding to poly(A)+RNA in IR-exposed cells. The functional analysis of DDX54 gene gene, a candidate genotoxic stress responsive RNA helicase, revealed that this Protein Info is an immediate-to-early DDR1 wt Allele regulator required for the splicing efficacy of its target IR-induced pre-mRNAs. Upon IR exposure, DDX54 gene gene acts by increased interaction with a well-defined class of pre-mRNAs that harbor Introns with weak Splice Acceptor Site, as well as by Protein Info-Protein Info contacts within components of U2 snRNP and Spliceosomes, resulting in lower intron retention and higher processing rates of its target transcripts. Because DDX54 gene gene promotes survival after exposure to IR, its expression and/or mutation rate may impact DDR1 wt Allele-related pathologies. Our work indicates the relevance of many uncharacterized RBPs potentially involved in the DDR1 wt Allele., The functional analysis of DDX54 gene gene, a candidate genotoxic stress responsive RNA helicase, revealed that this Protein Info is an immediate-to-early DDR1 wt Allele regulator required for the splicing efficacy of its target IR-induced pre-mRNAs.[SEP]", "label": "yes"}
{"original_question": "Is single-cell analysis (SCA) possible in proteomics?", "id": "converted_274", "sentence1": "Is single-cell analysis (Structure of superior cerebellar artery) possible in proteomics?", "sentence2": "Toward Single Cell Analysis by Plume Collimation in Laser Ablation Electrospray Ionization Mass Spectrometry., he advent of proteomics and genomics at a single-cell level has set the basis for an outstanding improvement in analytical technology and data acquisition., The new-generation technology of single-cell analysis is able to better characterize a cell's population, identifying and differentiating outlier Cells, in order to provide both a single-cell experiment and a corresponding bulk measurement, through the identification, quantification and characterization of all system biology aspects (genomics, transcriptomics, proteomics, metabolomics, degradomics and fluxomics). The movement of omics into single-cell analysis represents a significant and outstanding shift., Laser ablation electrospray ionization (LAESI) is a novel method for the direct imaging of biological tissues by mass spectrometry. By performing ionization in the ambient environment, this technique enables in vivo studies with potential for single-cell analysis., Other approaches for MS-based chemical imaging and profiling include those based on near-field laser ablation and inductively-coupled plasma MS analysis, which offer complementary capabilities for subcellular chemical imaging and profiling., Mass spectrometry imaging and profiling of single Cells., his is rapidly changing with the recent examples of single cell genomics, transcriptomics, proteomics and metabolomics. The rate of change is expected to accelerate owing to emerging technologies that range from micro/nanofluidics to microfabricated interfaces for mass spectrometry to third- and fourth-generation automated DNA sequencers, Single-cell analysis (Structure of superior cerebellar artery) has been increasingly recognized as the key technology for the elucidation of cellular functions, which are not accessible from bulk measurements on the population level. Thus far, Structure of superior cerebellar artery has been achieved by miniaturization of established engineering concepts to match the dimensions of a single cell, Single-cell proteomic chip for profiling Protoplasm signaling pathways in single tumor Cells., The amount of single Proteins in single Cells can be as low as one copy per cell and is for most Proteins in the attomole range or below; usually considered as insufficient for proteomic analysis., n Arabidopsis thaliana <plant> <plant>, we have successfully identified nine unique Proteins in a single-cell sample and 56 Proteins from a pool of 15 single-cell samples from glucosinolate-rich S-Cells by nanoLC-MS/MS proteomic analysis, thus establishing the proof-of-concept for true single-cell proteomic analysis, A first step towards practical single cell proteomics: a microfluidic antibody capture chip with TIRF detection.[SEP]", "label": "no"}
{"original_question": "Is there a relation between ANP and transcapillary albumin escape?", "id": "converted_1377", "sentence1": "Is there a relation between Atrial Natriuretic Factor and transcapillary ALB gene escape?", "sentence2": "Thus, in a large ethnically homogeneous cohort of diabetic subjects, our data show: (1) a significant association of C708/T Genetic Polymorphism with Microalbuminuria in long-term Diabetes Mellitus and with both lower plasma Atrial Natriuretic Factor levels and widespread ALB gene leakage, hese results suggest a possible role of PND gene in conferring protection from Kidney Diseases and microvascular damage in type 1 Diabetes Mellitus., Moreover, the increased susceptibility of the Glomerular capillaries structure in diabetics to Atrial Natriuretic Factor seems to be part of a more generalized capillary abnormality, because Atrial Natriuretic Factor also increases the transcapillary escape of ALB gene., In summary, low dose Atrial Natriuretic Factor infusion in healthy subjects caused a shift of plasma water and Electrolyte [EPC] from the circulation, with ALB gene escape as a secondary phenomenon.[SEP]", "label": "yes"}
{"original_question": "Is CD56 useful in Ewing sarcoma prognosis?", "id": "converted_76", "sentence1": "Is NCAM1 wt Allele useful in Ewings sarcoma prognosis?", "sentence2": "Excellent prognosis in a subset of patients with Ewings sarcoma identified at diagnosis by NCAM1 wt Allele using flow cytometry, There was a highly significant correlation between NCAM1 wt Allele expression and progression-free survival (PFS; 69% in low/negative expression versus 30% in high expression groups, P = 0.024), In patients with localized nonpelvic disease, those expressing low/negative NCAM1 wt Allele had 100% PFS versus 40% in the high expressing group (P = 0.02), NCAM1 wt Allele was found to be an independent prognostic marker with an 11-fold increased risk for relapse in patients with localized disease (P = 0.006), NCAM1 wt Allele expression could be used to reveal ES patients with excellent prognosis or patients predisposed to relapse, thus improving treatment stratification and implementation of personalized therapy, Excellent prognosis in a subset of patients with Ewings sarcoma identified at diagnosis by NCAM1 wt Allele using flow cytometry., Three years after diagnosis the patient presented with severe respiratory difficulty and following resection, the final pathology revealed Multiple tumors with Focal of High Grade Sarcoma compatible with primitive Neuroectodermal Tumors/extraskeletal Ewings sarcoma based on morphology and immunohistochemistry (CD99 antigen antigen, NCAM1 wt Allele)., NCAM1 wt Allele expression could be used to reveal ES patients with excellent prognosis or patients predisposed to relapse, thus improving treatment stratification and implementation of personalized therapy., Identification of NCAM1 wt Allele and B3GAT1 wt Allele by flow cytometry in Ewing's sarcoma of bone of bone or primitive Neuroectodermal Tumors., NCAM1 wt Allele expression could be used to reveal ES patients with excellent prognosis or patients predisposed to relapse, thus improving treatment stratification and implementation of personalized therapy.[SEP]Relations: Ewings sarcoma of bone has relations: disease_disease with Ewings sarcoma, disease_disease with Ewings sarcoma. Ewings sarcoma has relations: disease_phenotype_positive with Ewings sarcoma, disease_phenotype_positive with Ewings sarcoma.", "label": "yes"}
{"original_question": "Can zinc finger nucleases be used to combat disease?", "id": "converted_288", "sentence1": "Can Zinc Fingers nucleases be used to combat disease?", "sentence2": "Genetic engineering has emerged as a powerful mechanism for understanding biological systems and a potential approach for redressing Congenital Disorders., This is of particular importance, given the momentum currently behind ZFNs in moving into phase I clinical trials. This study provides a historical account of the origins of Zinc Finger Nucleases technology, an analysis of current techniques and applications, and an examination of the ethical issues applicable to translational Zinc Finger Nucleases genetic engineering in early phase clinical trials., This broad range of tractable species renders ZFNs a useful tool for improving the understanding of complex physiological systems, to produce Animals, Transgenic, Cultured Cell Line, and Plants, and to treat Homo sapiens disease., We observe comparably high frequencies in Homo sapiens T cells, raising the possibility of strategies based on zinc-finger nucleases for the treatment of disease., Using engineered nucleases, such as Zinc Finger Nucleases (ZFNs) or Transcription Activator-Like Effector Nucleases (Transcription Activator-Like Effector Nucleases), to make targeted genomic modifications has become a common technique to create new model organisms and custom Cultured Cell Line, and has shown great promise for disease treatment., Zinc Finger nucleases (ZFNs) have been used to create precise genome modifications at frequencies that might be therapeutically useful in gene therapy., Zinc finger nucleases as tools to understand and treat Homo sapiens diseases., Evaluation of novel design strategies for developing Zinc Fingers nucleases tools for treating Homo sapiens diseases., An over expression APP model for anti-Alzheimer disease drug screening created by Zinc Fingers nuclease technology., Oxidase-deficient neutrophils from Granulomatous Disease, Chronic, X-Linked Induced Pluripotent Stem Cells: functional correction by Zinc Fingers nuclease-mediated safe harbor targeting., Recently, it has been shown that targeted Mutagenesis Procedure using zinc-finger nucleases (ZFNs) and transcription activator-like effector nucleases (Transcription Activator-Like Effector Nucleases) can be used to generate knockout Zebrafish lines for analysis of their function and/or developing disease models, Using engineered nucleases, such as Zinc Finger Nucleases (ZFNs) or Transcription Activator-Like Effector Nucleases (Transcription Activator-Like Effector Nucleases), to make targeted genomic modifications has become a common technique to create new model organisms and custom Cultured Cell Line, and has shown great promise for disease treatment, Gene correction by homologous recombination with Zinc Fingers nucleases in primary cells from a mouse model of a generic recessive genetic disease., raising the possibility of strategies based on zinc-finger nucleases for the treatment of disease.[SEP]", "label": "yes"}
{"original_question": "Is periampullary carcinoma (PAC) a relatively rare genitourinary malignancy", "id": "converted_4416", "sentence1": "Is periampullary carcinoma (cisplatin/cyclophosphamide/doxorubicin protocol) a relatively rare genitourinary malignancy", "sentence2": "Pancreaticobiliary subtype of Periampullary carcinoma (cisplatin/cyclophosphamide/doxorubicin protocol) has a poor prognosis in comparison to the Intestines subtype., MUC1 wt Allele wt Allele, KRT20 wt Allele, and Caudal-type homeobox protein 2 Ag immunohistochemical markers can sub-classify periampullary carcinomas into pancreaticobiliary, Intestines, and mixed subtypes., Pancreaticoduodenectomy (Lugano Lymphoma Response Classification Progressive Disease by PET) is a complex surgical procedure involving resection of the Duodenum and Duodenum and duodenum, the Head of pancreas and uncinate process, and the distal common bile duct. It is most commonly performed for periampullary malignancy but may also be indicated in select cases of chronic pancreatitis or benign periampullary tumors., In patients suspected of Pancreatic Hormones or periampullary cancer, abdominal contrast-enhanced computed tomography (X-Ray Computed Tomography) is the standard diagnostic modality., The pre-operative neutrophil-to-lymphocyte ratio (NLR), when ≥5 has been associated with reduced survival for patients with various Malignant neoplasm of gastrointestinal tract, however, it's prognostic value in patients with periampullary tumour has not been reported to date., Comparison Of Biliary Stenting And Surgical Bypass In Palliative Management Of Irresectable Periampullary Carcinoma.,  Some 20-40% of the periampullary carcinoma is irresectable at the time of diagnosis. Biliary stenting and surgical bypass are commonly used palliative procedure., Whereas Periampulary AdenoCarcinoma (cisplatin/cyclophosphamide/doxorubicin protocol) having four anatomic subtypes, Pancreatic Hormones, Common Bile Duct (OPN1MW gene), ampullary and Duodenum and Duodenum and duodenum shows relative better prognosis, DEFINITION: Periampullary carcinomas are rare and constitute a special entity, as diagnosed earlier and having a better prognosis than other duodenal tumors.METHODS: In the present study, we retrospectively reviewed the medical records of 16 patients with periampullary carcinomas over 10 years.RESULTS: 16 patients, 10 men and 6 women (median age 66.7 years, range 42-80) had a , Periampullary carcinomas: a special entity of duodenal tumors., Periampullary adenocarcinomas are rare neoplasm that originates from the Head of pancreas, the ampulla of vater, the distal bile duct or the Duodenum and Duodenum and duodenum.[SEP]", "label": "no"}
{"original_question": "Are genomic regulatory blocks (GRBs) any different than TADs?", "id": "converted_3336", "sentence1": "Are genomic regulatory blocks (GRBs) any different than Tietz syndrome?", "sentence2": "Topologically associating domains are ancient features that coincide with Metazoan clusters of extreme noncoding conservation., Clusters of CNEs define the span of regulatory inputs for many important developmental regulators and have been described previously as genomic regulatory blocks (GRBs). Their function and distribution around important Genes, Regulator raises the question of how they relate to 3 Days conformation of these loci. Here, we show that clusters of CNEs strongly coincide with topological organisation, predicting the boundaries of hundreds of topologically associating domains (Tietz syndrome) in human and Drosophila <basidiomycetes> <basidiomycetes>. The set of Tietz syndrome that are associated with high levels of noncoding conservation exhibit distinct properties compared to Tietz syndrome devoid of extreme noncoding conservation. The close correspondence between extreme noncoding conservation and Tietz syndrome suggests that these Tietz syndrome are ancient, revealing a regulatory architecture conserved over hundreds of millions of years.Metazoan genomes contain many clusters of conserved noncoding elements. Here, the authors provide evidence that these clusters coincide with distinct topologically associating domains in Homo sapiens and Drosophila <basidiomycetes> <basidiomycetes>, revealing a conserved regulatory genomic architecture.[SEP]", "label": "no"}
{"original_question": "Is nintedanib effective for Idiopathic Pulmonary Fibrosis?", "id": "converted_384", "sentence1": "Is nintedanib effective for Idiopathic Pulmonary Fibrosis?", "sentence2": "In this review, we present the positive results of recently published clinical trials regarding therapy for Idiopathic Pulmonary Fibrosis, with emphasis on pirfenidone and nintedanib., Nintedanib: evidence for its therapeutic potential in idiopathic pulmonary fibrosis,  In the Phase II TOMORROW trial, treatment with 150 mg of nintedanib twice daily showed a trend to slow the decline in lung function and significantly decrease acute exacerbations in patients with Idiopathic Pulmonary Fibrosis, while showing an acceptable safety profile. The Phase III INPULSIS trials demonstrated a significant decrease in the annual rate of decline in forced vital capacity in Idiopathic Pulmonary Fibrosis patients treated with 150 mg nintedanib twice daily. In the INPULSIS-2 trial, the time to the first acute exacerbation significantly increased in Idiopathic Pulmonary Fibrosis patients who were treated with 150 mg of nintedanib twice daily.,  Effects on collagen secretion were compared with those of the drugs nintedanib and pirfenidone, recently approved for Idiopathic Pulmonary Fibrosis., Nintedanib, an orally available, small-molecule Protein Tyrosine Kinase inhibitor with selectivity for Recombinant Vascular Endothelial Growth Factor (Vascular Endothelial Growth Factor A), Platelet-Derived Growth Factor (PDGF) and Recombinant Fibroblast Growth Factor 1 (FGF) receptors has recently been shown, in two pivotal phase III studies, to effectively slow Idiopathic Pulmonary Fibrosis Disease progression. Consequently, nintedanib was given accelerated approval by the FDA in October 2014 for the treatment of Idiopathic Pulmonary Fibrosis. , Most recently, pirfenidone and nintedanib, two compounds with pleiotropic anti-fibrotic properties, have been proven effective in reducing functional decline and Disease progression in Idiopathic Pulmonary Fibrosis. , Meningococcal group B vaccine (Trumenba) to prevent more types of invasive meningococcal Disease; Factor VIII: C assay (recombinant), porcine sequence (Obizur) to treat Hemorrhage from acquired Hemophilia, NOS; and pirfenidone (Esbriet) and nintedanib (Ofev) for idiopathic pulmonary fibrosis.,  More importantly, the period ends with the publication of two groundbreaking studies that confirmed that two drugs, pirfenidone and nintedanib, slowed Disease progression, leading to a historic approval by the FDA. , Nintedanib (Ofev(®)) is an orally available, small, multiple receptor Protein Tyrosine Kinase inhibitor developed by Boehringer Ingelheim for the treatment of idiopathic pulmonary fibrosis (Idiopathic Pulmonary Fibrosis) and Primary malignant neoplasm. Nintedanib received its first global approval in the US in October 2014 for the treatment of Idiopathic Pulmonary Fibrosis. Nintedanib has received a positive opinion from the European Medicines Agency's Committee for Pharmaceutical Preparations for Homo sapiens Use for the treatment of Idiopathic Pulmonary Fibrosis, and for the second-line treatment in combination with docetaxel of locally advanced, metastatic or locally recurrent non-small cell lung Primary malignant neoplasm of adenocarcinoma tumour histology. , This article summarizes the milestones in the development of nintedanib leading to this first approval for Idiopathic Pulmonary Fibrosis., Efficacy and safety of nintedanib in idiopathic pulmonary fibrosis., Nintedanib: a novel therapeutic approach for idiopathic pulmonary fibrosis., Nintedanib is in clinical development as a treatment for idiopathic pulmonary fibrosis (Idiopathic Pulmonary Fibrosis)., Reducing lung function decline in patients with idiopathic pulmonary fibrosis: potential of nintedanib., These results suggest that nintedanib may impact the progressive course of fibrotic lung diseases such as idiopathic pulmonary fibrosis., Findings from recently published placebo-controlled trials in idiopathic pulmonary fibrosis have established that pirfenidone and nintedanib prevent about 50% of the decline in forced vital capacity typically seen in this Disease; future trials are therefore unlikely to use placebo as a control group for ethical reasons., The Protein Tyrosine Kinase inhibitor nintedanib (BIBF 1120) is in clinical development for the treatment of idiopathic pulmonary fibrosis., A phase 2 trial suggested that treatment with 150 mg of nintedanib twice daily reduced lung-function decline and acute exacerbations in patients with idiopathic pulmonary fibrosis., A phase 2 trial suggested that treatment with 150 mg of nintedanib twice daily reduced lung-function decline and acute exacerbations in patients with idiopathic pulmonary fibrosis. , Data from the Phase II TOMORROW study suggested that nintedanib 150�mg twice daily had clinical benefits with an acceptable safety profile.METHODS: The INPULSIS� trials are replicate Phase III, randomized, double-blind, studies comparing the efficacy and safety of nintedanib 150�mg twice daily with placebo in patients with Idiopathic Pulmonary Fibrosis. , Nintedanib received its first global approval in the US in October 2014 for the treatment of Idiopathic Pulmonary Fibrosis. , The most frequent adverse event in the nintedanib groups was Diarrhea, with rates of 61.5% and 18.6% in the nintedanib and placebo groups, respectively, in INPULSIS-1 and 63.2% and 18.3% in the two groups, respectively, in INPULSIS-2. CONCLUSIONS: In patients with idiopathic pulmonary fibrosis, nintedanib reduced the decline in FVC, which is consistent with a slowing of Disease progression; nintedanib was frequently associated with Diarrhea, which led to discontinuation of the study medication in less than 5% of patients. , A phase 2 trial suggested that treatment with 150 mg of nintedanib twice daily reduced lung-function decline and acute exacerbations in patients with idiopathic pulmonary fibrosis. METHODS: We conducted two replicate 52-week, randomized, double-blind, phase 3 trials (INPULSIS-1 and INPULSIS-2) to evaluate the efficacy and safety of 150 mg of nintedanib twice daily as compared with placebo in patients with idiopathic pulmonary fibrosis. , Nintedanib (Ofev(�)) is an orally available, small, multiple receptor Protein Tyrosine Kinase inhibitor developed by Boehringer Ingelheim for the treatment of idiopathic pulmonary fibrosis (Idiopathic Pulmonary Fibrosis) and Primary malignant neoplasm. Nintedanib received its first global approval in the US in October 2014 for the treatment of Idiopathic Pulmonary Fibrosis. , Nintedanib: evidence for its therapeutic potential in idiopathic pulmonary fibrosis., A phase 2 trial suggested that treatment with 150 mg of nintedanib twice daily reduced lung-function decline and acute exacerbations in patients with idiopathic pulmonary fibrosis. We conducted two replicate 52-week, randomized, double-blind, phase 3 trials (INPULSIS-1 and INPULSIS-2) to evaluate the efficacy and safety of 150 mg of nintedanib twice daily as compared with placebo in patients with idiopathic pulmonary fibrosis.[SEP]", "label": "yes"}
{"original_question": "Is there an increased risk for meningiomas in childhood leukemia survivors?", "id": "converted_3683", "sentence1": "Is there an increased risk for Meningioma in childhood leukemia Survivors?", "sentence2": "Cranial radiotherapy improves survival of the most common childhood cancers, including Brain Neoplasms and leukemia. Unfortunately, long-term Survivors are faced with consequences of secondary neoplasia, including radiation-induced Meningioma (RIMs). , Combined chemotherapy and prophylactic Cranial Irradiation has improved the prognosis of children with Acute leukemia. However Cranial Irradiation carries a latent risk of the induction of secondary Neoplasms, Intracranial. We encountered a patient who developed multiple intracranial radiation-induced Meningioma (RIMs) 25 years after prophylactic Cranial Irradiation for the treatment of Acute leukemia in childhood. , Focal cranial hyperostosis from Benign Meningioma: a complication from previous radiation treatment for childhood T-cell Pre B-cell Pre B-cell acute lymphoblastic leukemia., Presented is a case of a 20 year Homo sapiens with a history of T-cell lymphoblastic leukemia diagnosed at age 22 months, treated with chemotherapy and Cranial Irradiation. He had developed increasing prominence of the top of his Head - Component of Device over several months. Plain radiograph showed frontal calvarium thickening with Focal \"hair-on-end\" periosteal reaction. Magnetic resonance imaging revealed an enhancing dural-based mass with transcalvarial extension, confirmed after resection to be Benign Meningioma (World Health Organization Grade I). , RESULTS: Acute myeloid leukemia (Leukemia, Myelocytic, Acute; n = 186), MYELODYSPLASTIC SYNDROME (Miller Dieker syndrome; n = 69), and nonmeningioma brain tumor (n = 116) were the most common types of SMNs and had the poorest outcome (5-year survival rate, 18.1% ± 2.9%, 31.1% ± 6.2%, and 18.3% ± 3.8%, respectively). , Radiation-induced World Health Organization grade II Meningioma in young patients following prophylactic Cranial Irradiation for Pre B-cell Pre B-cell acute lymphoblastic leukemia in childhood. Three case reports., Current chemotherapeutic regimens have been used to successfully treat many children with Pre B-cell Pre B-cell acute lymphoblastic leukemia (Acute lymphocytic leukemia), but have resulted in an increased risk of late central nervous system tumors, most commonly Benign Meningioma, particularly in patients who have received Cranial Irradiation. , RESULTS: Fifty-nine MRI abnormalities (32 cavernomas, nine Focal areas of gliosis, seven dystrophic mineralizations, five cerebral atrophies, four pituitary atrophies, one diffuse radiation leukoencephalopathy, and one Benign Meningioma) were found in 43 patients. , Intraventricular Benign Meningioma after Cranial Irradiation for childhood leukemia., Radiation-induced Meningioma may also have predilection to recur. The authors describe a case of an intraventricular Benign Meningioma occurring 23 years after Cranial Irradiation for childhood Pre B-cell Pre B-cell acute lymphoblastic leukemia., Cumulative incidence at 30 years after the childhood Primary malignant neoplasm diagnosis was 20.5% (95% confidence interval [CI] = 19.1% to 21.8%) for all subsequent Neoplasms, 7.9% (95% CI = 7.2% to 8.5%) for second malignant Neoplasms (excluding nonmelanoma skin Primary malignant neoplasm), 9.1% (95% CI = 8.1% to 10.1%) for nonmelanoma skin Primary malignant neoplasm, and 3.1% (95% CI = 2.5% to 3.8%) for Benign Meningioma. , Radiation-induced Meningioma: a shadow in the success story of childhood leukemia., Although the cohort is small, it seems probable that the increasing incidence of Benign Meningioma will shadow the future of cranially irradiated leukemia Survivors., Age at the time of irradiation, gender, or cumulative doses of chemotherapeutic agents showed no significant association with the development of Meningioma., Meningioma Screening With MRI in Childhood Leukemia Survivors Treated With Cranial Radiation., High incidence of Benign Meningioma in cranial irradiated Survivors of childhood Pre B-cell Pre B-cell acute lymphoblastic leukemia., Radiation-induced World Health Organization grade II Meningioma in young patients following prophylactic Cranial Irradiation for Pre B-cell Pre B-cell acute lymphoblastic leukemia in childhood., Radiation-induced Benign Meningioma following prophylactic radiotherapy for Pre B-cell Pre B-cell acute lymphoblastic leukemia in childhood., Current chemotherapeutic regimens have been used to successfully treat many children with Pre B-cell Pre B-cell acute lymphoblastic leukemia ( Acute lymphocytic leukemia) , but have resulted in an increased risk of late central nervous system tumors , most commonly Benign Meningioma , particularly in patients who have received Cranial Irradiation, Survivors of childhood Acute lymphocytic leukemia treated with high-dose Cranial Irradiation are at risk both for early radiation injury in radiosensitive Organ , such as the Lens <bivalves> and pituitary gland , and for the later development of a radiation-induced Benign Meningioma, Radiation-induced Meningioma: a shadow in the success story of childhood leukemia, We treated 3 young patients with World Health Organization grade II Meningioma who had previously received Cranial Irradiation for the treatment of childhood Acute lymphocytic leukemia: a cerebellopontine angle tumor in a 19-year-old woman , a petroclival tumor in a 28-year-old Homo sapiens , and a frontal parasagittal tumor in a 19-year-old woman, We treated 3 young patients with World Health Organization grade II Meningioma who had previously received Cranial Irradiation for the treatment of childhood Acute lymphocytic leukemia: a cerebellopontine angle tumor in a 19-year-old woman, a petroclival tumor in a 28-year-old Homo sapiens, and a frontal parasagittal tumor in a 19-year-old woman., Current chemotherapeutic regimens have been used to successfully treat many children with Pre B-cell Pre B-cell acute lymphoblastic leukemia (Acute lymphocytic leukemia), but have resulted in an increased risk of late central nervous system tumors, most commonly Benign Meningioma, particularly in patients who have received Cranial Irradiation., Current chemotherapeutic regimens have been used to successfully treat many children with Pre B-cell Pre B-cell acute lymphoblastic leukemia (Acute lymphocytic leukemia), but have resulted in an increased risk of late central nervous system tumors, most commonly Benign Meningioma, particularly in patients who have received Cranial Irradiation., Long-term Survivors who received radiotherapy for Acute lymphocytic leukemia in childhood are at risk for late complications, including radiation-induced Benign Meningioma.[SEP]Relations: childhood leukemia has relations: disease_disease with Pre B-cell acute lymphoblastic leukemia, disease_disease with Pre B-cell acute lymphoblastic leukemia. acute lymphoblastic/lymphocytic leukemia has relations: disease_disease with Pre B-cell acute lymphoblastic leukemia, disease_disease with Pre B-cell acute lymphoblastic leukemia.", "label": "yes"}
{"original_question": "Is avelumab effective for urothelial carcinoma?", "id": "converted_3960", "sentence1": "Is avelumab effective for Urothelial Carcinoma?", "sentence2": "ince then, additional checkpoint inhibitors, including avelumab, durvalumab, and nivolumab, have gained approval. , Avelumab, an anti-programmed death-ligand 1 monoclonal immunoglobulin complex location approved for the treatment of metastatic Merkel cell carcinoma and platinum-treated Urothelial Carcinoma, was initially approved with a 10 mg/kg weight-based dose. , Five new PDCD1 wt Allele/CD274 wt Allele checkpoint inhibitors have been approved for the treatment of metastatic Urothelial Carcinoma (Ulcerative Colitis): pembrolizumab, atezolizumab, durvalumab, nivolumab, and avelumab. , We reviewed the literature for prospective studies evaluating PDCD1 wt Allele/CD274 wt Allele inhibitors in refractory Urothelial Carcinoma patients, which formed the basis for US Food and Drug Administration approval of 5 different antagonistic Antibodies, in vitro diagnostic targeting PDCD1 wt Allele or CD274 wt Allele (atezolizumab, durvalumab, avelumab, nivolumab, and pembrolizumab)., Nowadays, five immune checkpoint inhibitors blocking PDCD1 wt Allele (pembrolizumab, nivolumab) or CD274 wt Allele (atezolizumab, durvalumab, and avelumab) have been approved by the United States Food and Drug Administration (US FDA) for the first- or second-line use in Urothelial Carcinoma, based on durable response and manageable safety profiles observed in relevant clinical trials. , RETATION: Avelumab showed antitumour activity in the treatment of patients with platinum-refractory metastatic Urothelial Carcinoma; a manageable safety profile was reported in all avelumab-treated patients. These, data provide the rationale for therapeutic use of avelumab in metastatic Urothelial Carcinoma and it has received accelerated US FDA approval in this setting on this basis.FUNDIN, BACKGROUND: Anti-programmed cell death ligand 1 (CD274 wt Allele)/programmed cell death 1 Antibodies, in vitro diagnostic have shown clinical activity in platinum-treated metastatic Urothelial Carcinoma, resulting in regulatory approval of several agents, including avelumab (anti-CD274 wt Allele)., Avelumab as second-line therapy for metastatic, platinum-treated Urothelial Carcinoma in the phase Ib JAVELIN Solid Tumor study: 2-year updated efficacy and safety analysis., BACKGROUND: Avelumab has recently been approved by the Food and Drug Administration for the therapy of Merkel cell carcinoma and Urothelial Carcinoma., SIONS: Maintenance avelumab plus best supportive care significantly prolonged overall survival, as compared with best supportive care alone, among patients with urothelial cancer who had Disease that had not progressed with first-line chemotherapy. (Fund, By the emergence of modern immunotherapies with active agents like PDCD1 wt Allele (nivolumab, pembrolizumab) and CD274 wt Allele immune checkpoint blockers (atezolizumab, avelumab, durvalumab), new therapeutic options have become available for the treatment of patients with locally advanced and metastatic Urothelial Carcinoma., Avelumab, an anti-programmed death-ligand 1 monoclonal immunoglobulin complex location approved for the treatment of metastatic Merkel cell carcinoma and platinum-treated Urothelial Carcinoma, was initially approved with a 10 mg/kg weight-based dose., By the emergence of modern immunotherapies with active agents like PDCD1 wt Allele (nivolumab, pembrolizumab) and CD274 wt Allele immune checkpoint blockers (atezolizumab, avelumab, durvalumab), new therapeutic options have become available for the treatment of patients with locally advanced and metastatic Urothelial Carcinoma. Accor, ACQUISITION: Five Antibodies, in vitro diagnostic including pembrolizumab (CD274 wt Allele immunoglobulin complex location), atezolizumab (PDCD1 wt Allele immunoglobulin complex location), nivolumab (PDCD1 wt Allele immunoglobulin complex location), avelumab and durvalumab (CD274 wt Allele Antibodies, in vitro diagnostic) have been approved in the treatment of advanced Urothelial Carcinoma in first- and second-line treatment setting., INTERPRETATION: Avelumab showed antitumour activity in the treatment of patients with platinum-refractory metastatic Urothelial Carcinoma; a manageable safety profile was reported in all avelumab-treated patients., Conclusion Avelumab was well tolerated and associated with durable responses and prolonged survival in patients with refractory metastatic Ulcerative Colitis., Avelumab: A Novel Anti-CD274 wt Allele Agent in the Treatment of Merkel Cell Carcinoma and Urothelial Cell Carcinoma., In early 2017, avelumab (Bavencio®), a CD274 wt Allele-blocking monoclonal immunoglobulin complex location agent, was approved for the treatment of metastatic MCC and Ulcerative Colitis., Expert opinion: Avelumab has shown clinical efficacy for metastatic and advanced Ulcerative Colitis in phase I studies after the failure of platinum-based therapy with a well-tolerated safety profile., Avelumab has been approved by the U.S. FDA for the treatment of metastatic Merkel cell carcinoma and metastatic Urothelial Carcinoma that has progressed during or following treatment with a platinum-based regimen.[SEP]", "label": "yes"}
{"original_question": "Are Tregs CD4(+)CD25(+) regulatory T cells a positive regulator of the immune response?", "id": "converted_4585", "sentence1": "Are Tregs T-Cell Surface Glycoprotein CD4, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes a positive regulator of the immune response?", "sentence2": "The immunosuppressive effects of T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+ IL2RA wt Allele high regulatory Therapeutic gamma delta T-lymphocytes (Tregs) interfere with Antitumor immune responses in cancer patients., Alteration of regulatory Therapeutic gamma delta T-lymphocytes (Tregs) may contribute to ineffective suppression of proinflammatory cytokines in type 1 diabetes.AIM, Regulatory Therapeutic gamma delta T-lymphocytes (Tregs) suppress excessive immune responses in Iris (Eye), T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are negative regulators of the immune system that induce and maintain immune tolerance., PTPRF gene to chronic patients, Treg from patients with Prostate Health Index inhibited the proliferation of purified tuberculin (PPD) and HIV p24 activated CD4CD25 Therapeutic gamma delta T-lymphocytes. T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens,  demonstrate that aTregs are necessary for tolerance, DBA/2 skin was transplanted onto C57BL/6-RAG-1-deficient recipients adoptively transferred with purified sorted CD4CD25 Therapeutic gamma delta T-lymphocytes; half of the recipients undergo tolerance induction treatment.RE, It is well established that CD4CD25 regulatory Therapeutic gamma delta T-lymphocytes (Tregs) downregulate inflammatory immune responses and help to maintain immune homeostasis., In vitro expanded Homo sapiens T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+IL2RA wt Allele+ regulatory Therapeutic gamma delta T-lymphocytes are potent suppressors of T-cell-mediated xenogeneic responses., BACKGROUND: Regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are essential in the control of tolerance., T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are critical for the Peripheral immune tolerance., T regulatory Cells (Tregs) have a role in immunosuppression and control of Autoimmune Diseases, and are currently an important topic in the study of immune response to Specimen Source Codes - Tumor Cells, uncertain whether benign or malignant., T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+IL2RA wt Allele+ regulatory Therapeutic gamma delta T-lymphocytes attenuate lipopolysaccharide-induced systemic inflammatory responses and promotes survival in Mus Escherichia coli infection., OBJECTIVES: CD4CD25 regulatory Therapeutic gamma delta T-lymphocytes (Tregs) play a key role in the prevention of various inflammatory and autoimmune disorders by suppressing immune responses., IL2RA wt Allele(High) T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+ regulatory Therapeutic gamma delta T-lymphocytes (Regulatory T-Lymphocytes) have been described as key players in immune regulation, preventing infection-induced immune pathology and limiting collateral tissue damage caused by vigorous anti-parasite immune response. In t, ic subset of Therapeutic gamma delta T-lymphocytes, currently recognized as FOXP3(+) IL2RA wt Allele(+) T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs), are pivotal in suppressing Autoimmune Diseases and maintaining immune homeostasis by mediating self-tolerance at the periphery as shown in autoimmune diseases and Malignant Neoplasms. A growing body of , T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+IL2RA wt Allele+ regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are essential negative regulators of immune responses. , Accumulating evidence has demonstrated that naturally occurring T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are critical for maintenance of immunological tolerance and have been shown to be important in regulating the immune responses in many diseases. Curcu, 4+IL2RA wt Allele+ Forkhead Box Protein P3+ regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are recognized as one of the major regulatory factors in immune tolerance and inflammatory responses. Si, lly occurring T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) have a key role in the prevention of various inflammatory and autoimmune disorders by suppressing immune responses. We tested t, T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are considered to play a key role as suppressors of immune mediated reactions. The a, T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+ IL2RA wt Allele+ T regulatory Cells (Tregs) are classified as a subset of Therapeutic gamma delta T-lymphocytes whose role is the suppression and regulation of immune responses to self and non-self. , T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are potent modulators of immune responses., T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+ Therapeutic gamma delta T-lymphocytes naturally expressing IL2RA wt Allele molecules (natural T regulatory Cells (Tregs)) have a role in maintaining self tolerance and in regulating responses to infectious agents, transplantation Ags, and Specimen Source Codes - Specimen Source Codes - tumor Ags., Naturally occurring T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are essential for the active suppression of Autoimmune Diseases., Amongst these, naturally occurring T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) Regulatory T-Lymphocytes (nTreg) represent a major lymphocyte population engaged in the dominant control of self-reactive T responses and maintaining tolerance in several models of Autoimmune Diseases., T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+IL2RA wt Allele+ regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are essential negative regulators of immune responses., Naturally occurring T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+)FoxP3(+) regulatory Therapeutic gamma delta T-lymphocytes (IL2RA wt Allele(+) Tregs) constitute a specialized population of Therapeutic gamma delta T-lymphocytes that is essential for the maintenance of Peripheral self-tolerance., One of the subpopulations of T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+ Therapeutic gamma delta T-lymphocytes that express IL2RA wt Allele+ and the transcription factor FOXP3, known as Regulator Therapeutic gamma delta T-lymphocytes (TReg), plays an essential role in maintaining tolerance and immune homeostasis preventing autoimmune diseases, minimalize chronic inflammatory diseases by enlisting various immunoregulatory mechanisms., Regulatory Therapeutic gamma delta T-lymphocytes (Tregs) are T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(bright)CD62L(high) Cells that actively down-regulate immune responses., T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+)IL2RA wt Allele(+) regulatory Therapeutic gamma delta T-lymphocytes (Treg) play a central role in the prevention of Autoimmune Diseases and in the control of immune responses by down-regulating the function of effector T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+) or CD8(+) Therapeutic gamma delta T-lymphocytes., FoxP3(+)IL2RA wt Allele(+)T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+) regulatory Therapeutic gamma delta T-lymphocytes (Tregs) suppress a variety of normal physiological and pathological immune responses via several pathways, such as inhibitory cytokine secretion, direct cytolysis induction, and Antigen-Presenting Cells functional modulation., Regulatory T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens(+) IL2RA wt Allele(+) T (Treg) Cells with the ability to suppress host immune responses against self- or non-self antigens play important roles in the processes of Autoimmune Diseases, transplant rejection, infectious diseases and Malignant Neoplasms., BACKGROUND: Evidence indicating that T-Cell Surface Glycoprotein T-Cell Surface Glycoprotein CD4, Homo sapiens, Homo sapiens+IL2RA wt Allele+ regulatory T (Treg) Cells play a crucial role in the maintenance of Peripheral T-Lymphocyte tolerance to allergens has been [SEP]", "label": "no"}
{"original_question": "Is a mutation of the  ZIKV's membrane protein prM responsible for the microcephaly in new-born infants?", "id": "converted_2671", "sentence1": "Is a mutation of the  ZIKV's membrane protein prM responsible for the Microcephaly (physical finding) in new-born infants?", "sentence2": "Here we show that a single serine-to-asparagine substitution [Ser139→Asn139(S139N)] in the viral polyprotein substantially increased ZIKV infectivity in both Homo sapiens and Mus sp. neural progenitor cells (NPCs) and led to more severe Microcephaly (physical finding) in the Mus sp. fetus, as well as higher mortality rates in neonatal CASP14 gene., A single mutation in the prM protein of Zika virus contributes to fetal Microcephaly (physical finding).[SEP]", "label": "yes"}
{"original_question": "Is the Philadelphia chromosome a fusion between parts of chromosomes 1 and 9?", "id": "converted_3193", "sentence1": "Is the Philadelphia Chromosome a fusion between parts of chromosomes 1 and 9?", "sentence2": " The Philadelphia Chromosome, t(9;22)(q34;q11), is present in 95% of Myeloid Leukemia, Chronic patients, resulting in constitutive tyrosine kinase activity; however, ~5% of Myeloid Leukemia, Chronic patients possess a Philadelphia variant. , Chronic Myeloid Leukemia (Myeloid Leukemia, Chronic) is Chronic myeloproliferative disorder characterized by Philadelphia Chromosome which is a balanced translocation between Chromosomes, Human, Pair 9 and 22 in 90% of cases., Philadelphia Chromosome positive chronic myelogenous leukemia is a stem cell disease with the presence of Philadelphia Chromosome generated through reciprocal translocation of Chromosomes, Human, Pair 9 and 22. [SEP]", "label": "no"}
{"original_question": "Does HuR protein regulate the splicing process?", "id": "converted_1477", "sentence1": "Does ELAVL1 gene Protein Info regulate the splicing process?", "sentence2": "ELAVL1 gene and TIA1/TIAL1 are involved in regulation of alternative splicing of Sirtuin 1 pre-mRNA, Here we describe experiments showing that ELAVL1 gene and TIA1/TIAL1, two kinds of RNA-binding proteins, were involved in the regulation of alternative splicing of Sirtuin 1 pre-mRNA under normal and stress circumstances, ELAVL1 gene increased Sirtuin 1-∆Exon8 by promoting Sirtuin 1 exon 8 exclusion, whereas TIA1/TIAL1 inhibition of the exon 8 exclusion led to a decrease in Sirtuin 1-∆Exon8 mRNA levels. , ELAVL1 gene regulates alternative splicing of the TRA2β gene in Homo sapiens colon cancer cells under oxidative stress, Hu antigen R (ELAVL1 gene) regulates stress responses through stabilizing and/or facilitating the translation of target mRNAs, We show here that the RBP embryonic lethal Abnormal vision like 1 (ELAVL1, also know as ELAVL1 gene) regulates the alternative splicing of EIF4ENIF1 gene (Eif4enif1), which encodes an eukaryotic translation initiation factor 4E transporter (4E-T) Protein Info and suppresses the expression of capped mRNAs, Further, endothelial-specific Elavl1 knockout mice exhibited reduced revascularization after hind limb Ischemia Procedure and tumor angiogenesis in oncogene-induced mammary cancer, resulting in attenuated blood flow and tumor growth, respectively. , Changes in Cells mRNA stability, splicing, and polyadenylation through ELAVL1 gene Protein Info sequestration by a cytoplasmic RNA virus, Furthermore, significant changes can be observed in nuclear alternative polyadenylation and splicing events on Cells pre-mRNAs as a result of sequestration of ELAVL1 gene Protein Info by the 3' Untranslated Regions of RNA Transcript of this cytoplasmic RNA virus., Here we demonstrate that expression of 2A(pro) induces a selective nucleo-cytoplasm translocation of several important RNA-Binding Proteins and RNA Splicing Factors. Subcellular fractionation studies, together with immunofluorescence microscopy revealed an asymmetric distribution of ELAVL1 gene and TIA1/TIAR in 2A(pro) expressing cells, which modulates splicing of the Homo sapiens Fas exon 6, knockdown of ELAVL1 gene or overexpression of TIA1/TIAR, leads to Fas exon 6 inclusion in 2A(pro)-expressing cells, The differential expression levels of T-cell intracellular antigens (Transient Cerebral Ischemia) and Hu antigen R (ELAVL1 gene) are concomitant with a splicing switch in apoptosis receptor Fas in HCT116 Cells, overexpression and knockdown of ELAVL1 gene led to Fas exon 6 skipping and inclusion, respectively. These results suggest that the Transient Cerebral Ischemia and ELAVL1 gene Cells ratio influences cell-type specific Fas exon 6 splicing pattern., Hu antigen R (ELAVL1 gene) functions as an alternative pre-RNA, Messenger, Splicing regulator of Fas apoptosis-promoting receptor on exon definition, antiapoptotic regulator Hu antigen R (ELAVL1 gene, ELAVL1), a member of the embryonic lethal, Abnormal vision, Drosophila-like (ELAVL) family, promotes Fas exon 6 skipping by binding to an exonic splicing silencer, ELAV/Hu proteins bind to AU-rich elements (are unit of measure) in mRNAs and regulate their stability from splicing to translation, and the ubiquitous ELAVL1 gene Protein Info has been implicated in cancerous cell growth., The ELAVL1 gene Protein Info regulates the expression of thousands of Cells RNA Transcript by modulating RNA, Messenger, Splicing, trafficking, translation, and stability., Hu antigen R (ELAVL1 gene) functions as an alternative pre-RNA, Messenger, Splicing regulator of Fas apoptosis-promoting receptor on exon definition., I report that antiapoptotic regulator Hu antigen R (ELAVL1 gene, ELAVL1), a member of the embryonic lethal, Abnormal vision, Drosophila-like (ELAVL) family, promotes Fas exon 6 skipping by binding to an exonic splicing silencer. , Changes in Cells mRNA stability, splicing, and polyadenylation through ELAVL1 gene Protein Info sequestration by a cytoplasmic RNA virus., Further, the silencing capacity of ELAVL1 gene as splicing regulator resides in the RRM1 Protein Info, Homo sapiens Protein Info, Homo sapiens and hinge-RRM3 domains. , ELAVL1 gene and TIA1/TIAL1 are involved in regulation of alternative splicing of Sirtuin 1 pre-mRNA., ELAVL1 gene regulates alternative splicing of the TRA2β gene in Homo sapiens colon cancer cells under oxidative stress., The ELAVL1 gene Protein Info regulates the expression of thousands of Cells RNA Transcript by modulating RNA, Messenger, Splicing, trafficking, translation, and stability. , Further, the silencing capacity of ELAVL1 gene as splicing regulator resides in the RRM1 Protein Info, Homo sapiens Protein Info, Homo sapiens and hinge-RRM3 domains. Taken together, these results support a functional link between ELAVL1 gene as Transcription Repressor/Corepressor of alternative Fas splicing and the molecular mechanisms modulating programmed cell death., We are interested in interactions involving Heterogeneous-Nuclear Ribonucleoproteins Proteins participating in several steps of mRNA processing (mainly pre-RNA, Messenger, Splicing) and ELAVL1 gene with an established role in stability/translation of associated mRNAs. Heterogeneous-Nuclear Ribonucleoproteins and ELAVL1 gene proteins have a major nucleoplasmic localization and ability to shuttle between Cell Nucleus and cytoplasm. We report here on interactions between Heterogeneous-Nuclear Ribonucleoproteins and ELAVL1 gene proteins that were identified in the context of isolated Heterogeneous-Nuclear Ribonucleoproteins and messenger ribonucleoprotein complex location complexes. , Despite the fact that ELAVL1 gene sites are observed in intronic regions, our data do not support a role for ELAVL1 gene in regulating splicing.[SEP]Relations: ELAVL1 has relations: cellcomp_protein with Cell Nucleus, cellcomp_protein with Cell Nucleus. Protein Info binding has relations: molfunc_protein with RRM1 Protein Info, Homo sapiens, molfunc_protein with RRM1 Protein Info, Homo sapiens. EIF4ENIF1 has relations: cellcomp_protein with Cell Nucleus, cellcomp_protein with Cell Nucleus.", "label": "yes"}
{"original_question": "Can simvastatin alleviate depressive symptoms?", "id": "converted_2799", "sentence1": "Can simvastatin alleviate depressive symptoms?", "sentence2": "Simvastatin-treated patients experienced significantly more reductions in HDRS scores compared to the placebo group by the end of the trial (p=0.02). Early improvement and response rates were significantly greater in the simvastatin group than the placebo group (p=0.02 and p=0.01, respectively) but remission rate was not significantly different between the two groups (p=0.36)., In conclusion, simvastatin seems to be a safe and effective adjuvant therapy for patients suffering from major depressive disorder.[SEP]", "label": "yes"}
{"original_question": "Is there any functional association during viral replication between flaviviridae viral RNA depended RNA polymerase and viral helicase?", "id": "converted_836", "sentence1": "Is there any functional association during viral replication between flaviviridae viral RNA depended RNA polymerase and viral helicase?", "sentence2": "Several labs have obtained evidence for a Protein complex that involves many of the nonstructural (NS) Proteins encoded by the Virus. NOONAN SYNDROME 3, NS4A, NS4B, NS5A, and NS5B appear to interact structurally and functionally. In this study, we investigated the interaction between the helicase, NOONAN SYNDROME 3, and the RNA polymerase, NS5B. Pull-down experiments and surface plasmon resonance data indicate a direct interaction between NOONAN SYNDROME 3 and NS5B that is primarily mediated through the Protease Domain of NOONAN SYNDROME 3. This interaction reduces the basal Adenosine Triphosphatases activity of NOONAN SYNDROME 3. However, NS5B stimulates product formation in RNA unwinding experiments under conditions of excess Nucleic Acids substrate. When the concentrations of NOONAN SYNDROME 3 and NS5B are in excess of Nucleic Acids substrate, NS5B reduces the rate of NOONAN SYNDROME 3-catalyzed unwinding. Under pre-steady-state conditions, in which NOONAN SYNDROME 3 and substrate concentrations are similar, product formation increased in the presence of NS5B. The increase was consistent with 1:1 complex formed between the two Proteins. A fluorescently labeled form of NOONAN SYNDROME 3 was used to investigate this interaction through fluorescence polarization binding assays. Results from this assay support interactions that include a 1:1 complex formed between NOONAN SYNDROME 3 and NS5B., Contradictory results have been reported regarding NOONAN SYNDROME 3 in RNA synthesis. To investigate the effect of NOONAN SYNDROME 3 on classical swine fever Virus (CSFV) NS5B RNA-dependent RNA polymerase activity (RNA-directed RNA polymerase activity) activity and NOONAN SYNDROME 3-NS5B interaction, RNA-directed RNA polymerase activity reactions, GST-pull-down assays and co-immunoprecipitation analyses containing NS5B and either of NOONAN SYNDROME 3 protein and the different truncated NOONAN SYNDROME 3 Mutant were performed, respectively. We found that NOONAN SYNDROME 3 stimulated NS5B RNA-directed RNA polymerase activity activity in a dose-dependent manner by binding to Noonan Syndrome 5 through a NOONAN SYNDROME 3 Protease Domain. Furthermore, mapping important regions of the NOONAN SYNDROME 3 Protease Domain was carried out by Deletion Mutagenesis, associated with RNA-directed RNA polymerase activity reactions, GST-pull-down assays and co-immunoprecipitation analyses. Results showed that stimulation of CSFV NS5B RNA-directed RNA polymerase activity activity was obtained by NOONAN SYNDROME 3 binding to NS5B through a 31-amino acid fragment at the N-terminal end of NOONAN SYNDROME 3 Protease Domain, which mediated a specific NOONAN SYNDROME 3-NS5B interaction., The protocols detailed in this unit are used to purify three recombinant enzymes that are widely used in HCV research: the HCV NOONAN SYNDROME 3 Protease Domain, the helicase Superkingdom (taxonomic category) as an NOONAN SYNDROME 3+NS4A complex, and the NS5B RNA-dependent RNA polymerase. The active enzymes are purified to homogeneity by two-column chromatography to support a screening program for HCV inhibitors., Among potential targets are viral entry factors, including scavenger receptor type B1 (SCARB1 wt Allele) and CD81 antigen antigen, as well as Antibodies, Neutralizing against the viral glycoproteins. Popular targets related to translation and replication are the NOONAN SYNDROME 3/4A protease (inhibited by telaprevir and boceprevir) and the NS5B polymerase, as well as the NS2/3 autoprotease, the NOONAN SYNDROME 3 helicase, and nonenzymatic targets such as NS4B and NS5A Proteins. , The NOONAN SYNDROME 3 helicase Superkingdom (taxonomic category) competes with NOONAN SYNDROME 3 full-length for Noonan Syndrome 5 RNA-directed RNA polymerase activity binding, with a K(d.) of 2.5μM. Since NOONAN SYNDROME 3 and Noonan Syndrome 5 are required for DENV replication, this fascile assay could be used to screen for non-nucleoside, allosteric inhibitors that disrupt the interaction between the two Proteins.[SEP]", "label": "yes"}
{"original_question": "Are the genes for marneral biosynthesis scattered in the genome of A. thaliana?", "id": "converted_2049", "sentence1": "Are the Genes for marneral biosynthesis scattered in the genome of Arabidopsis thaliana <plant>?", "sentence2": "Here we characterize a second operon-like triterpene cluster (the marneral cluster) from Arabidopsis thaliana <plant>, compare the features of these two clusters, and investigate the evolutionary events that have led to cluster formation, Here we characterize a second operon-like triterpene cluster (the marneral cluster) from Arabidopsis thaliana <plant>, compare the features of these two clusters, and investigate the evolutionary events that have led to cluster formation., Previously in thale cress (Arabidopsis thaliana) we identified an operon-like gene cluster that is required for the synthesis and ResponseLevel - ResponseLevel - modification of the triterpene thalianol., Prediction of operon-like gene clusters in the Arabidopsis thaliana genome based on co-expression analysis of neighboring Genes, Here we characterize a second operon-like triterpene cluster (the marneral cluster) from Arabidopsis thaliana <plant>, compare the features of these two clusters, and investigate the evolutionary events that have led to cluster formation. , Here we characterize a second operon-like triterpene cluster (the marneral cluster) from A., the cyclic hydroxamic acid pathways in maize, the avenacin biosynthesis gene clusters in oat, the thalianol pathway in Arabidopsis thaliana, and the diterpenoid momilactone cluster in rice., Prediction of operon-like gene clusters in the Arabidopsis thaliana genome based on co-expression analysis of neighboring Genes.[SEP]", "label": "no"}
{"original_question": "Is ibudilast effective for multiple sclerosis?", "id": "converted_2801", "sentence1": "Is ibudilast effective for Multiple Sclerosis?", "sentence2": "ibudilast slowed brain atrophy in Parts per million (qualifier value) and SPMS patients in a multicenter phase 2b study.,  ibudilast inhibits several CNP gene, macrophage migration inhibitory factor, and toll-like receptor 4 and can cross the blood-brain barrier, with potential salutary effects in progressive Multiple Sclerosis., CONCLUSIONS: In a phase 2 trial involving patients with progressive Multiple Sclerosis, ibudilast was associated with slower progression of brain atrophy than placebo but was associated with higher rates of gastrointestinal side effects, Headache, and Cancer patients and suicide and Cancer patients and suicide and depression., Specifically, the current evidence regarding treatment of progressive MS with ocrelizumab, simvastatin, ibudilast, thioctic acid, high-dose biotin, siponimod, and cell-based therapies are discussed., Based on our knowledge of pathophysiology, three therapeutic strategies are proposed: anti-inflammatory (ocrelizumab, siponimod…); remyelinating (opicinumab); and neuroprotective (high-dose biotin, ibudilast, simvastatin…). , Current article provides an overview of the pharmacology of Irritable Bowel Syndrome with a focus on preclinical and clinical data supporting its potential neuroprotective benefits for neurological conditions, including Multiple Sclerosis, Neuropathic pain, medication overuse Headache, Cerebrovascular accident, Opioids, Alcohol - Recreational Drug Use Code and methamphetamine abuse., Design, rationale, and baseline characteristics of the randomized double-blind phase II clinical trial of ibudilast in progressive Multiple Sclerosis., METHODS: SPRINT-MS is a randomized, placebo-controlled, phase II trial of ibudilast in patients with POLYDACTYLY, POSTAXIAL, WITH PROGRESSIVE MYOPIA., CONCLUSION: SPRINT-MS is designed to evaluate the safety and efficacy of ibudilast as a treatment for POLYDACTYLY, POSTAXIAL, WITH PROGRESSIVE MYOPIA while simultaneously validating five different imaging biomarkers as outcome metrics for use in future phase II proof-of-concept POLYDACTYLY, POSTAXIAL, WITH PROGRESSIVE MYOPIA trials., ibudilast for the treatment of Multiple Sclerosis., AREAS COVERED: This article reviews various studies looking at ibudilast as a potential therapy for MS. It summarizes prior and current clinical trials of ibudilast in MS as well as its pharmacology.EXPERT OPINION: Although ibudilast has not been found to decrease the focal inflammatory activity in relapsing MS, it was shown to have an effect on preserving brain volume and disability progression. ibudilast may have a role in the treatment of progressive MS phenotypes., Adverse events with ibudilast included No gastrointestinal symptom, Headache, and Cancer patients and suicide and Cancer patients and suicide and depression.<br><b>CONCLUSIONS</b>: In a phase 2 trial involving patients with progressive Multiple Sclerosis, ibudilast was associated with slower progression of brain atrophy than placebo but was associated with higher rates of gastrointestinal side effects, Headache, and Cancer patients and suicide and Cancer patients and suicide and depression., It summarizes prior and current clinical trials of ibudilast in MS as well as its pharmacology.<br><b>EXPERT OPINION</b>: Although ibudilast has not been found to decrease the focal inflammatory activity in relapsing MS, it was shown to have an effect on preserving brain volume and disability progression.[SEP]", "label": "yes"}
{"original_question": "Does HER2 under-expression lead to favorable response to trastuzumab?", "id": "converted_1267", "sentence1": "Does ERBB2 wt Allele under-expression lead to favorable response to trastuzumab?", "sentence2": "over-expression of ERBB2 wt Allele is reported in approximately 20% of gastric tumours, challenging the use of targeted therapies. , In patients with advanced gastric or gastro-oesophageal junction cancer, addition of trastuzumab to chemotherapy significantly improved overall survival compared with chemotherapy alone. Addition of trastuzumab to chemotherapy did not increase the incidence of adverse events., treatment of ERBB2 wt Allele-overexpressing Malignant neoplasm of Breast: trastuzumab,, Trastuzumab has demonstrated clinical activity in several types of ERBB2 wt Allele-overexpressing epithelial tumors, such as Breast and metastatic gastric or gastroesophageal junction cancer. , An example is the established benefit of trastuzumab as adjuvant therapy for Malignant neoplasm of Breast; a clear definition of ERBB2 wt Allele-positivity and the assay reproducibility have, however, remained unanswered. , Trastuzumab is a monoclonal antibody CAL CAL targeted to the Her2 receptor and approved for treatment of Her2-positive Malignant neoplasm of Breast., epidermal growth factor receptor 2, human (ERBB2 wt Allele/neu) is an important target for the treatment of the Breast cancers in which it is overexpressed. However, no approved anti-ERBB2 wt Allele/neu therapy is available for the majority of Malignant neoplasm of Breast patients, who express ERBB2 wt Allele/neu at low levels (with scores of 1+ or 2+/fluorescence in situ hybridization-negative)., The humanized anti-ERBB2 wt Allele monoclonal antibody CAL CAL trastuzumab (Herceptin) is useful in the treatment of ErbB2-overexpressing Breast cancers,, HercepTestTM (DAKO A/S, Glostrup, Denmark) is an immunohistochemical assay that detects ERBB2 wt Allele/neu gene products, and evaluates the overexpression status of the ERBB2 wt Allele/neu protein in determining eligibility for the Trastuzumab (HerceptinR, Genentech, San Francisco, cyclophosphamide/doxorubicin protocol, USA) therapy. [SEP]", "label": "no"}
{"original_question": "Are Ultra-conserved elements (UCEs) enriched in segmental duplications?", "id": "converted_1959", "sentence1": "Are Ultra-conserved elements (UCEs) enriched in segmental duplications?", "sentence2": "Here we address the process by which CNVs become depleted of UCEs., We begin by showing that depletion for UCEs characterizes the most recent large-scale Homo sapiens CNV datasets and then find that even newly formed de novo CNVs, which have passed through meiosis at most once, are significantly depleted for UCEs., In striking contrast, CNVs arising specifically in Primary malignant neoplasm cells are, as a rule, not depleted for UCEs and can even become significantly enriched., Alternatively, lack of depletion for UCEs from Primary malignant neoplasm CNVs may reflect the diseased state. , ULEs are located in intergenic or intronic regions and are depleted from segmental duplications., Interestingly, Homo sapiens UCEs have been reported to be strongly depleted among segmental duplications and benign copy number variants (CNVs)., In addition, here we show that these elements are preferentially found in pathogenic deletions (enrichment ratio 3.6 vs. 0.5 in duplications), and that this association is not related with a higher content of Genes., In contrast, pathogenic CNVs lacking UCEs showed almost a threefold higher content in Genes, We have demonstrated that nonexonic UCEs are depleted among segmental duplications (SDs) and copy number variants (CNVs) and proposed that their ultraconservation may reflect a mechanism of copy counting via comparison., Mammalian ultraconserved elements are strongly depleted among segmental duplications and copy number variants., Here, we show that UCEs are significantly depleted among segmental duplications and copy number variants. Notably, of the UCEs that are found in segmental duplications or copy number variants, the majority overlap Exons, indicating, along with other findings presented, that UCEs overlapping Exons represent a distinct subset., Ultraconserved elements (UCEs) are strongly depleted from segmental duplications and copy number variations (CNVs) in the Homo sapiens genome, suggesting that Gene Deletion Abnormality or duplication of a NAGPA gene can be deleterious to the Mammalian Cell., Here, we show that UCEs are significantly depleted among segmental duplications and copy number variants., We have demonstrated that nonexonic UCEs are depleted among segmental duplications (SDs) and copy number variants (CNVs) and proposed that their ultraconservation may reflect a mechanism of copy counting via comparison., Here, we show that UCEs are significantly depleted among segmental duplications and copy number variants., Ultraconserved elements (UCEs) are strongly depleted from segmental duplications and copy number variations (CNVs) in the Homo sapiens genome, suggesting that Gene Deletion Abnormality or duplication of a NAGPA gene can be deleterious to the Mammalian Cell, melanogaster genome revealed depletion of the P-element and piggyBac Clinical act of insertion in and around the Sophophora UCEs., Mammalian ultraconserved elements are strongly depleted among segmental duplications and copy number variants., Here, we show that UCEs are significantly depleted among segmental duplications and copy number variants., Interestingly, Homo sapiens UCEs have been reported to be strongly depleted among segmental duplications and benign copy number variants (CNVs).[SEP]Relations: malignant giant cell tumor has relations: disease_disease with Primary malignant neoplasm, disease_disease with Primary malignant neoplasm.", "label": "no"}
{"original_question": "Is dexamethasone recommended for treatment of intracerebral hemorrhage?", "id": "converted_2176", "sentence1": "Is dexamethasone recommended for treatment of intracerebral hemorrhage?", "sentence2": "dexamethasone and other glucocorticoids should be avoided. , During the third interim analysis, the Cessation of life rate at the 21st day was identical in the two groups (dexamethasone vs. placebo, 21 of 46 vs. 21 of 47; chi-square = 0.01, P = 0.93). In contrast, the rate of complications (mostly Infections of musculoskeletal system and complications of Diabetes Mellitus) was much higher in the dexamethasone group (chi-square = 10.89, P less than 0.001), leading to early termination of the study. In the light of the absence of a demonstrable beneficial effect and the presence of a significant harmful effect, current practices of using dexamethasone for treatment of primary supratentorial hemorrhage should be reconsidered., In the light of the absence of a demonstrable beneficial effect and the presence of a significant harmful effect, current practices of using dexamethasone for treatment of primary supratentorial hemorrhage should be reconsidered.[SEP]", "label": "no"}
{"original_question": "Do thyroid hormone receptors change after brain injury?", "id": "converted_1507", "sentence1": "Do thyroid hormone receptors change after brain injury?", "sentence2": "For example, the T3 thoracic segmental innervation thoracic segmental innervation receptor alpha was predominantly expressed in stroke-tissue, indicating that regeneration of nerves in stroke tissue may be facilitated by increased T3 thoracic segmental innervation thoracic segmental innervation receptor alpha expression., TRα expression was also increased in Homo sapiens infants with IVH. , Thus, in infants with IVH the combined elevation in deiodinase-3 and reduction in deiodinase-2 decreases TH signaling that can be worsened by an increase in unliganded TRα. , A rapid increase of the total number of Binding Sites for T3 thoracic segmental innervation thoracic segmental innervation appeared within 30 min of Ischemia Procedure and reached over 40% by 3 h. During the same 3-h period, the relative binding affinity was reduced by 25%. Upon recirculation after 30 min or 3 h of Ischemia Procedure, a rapid reversal of measured T3 thoracic segmental innervation thoracic segmental innervation Binding Sites occurred, which progressed to 20-30% below the control value by the recirculation period of 3 h. [SEP]", "label": "yes"}
{"original_question": "Is low T3 syndrome a prognostic marker in patients with renal insufficiency?", "id": "converted_248", "sentence1": "Is low SLC25A5 gene syndrome a prognostic marker in patients with renal insufficiency?", "sentence2": "Low SLC25A5 gene was particularly common (44.3 %), and clearly associated with increased 6- and 12-month mortality and decreased overall survival (log rank test, P=0.007). , Increased rT3 may be more common in Kidney Failure, Chronic patients than previously described, and together with decreased SLC25A5 gene it may serve as an indicator of poor prognosis in subsequent months., The presence of Thyroid Function Tests alterations seems to not be associated with clinical and prognostic implications in Blighia sapida patients., Multivariate analysis, according to receiver operating characteristic (ROC) curves, showed that mortality was best predicted by total triiodothyronine (SLC25A5 gene)., Finally, low SLC25A5 gene but not low free triiodothyronine was associated with worse all-cause (Likelihood ratio = 45.4; P < 0.0001) and Cardiovascular system mortality (Likelihood ratio = 47.8; P < 0.0001) after adjustment for confounding factors.,  In Cox analyses, fT3 was a significant predictor of mortality independent of the main traditional as well as non-traditional risk factors., All-cause and CV mortality rates were significantly higher in patients with 'lower' SLC25A5 gene levels than in the 'higher' SLC25A5 gene group (113.4 vs 18.2 events per 1000 patient-years, P<0.001, and 49.8 vs 9.1 events per 1000 patient-years, P=0.001, respectively). The Kaplan-Meier analysis also showed significantly worse cumulative survival rates in the 'lower' SLC25A5 gene group (P<0.001). In the Cox regression analysis, low SLC25A5 gene was an independent predictor of all-cause mortality even after adjusting for traditional risk factors (hazard ratio=3.76, P=0.021). , In Chronic Kidney Diseases patients with Proteinuria, low SLC25A5 gene concentration predicted all-cause mortality and Cardiovascular system event independently of the severity of Proteinuria., Low-SLC25A5 gene syndrome is a frequent finding among Hodgkin Disease patients, but it does not predict outcome. However, serum fT3 level is a strong and inverse mortality predictor, in part explained by its underlying association with nutritional state and Inflammation., These data suggest that low cubic foot levels are not predictive for mortality in a subgroup of stable Hodgkin Disease patients who could survive more than 12 months., Low fT3 is an independent predictor of Cessation of life in hemodialysis patients. These data lend support to the hypothesis that Thyroid dysfunction is implicated in the high risk of the Kidney Failure, Chronic population.[SEP]", "label": "yes"}
{"original_question": "Is Semagacestat effective for Alzheimer's Disease?", "id": "converted_3788", "sentence1": "Is Semagacestat effective for Alzheimer's Disease?", "sentence2": "However, a large phase 3 trial of semagacestat, a potential non-transition state analog (non-TSA) GSI, in patients with ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) was terminated due to unexpected aggravation of Cognition Disorders and side effects. , BACKGROUND: In a recent report, 76 weeks' treatment with a gamma-secretase inhibitor (semagacestat) was associated with poorer cognitive outcomes in ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol)., CONCLUSION: In participants with mild to moderate cytarabine/daunorubicin protocol, high dose semagacestat treatment was associated with greater severity and faster worsening of Nail-Patella Syndrome in a pattern resembling an agitated depression. , INTRODUCTION: The negative efficacy study examining the γ-secretase inhibitor semagacestat in mild to moderate ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) included a number of biomarkers of the Disease as well as safety outcomes., A clinical trial with the wide-spectrum γ-secretase inhibitor semagacestat has, however, demonstrated that global inhibition of all γ-secretases causes serious Toxic effect. , ESULTS: Semagacestat treatment was associated with increased reporting of suspected Notch-related adverse events (Gastrointestinal:-:Point in time:^Patient:-, infection, and Malignant neoplasm of skin related). Other relevant safety findings associated with semagacestat treatment included cognitive and functional worsening, skin-related TEAEs, Kidney and hepatic changes, increased QT interval, and Measured Measured weight loss (observable entity) (observable entity). , CONCLUSIONS: As compared with placebo, semagacestat did not improve cognitive status, and patients receiving the higher dose had significant worsening of functional ability., RESULTS: The trial was terminated before completion on the basis of a recommendation by the data and safety monitoring board., The ADAS-cog scores worsened in all three groups (mean change, 6.4 points in the placebo group, 7.5 points in the group receiving 100 mg of the study Pharmacologic Substance, and 7.8 points in the group receiving 140 mg; P=0.15 and P=0.07, respectively, for the comparison with placebo). The ADCS-ADL scores also worsened in all groups (mean change at week 76, -9.0 points in the placebo group, -10.5 points in the 100-mg group, and -12.6 points in the 140-mg group; P=0.14 and P<0.001, respectively, for the comparison with placebo). Patients treated with semagacestat lost more weight and had more skin cancers and Infections of musculoskeletal system, treatment discontinuations due to adverse events, and serious adverse events (P<0.001 for all comparisons with placebo). , Recently disclosed Phase III findings on semagacestat indicated that ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) patients on this Pharmacologic Substance showed significantly worsened cognitive function compared to those treated with placebo., The recent failure of semagacestat in two large Phase III studies questions the value of γ-secretase inhibitors in treating ALZHEIMER DISEASE, FAMILIAL, 1., ntly disclosed Phase III findings on semagacestat indicated that ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) patients on this Pharmacologic Substance showed significantly worsened cognitive function compared to those treated with placebo. Since, ts from Phase III studies showed that semagacestat failed to slow Disease progression, and it was associated with worsening of clinical measures of cognition and the ability to perform activities of daily living. Furthermore, sem, rge Phase III clinical trials of semagacestat in mild-to-moderate cytarabine/daunorubicin protocol patients were prematurely interrupted because of the observation of a detrimental cognitive and functional effect of the Pharmacologic Substance. These detrimental ef, BACKGROUND: In a recent report, 76 weeks' treatment with a gamma-secretase inhibitor (semagacestat) was associated with poorer cognitive outcomes in Alzheimer's d, However, a large phase 3 trial of semagacestat, a potential non-transition state analog (non-TSA) GSI, in patients with ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) was terminated due to unexpected aggravation of Cognition Disorders and side effects., However, the preliminary equivocal cognitive results obtained with bapineuzumab as well as the detrimental cognitive effects observed with semagacestat, a potent γ-secretase inhibitor, raise the possibility that targeting Aβ may not be clinically efficacious in cytarabine/daunorubicin protocol.[SEP]", "label": "no"}
{"original_question": "Is the gene SLC6A2 associated with orthostatic intolerance?", "id": "converted_1548", "sentence1": "Is the gene SLC6A2 protein, Homo sapiens associated with orthostatic intolerance?", "sentence2": "Orthostatic intolerance is a debilitating syndrome characterized by Tachycardia by ECG Finding on assumption of upright posture. The norepinephrine (NE) transporter (NET) has been implicated in a genetic form of the disorder. , Thus attenuated baroreflex function and reduced sympathetic outflow may contribute to the orthostatic intolerance of severe NET deficiency., A Mutation Abnormality in the Homo sapiens Norepinephrine Plasma Membrane Transport Proteins (SLC6A2 protein, Homo sapiens protein, Homo sapiens) associated with orthostatic intolerance disrupts surface expression of Mutant and wild-type transporters.,  Recently, our laboratory reported a Genetic Polymorphism in the Homo sapiens NET (hNET) gene A457P in an individual with the autonomic disorder orthostatic intolerance (Osteogenesis Imperfecta). , Nonsynonymous single nucleotide polymorphisms (SNPs) in the Homo sapiens NET (hNET) gene that influence transporter function can contribute to disease, such as the nonfunctional transporter, A457P, identified in orthostatic intolerance. , Orthostatic intolerance is not necessarily related to a specific Mutation Abnormality (Ala457Pro) in the Homo sapiens Norepinephrine Plasma Membrane Transport Proteins., We propose that chromatin-modifying events associated with SLC6A2 protein, Homo sapiens protein, Homo sapiens gene suppression may constitute a mechanism of POTS., The goal of the present study was to further characterize the role and regulation of the SLC6A2 protein, Homo sapiens protein, Homo sapiens gene in POTS., In the absence of altered SLC6A2 protein, Homo sapiens protein, Homo sapiens gene sequence or promoter methylation, this reduced expression was directly correlated with chromatin modifications.  We propose that chromatin-modifying events associated with SLC6A2 protein, Homo sapiens protein, Homo sapiens gene suppression may constitute a mechanism of POTS., A coding Mutation Abnormality in the Norepinephrine Plasma Membrane Transport Proteins (SLC6A2 protein, Homo sapiens protein, Homo sapiens) sequence has been reported in 1 family kindred only. The goal of the present study was to further characterize the role and regulation of the SLC6A2 protein, Homo sapiens protein, Homo sapiens gene in POTS.[SEP]Relations: Defective SLC6A2 protein, Homo sapiens causes orthostatic intolerance (Osteogenesis Imperfecta) has relations: pathway_protein with SLC6A2 protein, Homo sapiens, pathway_protein with SLC6A2 protein, Homo sapiens.", "label": "yes"}
{"original_question": "Are there any DNMT3 proteins present in plants?", "id": "converted_216", "sentence1": "Are there any DNMT3 proteins present in plants?", "sentence2": "De novo DNA methylation in Arabidopsis sp. sp. thaliana is catalyzed by the methyltransferase DRM2, a Homologous Gene of the Mammals de novo methyltransferase DNMT3., Here we describe DNA Modification Methylases Genes from both Arabidopsis sp. sp. and maize that show a high level of Sequence - ParameterizedDataType similarity to DNMT3 Family, suggesting that they encode Plant allergen de novo Methyltransferase. Relative to all known eukaryotic Methyltransferase, these Plant Proteins contain a novel arrangement of the motifs required for DNA Modification Methylases catalytic activity. The N termini of these Methyltransferase contain a series of ubiquitin-associated (UBA) domains. , BLASTX searches and phylogenetic analysis suggested that five cDNAs belonged to four classes (DNMT1 wt Allele, TRDMT1 wt Allele, CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate and DNMT3 Family) of DNA Modification Methylases Genes.[SEP]", "label": "yes"}
{"original_question": "Can Levoxyl (levothyroxine sodium) cause insomnia?", "id": "converted_87", "sentence1": "Can Levoxyl (levothyroxine sodium) cause insomnia?", "sentence2": "METHODS: Seventy-one patients diagnosed with Acquired hypothyroidism were randomly allocated into two study groups: the first group received usual dose of levothyroxine and the second group received combination of levothyroxine and liothyronine for at least 4 months. The main outcomes were psychosocial problems (Goldberg's General Health Questionnaire, GHQ-28), bodyweight, heart rate, blood pressure, and serum lipid levels. RESULTS: In both groups serum thyroid-stimulating hormone levels remained unchanged compared with baseline. Psychosocial scores, body weight, heart rate, blood pressure, and lipid profile in the two groups remained constant. The only exception was a small but significant reduction in anxiety/insomnia in combined treatment group as compared with monotherapy. [SEP]", "label": "yes"}
{"original_question": "Is cariprazine effective for treatment of bipolar disorder?", "id": "converted_2780", "sentence1": "Is cariprazine effective for treatment of Bipolar Disorder Type 2?", "sentence2": "BACKGROUND: We evaluated the safety/tolerability of longer-term open-label treatment with cariprazine in patients who had responded to cariprazine for acute bipolar mania., Clinically relevant response and remission outcomes in cariprazine-treated patients with Bipolar I disorder., cariprazine is FDA approved for the acute treatment of SCHIZOPHRENIA 2 (disorder) and Manic mood or mixed episodes associated with Bipolar I disorder in adults., DISCUSSION: cariprazine-treated patients with Bipolar I disorder attained clinically significant improvement in Manic mood symptoms as shown by significantly greater rates of response and remission versus placebo; improvement in Manic mood symptoms did not induce depressive symptoms., OBJECTIVE: cariprazine, a dopamine D3/D2 partial agonist atypical antipsychotic with preferential binding to D3 receptors, is approved for the treatment of SCHIZOPHRENIA 2 (disorder) and Manic mood or mixed episodes associated with Bipolar I disorder., <b>BACKGROUND</b>: cariprazine was approved for treating SCHIZOPHRENIA 2 (disorder) and Bipolar Disorder Type 2, and currently is being evaluated for treating Cancer patients and suicide and Cancer patients and suicide and depression in clinical trials in the United States.[SEP]Relations: Dopamine has relations: drug_drug with cariprazine, drug_drug with cariprazine.", "label": "yes"}
{"original_question": "Does RNA polymerase II have RNA cleavage activity?", "id": "converted_2244", "sentence1": "Does 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 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 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 RNA Polymerase II., Complexes of yeast 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 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 RNA Polymerase II away from the transcriptional impediment and/or permit RNA Polymerase II multiple attempts at RNA elongation., SII is an RNA Polymerase II-binding protein that stimulates transcription elongation and also activates nascent RNA Transcript cleavage by RNA Polymerase II in elongation complexes in vitro, The 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 RNA Polymerase II elongation complexes., transcription factor S-II (also known as TCEA1 wt Allele) is an 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 RNA Polymerase II in a stalled elongation complex., POLR2I gene, a small subunit of 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 RNA Polymerase II., It is also possible that the RNA Transcript cleavage activity of RNA Polymerase II represents a proofreading function of the Enzyme [APC].., Nascent RNA cleavage by arrested RNA Polymerase II does not require upstream translocation of the elongation complex on DNA., Intrinsic RNA Transcript cleavage in yeast RNA Polymerase II elongation complexes.[SEP]", "label": "yes"}
{"original_question": "Does the 3D structure of  the genome remain stable during cell differentiation?", "id": "converted_1450", "sentence1": "Does the 3 Days structure of  the Genome - anatomical entity remain stable during \"U\" lymphocyte differentiation?", "sentence2": "We identify large, megabase-sized local chromatin location location interaction domains, which we term 'topological domains', as a pervasive structural feature of the Genome - anatomical entity organization., The domains are stable across different \"U\" lymphocyte types and highly conserved across species, indicating that topological domains are an inherent property of mammalian genomes, Insulators are involved in 3 Days Genome - anatomical entity organization at multiple spatial scales and are important for dynamic reorganization of chromatin location location structure during reprogramming and differentiation., The relation between alterations in chromatin location location structure and changes in gene expression during \"U\" lymphocyte differentiation has served as a paradigm to understand the link between Genome - anatomical entity organization and function., Architectural Proteins orchestrate higher-order chromatin location location organization through the establishment of interactions between regulatory elements across multiple spatial scales. The regulation of these Proteins, their interaction with DNA, and their co-occurrence in the Genome - anatomical entity, may be responsible for the plasticity of 3 Days chromatin location location architecture that dictates \"U\" lymphocyte and time-specific blueprints of gene expression., The role of 3 Days Genome - anatomical entity organisation in the control and execution of lineage-specific transcription programmes during the development and differentiation of Multipotent Stem Cells into specialised \"U\" lymphocyte types remains poorly understood., Chromatin structural states and their remodelling, including higher-order chromatin location location folding and three-dimensional (3 Days) Genome - anatomical entity organisation, play an important role in the control of gene expression, Here, we show that substantial remodelling of the higher-order chromatin location location structure of the LORICRIN gene (Electrodesiccation with curettage), a keratinocyte lineage-specific gene locus on mouse chromosome 3, occurs during epidermal morphogenesis., Many studies have suggested a link between the spatial organization of genomes and fundamental biological processes such as Genome - anatomical entity reprogramming, gene expression, and differentiation., Moreover, we reveal that formation of such highly condensed, transcriptionally repressed Heterochromatin promotes transcriptional activation of differentiation genes and loss of pluripotency., The open chromatin location location of Embryonic Stem Cells (Enhanced S-Cone Syndrome) condenses into repressive Heterochromatin as Cells exit the pluripotent state., we find that localized Heterochromatin condensation of Ribosomal RNA Genes initiates establishment of highly condensed chromatin location location structures outside of the Cell Nucleolus, We focus on the emerging relationship between Genome - anatomical entity organization and lineage-specific transcriptional regulation, which we argue are inextricably linked., Cells face the challenge of storing two meters of DNA in the three-dimensional (3 Days) space of the Cell Nucleus that spans only a few microns. The nuclear organization that is required to overcome this challenge must allow for the accessibility of the gene regulatory machinery to the DNA and, in the case of Embryonic Stem Cells (Enhanced S-Cone Syndrome), for the transcriptional and epigenetic changes that accompany differentiation, In this review we summarize some of the recent findings illuminating the 3 Days structure of the eukaryotic Genome - anatomical entity, as well as the relationship between Genome - anatomical entity topology and function from the level of whole chromosomes to enhancer-promoter loops with a focus on features affecting Genome - anatomical entity organization in Enhanced S-Cone Syndrome and changes in nuclear organization during differentiation, We observe that although self-associating chromatin location location domains are stable during differentiation, chromatin location location interactions both within and between domains change in a striking manner, altering 36% of active and inactive chromosomal compartments throughout the Genome - anatomical entity[SEP]", "label": "no"}
{"original_question": "Are there any urine biomarkers for bladder cancer diagnosis?", "id": "converted_677", "sentence1": "Are there any urine biomarkers for Malignant neoplasm of urinary bladder diagnosis?", "sentence2": "CONCLUSIONS: Several gene-based urinary biomarkers have demonstrated promise in initial studies, which now need to be rigorously validated in the clinical setting for them to be translated into clinically useful tests in diagnosis, surveillance or risk-stratification of Malignant neoplasm of urinary bladder,  Novel promising markers are in various stages of clinical testing, and a panel of biomarkers may serve in the future as a feasible alternative to urine cytology and Cystoscopy for the screening, detection, and follow-up of non-muscle invasive Malignant neoplasm of urinary bladder., RESULTS: Seven of the 8 urine biomarkers were increased in subjects with Malignant neoplasm of urinary bladder relative to those without Malignant neoplasm of urinary bladder. The 7 biomarkers were assessed in a new model, which had an AUROC of 0.88 (95% CI 0.84-0.93), and 74% sensitivity and 90% specificity., The study provides further evidence that the reported panel of diagnostic biomarkers can reliably achieve the noninvasive detection of Malignant neoplasm of urinary bladder with higher sensitivity than currently available urine based assays., The urinary concentrations of 14 biomarkers (interleukin-8 receptor binding activity, Matrix Metalloproteinase 9, MMP10 protein, human, SDC1 gene gene, CCL18 gene gene, Plasminogen Activator Inhibitor 1, CD44 Antigens Antigens, Vascular Endothelial Growth Factor A, ANG protein, human protein, human, CA9 wt Allele wt Allele, alpha 1-proteinase inhibitor, human, SPP1 wt Allele, PITX3 gene, and Apolipoprotein E) were assessed by enzyme-linked immunosorbent assay (ELISA). Diagnostic performance of each biomarker and multivariate models were compared using receiver operating characteristic curves and the chi-square test. An 8-biomarker model achieved the most accurate Bicinchoninic Acid Assay diagnosis (sensitivity 92%, specificity 97%), but a combination of 3 of the 8 biomarkers (interleukin-8 receptor binding activity, Vascular Endothelial Growth Factor A, and Apolipoprotein E) was also highly accurate (sensitivity 90%, specificity 97%). For comparison, the commercial BTA-Trak ELISA test achieved a sensitivity of 79% and a specificity of 83%, and voided urine cytology detected only 33% of Bicinchoninic Acid Assay cases in the same cohort. These data show that a multivariate urine-based assay can markedly improve the accuracy of non-invasive Bicinchoninic Acid Assay detection, : Histopathological grading of papillary urothelial tumors (PUTs) of the urinary bladder is subjective and poorly reproducible. We investigated the relationship between the expression of frequently deregulated MicroRNAs (miRNAs) as well as their target Genes (ZEB1/ZEB2) and Malignant neoplasm of urinary bladder histopathological grade in an attempt to find a miRNA that might allow more reliable grading of PUTs., The MCM5 protein, human immunoassay is a non-invasive test for identifying patients with urothelial cancers with similar accuracy to the FDA-approved Nuclear matrix protein 22 ELISA Test Kit. The combination of MCM5 protein, human plus Nuclear matrix protein 22 improves the detection of UCC and identifies 95% of clinically significant disease. Trials of a commercially developed MCM5 protein, human assay suitable for an end-user laboratory alongside Nuclear matrix protein 22 are required to assess their potential clinical utility in improving diagnostic and surveillance care pathways., HYAL1 gene and HNF1A-AS1 gene expression predicted Bicinchoninic Acid Assay metastasis, and HYAL1 gene expression also predicted disease-specific survival. Furthermore, the combined HAS2-HYAL1 gene biomarker detected Bicinchoninic Acid Assay and significantly predicted its recurrence., Cancer biomarkers are the backbone for the implementation of individualized approaches to Malignant neoplasm of urinary bladder (Bicinchoninic Acid Assay). , Through Genome and proteomic profiling of urine, we have identified a panel of biomarkers associated with the presence of Bicinchoninic Acid Assay. In this study, we evaluated the utility of three of these biomarkers, interleukin-8 (interleukin-8 receptor binding activity), Matrix metallopeptidase 9 (Matrix Metalloproteinase 9) and syndecan 1 protein in the diagnosis of Bicinchoninic Acid Assay through urinalysis. METHODS: Voided urines from 127 subjects, cancer subjects (n = 64), non-cancer subjects (n = 63) were analyzed. The protein concentrations of interleukin-8 receptor binding activity, Matrix Metalloproteinase 9, and syndecan 1 protein were assessed by enzyme-linked immunosorbent assay (ELISA)., . There was an association between differences in individual biomarkers and differences in protein levels over time, particularly in control patients. Collectively, our findings identify caveats intrinsic to the common practice of protein standardization in biomarker discovery studies conducted on urine, particularly in patients with Hematuria[SEP]", "label": "yes"}
{"original_question": "Is poliosis circumscripta another term for a white or unpigmented patch of hair or skin?", "id": "converted_3639", "sentence1": "Is poliosis circumscripta another term for a white or unpigmented patch of hair or skin?", "sentence2": "\"white forelock,\" poliosis circumscripta, defined as a localized patch of white hair in a group of hair follicle, Although traditionally known as \"white forelock,\" poliosis circumscripta, defined as a localized patch of white hair in a group of hair follicles, can involve any hairy area on the body including the Scalp structure, Eyebrow structure, and Eyelash., Although traditionally known as \" white forelock , \" poliosis circumscripta , defined as a localized patch of white hair in a group of hair follicles , can involve any hairy area on the body including the Scalp structure , Eyebrow structure , and Eyelash, Although traditionally known as \"white forelock,\" poliosis circumscripta, defined as a localized patch of white hair in a group of hair follicles, can involve any hairy area on the body including the Scalp structure, Eyebrow structure, and Eyelash.[SEP]", "label": "yes"}
{"original_question": "Does temsirolimus improve survival of glioblastoma patients?", "id": "converted_2590", "sentence1": "Does temsirolimus improve survival of glioblastoma patients?", "sentence2": "RESULTS: fourteen randomized clinical trials were identified (7 with bevacizumab, 2 Cilengitide, 1 enzastaurin, 1 dasatinib, 1 vandetanib, 1 temsirolimus, 1 cediranib) including 4330 patients. Antiangiogenic drugs showed no improvement in overall survival with a pooled HR of 1.00, a trend for an inferior outcome, in terms of overall survival, was observed in the group of patients receiving antiangiogenic drug alone compared to cytotoxic drug alone (HR=1.24, p=0.056)., CONCLUSIONS: temsirolimus was not superior to temozolomide in patients with an unmethylated MGMT promoter., The actuarial 1-year survival was 72.2% [95% confidence interval (NDUFB6 gene), 58.2-82.2] in the temozolomide arm and 69.6% (95% NDUFB6 gene, 55.8-79.9) in the temsirolimus arm [hazard ratio (HR) 1.16; 95% NDUFB6 gene, 0.77-1.76; P = 0.47]., CONCLUSION: The combination of bevacizumab with temsirolimus was well-tolerated and resulted in stable Disease of at least four months/partial response in three out of six pediatric patients with chemorefractory CNS Neoplasms., CONCLUSIONS: temsirolimus administered weekly at the dose of 75 mg/m(2) did not meet the primary objective efficacy threshold in children with Malignant Glioma, Neuroblastoma or Anal Rhabdomyosarcoma; however, meaningful prolonged stable Disease merits further evaluation in combination therapy., Novel targeted agents such as bevacizumab, imatinib, erlotinib, temsirolimus, immunotherapy, Cilengitide, talampanel, etc. are helping classical chemotherapeutic agents, like temozolomide, to achieve an increase in overall survival., CONCLUSIONS: CCI 779 was well tolerated at this dose schedule; however, there was no evidence of efficacy in patients with recurrent Glomerular Basement Membrane, The addition of temsirolimus to human leukocyte human leukocyte interferon did not improve survival., CONCLUSIONS temsirolimus was not superior to temozolomide in patients with an unmethylated MGMT promoter., The addition of temsirolimus to human leukocyte human leukocyte interferon did not improve survival.[SEP]Relations: Vandetanib has relations: drug_drug with temsirolimus, drug_drug with temsirolimus. Erlotinib has relations: drug_drug with temsirolimus, drug_drug with temsirolimus. Bevacizumab has relations: drug_drug with temsirolimus, drug_drug with temsirolimus. Temozolomide has relations: drug_drug with temsirolimus, drug_drug with temsirolimus. Dasatinib has relations: drug_drug with temsirolimus, drug_drug with temsirolimus. Imatinib has relations: drug_drug with temsirolimus, drug_drug with temsirolimus.", "label": "no"}
{"original_question": "Can administration of the thyrotropin releasing hormone reduce fatigue in cancer patients?", "id": "converted_1270", "sentence1": "Can administration of the thyrotropin releasing hormone reduce Fatigue in cancer patients?", "sentence2": "Pro-Thyrotropin-Releasing Hormone, human administration was associated with significant improvement (p < 0.05) in Fatigue levels as measured by the Visual Analog Scale-Energy (VAS-E), was associated with significant (p < 0.05) improvement in sleep disturbances and improved quality of life. , This decrease in C-reactive protein level with Pro-Thyrotropin-Releasing Hormone, human administration was associated with improvement in energy levels as measured by the VAS-E. , In the present pilot, randomized, placebo-controlled, crossover study, we investigated the efficacy and safety of Pro-Thyrotropin-Releasing Hormone, human as a treatment for cyclophosphamide/fluorouracil., Pro-Thyrotropin-Releasing Hormone, human administration was associated with significant improvement in Fatigue level as measured by the VAS-E, the Fatigue and vigor subscales of the Profile of mood states, and the Fatigue subscale of FACIT-F (p < 0.05). , Pro-Thyrotropin-Releasing Hormone, human administration was efficacious, safe, and tolerable in the treatment of cyclophosphamide/fluorouracil with a positive impact on quality of life. These results provide a crucial impetus for pursuing Pro-Thyrotropin-Releasing Hormone, human therapeutics to treat cyclophosphamide/fluorouracil., Thyrotropin-Releasing Hormone, human can relieve cancer-related Fatigue: hypothesis and preliminary observations., Global assessment using both subjective and objective parameters showed that Pro-Thyrotropin-Releasing Hormone, human exerted clear anti-Fatigue effects in four of the six Pro-Thyrotropin-Releasing Hormone, human treatments. , These initial findings support the proposal that Pro-Thyrotropin-Releasing Hormone, human can ameliorate cancer-related Fatigue.[SEP]", "label": "yes"}
{"original_question": "Are there telemedicine applications for chronic pain management?", "id": "converted_573", "sentence1": "Are there telemedicine applications for Chronic pain management?", "sentence2": "An Integrated cognitive-behavioral and physical therapy group protocol has been developed and then implemented at remote sites using videoconferencing technology to provide pain management for veterans. , Tele-pain management: use of videoconferencing technology in the delivery of an Integrated cognitive-behavioral and physical therapy group intervention., It is feasible to provide treatment to women veterans living in rural areas by utilizing video-teleconferencing technology between larger VA medical centers and facilities at CBOCs in more rural settings, The results suggest that a smartphone-delivered intervention with diaries and personalized feedback can reduce catastrophizing and prevent increases in functional impairment and symptom levels in women with chronic widespread pain following inpatient rehabilitation.,  Of the studies available, there are very few randomized trials of telehealth pain care and only one general overview of e-health and Chronic pain, which dedicates just a few paragraphs to telehealth., therapy adaptation and the resultant specification for the SMART2 project-a technology-based self-management system for assisting long-term health conditions, including Chronic pain, Results showed the use of videoconferencing for this group of patients is useable and satisfactory for both patients and staff, that the patients save time and money, and that for a system where videoconferencing equipment is already in use, it is also cost effective. Staff were able to identify new patient problems. , This pilot study indicates that telemedicine follow-up consultations for Chronic pain patients are feasible and cost-saving. Patients and anesthesiologists were highly satisfied with telemedicine consultation.[SEP]", "label": "yes"}
{"original_question": "Is transcapillary  albumin escape altered in diabetic patients?", "id": "converted_807", "sentence1": "Is transcapillary  albumin escape altered in diabetic patients?", "sentence2": "On the contrary, altered TERalb and increased carotid artery intimal thickness are shown by all hypertensive type 2 diabetic patients, both with normal and altered patterns of Smooth Endoplasmic Reticulum., Altered systemic capillary permeability characterizes insulin-resistant hypertensive patients with Metabolic Syndrome X X., TERalb is increased in normo-albuminuric type 1 diabetic patients. [SEP]", "label": "yes"}
{"original_question": "Is enzastaurin effective treatment of glioblastoma?", "id": "converted_2280", "sentence1": "Is enzastaurin effective treatment of Glioblastoma Multiforme?", "sentence2": "RESULTS: fourteen randomized clinical trials were identified (7 with bevacizumab, 2 Cilengitide, 1 enzastaurin, 1 dasatinib, 1 vandetanib, 1 temsirolimus, 1 cediranib) including 4330 patients. Antiangiogenic drugs showed no improvement in overall survival with a pooled HR of 1.00, a trend for an inferior outcome, in terms of overall survival, was observed in the group of patients receiving antiangiogenic drug alone compared to cytotoxic drug alone (HR=1.24, p=0.056). , Enzastaurin (LY317615.HCl.HCl) in combination with bevacizumab for recurrent malignant gliomas is well-tolerated, with response and progression-free survival similar to bevacizumab monotherapy., So far, inhibition of angiogenesis by compounds such as bevacizumab, cediranib, enzastaurin or Cilengitide as well as alternative dosing schedules of temozolomide did not prolong survival, neither at primary diagnosis nor at recurrent disease., Despite promising phase II clinical trial results and patient benefit in terms of clinical improvement and longer progression-free survival, an overall survival benefit has not been demonstrated in four randomized phase III trials of bevacizumab or Cilengitide in newly diagnosed Glioblastoma Multiforme or cediranib or enzastaurin in recurrent Glioblastoma Multiforme., CONCLUSIONS: PFS-6 missed the primary planned outcome of 55%. , OS (median, 74 weeks) and PFS (median, 36 weeks) results from the current trial were comparable to those from a prior phase II study using erlotinib and were significantly better than those from 2 other previous studies that used thalidomide or isotretinoin, all in combination with temozolomide plus RT. , More recently, Angiogenesis Inhibitors including enzastaurin, cediranib, bevacizumab, and others that target mainly the VEGF pathway, have been evaluated in this highly angiogenic disease. Among them, only bevacizumab has been associated with clear anti-tumor activity, although the lack of control studies limits the impact of the results to date., Enzastaurin has anti-glioma activity in patients with recurrent high-grade glioma, but does not appear to have enough single-agent activity to be useful as monotherapy., Several signal transduction inhibitors have been examined in preclinical and clinical malignant glioma trials, including Angiogenesis Inhibitors (bevacizumab, enzastaurin), and inhibitors of Epidermal Growth Factor Receptor tyrosine kinase (gefitinib and erlotinib), mammalian target of rapamycin (temsirolimus, everolimus) and Integrins (Cilengitide). Although preliminary clinical results of the use of targeted agents have not translated into significantly better survival, more recent phase II trials are exploring the combination of multitargeted drugs with cytotoxic chemotherapy and radiotherapy in order to overcome the resistance of Neoplasms to single-agent targeted therapies., Several drugs have been tested, including Epidermal Growth Factor Receptor (EGFR) Protein-tyrosine kinase inhibitor (disposition) (gefitinib and erlotinib), mammalian target of rapamycin (mTOR) inhibitors (temsirolimus and everolimus), and Vascular Endothelial Growth Factor Receptor-1 (Vascular Endothelial Growth Factor Receptor), protein kinase C-beta, and other angiogenesis pathways inhibitors (vatalanib, bevacizumab, and enzastaurin). Although preliminary efficacy results of most trials in recurrent disease have fallen short on expectations, substantial advances have been achieved by associated translational research. , So far, inhibition of angiogenesis by compounds such as bevacizumab, cediranib, enzastaurin or Cilengitide as well as alternative dosing schedules of temozolomide did not prolong survival, neither at primary diagnosis nor at recurrent disease.[SEP]", "label": "no"}
{"original_question": "Is apremilast effective for psoriatic arthritis?", "id": "converted_2231", "sentence1": "Is apremilast effective for Arthritis, Psoriatic?", "sentence2": "apremilast, an oral phosphodiesterase 4 inhibitor, in patients with Arthritis, Psoriatic and current Skin Specimen Source Code involvement: a phase III, randomised, controlled trial (PALACE 3)., OBJECTIVE: To evaluate apremilast treatment in patients with active Arthritis, Psoriatic, including current Skin Specimen Source Code involvement, despite prior therapy with conventional disease-modifying antirheumatic drugs and/or Biological Factors., CONCLUSIONS: apremilast demonstrated clinically meaningful improvements in Arthritis, Psoriatic and Psoriasis at week 16; sustained improvements were seen with continued treatment through 52 weeks. , apremilast: A Novel Drug for Treatment of Psoriasis and Psoriatic Arthritis., OBJECTIVE: To review the pharmacology, efficacy, and safety of apremilast and determine its role relative to other agents in the treatment of Psoriasis and Arthritis, Psoriatic., CONCLUSIONS: apremilast has a novel mechanism of action and is safe and effective for the management of Psoriasis and Arthritis, Psoriatic. ,  In particular, apremilast has been recently approved for the treatment of Psoriasis and Arthritis, Psoriatic., apremilast, an oral phosphodiesterase 4 inhibitor, has an acceptable safety profile and is effective for treatment of plaque Psoriasis and Arthritis, Psoriatic., As part of the National Institute for Health and Clinical Excellence (NICE) single technology appraisal (GROWTH CONTROL, Y-CHROMOSOME INFLUENCED) process, the manufacturer of apremilast was invited to submit evidence for its clinical and cost effectiveness for the treatment of active Arthritis, Psoriatic (Prostate-Specific Antigen) for whom disease-modifying anti-rheumatic drugs (DMARDs) have been inadequately effective, not tolerated or contraindicated., Psoriatic Arthritis Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active Arthritis, Psoriatic despite prior traditional disease-modifying antirheumatic Pharmacologic Substance (DMARD) and/or biologic therapy., In patients with Arthritis, Psoriatic, there are no clinical trials comparing apremilast with TNF alpha antagonists, and no interpretable trials of apremilast after failure of a TNF alpha antagonist., Psoriatic Arthritis Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active Arthritis, Psoriatic despite prior traditional disease-modifying antirheumatic Pharmacologic Substance (DMARD) and/or biologic therapy.In the 24-week, placebo-controlled phase of PALACE 1, patients (N=504) were randomised (1:1:1) to placebo, apremilast 20 mg twice a day (Twice a day) or apremilast 30 mg Twice a day, No imbalance in major adverse cardiac events, serious or Opportunistic Infections, Malignant Neoplasms or laboratory abnormalities was observed.apremilast was effective in the treatment of Arthritis, Psoriatic, improving signs and symptoms and physical function, apremilast is a novel oral PDE4 Enzyme Inhibitor [APC] capable of blocking leukocyte production of Recombinant Interleukin-12, interleukin-23 binding activity, TNF protein, human, INF- with subsequent suppression of NELFCD wt Allele and Th17-mediated immune responses, and proven clinical efficacy for Psoriasis as well as rheumatoid and Arthritis, Psoriatic.Cutaneous Lupus Erythematosus Disease Area and Severity Index (CLASI) showed a significant (P&lt;0.05) decrease after 85 days of treatment with apremilast 20 mg twice daily in 8 patients with active discoid lupus, The purpose of this study is to give an overview of the new treatments approved by the U.S. Food and Drug Administration (FDA) for use in Arthritis, Psoriatic (Prostate-Specific Antigen).FDA has approved three new drugs for Prostate-Specific Antigen: Certolizumab-pegol: a PEGylated Fc-free tumour necrosis factor inhibitor (TNFi); Ustekinumab Ab: an anti interleukin (IL)-12 and interleukin-23 binding activity mAb; and apremilast and oral phosphodiesterase 4 inhibitor., In all trials, the Pharmacologic Substance had an acceptable safety profile, with the most common adverse effects of Diarrhea, Nausea:Presence or Threshold:Point in time:^Patient:Ordinal, and Headache.apremilast has a novel mechanism of action and is safe and effective for the management of Psoriasis and Arthritis, Psoriatic., apremilast is a well-tolerated and effective phosphodiesterase type 4 inhibitor that is indicated for the treatment of moderate-to-severe plaque Psoriasis and Arthritis, Psoriatic., Psoriatic Arthritis Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active Arthritis, Psoriatic despite prior traditional disease-modifying antirheumatic Pharmacologic Substance (DMARD) and/or biologic therapy.In the 24-week, placebo-controlled phase of PALACE 1, patients (N=504) were randomised (1:1:1) to placebo, apremilast 20 mg twice a day (Twice a day) or apremilast 30 mg Twice a day., Newer drugs in the treatment armamentarium that have shown efficacy for both Psoriasis and Arthritis, Psoriatic consist of the anti-IL-17 agent, secukinumab, and a phosphodiesterase-4 inhibitor, apremilast., To review the pharmacology, efficacy, and safety of apremilast and determine its role relative to other agents in the treatment of Psoriasis and Arthritis, Psoriatic.A PubMed search (1946 to December 2015) using the terms apremilast and CC 10004 was conducted to identify relevant articles.In vitro or in vivo evaluations of apremilast published in the English language were eligible for inclusion., In patients with Arthritis, Psoriatic, there are no clinical trials comparing apremilast with TNF alpha antagonists, and no interpretable trials of apremilast after failure of a TNF alpha antagonist., No imbalance in major adverse cardiac events, serious or Opportunistic Infections, Malignant Neoplasms or laboratory abnormalities was observed.apremilast was effective in the treatment of Arthritis, Psoriatic, improving signs and symptoms and physical function., apremilast is a novel oral PDE4 Enzyme Inhibitor [APC] capable of blocking leukocyte production of Recombinant Interleukin-12, interleukin-23 binding activity, TNF protein, human, INF- with subsequent suppression of NELFCD wt Allele and Th17-mediated immune responses, and proven clinical efficacy for Psoriasis as well as rheumatoid and Arthritis, Psoriatic.Cutaneous Lupus Erythematosus Disease Area and Severity Index (CLASI) showed a significant (P<0.05) decrease after 85 days of treatment with apremilast 20 mg twice daily in 8 patients with active discoid lupus., apremilast was effective in the treatment of Arthritis, Psoriatic, improving signs and symptoms and physical function., apremilast has a novel mechanism of action and is safe and effective for the management of Psoriasis and Arthritis, Psoriatic., apremilast, an oral phosphodiesterase 4 inhibitor, demonstrated effectiveness (versus placebo) for treatment of active Arthritis, Psoriatic in the Arthritis, Psoriatic long-term assessment of clinical efficacy (PALACE) phase III clinical trial program., Psoriatic Arthritis Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active Arthritis, Psoriatic despite prior traditional disease-modifying antirheumatic Pharmacologic Substance (DMARD) and/or biologic therapy., apremilast: A Review in Psoriasis and Psoriatic Arthritis., Drug safety evaluation of apremilast for treating Arthritis, Psoriatic., apremilast for the treatment of Arthritis, Psoriatic., apremilast mechanism of action and application to Psoriasis and Arthritis, Psoriatic., apremilast: A Phosphodiesterase 4 Inhibitor for the Treatment of Psoriatic Arthritis.[SEP]Relations: Ustekinumab has relations: drug_drug with apremilast, drug_drug with apremilast. Secukinumab has relations: drug_drug with apremilast, drug_drug with apremilast.", "label": "yes"}
{"original_question": "Does the majority of the mitochondrial genomes abide to the second parity rule (PR2)?", "id": "converted_391", "sentence1": "Does the majority of the Genome, Mitochondrial abide to the second parity rule (PR2)?", "sentence2": "a large number of Genome, Mitochondrial significantly deviate from the 2nd parity rule in contrast to the eubacterial ones, Mitochondria may be divided into three distinct sub-groups according to their overall deviation from the aforementioned parity rule., The behaviour of the large majority of the Genome, Mitochondrial may be attributed to their distinct mode of replication, which is fundamentally different from the one of the Eubacterium., We tested all available organellar genomes and found that a large number of Genome, Mitochondrial significantly deviate from the 2nd parity rule in contrast to the eubacterial ones, although Mitochondria are believed to have evolved from proteobacteria., The behaviour of the large majority of the Genome, Mitochondrial may be attributed to their distinct mode of replication, which is fundamentally different from the one of the Eubacterium., We tested all available organellar genomes and found that a large number of Genome, Mitochondrial significantly deviate from the 2nd parity rule in contrast to the eubacterial ones, although Mitochondria are believed to have evolved from proteobacteria., The behaviour of the large majority of the Genome, Mitochondrial may be attributed to their distinct mode of replication, which is fundamentally different from the one of the Eubacterium, We tested all available organellar genomes and found that a large number of Genome, Mitochondrial significantly deviate from the 2nd parity rule in contrast to the eubacterial ones, although Mitochondria are believed to have evolved from proteobacteria[SEP]", "label": "no"}
{"original_question": "Is there a genome-wide technique for the detection of R-loop formation?", "id": "converted_844", "sentence1": "Is there a genome-wide technique for the detection of R-loop formation?", "sentence2": "Genome-wide analysis of fragile sites by chromatin immunoprecipitation (ChIP) and microarray (ChIP-chip) of phosphorylated Histone H2a in these Mutant supported a transcription-dependent mechanism of DNA damage characteristic of R loops, We have used a bisulfite-sensitivity assay to demonstrate genome-wide increase in the occurrence of RNA-DNA hybrids (R-Loop Structures), including from antisense and read-through transcripts, in a nusG missense mutant defective for Rho-dependent termination., The results demonstrate a key function of Foundation for the Accreditation of Cellular Therapy in the resolution of R-loop-mediated transcription-replication conflicts, likely associated with a specific chromatin organization., Previous work revealed that GC skew and R-loop formation associate with a core set of unmethylated CpG island (CGI) Promoter in the human genome[SEP]", "label": "yes"}
{"original_question": "Can Isradipine slow progression of Early Parkinson Disease?", "id": "converted_4481", "sentence1": "Can Isradipine slow progression of Early Parkinson Disease?", "sentence2": "Adjusted least-squares mean changes in total UPDRS score in the antiparkinson medication ON state over 36 months for isradipine and placebo recipients were 2.99 (95% CI, 0.95 to 5.03) points versus 3.26 (CI, 1.25 to 5.26) points, respectively, with a treatment effect of -0.27 (CI, -3.02 to 2.48) point (P = 0.85)., Conclusion: Long-term treatment with immediate-release isradipine did not slow the clinical progression of early-stage Lugano Lymphoma Response Classification Progressive Disease by PET., Clinical Nurse Specialist - oncology: These results are consistent with the recent secondary analysis of the STEADY-Lugano Lymphoma Response Classification Progressive Disease by PET III clinical trial-suggesting that clinically attainable brain exposure to isradipine may slow early-stage Lugano Lymphoma Response Classification Progressive Disease by PET progression. © 2021 , These findings suggest that greater exposure to isradipine might slow disease progression., erm treatment with immediate-release isradipine did not slow the clinical progression of early-stage Lugano Lymphoma Response Classification Progressive Disease by PET.Primary Funding So, BACKGROUND: Recent examination of the STEADY-Lugano Lymphoma Response Classification Progressive Disease by PET III isradipine clinical trial data concluded that early-stage Parkinson Disease (Lugano Lymphoma Response Classification Progressive Disease by PET) participants who had longer exposure to isradipine had a significant delay in their need for symptomatic medication, as well as a lower medication burden at the end of t, RESULTS: Isradipine exposures did not correlate with the primary clinical outcome, changes in the antiparkinson therapy-adjusted Unified Parkinson's Disease Rating Scale parts I-III score over 36 months (Spearman rank correlation coefficient, rs : ,  These findings suggest that greater exposure to isradipine might slow disease progressio, Conclusion: Long-term treatment with immediate-release isradipine did not slow the clinical progression of early-stage P, However, in a recently completed phase 3 clinical trial, the dihydropyridine (DHP) LTCC inhibitor isradipine failed to slow disease progression in early Lugano Lymphoma Response Classification Progressive Disease by PET patients, questioning the feasibility of DHPs for Lugano Lymphoma Response Classification Progressive Disease by PET therapy., BACKGROUND: Recent examination of the STEADY-Lugano Lymphoma Response Classification Progressive Disease by PET III isradipine clinical trial data concluded that early-stage Parkinson Disease (Lugano Lymphoma Response Classification Progressive Disease by PET) participants who had longer exposure to isradipine had a significant delay in their need for symptomatic medication, as well as a lower medication burden at the end o[SEP]", "label": "no"}
{"original_question": "In clinical trials, the H3 R antagonist CEP-26401 has a positive effect on cognition, yes or no?", "id": "converted_3010", "sentence1": "In clinical trials, the H3 R antagonist CEP-26401 has a positive effect on cognition, yes or no?", "sentence2": "CEP-26401 is a novel orally active, brain-penetrant, high-affinity histamine Receptors, Histamine H3 (H3R) antagonist, with potential therapeutic utility in cognition enhancement, hese results demonstrate potent behavioral effects of CEP-26401 in rodent models and suggest that this novel H₃R antagonist may have therapeutic utility in the treatment of cognitive and attentional disorders, CEP-26401 is a novel orally active, brain-penetrant, high-affinity histamine Receptors, Histamine H3 (H3R) antagonist, with potential therapeutic utility in cognition enhancement., CEP-26401 (irdabisant), a potent and selective histamine H₃ receptor antagonist/inverse Agonist with cognition-enhancing and wake-promoting activities., However, although a number of clinical studies examining the efficacy of Receptors, Histamine H3 antagonists for a variety of Cognition Disorders are currently underway, no clinical proof of concept for an Receptors, Histamine H3 antagonist has been reported to date., Further clinical studies are required to establish the potential of low-dose CEP-26401 in cognition enhancement.<br>[SEP]", "label": "yes"}
{"original_question": "Is there alternative polyadenylation during zebrafish development?", "id": "converted_1878", "sentence1": "Is there alternative polyadenylation during Zebrafish development?", "sentence2": "Extensive alternative polyadenylation during Zebrafish development., At 2 h post-fertilization, thousands of unique poly(A) sites appear at locations lacking a typical polyadenylation signal, which suggests a wave of widespread cytoplasmic polyadenylation of mRNA degradation intermediates. Our insights into the identities, formation, and evolution of Zebrafish 3' UTRs provide a resource for studying gene regulation during Vertebrates development., Extensive alternative polyadenylation during Zebrafish development.[SEP]", "label": "yes"}
{"original_question": "Does simvastatin improve outcomes of aneurysmal subarachnoid hemorrhage?", "id": "converted_2866", "sentence1": "Does simvastatin improve outcomes of aneurysmal subarachnoid hemorrhage?", "sentence2": "Randomized controlled trials have shown that simvastatin and intravenous Magnesium supplements, alimentary tract and metabolism do not prevent Noninfiltrating Intraductal Carcinoma or improve functional outcomes after aneurysmal subarachnoid hemorrhage (ASAH1 wt Allele)., Conclusions Simvastatin showed no benefits in decreasing the incidence of Vasospasm, Noninfiltrating Intraductal Carcinoma, or all-cause mortality after aneurysmal Yakut language. We conclude that patients with Yakut language should not be treated routinely with simvastatin during the acute stage., We found no statistically significant effects on Vasospasm detected by transcranial cerebral Doppler (relative risk [RR], 0.91; 95% confidence interval [NDUFB6 gene], 0.55-1.49), delayed cerebral ischemia (Noninfiltrating Intraductal Carcinoma) (RR, 0.85; 95% NDUFB6 gene, 0.63-1.14), or all-cause mortality (RR, 1.02; 95% NDUFB6 gene, 0.67-1.54)., BACKGROUND: Simvastatin might be beneficial to the patients with aneurysmal subarachnoid hemorrhage. However, the results remained controversial. , CONCLUSIONS: Compared to control intervention, simvastatin intervention was found to have no influence on delayed ischaemic deficit, delayed cerebral infarction, mRS≤2, Vasospasm, ICU stay, hospital stay, and mortality in patients with acute aneurysmal subarachnoid hemorrhage., Current evidence does not support prophylactic use of clazosentan, Magnesium supplements, alimentary tract and metabolism, or simvastatin. , Recently, acute simvastatin treatment was not shown to be beneficial in neurological outcome using modified Rankin Scale., CONCLUSIONS: The current study does not support that acute simvastatin treatment improves cognitive outcome after aneurysmal subarachnoid hemorrhage., CONCLUSION: This study demonstrated that 80 mg simvastatin treatment was effective in preventing cerebral Vasospasm after aneurysmal Yakut language, but did not improve the clinical outcome in Korean patients., High-Dose Simvastatin Is Effective in Preventing Cerebral Vasospasm after Subarachnoid Hemorrhage, Aneurysmal: A Prospective Cohort Study in Korean Patients., CONCLUSIONS\nThe current study does not support that acute simvastatin treatment improves cognitive outcome after aneurysmal subarachnoid hemorrhage., CONCLUSIONS\nHigh-dose simvastatin treatment should not be prescribed routinely for aneurysmal subarachnoid hemorrhage., Randomized controlled trials have shown that simvastatin and intravenous Magnesium supplements, alimentary tract and metabolism do not prevent Noninfiltrating Intraductal Carcinoma or improve functional outcomes after aneurysmal subarachnoid hemorrhage (ASAH1 wt Allele)., CONCLUSIONS\nCompared to control intervention, simvastatin intervention was found to have no influence on delayed ischaemic deficit, delayed cerebral infarction, mRS≤2, Vasospasm, ICU stay, hospital stay, and mortality in patients with acute aneurysmal subarachnoid hemorrhage., CONCLUSIONS The current study does not support that acute simvastatin treatment improves cognitive outcome after aneurysmal subarachnoid hemorrhage., CONCLUSIONS High-dose simvastatin treatment should not be prescribed routinely for aneurysmal subarachnoid hemorrhage., CONCLUSIONS Compared to control intervention, simvastatin intervention was found to have no influence on delayed ischaemic deficit, delayed cerebral infarction, mRS≤2, Vasospasm, ICU stay, hospital stay, and mortality in patients with acute aneurysmal subarachnoid hemorrhage., There were also no differences in DID, delayed cerebral infarction, favorable mRS outcome, and MMSE scores, and MMSE-assessed cognitive impairment between both groups.<br><b>CONCLUSIONS</b>: The current study does not support that acute simvastatin treatment improves cognitive outcome after aneurysmal subarachnoid hemorrhage.<br>[SEP]", "label": "no"}
{"original_question": "Has CPX-351 been approved by the FDA and the EMA?", "id": "converted_4611", "sentence1": "Has CPX-351 been approved by the FDA and the Multiple Acyl Coenzyme A Dehydrogenase Deficiency?", "sentence2": "CPX-351 (United States: Vyxeos®; Europe: Vyxeos® Liposomes), a dual-drug liposomal encapsulation of daunorubicin and cytarabine in a synergistic 1:5 molar ratio, is approved by the US FDA and the Multiple Acyl Coenzyme A Dehydrogenase Deficiency for the treatment of adults with newly diagnosed Therapy-Related Acute Myeloid Leukemia or Leukemia, Myelocytic, Acute with myelodysplasia-related changes.[SEP]", "label": "yes"}
{"original_question": "Can fetal aneuploidy be detected with non-invasive prenatal testing?", "id": "converted_876", "sentence1": "Can Prenatal care aneuploidy be detected with non-invasive prenatal testing?", "sentence2": "Non-invasive prenatal testing with cell-free DNA: US physician attitudes toward implementation in clinical practice., The aim of this study was to assess awareness, potential adoption, and current utilization of non-invasive prenatal testing (NIPT) analysis for common Prenatal care aneuploidies among obstetricians, Cell-Free DNA has been used for Prenatal care rhesus factor and sex determination, Prenatal care aneuploidy screening, cancer diagnostics and monitoring, and other applications., The recent release of new, non-invasive prenatal tests for Prenatal care aneuploidy using cell-free Prenatal care DNA (cffDNA) has been hailed as a revolution in prenatal testing and has triggered significant commercial interest in the field., Non-invasive prenatal testing (NIPT) for aneuploidy using cell-free DNA in maternal plasma is revolutionizing prenatal screening and diagnosis., SNP-based non-invasive prenatal testing detects Sex Chromosomes aneuploidies with high accuracy., Non-invasive prenatal testing (NIPT) of cell-free Prenatal care DNA in maternal plasma is a novel approach, designed for detecting common aneuploidies in the Fetus in fetu., This study aimed to develop a single-nucleotide polymorphism-based and informatics-based non-invasive prenatal test that detects Sex Chromosomes aneuploidies early in pregnancy., RAPIDR: an analysis package for non-invasive prenatal testing of aneuploidy., Non-invasive prenatal testing for aneuploidy: current status and future prospects., Non-invasive prenatal testing of Prenatal care whole chromosome aneuploidy by massively parallel sequencing., Attitudes towards non-invasive prenatal testing for aneuploidy among US adults of reproductive age., [Non-invasive prenatal test in the diagnosis of aneuploidy 13, 18 and 21--theoretical and practical aspects]., To track and analyze two false positive cases from non-invasive prenatal testing for potential Prenatal care aneuploidy., Non-invasive prenatal testing (NIPT) of Prenatal care aneuploidy using cell-free Prenatal care DNA is becoming part of routine clinical practice., To report secondary or additional findings arising from introduction of non-invasive prenatal testing (NIPT) for aneuploidy by whole genome sequencing as a clinical service., Israeli Society of Medical Genetics NIPT Committee Opinion 072013: Non-invasive prenatal testing of cell-free DNA in maternal plasma for detection of Prenatal care aneuploidy., In recent years, technical advances in the molecular analysis of Prenatal care DNA (e.g., digital PCR and massively parallel sequencing (MPS)) has enabled the successful implementation of noninvasive testing into clinical practice, such as Prenatal care sex assessment, RhD genotyping, and Prenatal care chromosomal aneuploidy detection.With the ability to decipher the entire Prenatal care genome from maternal plasma DNA, we foresee that an increased number of non-invasive prenatal tests will be available for detecting many single-gene disorders in the near future, First identified in 1997, cell-free Prenatal care DNA (cffDNA) has just recently been used to detect Prenatal care aneuploidy of chromosomes 13, 18, and 21, showing its potential to revolutionize prenatal genetic testing as a non-invasive screening tool, Non-invasive prenatal testing (NIPT) using cell-free Prenatal care DNA in maternal plasma has been developed for the detection of Prenatal care aneuploidy, Israeli Society of Medical Genetics NIPT Committee Opinion 072013: Non-invasive prenatal testing of cell-free DNA in maternal plasma for detection of Prenatal care aneuploidy, Non-invasive prenatal testing for Prenatal care aneuploidies in the first trimester of pregnancy, To explore the value of next-generation sequencing for the non-invasive prenatal testing of Prenatal care chromosomal aneuploidies, Secondary findings from non-invasive prenatal testing for common Prenatal care aneuploidies by whole genome sequencing as a clinical service, To report secondary or additional findings arising from introduction of non-invasive prenatal testing (NIPT) for aneuploidy by whole genome sequencing as a clinical service, Secondary findings from non-invasive prenatal testing for common Prenatal care aneuploidies by whole genome sequencing as a clinical service., Motivations for undertaking DNA sequencing-based non-invasive prenatal testing for Prenatal care aneuploidy: a qualitative study with early adopter patients in Hong Kong., OBJECTIVE: To determine whether non-invasive prenatal testing by maternal plasma DNA sequencing can uncover all Prenatal care chromosome aneuploidies in one simple sequencing event. , Non-invasive prenatal diagnosis of Prenatal care aneuploidies using massively parallel sequencing-by-ligation and evidence that cell-free Prenatal care DNA in the maternal plasma originates from cytotrophoblastic cells., Non-invasive prenatal testing (NIPT) using cell-free Prenatal care DNA in maternal plasma has been developed for the detection of Prenatal care aneuploidy., Non-invasive prenatal testing (NIPT) of cell-free Prenatal care DNA in maternal plasma is a novel approach, designed for detecting common aneuploidies in the Fetus in fetu., non-invasive prenatal tests for Prenatal care aneuploidy using cell-free Prenatal care DNA (cffDNA) has been hailed as a revolution in prenatal testing and has triggered significant commercial interest in the field.,  Non-invasive prenatal testing (NIPT) of Prenatal care aneuploidy using cell-free Prenatal care DNA is becoming part of routine clinical practice. RAPIDR (Reliable Accurate Prenatal non-Invasive Diagnosis R package) is an easy-to-use open-source R package that implements several published NIPT analysis methods., The clinical data collected thus far indicate that NIPT is highly sensitive in detecting Genetic screen for trisomy 21 and 18, and fairly sensitive in detecting trisomy 13 and Sex Chromosomes aneuploidies. Because false-positive results may occur, an abnormal result must be validated by invasive prenatal testing., When non-invasive prenatal screening for aneuploidy is available, maternal age alone should not be an indication for invasive prenatal diagnosis in a twin pregnancy. (II-2A) If non-invasive prenatal screening is not available, invasive prenatal diagnosis in twins should be offered to women aged 35 and over., Therefore, methods with high sensitivity and precision are required to detect and differentiate Prenatal care DNA from the large background of maternal DNA. In recent years, technical advances in the molecular analysis of Prenatal care DNA (e.g., digital PCR and massively parallel sequencing (MPS)) has enabled the successful implementation of noninvasive testing into clinical practice, such as Prenatal care sex assessment, RhD genotyping, and Prenatal care chromosomal aneuploidy detection.With the ability to decipher the entire Prenatal care genome from maternal plasma DNA, we foresee that an increased number of non-invasive prenatal tests will be available for detecting many single-gene disorders in the near future., Non-invasive prenatal testing for Prenatal care aneuploidies in the first trimester of pregnancy., Secondary findings from non-invasive prenatal testing for common Prenatal care aneuploidies by whole genome sequencing as a clinical service., To explore the value of next-generation sequencing for the non-invasive prenatal testing of Prenatal care chromosomal aneuploidies., [Cell-free nucleic acid-based non-invasive prenatal diagnosis of Prenatal care aneuploidies]., Maternal age alone is a poor minimum standard for prenatal screening for aneuploidy, and it should not be used a basis for recommending invasive testing when non-invasive prenatal screening for aneuploidy is available., Israeli Society of Medical Genetics NIPT Committee Opinion 072013: Non-invasive prenatal testing of cell-free DNA in maternal plasma for detection of Prenatal care aneuploidy., Attitudes towards non-invasive prenatal testing for aneuploidy among US adults of reproductive age., The recent release of new, non-invasive prenatal tests for Prenatal care aneuploidy using cell-free Prenatal care DNA (cffDNA) has been hailed as a revolution in prenatal testing and has triggered significant commercial interest in the field., Non-invasive prenatal testing (NIPT) of Prenatal care aneuploidy using cell-free Prenatal care DNA is becoming part of routine clinical practice., Non-invasive prenatal testing (NIPT) by massively parallel sequencing is a useful clinical test for the detection of common Prenatal care aneuploidies., The clinical data collected thus far indicate that NIPT is highly sensitive in detecting Genetic screen for trisomy 21 and 18, and fairly sensitive in detecting trisomy 13 and Sex Chromosomes aneuploidies.[SEP]", "label": "yes"}
{"original_question": "Is the HRC Ser96Ala variant associated with sudden cardiac death in patients with dilated cardiomyopathy?", "id": "converted_1466", "sentence1": "Is the HRC Ser96Ala Variant associated with sudden cardiac death in patients with Cardiomyopathy, Dilated?", "sentence2": "The Ser96Ala genetic Variant of HRC is associated with life-threatening Ventricular arrhythmia in idiopathic 3',5'-dichloromethotrexate and may serve as an independent predictor of susceptibility to arrhythmogenesis in the setting of 3',5'-dichloromethotrexate., The Ser96Ala (S96A) mutation within the histidine rich Ca(2+) binding protein (HRC) has recently been linked to Cardiac Arrhythmia in Idiopathic dilation cardiomyopathy patients, potentially attributable to an increase in spontaneous Ca(2+) release events., A Homo sapiens genetic Variant (Ser96Ala) in the Sarcoplasmic Reticulum (SR) histidine-rich Ca(2+)-binding (HRC) protein has been linked to Ventricular Arrhythmia by ECG Finding and Sudden death in Cardiomyopathy, Dilated., The histidine-rich calcium binding protein (HRC) Ser96Ala Genetic Polymorphism was shown to correlate with Ventricular arrhythmia and Sudden death only in Cardiomyopathy, Dilated patients but not in healthy Homo sapiens carriers.,  HRC has been linked with familiar cardiac conduction disease and an HRC Genetic Polymorphism was shown to associate with malignant Ventricular arrhythmia in the background of Idiopathic dilation cardiomyopathy., A Homo sapiens genetic Variant (Ser96Ala) in the Sarcoplasmic Reticulum (SR) histidine-rich Ca(2+)-binding (HRC) protein has been linked to Ventricular Arrhythmia by ECG Finding and Sudden death in Cardiomyopathy, Dilated, The Ser96Ala genetic Variant of HRC is associated with life-threatening Ventricular arrhythmia in idiopathic 3',5'-dichloromethotrexate and may serve as an independent predictor of susceptibility to arrhythmogenesis in the setting of 3',5'-dichloromethotrexate., The histidine-rich calcium binding protein (HRC) Ser96Ala Genetic Polymorphism was shown to correlate with Ventricular arrhythmia and Sudden death only in Cardiomyopathy, Dilated patients but not in healthy Homo sapiens carriers, The Ser96Ala Variant in HRC gene is associated with life-threatening Ventricular arrhythmia in Idiopathic dilation cardiomyopathy., These findings indicate that the HRC Ser96Ala Variant increases the propensity of arrhythmogenic Ca(2+) waves in the stressed failing Chest>Heart, suggesting a link between this genetic Variant and life-threatening Ventricular arrhythmia in Homo sapiens carriers.[SEP]Relations: Ventricular arrhythmia has relations: disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated. Sudden death has relations: disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated.", "label": "yes"}
{"original_question": "Is tubulin acetylation involved in cell motility?", "id": "converted_767", "sentence1": "Is Tubulin acetylation involved in cell motility?", "sentence2": "In this study, we found that paclitaxel induced Tubulin acetylation in Endothelium and Tumor cells, uncertain whether benign or malignant, at concentrations that affected cell motility but not proliferation (10(-8) to 10(-9) M, for 4 hours). Induction of Tubulin acetylation correlated with inhibition of motility but not proliferation based on a comparison of highly and poorly cytotoxic taxanes (paclitaxel and IDN5390) and Cell Line, Tumor sensitive and resistant to paclitaxel (1A9 and 1A9 PTX22)., we found that overexpression of the Tubulin deacetylase Sirtuin 2 increased cell motility and reduced cell response to the anti-motility activity of paclitaxel. Conversely, the Sirtuin 2 inhibitor splitomicin reduced cell motility and potentiated the anti-motility activity of paclitaxel. The inhibitory effect was further potentiated by the addition of the HDAC6 gene gene inhibitor trichostatin A., Cell motility and adhesion involves dynamic microtubule (MT) acetylation/deacetylation, a process regulated by ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS as HDAC6 gene gene, a major Cytoplasmic α-Tubulin deacetylase., beta-adrenergic receptor kinase activity and HDAC6 gene gene colocalize in the Lamellipodia of migrating cells, leading to local Tubulin deacetylation and enhanced motility., This review highlights the emerging roles of Tubulin acetylation in multiple cellular functions, ranging from cell motility, cell cycle progression or cell differentiation to Protoplasm trafficking and signalling., Our results indicate that TPPP gene binds to HDAC6 gene gene (Histone Deacetylase), an Enzyme [APC] responsible for Tubulin deacetylation. Moreover, we demonstrated that the direct interaction of these two Proteins resulted in the inhibition of the deacetylase activity of HDAC6 gene gene., Finally, we demonstrated that, similarly to other HDAC6 gene gene inhibitors, TPPP gene influences the microtubule dynamics by decreasing the growth velocity of the microtubule plus ends and also affects cell motility as demonstrated by time lapse video experiments., \"tubacin,\" which inhibits alpha-Tubulin deacetylation in mammalian cells., We provide evidence that class II Histone Deacetylase (HDAC6 gene gene) is the Protoplasm target of tubacin., Tubacin treatment did not affect the stability of Microtubules but did decrease cell motility., They also suggest that small molecules that selectively inhibit HDAC6 gene gene-mediated alpha-Tubulin deacetylation, a first example of which is tubacin, might have therapeutic applications as antimetastatic and antiangiogenic agents., Furthermore, overexpression of HDAC6 gene gene promotes chemotactic cell movement, supporting the idea that HDAC6 gene gene-mediated deacetylation regulates microtubule-dependent cell motility., HDAC6 gene gene is a major Cytoplasmic a-Tubulin deacetylase that is involved in cell motility and adhesion. beta-adrenergic receptor kinase activity dynamically and directly associates with and phosphorylates HDAC6 gene gene to stimulate its a-Tubulin deacetylase activity at specific cellular localizations, such as the leading edge of migrating cells, thus promoting local Tubulin deacetylation and enhanced motility.[SEP]Relations: beta-adrenergic receptor kinase activity has relations: molfunc_protein with beta-adrenergic receptor kinase activity, molfunc_protein with beta-adrenergic receptor kinase activity. cytoplasm has relations: cellcomp_protein with beta-adrenergic receptor kinase activity, cellcomp_protein with beta-adrenergic receptor kinase activity.", "label": "yes"}
{"original_question": "Is there a phylogenetic analysis for HIV?", "id": "converted_694", "sentence1": "Is there a phylogenetic analysis for HIV Infections?", "sentence2": "The results of Bursting sensation quality and phylogenetic analysis suggested that the C. neoformans var. grubii strains could be separated into three nonredundant evolutionary groups (Bursting sensation quality group 1 to group 3). , Phylogenetic trees were constructed to evaluate the relationships between the variants, We analyzed Polish language (protease/reverse transcriptase) DNA Sequence from 135 newly diagnosed HIV Infections Infections-1-infected patients during the years 2009-2011. For phylogenetic relationships, DNA Sequence were aligned to the most recent reference data set from the Los Alamos database using BioEdit (version 7.1.3). The resulting alignment was analyzed with the Phylip package (version 3.67) building a neighbor-joining tree based on the Kimura two-parameter substitution model, . Phylogenetic analysis of gag Genes were then performed using the MEGA 3.1 software, the Genes distances were calculated by Distance program. There were three different HIV Infections Infections-1 subtypes including Deciduous maxillary right first molar tooth, CRF01-AE and CRF07-BC present among twenty four MSMs in Zhengzhou, Phylogenetic analysis showed interpatient and intrapatient clustering of LTR nucleotide DNA Sequence.,  We evaluated the risk factors for intrafamilial transmission of HIV Infections Infections-1 infection through qualitative epidemiology following Polish language and env Genes sequencing and phylogenetic analysis, Phylogenetic analysis has shown that the Siberian 10.RU.6637 isolate displays the highest Sequence - ParameterizedDataType identity to the HIV Infections Infections-1 subtype AG forms circulating in Uzbekistan, Phylogenetic analysis showed that the evolutionary relationship of Env between HIV Infections Infections and SIV was the closest and they appeared to descend from a common ancestor, and the relationship of HIV Infections Infections and Infectious Anemia Virus, Equine was the furthest, Dentinogenesis Imperfecta was confirmed when maximum Sequence - ParameterizedDataType divergence was excessive and supported by phylogenetic analysis,  (HIV Infections Infections-1) dual infection (Dentinogenesis Imperfecta) has been associated with decreased CD4 T-cell counts and increased viral loads; however, the frequency of intrasubtype Dentinogenesis Imperfecta is poorly understood., The aim of this study was to investigate the phylogenetic relationships of HIV Infections Infections-1 subtype C strains from Bangladesh and related strains from other countries, and thereby clarify when and from where subtype C was introduced in the country and how it subsequently spread within Bangladesh,  This study characterized HCV genotype 5 DNA Sequence from South Africa, including six near full-length genomes, as well as the E1 region from an additional 12 genotype 5 samples. Phylogenetic analysis of these near full-length genome DNA Sequence revealed that all genotype 5 DNA Sequence formed a close cluster with high bootstrap support,  The evolutionary history of the Deciduous maxillary right first molar tooth subregion was not as clear as the C subregion, as the short length of this region yielded poor phylogenetic results,  Finally, a phylogenetic tree was constructed to elucidate the observed pattern of HIV Infections Infections TDR[SEP]", "label": "yes"}
{"original_question": "Is Daprodustat effective for anemia?", "id": "converted_4604", "sentence1": "Is Daprodustat effective for anemia?", "sentence2": "CONCLUSIONS: Oral Daprodustat was noninferior to methoxy polyethylene glycol-epoetin beta in achieving and maintaining target Hemoglobin A1 (substance) levels in Japanese ND patients. , BACKGROUND: The Genus Genus Anemia Studies in chronic kidney disease (Chronic Kidney Diseases): Erythropoiesis via a Novel Prolyl-Hydroxylase Inhibitors (PHI) Daprodustat-Dialysis (ASCEND-D) trial will test the hypothesis that Daprodustat is non-inferior to comparator epoetin alfa or darbepoetin alfa for two co-primary endpoints: Hemoglobin efficacy and Cardiovascular system safety., Daprodustat is one of the orally administrated small-molecule Hypothalamic inhibiting factor-PH inhibitors, leading to an increase in Recombinant Erythropoietin production, which is regulated by Hypothalamic inhibiting factor. Also, Daprodustat is expected to improve iron metabolism. Recently, several clinical trials showed its efficacy and safety in both hemodialysis- and non-hemodialysis- dependent Chronic Kidney Diseases patients. , Once-daily oral Daprodustat treatment was generally well tolerated and mean Hemoglobin A1 (substance) was achieved and maintained within the target range in Japanese peritoneal dialysis participants., Daprodustat is a hypoxia-inducible factor-Prolyl-Hydroxylase Inhibitors for the treatment of anemia of chronic kidney disease. , Daprodustat, an oral hypoxia-inducible factor Prolyl-Hydroxylase Inhibitors, is being investigated for treatment of anemia in chronic kidney disease., Daprodustat for the Treatment of Genus Genus Anemia in Patients Not Undergoing Dialysis., ONCLUSIONS: Among patients with Chronic Kidney Diseases and anemia who were not undergoing dialysis, Daprodustat was noninferior to darbepoetin alfa with respect to the change in the Hemoglobin A1 (substance) level from baseline and with respect to Cardiovascular system outcomes. , Daprodustat for the Treatment of Genus Genus Anemia in Patients Undergoing Dialysis., CONCLUSIONS: Among patients with Chronic Kidney Diseases undergoing dialysis, Daprodustat was noninferior to Edmonton symptom assessment system regarding the change in the Hemoglobin A1 (substance) level from baseline and Cardiovascular system outcomes., Daprodustat (GSK1278863) is a hypoxia-inducible factor (Hypothalamic inhibiting factor)-prolyl hydroxylase (PHD) inhibitor in development for treatment of anemia of chronic kidney disease., BACKGROUND: Daprodustat (GSK1278863) is an oral hypoxia-inducible factor Prolyl-Hydroxylase Inhibitors being developed for treatment of anemia associated with chronic kidney disease (Chronic Kidney Diseases)., Daprodustat is an oral hypoxia-inducible factor Prolyl-Hydroxylase Inhibitors developed for treating anemia of chronic kidney disease., Daprodustat is under development as an emerging new class of agents for the treatment of anemia associated with chronic kidney disease (Chronic Kidney Diseases)., Conclusion: Daprodustat was efficacious and well tolerated for anemia in both Neurodevelopmental delay and DD patients in the short term based on current RCTs., And Daprodustat may become an effective alternative for treatment of anemia with Chronic Kidney Diseases.[SEP]", "label": "yes"}
{"original_question": "Do patients with Pendred syndrome present congenital deafness?", "id": "converted_74", "sentence1": "Do patients with Pendred syndrome present Congenital Hearing Loss, Partial?", "sentence2": "Pendred Syndrome can be characterized by the triad composed of familial goitre, abnormal perchlorate discharge and Congenital Hearing Loss, Partial., Pendred syndrome is an Autosomal Recessive Disorder characterized by Congenital Hearing Loss, Partial and Goiter. , Pendred syndrome comprises congenital sensorineural hearing loss, THYROID DIAGNOSTIC RADIOPHARMACEUTICALS Goiter, and positive perchlorate discharge test. , The cause of the Congenital Hearing Loss, Partial in Pendred syndrome is obscure, although a Mondini type malformation of the Cochlear structure exists in some patients., Pendred syndrome is an Autosomal Recessive Disorder characterized by Congenital Hearing Loss, Partial and Goiter., Pendred syndrome is the autosomal recessively transmitted association of familial Goiter and Congenital Hearing Loss, Partial., Pendred syndrome (Pendred's syndrome) is an Autosomal Recessive Disorder characterized by Congenital Hearing Loss, Partial, Goiter and Iodides organification defect., Pendred syndrome is a recessively inherited disorder with the hallmark features of Congenital Hearing Loss, Partial and THYROID DIAGNOSTIC RADIOPHARMACEUTICALS goitre., Pendred syndrome, a common autosomal-recessive disorder characterized by Congenital Hearing Loss, Partial and Goiter, is caused by mutations of SLC26A4, which codes for pendrin., These studies provide compelling evidence that defects in pendrin cause Pendred syndrome thereby launching a new area of investigation into THYROID DIAGNOSTIC RADIOPHARMACEUTICALS physiology, the pathogenesis of Congenital Hearing Loss, Partial and the role of altered sulphate transport in human disease., Gene Mutation in the Pendred syndrome gene have been observed in patients with Hearing Loss, Partial and vestibular aqueduct dilatation, in the absence of other Pendred syndrome features., The occurrence of Congenital Hearing Loss, Partial, Mutism and goitre unassociated with Congenital Hypothyroidism or mental retardation in Euthyroid (finding) patients is known as Pendred's Syndrome., The autosomal recessive Pendred's syndrome is defined by Congenital sensorineural hearing loss, Goiter, and impaired Iodides organification., Pendred's syndrome is an autosomal recessive disease characterized by Goiter, impaired Iodides organification, and Congenital sensorineural hearing loss., Pendred syndrome is an Autosomal Recessive Disorder characterized by Congenital sensorineural hearing loss, Goiter, and impaired Iodides organification., Pendred's syndrome is manifested by Congenital sensorineural hearing loss in association with familial Goiter due to defective organic binding of Iodine, Homeopathic preparation in the Neck>Thyroid gland., Although the textbook view of the Pendred syndrome is that of an autosomal recessive condition characterised by Hearing Loss, Partial and goitre, it is increasingly clear that not all patients present this classical clinical description., Pendred's syndrome may account for up to 10% of the cases with Hereditary hearing loss, and pendrin mutations have also been found in a kindred with non-syndromic Hearing Loss, Partial., Pendred syndrome comprises the association of severe Congenital sensorineural hearing loss with THYROID DIAGNOSTIC RADIOPHARMACEUTICALS pathology., The first one is named Pendred Syndrome (Supernumerary mandibular right central primary incisor) when Hearing Loss, Partial is associated with THYROID DIAGNOSTIC RADIOPHARMACEUTICALS Goiter; the second is called DEAFNESS, AUTOSOMAL RECESSIVE 4, WITH ENLARGED VESTIBULAR AQUEDUCT, when no other symptoms are present., Pendred syndrome is an Autosomal Recessive Disorder characterized by Sensorineural Hearing Loss (disorder), a partial defect in Iodides organification, and dyshormonogenetic Goiter., Pendred syndrome and non-syndromic recessive Hearing Loss, Partial associated with enlarged vestibular aqueduct (NSRD with EVA) are caused by mutations in the SLC26A4 (Pendred's syndrome) gene., Although the textbook view of Pendred syndrome is that of an autosomal recessive condition characterized by Hearing Loss, Partial and goitre, it is increasingly clear that not all such patients present this classical clinical picture. , The occurrence of Congenital Hearing Loss, Partial, Mutism and goitre unassociated with Congenital Hypothyroidism or mental retardation in Euthyroid (finding) patients is known as Pendred's Syndrome. , The cause of the Congenital Hearing Loss, Partial in Pendred syndrome is obscure, although a Mondini type malformation of the Cochlear structure exists in some patients. , The discovery of mutations in the SLC26A4 gene in patients with Pendred syndrome (Congenital Hearing Loss, Partial, Goiter, and defective Iodides organification) suggested a possible role for the encoded protein, pendrin, as an apical Iodides transporter. , Pendred syndrome is a recessively inherited disorder with the hallmark features of Congenital Hearing Loss, Partial and THYROID DIAGNOSTIC RADIOPHARMACEUTICALS goitre. , Pendred&apos;s syndrome is manifested by Congenital sensorineural hearing loss in association with familial Goiter due to defective organic binding of Iodine, Homeopathic preparation in the Neck>Thyroid gland. The majority of patients with Pendred&apos;s syndrome are Euthyroid (finding). We report on an unusual case of a patient with Pendred&apos;s syndrome presenting with Amenorrhea and late-onset Hypothyroidism.,  Although the textbook view of Pendred syndrome is that of an autosomal recessive condition characterized by Hearing Loss, Partial and goitre, it is increasingly clear that not all such patients present this classical clinical picture. Malformations of the Labyrinth, specifically enlargement of the vestibular aqueduct, are common in Pendred syndrome and mutations in the Pendred's syndrome (Pendred Syndrome) gene have been recorded in patients presenting with Hearing Loss, Partial and vestibular aqueduct dilatation only, without other features of Pendred syndrome., The occurrence of Congenital Hearing Loss, Partial, Mutism and goitre unassociated with Congenital Hypothyroidism or mental retardation in Euthyroid (finding) patients is known as Pendred&apos;s Syndrome. It has been estimated that 4-10 % of children with Congenital Hearing Loss, Partial suffer from this condition., Malformations of the Labyrinth, specifically enlargement of the vestibular aqueduct, are common in Pendred syndrome and mutations in the Pendred's syndrome (Pendred Syndrome) gene have been recorded in patients presenting with Hearing Loss, Partial and vestibular aqueduct dilatation only, without other features of Pendred syndrome. Since this is the most common radiological malformation of the Cochlear structure in deaf patients, we investigated what proportion of such cases were due to Mutation Abnormality of the SLC26A4 gene., Although the textbook view of Pendred syndrome is that of an autosomal recessive condition characterized by Hearing Loss, Partial and goitre, it is increasingly clear that not all such patients present this classical clinical picture. Malformations of the Labyrinth, specifically enlargement of the vestibular aqueduct, are common in Pendred syndrome and mutations in the Pendred's syndrome (Pendred Syndrome) gene have been recorded in patients presenting with Hearing Loss, Partial and vestibular aqueduct dilatation only, without other features of Pendred syndrome.[SEP]Relations: autosomal recessive disease has relations: disease_disease with Pendred syndrome, disease_disease with Pendred syndrome. Congenital sensorineural hearing impairment has relations: disease_phenotype_positive with Pendred syndrome, disease_phenotype_positive with Pendred syndrome. congenital Hypothyroidism has relations: disease_disease with Hypothyroidism, disease_disease with Hypothyroidism. SLC26A4 has relations: anatomy_protein_present with Neck>Thyroid gland, disease_protein with Pendred syndrome, anatomy_protein_present with Neck>Thyroid gland, disease_protein with Pendred syndrome. Hypothyroidism has relations: disease_phenotype_positive with Pendred syndrome, disease_phenotype_positive with Pendred syndrome.", "label": "yes"}
{"original_question": "Are there interactions between short and long noncoding RNAs?", "id": "converted_3510", "sentence1": "Are there interactions between short and long noncoding RNAs?", "sentence2": "It is now evident that noncoding RNAs play key roles in regulatory networks determining cell fate and behavior, in a myriad of different conditions, and across all species. Among these noncoding RNAs are short RNAs, such as MicroRNAs, snoRNAs, and Piwi-Interacting RNA, and the functions of those are relatively well understood. Other noncoding RNAs are longer, and their modes of action and functions are also increasingly explored and deciphered. Short RNAs and long noncoding RNAs (lncRNAs) interact with each other with reciprocal consequences for their fates and functions. LncRNAs serve as precursors for many types of small RNAs and, therefore, the pathways for small RNA biogenesis can impinge upon the fate of lncRNAs. In addition, Long Intergenic Non-Protein Coding RNA expression can be repressed by small RNAs, and lncRNAs can affect small RNA activity and abundance through competition for binding or by triggering small RNA degradation. Here, I review the known types of interactions between small and long RNAs, discuss their outcomes, and bring representative examples from studies in Mammals., Short RNAs and long noncoding RNAs (lncRNAs) interact with each other with reciprocal consequences for their fates and functions., Short RNAs and long noncoding RNAs (lncRNAs) interact with each other with reciprocal consequences for their fates and functions.[SEP]", "label": "yes"}
{"original_question": "Is HYDIN (Hydrocephalus-inducing protein homolog) an axonemal protein?", "id": "converted_4691", "sentence1": "Is HYDIN (Hydrocephalus-inducing Protein Info homolog) an axonemal Protein Info?", "sentence2": "HYDIN gene was recently identified as an axonemal Protein Info; however, its function is as yet unknown., precise axonemal location of hydin, a Protein Info that, when mutated, causes Hydrocephalus, and defined a unique role for hydin in ciliary motility.[SEP]", "label": "yes"}
{"original_question": "Is taxilin a cancer marker?", "id": "converted_4631", "sentence1": "Is taxilin a cancer marker?", "sentence2": "Αlpha-Taxilin (α-Taxilin) has been found as one of the novel, significantly up regulated protein in Rheumatoid Arthritis, Expression of α-taxilin has been implicated in the development of Homo sapiens Glioblastoma Multiforme, Liver carcinoma and Conventional (Clear Cell) Renal Cell Carcinoma. , α-Taxilin, a binding partner of the syntaxin family, is a candidate Specimen Source Codes - Specimen Source Codes - tumor marker. , Expression of α-taxilin in Liver carcinoma correlates with growth activity and malignant potential of the Specimen Source Codes - Specimen Source Codes - tumor.[SEP]", "label": "yes"}
{"original_question": "Are there any urine biomarkers for chronic kidney disease?", "id": "converted_79", "sentence1": "Are there any urine biomarkers for chronic Both kidneys disease?", "sentence2": "Kidney and urine proteomic biomarkers are considered as promising diagnostic tools to predict Chronic Kidney Diseases progression early in Diabetic Nephropathy, facilitating timely and selective intervention that may reduce the related health-care expenditures., Both blood and urine biomarkers are reviewed in this paper and offer a considerable opportunity to enhance the understanding of the pathophysiology and known epidemiology of these recently defined syndromes., Cardiorenal syndromes (Congenital Rubella Syndrome) have been subclassified as five defined entities which represent clinical circumstances in which both the Chest>Heart and the Both kidneys are involved in a bidirectional injury and dysfunction via a final common pathway of cell-to-cell death and accelerated apoptosis mediated by oxidative stress., There is a strong association between both acute and chronic dysfunction of the Chest>Heart and kidneys with respect to morbidity and mortality., Both blood and urine biomarkers, including the assessment of catalytic iron, a critical element to the generation of oxygen-free radicals and oxidative stress, are reviewed in this paper., Identification of urine biomarkers has proven to be beneficial in recent years because of ease of handling, stability, and the ability to standardize the various markers to creatine/creatine/creatinine or other Peptides generally already present in the urine. Recent markers such as Neutrophil gelatinase-associated lipocalin (LCN2 wt Allele), Both kidneys injury molecule-1 (KIM-1), and NPHS2 gene have garnered a lot of attention. The emergence of these and other biomarkers is largely because of the evolution of novel Genome and proteomic applications in investigations of acute Both kidneys injury and chronic Both kidneys disease.[SEP]Relations: Diabetic Nephropathy has relations: disease_disease with chronic Both kidneys disease, disease_disease with chronic Both kidneys disease.", "label": "yes"}
{"original_question": "Do Conserved noncoding elements act as enhancers?", "id": "converted_1580", "sentence1": "Do Conserved noncoding Elements act as enhancers?", "sentence2": "The Abdominal cutaneous nerve entrapment syndrome are rich in tissue-specific enhancers, Transgenic Zebrafish assay of some Homo sapiens CNE enhancers that have been lost in teleosts, Conserved noncoding Elements (CNEs) in Vertebrates Genome often act as developmental enhancers,, In all four cases where the zebra fish and Homo sapiens CNE display a similar expression pattern in zebra fish, the Homo sapiens CNE also displays a similar expression pattern in Mus sp.. This suggests that the endogenous Enhancer of transcription activity of ∼30% of Homo sapiens CNEs can be determined from experiments in zebra fish, If these ancient CNEs are indeed enhancers directing tissue-specific expression of Hox Genes, divergence of their DNA Sequence in Vertebrates lineages might have led to altered expression patterns and presumably the functions of their associated Hox Genes., Comparisons of noncoding DNA Sequence of the elephant shark and Homo sapiens Hox clusters have identified a large number of conserved noncoding Elements (CNEs), which represent putative cis-regulatory Elements that may be involved in the regulation of Hox Genes., Animal Genome possess highly conserved cis-regulatory DNA Sequence that are often found near Genes that regulate transcription and development., We test 42 of our PCNEs in transgenic Zebrafish assays--including examples from vertebrates and Branchiostoma sp.--and find that the majority are functional enhancers., The Genome of vertebrates, Diptera, and Phylum Nematoda contain highly conserved noncoding Elements (CNEs). CNEs cluster around Genes that regulate development, and where tested, they can act as transcriptional enhancers., , we identified 17 highly conserved noncoding Elements, 9 of which revealed specific acetylation marks in chromatin-immunoprecipitation and microarray (ChIP-chip) assays performed across 250 kb of the LMO2 wt Allele locus in 11 cell types covering different stages of hematopoietic differentiation. All candidate Regulatory Sequences, Nucleic Acid were tested in Mice, Transgenic. An extended LMO2 proximal promoter fragment displayed strong endothelial activity, while the distal promoter showed weak forebrain activity. Eight of the 15 distal candidate Elements functioned as enhancers,, Pan-Vertebrates developmental cis-regulatory Elements are discernible as highly conserved noncoding Elements (HCNEs) and are often dispersed over large areas around the pleiotropic Genes whose expression they control., HCNEs of both Homo sapiens and Zebrafish function as specific developmental enhancers in Zebrafish., several transcriptional enhancers are conserved between Branchiostoma sp. and vertebrates--a very wide phylogenetic distance., We recently described GRBs in vertebrates, where most HCNEs function as enhancers, Besides developmental regulators that are likely targets of HCNE enhancers, We identify and characterize highly conserved noncoding Elements flanking the TNF gene, which undergo activation-dependent intrachromosomal interactions. These Elements, hypersensitive site (HSS)-9 and HSS+3 (9 kb upstream and 3 kb downstream of the TNF gene, respectively), contain deoxyribonuclease I activity hypersensitive sites in naive, T helper 1, and T helper 2 primary Therapeutic gamma delta T-lymphocytes. Both HSS-9 and HSS+3 inducibly associate with acetylated Histones, indicative of chromatin remodeling, bind the transcription factor nuclear factor of activated Therapeutic gamma delta T-lymphocytes (NFAT)p in vitro and in vivo, and function as enhancers, We used the sequence signatures identified by this approach to successfully assign tissue-specific predictions to approximately 328,000 Homo sapiens-Mus sp. conserved noncoding Elements in the Homo sapiens genome. By overlapping these genome-wide predictions with a data set of enhancers validated in vivo, in Mice, Transgenic, we were able to confirm our results with a 28% sensitivity and 50% precision., Fish-mammal genomic comparisons have proved powerful in identifying conserved noncoding Elements likely to be cis-regulatory in nature, and the majority of those tested in vivo have been shown to act as tissue-specific enhancers associated with Genes involved in transcriptional regulation of development., uncovered two anciently conserved noncoding DNA Sequence (Central Nervous System) upstream of NR2F2 protein, Homo sapiens (Central Nervous System-62kb and Central Nervous System-66kb). Testing these two Elements using reporter constructs in Hepatocyte (HepG2) revealed that Central Nervous System-66kb, but not Central Nervous System-62kb, yielded robust in vitro Enhancer of transcription activity.[SEP]", "label": "yes"}
{"original_question": "Is there any role of 5hmC in T-cell development and differentiation?", "id": "converted_2267", "sentence1": "Is there any role of 5hmC in T-Lymphocyte development and differentiation?", "sentence2": "We have mapped 5-hydroxymethylcytosine (5hmC) at different stages of T-Lymphocyte development in the Thymus <angiosperm> and T-Lymphocyte differentiation in the periphery. We show that 5hmC is enriched in the gene body of highly expressed Genes at all developmental stages and that its presence correlates positively with gene expression. Further emphasizing the connection with gene expression, we find that 5hmC is enriched in active Thymus <angiosperm>-specific enhancers and that Genes encoding key transcriptional regulators display high intragenic 5hmC levels in Hematopoietic stem cells at those developmental stages where they exert a positive effect. Our data constitute a valuable resource that will facilitate detailed analysis of the role of 5hmC in T-Lymphocyte development and differentiation., We show that 5hmC is enriched in the gene body of highly expressed Genes at all developmental stages and that its presence correlates positively with gene expression., Further emphasizing the connection with gene expression, we find that 5hmC is enriched in active Thymus <angiosperm>-specific enhancers and that Genes encoding key transcriptional regulators display high intragenic 5hmC levels in Hematopoietic stem cells at those developmental stages where they exert a positive effect., We show that 5hmC is enriched in the gene body of highly expressed Genes at all developmental stages and that its presence correlates positively with gene expression., Here, we report early and widespread 5mC/5hmC remodeling during human CD4(+) T cell differentiation ex vivo at Genes and cell-specific enhancers with known T cell function., Our results support 5hmC-mediated DNA de-methylation as a key component of CD4(+) T cell biology in Homo sapiens, with important implications for gene regulation and lineage commitment., 5hmC plays important roles in regulation of gene expression and differentiation and has been implicated in T cell malignancies and Autoimmune Diseases.[SEP]", "label": "yes"}
{"original_question": "Does fibronectin constitute a serum biomarker for Duchenne muscular dystrophy?", "id": "converted_1723", "sentence1": "Does Fibronectins constitute a serum biomarker for Duchenne muscular dystrophy?", "sentence2": "FN1 gene is a serum biomarker for Duchenne muscular dystrophy, There was a significant increase in Fibronectins levels in Muscular Dystrophy, Duchenne patients compared to age-matched controls. FN1 gene levels in patients with Becker muscular dystrophy, BETHLEM MYOPATHY 2, or Myasthenia Gravis were comparable to control levels. Progressive elevation in Fibronectins levels was observed in longitudinal samples from 22 Muscular Dystrophy, Duchenne patients followed up for a period of 6 months up to 4 years, This study suggests that serum Fibronectins levels may constitute a promising biomarker to monitor disease progression in Muscular Dystrophy, Duchenne patients, FN1 gene is a serum biomarker for Duchenne muscular dystrophy., Progressive elevation in Fibronectins levels was observed in longitudinal samples from 22 Muscular Dystrophy, Duchenne patients followed up for a period of 6 months up to 4 years.CONCLUSION AND CLINICAL RELEVANCE: This study suggests that serum Fibronectins levels may constitute a promising biomarker to monitor disease progression in Muscular Dystrophy, Duchenne patients., There was a significant increase in Fibronectins levels in Muscular Dystrophy, Duchenne patients compared to age-matched controls., Progressive elevation in Fibronectins levels was observed in longitudinal samples from 22 Muscular Dystrophy, Duchenne patients followed up for a period of 6 months up to 4 years., This study suggests that serum Fibronectins levels may constitute a promising biomarker to monitor disease progression in Muscular Dystrophy, Duchenne patients., Progressive elevation in Fibronectins levels was observed in longitudinal samples from 22 Muscular Dystrophy, Duchenne patients followed up for a period of 6 months up to 4 years. This study suggests that serum Fibronectins levels may constitute a promising biomarker to monitor disease progression in Muscular Dystrophy, Duchenne patients., This study suggests that serum Fibronectins levels may constitute a promising biomarker to monitor disease progression in Muscular Dystrophy, Duchenne patients. © 2014 The Authors PROTEOMICS - Clinical Applications Published by Wiley-VCH Verlag GmbH & Co., There was a significant increase in Fibronectins levels in Muscular Dystrophy, Duchenne patients compared to age-matched controls. FN1 gene levels in patients with Becker muscular dystrophy, BETHLEM MYOPATHY 2, or Myasthenia Gravis were comparable to control levels., FN1 gene levels in patients with Becker muscular dystrophy, BETHLEM MYOPATHY 2, or Myasthenia Gravis were comparable to control levels. Progressive elevation in Fibronectins levels was observed in longitudinal samples from 22 Muscular Dystrophy, Duchenne patients followed up for a period of 6 months up to 4 years., FN1 gene is a serum biomarker for Duchenne muscular dystrophy., This study suggests that serum Fibronectins levels may constitute a promising biomarker to monitor disease progression in Muscular Dystrophy, Duchenne patients.[SEP]Relations: BETHLEM MYOPATHY 2 has relations: disease_protein with Muscular Dystrophy, Duchenne, disease_protein with Muscular Dystrophy, Duchenne. Duchenne muscular dystrophy has relations: disease_protein with Muscular Dystrophy, Duchenne, disease_protein with Muscular Dystrophy, Duchenne.", "label": "yes"}
{"original_question": "Is Mammaprint approved by the United States Food and Drug Administration?", "id": "converted_1365", "sentence1": "Is Mammaprint approved by the United States Food and Drug Administration?", "sentence2": "an FDA-cleared 70-gene signature of MammaPrint panel , on MammaPrint, the first and only assay for Malignant neoplasm of breast management that has been cleared by the FDA., The MammaPrint assay has the advantages of a 510(k) clearance by the US Food and Drug Administration, a larger gene number which may enhance further utility, and the potentially wider patient eligibility including lymph node-positive, ER-negative, , The MammaPrint assay has the advantages of a 510(k) clearance by the U.S. Food and Drug Administration, a larger gene number, which may enhance further utility, and a potentially wider patient eligibility, including lymph node-positive, estrogen receptor (ER)-negative, and younger patients being accrued into the prospective trial (Microarray in Node-Negative Disease May Avoid Chemotherapy). [SEP]", "label": "yes"}
{"original_question": "Do conserved noncoding elements co-occur with matrix-attachment regions?", "id": "converted_1131", "sentence1": "Do conserved noncoding elements co-occur with matrix-attachment regions?", "sentence2": "We hypothesized that some of these regions might be matrix-scaffold attachment regions, Planet Mars (or S/Planet Mars). Planet Mars comprise one of the few classes of eukaryotic noncoding DNA with an experimentally characterized function, being involved in the attachment of chromatin location location to the Nuclear Matrix, chromatin location location remodeling and transcription regulation. To test our hypothesis, we analyzed the co-occurrence of predicted Planet Mars with highly conserved noncoding DNA regions in Homo sapiens-Mus sp. genomic alignments. We found that 11% of the conserved noncoding DNA consists of predicted Planet Mars. Conversely, more than half of the predicted Planet Mars co-occur with one or more independently identified conserved sequence blocks. An excess of conserved predicted Planet Mars is seen in Intergenic Region preceding 5' ends of Genes, suggesting that these Planet Mars are primarily involved in transcriptional control, A significant fraction of conserved noncoding DNA in Homo sapiens and Mus sp. consists of predicted matrix attachment regions., To test our hypothesis, we analyzed the co-occurrence of predicted Planet Mars with highly conserved noncoding DNA regions in Homo sapiens-Mus sp. genomic alignments., To test our hypothesis, we analyzed the co-occurrence of predicted Planet Mars with highly conserved noncoding DNA regions in Homo sapiens-Mus sp. genomic alignments[SEP]", "label": "yes"}
{"original_question": "Do de novo truncating mutations in WASF1 cause cancer?", "id": "converted_3284", "sentence1": "Do de novo truncating mutations in WASF1 gene cause cancer?", "sentence2": "De Novo Truncating Gene Mutation in WASF1 gene gene Cause Intellectual Disability with Seizures., Here, using exome sequencing and whole-genome sequencing, we identified three de novo truncating mutations in WASF2 gene (WASF1 gene gene) in five unrelated individuals with moderate to profound Intellectual Disability with autistic features and Seizures. WASF1 gene gene, also known as WAVE1, is part of the SCAR complex and acts as a mediator between Rac-GTPase and actin to induce actin polymerization. The three mutations connected by Matchmaker Exchange were c.1516C>T (p.Arg506Ter), which occurs in three unrelated individuals, c.1558C>T (p.Gln520Ter), and c.1482delinsGCCAGG (p.Ile494MetfsTer23). All three Variant are predicted to partially or fully disrupt the C-terminal actin-binding WCA domain. Functional studies using Fibroblasts from two affected individuals with the c.1516C>T mutation showed a truncated WASF1 gene gene and a defect in actin remodeling. This study provides evidence that de novo heterozygous mutations in WASF1 gene gene cause a rare form of Intellectual Disability.[SEP]", "label": "no"}
{"original_question": "Is verubecestat effective for Alzheimer’s Disease?", "id": "converted_3003", "sentence1": "Is verubecestat effective for Alzheimer’s Disease?", "sentence2": " The lack of efficacy of verubecestat in mild-to-moderate cytarabine/daunorubicin protocol raises important questions about the timing of intervention with BACE-1 inhibitors, and anti-amyloid therapies in general, in cytarabine/daunorubicin protocol treatment., This reaction was applied to the preparation of verubecestat, which is currently undergoing clinical evaluation for the treatment of ALZHEIMER DISEASE, FAMILIAL, 1., Verubecestat is an PPP1R1A gene of β-site amyloid precursor protein cleaving enzyme 1 (BACE1 protein, human protein, human) being evaluated in clinical trials for the treatment of ALZHEIMER DISEASE, FAMILIAL, 1. , CONCLUSIONS: Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 and was associated with treatment-related adverse events. , Randomized Trial of Verubecestat for Mild-to-Moderate Alzheimer's Disease.Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 and was associated with treatment-related adverse events. , CONCLUSIONS\nVerubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 and was associated with treatment-related adverse events., Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 and was associated with treatment-related adverse events.[SEP]", "label": "no"}
{"original_question": "Is cabergoline used for treatment of the Nelson's syndrome ?", "id": "converted_3936", "sentence1": "Is cabergoline used for treatment of the Nelson Syndrome ?", "sentence2": "Due to a rapid regrowth of the Neoplasms, the patient did not receive gamma-knife therapy and was treated with cabergoline and Somatostatin Assay analogue for some time. , Identification of D(2) receptors in corticotroph tumors led to clinical trials of cabergoline therapy in limited cases of Nelson Syndrome, ectopic ACTH-secreting tumors, and recently Pituitary-dependent Pituitary-dependent Cushing's disease (CD).,  In our observation cabergoline at 2 mg per week seems to be efficient after a 3 and a half years follow-up, in accordance with some recent publications. , Clinical and biochemical stabilization of Nelson Syndrome with long-term Low-Dose Treatment cabergoline treatment., We report the results of long-term (6-year) treatment of Nelson Syndrome with the long-acting dopamine Agonist, cabergoline, in a 55-year-old woman., This case demonstrates that long-term cabergoline treatment may be efficient in patients with Nelson Syndrome., Therefore, in addition to Prolactinoma, targets of dopamine Agonist therapy are somatotroph tumors, nonfunctioning Pituitary Neoplasms, corticotroph Pituitary Neoplasms, Nelson Syndrome, gonadotropinomas, and thyrotropin-secreting Pituitary Neoplasms., Nelson Syndrome: complete remission with cabergoline but not with bromocriptine or cyproheptadine treatment., The results obtained show for the first time that a long-term treatment with cabergoline also brings about a complete remission of Nelson Syndrome in the presence of a Pituitary macroadenoma., Complete remission of Nelson Syndrome after 1-year treatment with cabergoline., In this case report we demonstrated that treatment with the long-acting D2 receptor Agonist cabergoline for 1 year induced normalization of plasma ACTH levels and disappearance of the pituitary tumor in a patient with Nelson Syndrome. , This case demonstrated that cabergoline treatment is able to induce the remission of Nelson Syndrome and may be a valid therapeutic alternative in this syndrome., However, some preliminary data suggest a potential use of cabergoline in combination with ketoconazole, or alone, in selected cases of Pituitary-dependent Pituitary-dependent Cushing's disease or Nelson Syndrome., We report the results of long-term (6-year) treatment of Nelson Syndrome with the long-acting dopamine Agonist, cabergoline, in a 55-year-old woman. The, actinomas. Identification of D(2) receptors in corticotroph tumors led to clinical trials of cabergoline therapy in limited cases of Nelson Syndrome, ectopic ACTH-secreting tumors, and recently Cushing's diseas, In order to investigate on the direct effect played by cabergoline treatment on the remission of Nelson Syndrome, the treatment was withdrawn., lactinomas. Identification of D(2) receptors in corticotroph tumors led to clinical trials of cabergoline therapy in limited cases of Nelson Syndrome, ectopic ACTH-secreting tumors, and recently Pituitary-dependent Pituitary-dependent Cushing's disease (CD).OBJECTIVE: To evaluate the long-term efficacy of cabergoline monotherapy in patients with CD.METHODS: Retrospective analysis of non-randomized clinical therapy with cabergoline in 30 patients with CD treated in academic cente[SEP]", "label": "yes"}
{"original_question": "Is there increased incidence of incontinence in athletes?", "id": "converted_1335", "sentence1": "Is there increased incidence of Incontinence in athletes?", "sentence2": "Urinary tract tract Incontinence affects women of all ages, including top female athletes, but is often under-reported. The highest prevalence of Urinary tract tract Incontinence is reported in those participating in high impact sports., The prevalence of female stress Urinary tract tract Incontinence is high, and young adults are also affected, including athletes, especially those involved in \"high-impact\" sports, Analysis of these data suggests that perineal pressure is decreased in female athletes compared with nonathlete women. A lower perineal pressure correlates with increased symptoms of Urinary tract tract Incontinence and pelvic floor dysfunction., Urinary tract tract Incontinence is a prevalent condition among athletes that is not openly discussed., High-level sport appears to be a significant independent risk factor for Aortic Valve Insufficiency in healthy young women. , The prevalence of LUTS was 54.7%, and 30% for Urinary tract tract Incontinence., LUTS and Incontinence are prevalent in female athletes., A relationship between sport or fitness activities and Urinary tract tract Incontinence (UI) previously has been described in women. , studies have also shown a high prevalence of SUI in young, physically fit female athletes. , There was Urinary tract tract Incontinence in female long-distance runners and a correlation with Eating Disorders., young female athletes participating in high-impact sports may be at higher risk for Urinary tract tract Incontinence., Results indicated that more than 25% of those completing surveys experienced Incontinence and that more than 90% had never told anyone about their problem and had no knowledge of preventive measures; 16% reported Incontinence negatively impacted their quality of life., There is a very high prevalence of Urinary tract tract Incontinence in women athletes., Women athletes should be counseled about the increased risk of Urinary tract tract Incontinence with ultra high-impact sports and Eating Disorders., Stress Urinary tract tract Incontinence is a barrier to women's participation in sport and fitness activities and, therefore, it may be a threat to women's health, self-esteem and well-being. The prevalence during sports among young, nulliparous elite athletes varies between 0% (golf) and 80% (trampolinists). The highest prevalence is found in sports involving high impact activities such as gymnastics, track and field, and some ball games, Urinary tract tract leakage is common among elite athletes and dancers, particularly during training, but also during daily life activities., There is a high prevalence of stress and urge Incontinence in female elite athletes. The frequency of SUI and urge Incontinence was significantly higher in eating disordered athletes compared with healthy athletes., High impact sports activities may produce Urinary tract tract Incontinence., Urinary tract tract Incontinence during physical stresses is common in young nulliparous wome, Incontinence during physical stresses is common in young, highly fit, nulliparous women.[SEP]Relations: Urinary tract Incontinence has relations: phenotype_phenotype with Stress Urinary tract Incontinence, phenotype_phenotype with Stress Urinary tract Incontinence.", "label": "yes"}
{"original_question": "Is c-met involved in the activation of the Akt pathway?", "id": "converted_61", "sentence1": "Is c-met involved in the activation of the Proto-Oncogene Proteins c-akt pathway?", "sentence2": "Amplification of methionine has been reported in approximately 5%-22% of Lung Neoplasms with acquired resistance to small-molecule inhibitors of the Epidermal Growth Factor Receptor (EGFR). Resistance to HER1 Antagonists is likely mediated through downstream activation of the phosphoinositide 3-kinase /AKT pathway., Simultaneous treatment of resistant tumors with a methionine PPP1R1A gene plus an EGFR PPP1R1A gene can abrogate activation of downstream effectors of cell growth, proliferation, and survival, thereby overcoming acquired resistance to HER1 Antagonists., Hepatocyte Growth Factor mediated both Mitogen-Activated Protein Kinases and Proto-Oncogene Proteins c-akt phosphorylation., Mitogen-Activated Protein Kinases/Proto-Oncogene Proteins c-akt signaling, but not the Smad pathway, may be one of the main processes in Hepatocyte Growth Factor-induced EMT,, The MAPK/Proto-Oncogene Proteins c-akt pathway is indispensable in Hepatocyte Growth Factor/c-Met signaling., Inhibition of c-Met activation sensitizes osteosarcoma cells to cisplatin via suppression of the 1-Phosphatidylinositol 3-Kinase-Proto-Oncogene Proteins c-akt signaling, Specifically, we demonstrated that inhibition of c-Met activity led to suppression of the 1-Phosphatidylinositol 3-Kinase-Proto-Oncogene Proteins c-akt pathway, thus enhancing cisplatin chemosensitivity., Our study clearly suggests that inhibition of c-Met activity can effectively sensitize osteosarcoma cells to cisplatin via suppression of the 1-Phosphatidylinositol 3-Kinase-Proto-Oncogene Proteins c-akt signaling., We found that a dual Met/VEGF receptor 2 kinase PPP1R1A gene, c-Met/VEGFR-2 Kinase Inhibitor c-Met/VEGFR-2 Kinase Inhibitor E7050, circumvented Hepatocyte Growth Factor-induced EGFR-TKI resistance in EGFR mutant Primary malignant neoplasm of lung cell lines by inhibiting the Met/Gab1/1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt pathway in vitro., Here, we report that i) treatment of RL95-2 cells with Hepatocyte Growth Factor resulted in phosphorylation of the Hepatocyte Growth Factor receptor c-Met, activation of Proto-Oncogene Proteins c-akt and IκB, translocation of NF-κB into the Cell Nucleus, and up-regulation of PTGS2 wt Allele mRNA;, Our data suggest that Hepatocyte Growth Factor possesses chemotactic ability, has anti-apoptosis action, and induces cellular infiltration via the 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt pathway;, Hepatocyte growth factor-induced SRC wt Allele-Phosphatidylinositol 3-Kinases-AKT-Mammals target of sirolimus pathway inhibits Antigen-Presenting Cells activation by blocking MAP Kinase Kinase Kinase activity, Activation of SRC wt Allele in turn establishes a complex consisting of Phosphatidylinositol 3-Kinases and c-methionine, and promotes downstream activation of the Phosphatidylinositol 3-Kinases/AKT pathway and Mammals target of sirolimus., Notably, hepatocyte growth factor-stimulated SRC wt Allele activation results in induction of Phosphatidylinositol 3-Kinases complexes p85α/p110α and p85α/p110δ, which is required for activation of Mammals target of sirolimus, and consequent inhibition of MAP Kinase Kinase Kinase and nuclear factor-κB activation., Our findings, for the first time, have identified the SRC wt Allele-Phosphatidylinositol 3-Kinases-AKT-Mammals target of sirolimus pathway that plays a pivotal role in mediating the inhibitory effects of hepatocyte growth factor on Antigen-Presenting Cells activation by blocking nuclear factor-κB signaling., CCN1 wt Allele siRNA inhibited a second phase of Proto-Oncogene Proteins c-akt phosphorylation measured 12 hours after cell stimulation with Hepatocyte Growth Factor and also inhibited Hepatocyte Growth Factor-induced phosphorylation of the Proto-Oncogene Proteins c-akt target glycogen synthase kinase 3alpha., Hepatocyte Growth Factor+epidermal growth factor treatment increased the duration of ERK1/2 and AKT activation compared to Hepatocyte Growth Factor or epidermal growth factor alone. All these data indicate that a crosstalk between the epidermal growth factor and Hepatocyte Growth Factor pathways in mammary epithelial cells may modulate the development of the Mammary gland., Hepatocyte growth factor and c-Met promote dendritic maturation during hippocampal neuron differentiation via the Proto-Oncogene Proteins c-akt pathway, Consistent with these results, Hepatocyte Growth Factor activated Proto-Oncogene Proteins c-akt, which phosphorylates glycogen synthase kinase-3beta (glycogen synthase kinase 3 beta) to inactivate it, and reduced phosphorylation of Microtubule-Associated Protein 2 (METAP2 gene), which can promote Microtubules polymerization and Dendrites elongation when dephosphorylated., Conversely, pharmacological inhibition of c-Met with its specific PPP1R1A gene, PHA 665752, or genetic knock-down of c-Met with short hairpin RNAs (shRNAs) suppressed Hepatocyte Growth Factor-induced phosphorylation of Proto-Oncogene Proteins c-akt and glycogen synthase kinase 3 beta, increased phosphorylation of METAP2 gene, and reduced Dendrites number and length in cultured hippocampal Neurons., Inhibiting Proto-Oncogene Proteins c-akt activity with the phosphoinositide-3-kinase PPP1R1A gene LY 294002 or Proto-Oncogene Proteins c-akt PPP1R1A gene X suppressed Hepatocyte Growth Factor-induced phosphorylation of glycogen synthase kinase 3 beta, increased METAP2 gene phosphorylation, and blocked the ability of Hepatocyte Growth Factor to enhance dendritic length., These observations indicate that Hepatocyte Growth Factor and c-Met can regulate the early stages of Dendrites maturation via activation of the Proto-Oncogene Proteins c-akt/glycogen synthase kinase 3 beta pathway., Involvement of 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt signaling pathway in hepatocyte growth factor-induced migration of uveal melanoma cells, Hepatocyte Growth Factor was found to enhance cell migration, and that Hepatocyte Growth Factor-induced migration depends on 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt pathway. The activation of 1-Phosphatidylinositol 3-Kinase/Proto-Oncogene Proteins c-akt pathway induced by the Hepatocyte Growth Factor/c-Met axis is involved in the downregulation of cell adhesion molecules E-Cadherin and CTNNB1 gene, contributing to the attenuation of cell-cell adhesion and promoting the enhanced motility and migration of uveal melanoma cells., Hepatocyte Growth Factor protects cultured cortical Neurons against hypoxia/reoxygenation induced cell injury via ERK1/2 and Pulmonary Valve Insufficiency-3K/Proto-Oncogene Proteins c-akt pathways, Hepatocyte Growth Factor stimulated both ERK1/2 and Proto-Oncogene Proteins c-akt activities in cortical Neurons., Inhibition of Mitogen-Activated Protein Kinases activation completely abolished the protective effects of Hepatocyte Growth Factor, and inhibition of Proto-Oncogene Proteins c-akt activation reduced, but did not completely eliminate the Hepatocyte Growth Factor mediated neuroprotection., It is suggested that the neuroprotection of Hepatocyte Growth Factor depend on ERK1/2 pathway, and, to a lesser extent, Pulmonary Valve Insufficiency-3K/Proto-Oncogene Proteins c-akt pathway. , Met signals hepatocyte survival by preventing Fas-triggered CFLAR wt Allele degradation in a PI3k-Proto-Oncogene Proteins c-akt-dependent manner, Thus, Met acting on 1-Phosphatidylinositol 3-Kinase and Proto-Oncogene Proteins c-akt ensures high levels of FLIPL, and disruption of this pathway contributes to hepatic apoptosis and possibly to Fas-related liver diseases., The Hepatocyte Growth Factor-induced increase in Nkx 2.5 expression was inhibited by co-treatment with the PI3 kinase inhibitors Wortmannin and LY 294002, but not by its inactive homolog LY 303511, suggesting an involvement of the PI3 kinase/Proto-Oncogene Proteins c-akt pathway in this effect., X-Linked PPP1R1A gene of apoptosis protein expression level in Malignant neoplasm of colon and/or rectum is regulated by hepatocyte growth factor/C-met pathway via Proto-Oncogene Proteins c-akt signaling, Activation of XIAP gene gene expression by Hepatocyte Growth Factor was inhibited by siRNA targeting AKT1 protein, human and AKT2 protein, human., Activation of methionine wt Allele enhances XIAP gene gene through the Proto-Oncogene Proteins c-akt pathway., Hepatocyte growth factor prevents ventricular remodeling and dysfunction in CASP14 gene via Proto-Oncogene Proteins c-akt pathway and angiogenesis, A significant reduction in apoptosis in the Hepatocyte Growth Factor-treated hearts was observed compared with control hearts, and was strongly associated with increased Proto-Oncogene Proteins c-akt activation., The antiapoptotic effect of Hepatocyte Growth Factor was mediated by activation of PI3-kinase/Proto-Oncogene Proteins c-akt pathway., The protective effect of Hepatocyte Growth Factor/SF against the ADR-induced apoptosis was abolished in the presence of either LY 294002, an PPP1R1A gene of phosphatidylinositols-3'-OH kinase (PI3-K) or 1L-6-hydroxymethyl-chiro-inositol 2-(R)-2-O-methyl-3-O-octadecylcarbonate, an PPP1R1A gene of Proto-Oncogene Proteins c-akt, thus implicating the activation of PI3-K-Proto-Oncogene Proteins c-akt signaling in the antiapoptotic action of Hepatocyte Growth Factor/SF., Immunoblotting analysis revealed that Hepatocyte Growth Factor/SF stimulated the sustained phosphorylation of Proto-Oncogene Proteins c-akt for several hours, Furthermore, ADR-induced activation of caspase-9, a downstream molecule of Proto-Oncogene Proteins c-akt, was inhibited for at least 24 h after Hepatocyte Growth Factor/SF stimulation,, These results indicate that Hepatocyte Growth Factor/SF, but not epidermal growth factor, transmitted protective signals against ADR-induced apoptosis by causing sustained activation of the PI3-K-Proto-Oncogene Proteins c-akt signaling pathway., Hepatocyte growth factor/scatter factor inhibits UVB-induced apoptosis of human keratinocytes but not of keratinocyte-derived cell lines via the Phosphatidylinositol 3-Kinases/AKT pathway, When we analyzed the signaling pathways initiated by the Hepatocyte Growth Factor/SF receptor c-met, we found that the phosphatidylinositols (Pulmonary Valve Insufficiency) 3-kinase and its downstream-element AKT and the mitogen-activated protein (MAP) kinase were activated., Inhibition of Pulmonary Valve Insufficiency 3-kinase led to a complete abrogation of the anti-apoptotic effect of Hepatocyte Growth Factor/SF, whereas blockade of the MAP kinase pathway had no effect., We now show in detached cells a cooperative effect of Hepatocyte Growth Factor and FN1 wt Allele in the activation of Pulmonary Valve Insufficiency 3-kinase and on the phosphorylation of PKB/Proto-Oncogene Proteins c-akt at serine 473., Pulmonary Valve Insufficiency 3-kinase activity is also required for the Hepatocyte Growth Factor- and fibronectin-induced survival responses, as well as anchorage-independent colony growth., Together, these results demonstrate that the Pulmonary Valve Insufficiency 3-kinase/Proto-Oncogene Proteins c-akt pathway is a key effector of the Hepatocyte Growth Factor- and fibronectin-induced survival response of breast carcinoma cells under detached conditions and corroborate an interaction between Integrins and Hepatocyte Growth Factor/ Met signalling pathways in the development of invasive breast cancer.[SEP]Relations: Epidermal Growth Factor Receptor binding has relations: molfunc_protein with epidermal growth factor, molfunc_protein with epidermal growth factor. METAP2 has relations: anatomy_protein_present with Mammary gland, anatomy_protein_present with Mammary gland. Microtubules associated complex has relations: cellcomp_protein with METAP2 gene, cellcomp_protein with METAP2 gene. Cisplatin has relations: drug_drug with Wortmannin, drug_drug with Wortmannin. Mammary gland has relations: anatomy_protein_present with Hepatocyte Growth Factor, anatomy_protein_present with methionine, anatomy_protein_present with METAP2 gene, anatomy_protein_present with epidermal growth factor, anatomy_protein_present with Hepatocyte Growth Factor, anatomy_protein_present with methionine, anatomy_protein_present with METAP2 gene, anatomy_protein_present with epidermal growth factor. Microtubules has relations: cellcomp_protein with METAP2 gene, cellcomp_protein with METAP2 gene. PPP1R1A has relations: anatomy_protein_present with Mammary gland, anatomy_protein_present with Mammary gland. Dendrites has relations: cellcomp_protein with METAP2 gene, cellcomp_protein with METAP2 gene. malignant colon neoplasm has relations: disease_disease with Malignant neoplasm of colon and/or rectum, disease_disease with Malignant neoplasm of colon and/or rectum. Sirolimus has relations: drug_drug with Wortmannin, drug_drug with Wortmannin. CTNNB1 has relations: protein_protein with methionine, protein_protein with epidermal growth factor, protein_protein with Hepatocyte Growth Factor, cellcomp_protein with Cell Nucleus, disease_protein with Primary malignant neoplasm of lung, disease_protein with Malignant neoplasm of colon and/or rectum, anatomy_protein_present with Mammary gland, protein_protein with methionine, protein_protein with epidermal growth factor, protein_protein with Hepatocyte Growth Factor, cellcomp_protein with Cell Nucleus, disease_protein with Primary malignant neoplasm of lung, disease_protein with Malignant neoplasm of colon and/or rectum, anatomy_protein_present with Mammary gland. lung neoplasm has relations: disease_protein with methionine, disease_disease with Primary malignant neoplasm of lung, disease_protein with methionine, disease_disease with Primary malignant neoplasm of lung.", "label": "yes"}
{"original_question": "Are mutations in the STXBP1 gene associated with epilepsy?", "id": "converted_1729", "sentence1": "Are mutations in the STXBP1 gene Genes associated with Epilepsy?", "sentence2": "leucovorin responsive Epilepsy in Ohtahara syndrome caused by STXBP1 gene Genes Mutation Abnormality., A novel Mutation Abnormality in STXBP1 gene Genes Genes in a child with epileptic Encephalopathies and an atypical electroclinical pattern., Gene Mutation in STXBP1 gene Genes Genes, encoding the syntaxin binding protein 1, have been recently described in Ohtahara syndrome, or early infantile epileptic Encephalopathies with suppression-burst pattern, and in other early-onset epileptic encephalopathies., STXBP1 gene Genes (MUNC18.1), encoding syntaxin binding protein 1, has been reported in Ohtahara syndrome, a rare epileptic Encephalopathies with suppression burst pattern on EEG, in patients with Infantile Spasm and in a few patients with nonsyndromic mental retardation without Epilepsy. , ed with severe developmental delay and poor prognosis. Gene Mutation and Gene Deletion in the STXBP1 gene Genes Genes are associated with Ohtahara syndrome, also known as \"early infantile epileptic Encephalopathies, Here we show that de novo heterozygous mutations in the Genes encoding STXBP1 gene Genes, also known as MUNC18-1, which is essential in Synaptic Vesicles release in multiple species, cause OS, STXBP1 gene Genes haploinsufficiency results in progressive Encephalopathies characterized by Intellectual Disability and may be accompanied by Epilepsy, Movement Disorders, and Autistic Disorder. , Gene Mutation of the syntaxin binding protein 1 (STXBP1 gene Genes) have been associated with severe infantile epileptic encephalopathies (Ohtahara syndrome and West Syndrome), but also with moderate to severe No No cognitive impairment and nonsyndromic Epilepsy., A novel STXBP1 gene Genes Mutation Abnormality causes focal Seizures with neonatal onset., STXBP1 gene Genes mutations in early infantile epileptic Encephalopathies with suppression-burst pattern., e novo STXBP1 gene Genes mutations have been found in individuals with early infantile epileptic Encephalopathies with suppression-burst pattern (EIEE), Gene Mutation in STXBP1 gene Genes are relatively frequent in patients with infantile epileptic encephalopathies. STXBP1 gene Genes-related Encephalopathies may present as drug-responsive Infantile Spasm with focal/lateralized discharges., De novo SCN1A gene Genes mutations in migrating partial Seizures of infancy., De novo mutations in the Genes encoding STXBP1 gene Genes (MUNC18-1) cause early infantile epileptic Encephalopathies., Gene Mutation in STXBP1 gene Genes have been identified in a subset of patients with early onset epileptic Encephalopathies (Eosinophilic esophagitis), but the full phenotypic spectrum remains to be delineated, and STXBP1 gene Genes-related West/Ohtahara syndromes, are due to a Mutation Abnormality in a unique Genes., This is the first case report showing that STXBP1 gene Genes mutations caused West Syndrome from the onset of Epilepsy. [SEP]Relations: Infantile spasms has relations: disease_phenotype_positive with West Syndrome, disease_phenotype_positive with West Syndrome.", "label": "yes"}
{"original_question": "Are Spinal Intradural Primary Malignant Peripheral Nerve Sheath Tumors(MPNST) rare in neurofibromatosis patients?", "id": "converted_3337", "sentence1": "Are Spinal Intradural Primary Malignant Peripheral Nerve Sheath Tumors(Malignant Peripheral Nerve Sheath Tumor) rare in NF1 gene patients?", "sentence2": "Spinal intradural primary malignant peripheral nerve sheath tumors (Malignant Peripheral Nerve Sheath Tumor) are rare in patients without NF1 gene., Primary malignant peripheral nerve sheath tumors (MPNSTs) are extremely rare in patients without a history of NF1 gene; only 18 cases have been reported in the English-language literature to this point.[SEP]", "label": "no"}
{"original_question": "Is Cabotegravir effective for HIV prevention?", "id": "converted_4240", "sentence1": "Is Cabotegravir effective for HIV Infections prevention?", "sentence2": "A new paradigm for antiretroviral delivery: long-acting cabotegravir and rilpivirine for the treatment and prevention of HIV Infections Infections., PURPOSE OF REVIEW: Cabotegravir (Carbonic Anhydrase 1 (enzyme), Human) and rilpivirine (RPV) is the first long-acting injectable antiretroviral therapy (ART) option approved for virologically suppressed adults with HIV Infections Infections-1. In addition, long-acting Carbonic Anhydrase 1 (enzyme), Human is a promising agent for HIV Infections Infections preexposure prophylaxis (HIV Infections Infections: HIV Infections: PrEP and PEP and PEP). , SUMMARY: Clinical trial results support the use of long-acting Carbonic Anhydrase 1 (enzyme), Human for HIV Infections Infections HIV Infections Infections: HIV Infections: PrEP and PEP and PEP and long-acting Carbonic Anhydrase 1 (enzyme), Human and RPV as a switch strategy for adults with HIV Infections Infections-1 who are first virologically suppressed with oral ART. , OBJECTIVE: We had previously shown that long-acting cabotegravir (Carbonic Anhydrase 1 (enzyme), Human-Latex Fixation Tests) injections fully protected Macaca from vaginal simian HIV Infections Infections (SHIV) infection., The Potential Impact of Long-Acting Cabotegravir for HIV Infections Infections Prevention in South Africa: A Mathematical Modeling Study.,  Long-acting cabotegravir (Carbonic Anhydrase 1 (enzyme), Human Latex Fixation Tests) is a potential new injectable formulation for Human immunodeficiency virus antigen (HIV Infections Infections) HIV Infections Infections: HIV Infections: PrEP and PEP and PEP being tested in phase III trials., Design and Testing of a Cabotegravir Implant for HIV Infections Infections Prevention., Cabotegravir and rilpivirine long-acting injectable antiretroviral therapy for the treatment of HIV Infections Infections-1 infection brings promise of a new mode of delivery and potential solutions to some problems of oral therapy, but also new challenges and unanswered questions., Cabotegravir is an investigational HIV Infections Infections Integrase Inhibitor in development for the treatment and pre-exposure prophylaxis of HIV Infections Infections-1 infection., Bictegravir, cabotegravir, dolutegravir, elvitegravir, and raltegravir are members of the latest class of antiretrovirals available to treat Human immunodeficiency virus antigen (HIV Infections Infections) infection, the integrase strand transfer inhibitors., PURPOSE OF REVIEW: Long-acting cabotegravir may provide a novel therapeutic option for both the treatment and prevention of HIV Infections Infections-1 infection that does not necessitate adherence, Long-acting injectable cabotegravir for the prevention of Human immunodeficiency virus II infection, BACKGROUND: The HIV Infections Infections Prevention Trials Network (HPTN) 083 trial demonstrated that long-acting cabotegravir (Carbonic Anhydrase 1 (enzyme), Human-Latex Fixation Tests) was more effective than tenofovir disoproxil fumarate-emtricitabine (TDF/FTC) in preventing Human immunodeficiency virus antigen (HIV Infections Infections) in cisgender men and transgender women who have sex with, Areas covered: Here, we review trials of cabotegravir (Carbonic Anhydrase 1 (enzyme), Human) as treatment of HIV Infections Infections-1 infection and its potential use as pre-exposure prophylaxis (HIV Infections Infections: HIV Infections: PrEP and PEP and PEP) in high risk individuals, including issues around oral lead in and potential resistance emergence. Exper, frequent dosing. This review focuses on the potential benefits and considerations for the study and use of 2 long-acting injectable agents, cabotegravir (GSK1265744LA, Carbonic Anhydrase 1 (enzyme), Human Latex Fixation Tests) and rilpivirine (TMC278LA, RPV Latex Fixation Tests), for use as chemoprophylaxis for HIV Infections Infections , An evaluation of cabotegravir for HIV Infections Infections treatment and prevention., Cabotegravir long-acting for HIV Infections Infections-1 prevention., Our findings suggest that cabotegravir should be evaluated in clinical trials as a potential option for antiretroviral therapy and preexposure prophylaxis in HIV Infections Infections-2-prevalent settings., Profile of cabotegravir and its potential in the treatment and prevention of HIV Infections Infections-1 infection: evidence to date., Long-Acting Cabotegravir for HIV Infections Infections/AIDS Prophylaxis., Cabotegravir for HIV Infections Infections Prevention in Cisgender Men and Transgender Women., Cabotegravir is a novel Human immunodeficiency virus antigen integrase enzyme inhibitor used for prevention and treatment of Human immunodeficiency virus II infection., PURPOSE OF REVIEW: Long-acting cabotegravir may provide a novel therapeutic option for both the treatment and prevention of HIV Infections Infections-1 infection that does not necessitate adherence , Cabotegravir in the treatment and prevention of Human Immunodeficiency Virus-1., Cabotegravir: its potential for antiretroviral therapy and preexposure prophylaxis., Satisfaction and acceptability of cabotegravir long-acting injectable suspension for prevention of HIV Infections Infections: Patient perspectives from the ECLAIR trial.[SEP]", "label": "yes"}
{"original_question": "Has proteomics been used in the study of the dry eye syndrome?", "id": "converted_1589", "sentence1": "Has proteomics been used in the study of the dry eye syndrome?", "sentence2": "Tear proteomic analysis of patients with type 2 diabetes and dry eye syndrome by two-dimensional nano-liquid chromatography coupled with tandem mass spectrometry., Dry Eye Syndromes in diabetic patients is associated with aberrant expression of tear proteins, and the findings could lead to identification of novel pathways for therapeutic targeting and new diagnostic markers.,  2D electrophoresis (2DE) and Differential gel electrophoresis (DIGE) was done to identify differentially expressed proteins. , Two dimensional electrophoretic analysis of Homo sapiens tears: collection method in dry eye syndrome., Identification of tear fluid biomarkers in dry eye syndrome using iTRAQ quantitative proteomics., This study demonstrated that iTRAQ technology combined with 2D-nanoLC-nanoESI-MS/MS quantitative proteomics is a powerful tool for biomarker discovery.[SEP]", "label": "yes"}
{"original_question": "Is HbA1c an ideal biomarker of well-controlled diabetes?", "id": "converted_3916", "sentence1": "Is Glycosylated hemoglobin A an ideal biomarker of well-controlled Diabetes Mellitus?", "sentence2": "Glycosylated hemoglobin A is a biomarker with a central role in the diagnosis and follow-up of patients with Diabetes Mellitus, although not a perfect one. Common comorbidities encountered in patients with Diabetes Mellitus mellitus, such as Kidney Failure, high output states (iron deficiency anaemia, Anemia, Hemolytic, Hemoglobinopathies and pregnancy) and intake of specific drugs could compromise the sensitivity and specificity of the biomarker. COVID-19 pandemic poses a pressing challenge for the diabetic population, since maintaining optimal blood glucose control is key to reduce morbidity and mortality rates.[SEP]", "label": "no"}
{"original_question": "Are immune cells affected in Amyotrophic Lateral Sclerosis?", "id": "converted_1535", "sentence1": "Are immune cells affected in Amyotrophic Lateral Sclerosis?", "sentence2": "Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to cyclophosphamide/prednisone activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived Specimen Source Codes - Macrophages and Foxp3(+) regulatory Therapeutic gamma delta T-lymphocytes, and elevation of the neurotrophic factors Insulin-Like Growth Factor I and Glial Cell Line-Derived Neurotrophic Factor in the diseased Spinal Cord parenchyma, Immunization with a Myelin-Derived Antigen Activates the Brain's Choroid Plexus for Recruitment of Immunoregulatory Cells to the Central Nervous System and Attenuates Disease Progression in a Mouse Model of ALS., Amyotrophic lateral sclerosis (ALS) is a rapidly progressing fatal Neurodegenerative Disorders characterized by the selective death of Neurons, Efferent (MNSs Blood-Group System) in the Spinal Cord, and is associated with local neuroinflammation., T-lymphocyte deficiency increases Neuronal loss in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, while boosting T-Lymphocyte levels reduces it., As disease accelerates, a shift occurs from beneficial immune responses (involving M2 Microglia and Regulatory T-Lymphocytes) to deleterious immune responses (involving M1 Microglia and T-helper cell type 1). In this review, we underscore the importance of immune-mediated mechanisms in the pathogenesis of ALS and discuss the alterations and distinct phenotypes of immune cells at the different stages of disease.,  Immunological disturbances have been implicated in the pathogenesis of Amyotrophic Lateral Sclerosis (ALS). Recombinant Chemokine are involved in the recruitment of immune cells., The immune system has been found to be involved with positive and negative effects in the nervous system of Amyotrophic Lateral Sclerosis (ALS) patients. In general, Therapeutic gamma delta T-lymphocytes, B-Lymphocytes, Natural Killer Cells, mast cell, Specimen Source Codes - Macrophages, Dendritic Cells, Microglia, Antibodies, in vitro diagnostic, complement and Recombinant Cytokines participate in limiting damage., Immunological disturbances have been implicated in the pathogenesis of Amyotrophic Lateral Sclerosis (ALS). Recombinant Chemokine are involved in the recruitment of immune cells., We propose the following mechanism for the effect of Mesenchymal Stem Cells (cyclic nucleotide-gated mechanosensitive ion channel activity) administered intrathecally in Amyotrophic Lateral Sclerosis (ALS): cyclic nucleotide-gated mechanosensitive ion channel activity increase infiltration of peripheral immune cells into Central Nervous System and skew the infiltrated immune cells toward regulatory T lymphocytes (Treg ) and Th2 lymphocytes., Immune Cell infiltration to the brain&apos;s territory was considered for decades to reflect a pathological process in which immune cells attack the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Central Nervous System); such a process is observed in the inflammatory autoimmune disease, Multiple Sclerosis (MS).[SEP]Relations: Spinal Cord has relations: anatomy_protein_present with cyclophosphamide/prednisone, anatomy_protein_present with cyclophosphamide/prednisone. glial cell-derived neurotrophic factor receptor binding has relations: molfunc_protein with Glial Cell Line-Derived Neurotrophic Factor, molfunc_protein with Glial Cell Line-Derived Neurotrophic Factor. Neuronal loss in CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS has relations: disease_phenotype_positive with Amyotrophic Lateral Sclerosis, disease_phenotype_positive with Amyotrophic Lateral Sclerosis. CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS has relations: anatomy_protein_present with cyclophosphamide/prednisone, anatomy_protein_present with cyclophosphamide/prednisone.", "label": "yes"}
{"original_question": "Do R-loops tend to form at sites of DNA replication?", "id": "converted_949", "sentence1": "Do R-loops tend to form at Site of DNA replication?", "sentence2": "Escherichia coli 2 2 rnhA Mutant devoid of Pancreatic ribonuclease HI exhibit constitutive stable DNA replication, cSDR, which is thought to be initiated from R-loops stabilized in the absence of Pancreatic ribonuclease HI., We propose that the organized structure of the R-Loop Structures is critical for Oligonucleotide Primers RNA function in vivo with important implications for the RNA processing and DNA replication machinery., The precursor Oligonucleotide Primers RNA exists as a persistent RNA-DNA hybrid, known as an R-Loop Structures, formed during transcription through the replication origin (Xu, B., and Clayton, D. A. (1996) EMBO J. 15, 3135-3143)., We found that overproduction of RecG protein drastically decreased copy numbers of ColE1-type Plasmids, which require R-Loop Structures formation between the template DNA and a Oligonucleotide Primers RNA transcript (RNA II) for the initiation of replication., These results suggest that overproduced RecG inhibits the initiation of replication by prematurely resolving the R-loops formed at the replication origin region of these Plasmids with its unique helicase activity. The possibility that RecG regulates the initiation of a unique mode of DNA replication, oriC-independent constitutive stable DNA replication, by its activity in resolving R-loops is discussed., We propose that downstream of a replication block, RNA at R-loops is extended by deoxyribonucleic polymerase I activity, opening up the DNA duplex and leading to the recruitment of the replisome. This would allow replication to proceed while the original block is repaired or bypassed, Furthermore, increased RNaseH expression significantly alleviated genomic instability in deficient Specimen Source Codes - Fibroblasts suggesting that cotranscriptional R-loops formation contributes to the genesis of replication-dependent DSBs in these Cells., Transcription is an important source of replicative stress and consequently, maintenance of Genome - anatomical entity integrity requires the protection of chromosomes from the deleterious effects arising from the interaction between nascent RNA and template DNA, leading to stable DNA-RNA hybrids (R-Loop Structures) formation., Strikingly, we found that attenuation of replication strongly suppresses R-Loop Structures-mediated DNA rearrangements in both E. coli and HeLa Cells., More importantly, we then show that R-Loop Structures formation causes DNA replication Orthopedic Fork stalling, and that this in fact underlies the effects of R loops on genomic stabilit, R-Loop Structures-mediated genomic instability is caused by impairment of replication Orthopedic Fork progression, When any of these processes are not properly coordinated, aberrant outcomes such as Orthopedic Fork reversal and R-Loop Structures formation arise and trigger unscheduled recombinogenic events and Genome - anatomical entity rearrangements. , Many studies show that Cells can manage R loop formation with efficiency, and can also process the R-loops already formed in the \"U\" lymphocyte, and by which, the bad effects of R-loops on DNA replication, TAF1 Gene Mutation and homologous recombination can be regulated., Here we propose that physiological R-Loop Structures formation at CpG island promoters can contribute to DNA replication origin specification at these regions, the most efficient replication initiation Site in mammalian Cells. , In agreement with this, we found that R-loops co-localize with the origin recognition complex location within the same CpG island region in a significant fraction of these efficient replication origins, precisely at the Positioning Attribute displaying the highest density of G4 motifs. , connection between transcription and replication in Human Cells and suggests that R-Loop Structures dysregulation at CpG island promoter-origins might contribute to the phenotype of DNA replication abnormalities and loss of Genome - anatomical entity integrity detected in Tumor Cells, malignant., We show that RNA:DNA hybrids (R-loops) form at Site of transcription/replication collisions and that Pancreatic ribonuclease H1 functions to suppress Chronic Fatigue Syndrome instability., R-loops and initiation of DNA replication in Human Cells: a missing link?, Stable RNA-DNA hybrids (R-loops) prime the initiation of replication in Escherichia coli 2 2 Cells., We propose that downstream of a replication block, RNA at R-loops is extended by deoxyribonucleic polymerase I activity, opening up the DNA duplex and leading to the recruitment of the replisome., Immediately after Communicable Diseases, RNA-DNA hybrids (R-loops) occur on (at least some) replication origins, with the annealed RNA serving as a Oligonucleotide Primers for leading-strand synthesis in one direction., Here we propose that physiological R-Loop Structures formation at CpG island promoters can contribute to DNA replication origin specification at these regions, the most efficient replication initiation Site in mammalian Cells., Plasmid ColE1 origins of replication and oriK Site initiate primosome complex complex assembly by an RNA-DNA hybrid structure known as R-Loop Structures., This scenario builds on the connection between transcription and replication in Human Cells and suggests that R-Loop Structures dysregulation at CpG island promoter-origins might contribute to the phenotype of DNA replication abnormalities and loss of Genome - anatomical entity integrity detected in Tumor Cells, malignant., The multiple cleavage Site on the R-Loop Structures substrate match the priming Site observed in vivo, suggesting that Pancreatic ribonuclease MRP alone is capable of generating virtually all of the leading-strand replication primers., Mechanisms of Oligonucleotide Primers RNA synthesis and D-loop/R-Loop Structures-dependent DNA replication in Escherichia coli 2 2., Alternative oriC-independent modes of replication initiation are possible, one of which is constitutive stable DNA replication (cSDR) from transcription-associated RNA-DNA hybrids or R-loops., Our results suggest that TOP1 protein, human execute this function by suppressing the formation of DNA-RNA hybrids during transcription, these so-called R-loops interfering with the progression of replication forks., Critical role of R-loops in processing replication blocks., The possibility that RecG regulates the initiation of a unique mode of DNA replication, oriC-independent constitutive stable DNA replication, by its activity in resolving R-loops is discussed., Competition between the RNA transcript and the nontemplate DNA strand during R-Loop Structures formation in vitro: a nick can serve as a strong R-Loop Structures initiation site., More importantly, we then show that R-Loop Structures formation causes DNA replication Orthopedic Fork stalling, and that this in fact underlies the effects of R loops on genomic stability. , Consistent with this hypothesis, the 3' ends of the Mitochondrial Inheritance R-Loop Structures formed by in vitro transcription are located close to the initiation Site of the Mitochondrial Inheritance DNA replication. , A hybrid G-quadruplex structure formed between RNA and DNA explains the extraordinary stability of the Mitochondrial Inheritance R-Loop Structures., Previous studies have shown that the newly synthesized primers form a stable and persistent RNA-DNA hybrid, a R-Loop Structures, near the leading-strand origin of DNA replication. , Escherichia coli 2 2 rnhA Mutant devoid of Pancreatic ribonuclease HI exhibit constitutive stable DNA replication, cSDR, which is thought to be initiated from R-loops stabilized in the absence of Pancreatic ribonuclease HI. [SEP]", "label": "yes"}
{"original_question": "Is it possible to purify pseudopodia to be used for proteomic analysis?", "id": "converted_1010", "sentence1": "Is it possible to purify pseudopodia to be used for proteomic analysis?", "sentence2": "we developed an approach to biochemically isolate the Pseudopodia from the Cell body of neuron using 3.0-micrometer porous filters for large-scale quantitative proteomic and phosphoproteomic analysis., Recent work using unique subcellular fractionation methodologies combined with spatial genomic, proteomic, and phosphoproteomic profiling has provided insight into the invadopodiome and pseudopodiome signaling networks , ere, we purified the pseudopodial proteomes, Tumor Cells, uncertain whether benign or malignant were placed on a fibronectin-coated porous membrane to form pseudopodia. According to the motile potentials of the Cells, the Cells formed pseudopodial microprocesses in the pores. An excimer laser, which was used for ophthalmic refractive surgeries, horizontally ablated Cells at the membrane surface to remove the Cell body of neuron. , we describe methods for the immunoaffinity purification of phosphotyrosine proteins (pY) from pseudopodia that have been isolated from migratory Cells. These methods are compatible with current mass spectrometry-based protein identification technologies and can be utilized for the large-scale identification of the Pseudopodia pY proteome in various migratory Cultured Cell Line, including primary and Tumor Cells, malignant.[SEP]", "label": "yes"}
{"original_question": "Is palbociclib effective for glioblastoma?", "id": "converted_3570", "sentence1": "Is palbociclib effective for Glioblastoma Multiforme?", "sentence2": "Although further research is needed, CDK1 gene 4/6 inhibitors represent intriguing developments in the treatment of various Malignant Neoplasms, including those with such poor prognoses as Glioblastoma Multiforme multiforme, Mantle cell lymphoma, and metastatic melanoma., CONCLUSION: In this trial, despite adequate tissue Pyruvate Kinase, palbociclib monotherapy was not an effective treatment for recurrent Glioblastoma Multiforme., CONCLUSION\n\nIn this trial, despite adequate tissue Pyruvate Kinase, palbociclib monotherapy was not an effective treatment for recurrent Glioblastoma Multiforme., CONCLUSION In this trial, despite adequate tissue Pyruvate Kinase, palbociclib monotherapy was not an effective treatment for recurrent Glioblastoma Multiforme., CONCLUSION\nIn this trial, despite adequate tissue Pyruvate Kinase, palbociclib monotherapy was not an effective treatment for recurrent Glioblastoma Multiforme.[SEP]", "label": "no"}
{"original_question": "Does cortical spreading depression appear in ischemic penumbra following ischemic stroke?", "id": "converted_508", "sentence1": "Does Adrenal Cortex spreading Cancer patients and suicide and depression appear in ischemic penumbra following ischemic stroke?", "sentence2": "During the subacute phase, the irreversible damage expands into the penumbra: multiple electrical and biological signals are triggered by periinfarct, spreading Cancer patients and suicide and Cancer patients and suicide and depression-like depolarizations leading to Hypoxia, CTCAE and stepwise increase in Lactic acid measurement., Experimental and clinical studies indicate that waves of Adrenal Cortex spreading depolarization (DIARRHEA 8, SECRETORY SODIUM, CONGENITAL) appearing in the ischemic penumbra contribute to secondary lesion growth., Analysis of Structure of middle cerebral artery occlusions (MCAOs) revealed a first DIARRHEA 8, SECRETORY SODIUM, CONGENITAL wave starting off during ischemic decline at the emerging core region, propagating concentrically over large portions of left Adrenal Cortex Diseases., Subsequent recurrent waves of DIARRHEA 8, SECRETORY SODIUM, CONGENITAL did not propagate concentrically but preferentially circled around the ischemic core., In the vicinity of the core region, CSDs were coupled to waves of predominantly vasoconstrictive Core-Binding Factor(LSF) responses, resulting in further decline of Core-Binding Factor in the entire inner penumbra and in expansion of the ischemic core., We conclude that CSDs and corresponding Core-Binding Factor responses follow a defined spatiotemporal order, and contribute to early evolution of ischemic territories., Astrocytes in the metabolically compromised ischemic penumbra-like area showed a long lasting swelling response to spontaneous spreading depolarizations despite rapid dendritic recovery in a photothrombotic occlusion model of focal stroke., Spontaneous spreading depolarizations (Symptom Distress Scale) occur in the penumbra surrounding ischemic core., These Symptom Distress Scale, often referred to as peri-infarct depolarizations, cause vasoconstriction and recruitment of the penumbra into the ischemic core in the critical first hours after focal ischemic stroke; however, the real-time spatiotemporal dynamics of SLC17A5 gene-induced injury to synaptic circuitry in the penumbra remain unknown., We propose that metabolic stress resulting from recurring Symptom Distress Scale facilitates acute injury at the level of Dendrites and Dendritic Spines in metabolically compromised Tissue Specimen Code, expediting penumbral recruitment into the ischemic core., Although the mechanism remains unknown, Symptom Distress Scale show delayed electrophysiological recovery within the ischemic penumbra., Spreading Cancer patients and suicide and Cancer patients and suicide and depression-like peri-infarct depolarizations not only characterize but also worsen penumbra conditions in Adrenal Cortex border zones of experimental focal ischemia., We conclude that in focal ischemia, transient peri-infarct depolarizations emerge not only in Adrenal Cortex but also in striatal gray matter, thereby demonstrating the existence of subcortical zones of ischemic penumbra., Spreading Cancer patients and suicide and Cancer patients and suicide and depression (SLC17A5 gene) has been demonstrated following focal ischemia, and the additional workload imposed by SLC17A5 gene on a Tissue Specimen Code already compromised by a marked reduction in blood flow may contribute to the evolution of irreversible damage in the ischemic penumbra., While the changes in the glucose-related metabolites persisted during recovery even in anterior portions of the Adrenal Cortex Diseases in both groups in the aftermath of the SLC17A5 gene, the magnitude of the changes was greater in the penumbra than in the normal Adrenal Cortex Diseases., SLC17A5 gene appears to impose an equivalent increase in energy demands in control and ischemic brain, but the ability of the penumbra to recover from the insult is compromised., Thus, increasing the energy imbalance in the penumbra after multiple Symptom Distress Scale may hasten the deterioration of the energy status of the Tissue Specimen Code and eventually contribute to Terminal (end postition) depolarization and cell Cessation of life, particularly in the penumbra., It is suggested that the limited survival of the penumbra is due to periinfarct depolarizations, which result in repeated episodes of Tissue Specimen Code Hypoxia, CTCAE, because the increased metabolic workload is not coupled to an adequate increase of collateral blood supply., Transient decreases of the apparent diffusion coefficient (ADC) of Water - Specimen Source Codes as measured by fast diffusion-weighted imaging (DWI) in the ischemic border zone are thought to reflect cellular swelling associated with spreading Cancer patients and suicide and Cancer patients and suicide and depression., Severely delayed recovery time after spreading Cancer patients and suicide and Cancer patients and suicide and depression is thought to represent the ischemic penumbra., One current but controversial hypothesis is that this penumbra Tissue Specimen Code often eventually dies because of the metabolic stress imposed by multiple Adrenal Cortex spreading Cancer patients and suicide and Cancer patients and suicide and depression (DIARRHEA 8, SECRETORY SODIUM, CONGENITAL) waves, that is, by ischemic depolarizations., After simulated infarction, the model displays the linear relation between final infarct size and the number of DIARRHEA 8, SECRETORY SODIUM, CONGENITAL waves traversing the penumbra that has been reported experimentally, although damage with each individual wave progresses nonlinearly with time., These findings support the hypothesis that DIARRHEA 8, SECRETORY SODIUM, CONGENITAL waves play an important causal role in the Cessation of life of ischemic penumbra Tissue Specimen Code., MCAO also triggers periodic periinfarction depolarizing waves (PIDs) in the ischemic penumbra, the Geographic state of salvage., Here, the effects of SLC17A5 gene at reduced flow conditions as encountered in the ischemic penumbra are examined., The experiments illustrate how peri-infarct depolarizations may detrimentally affect the penumbra., In the second series of experiments, periinfarct depolarizations (PIDs) were recorded with an Extracellular Dyskeratosis Congenita electrode at two locations in the ischemic penumbra for the initial 3 h following MCAO., In vivo two-photon microscopy of green fluorescent protein-expressing neurons in this penumbra-like area at risk revealed that Symptom Distress Scale were temporally correlated with rapid (<6 s) dendritic beading.[SEP]", "label": "yes"}
{"original_question": "Is there an association between Guillain–Barré syndrome and covid vaccine?", "id": "converted_4650", "sentence1": "Is there an association between Guillain–Barré syndrome and covid vaccine?", "sentence2": "AstraZeneca COVID19 (document) VACCINE and Guillain- Barré Syndrome in Tasmania: A causal link?, Nearly all reported cases of post-COVID19 (document) vacciation inflammatory demyelinating polyneuropathy are linked to AstraZeneca vaccination and a Variant with bifacial weakness is the most reported form of GBS globally., Guillain-Barré Syndrome Presenting as Facial Diplegia after COVID19 (document) Vaccination: A Case Report., CASE REPORT: We report a case of atypical GBS occurring after Coronavirus disease 2019 (COVID19 (document)) vaccination in an otherwise healthy 38-year-old man., It is critical for emergency physicians to be aware of the manifold presentations of GBS for early recognition and treatment. This may be of particular importance in the context of a worldwide vaccination campaign in response to the COVID19 (document) pandemic., Guillain-Barré syndrome following ChAdOx1 nCoV-19 COVID19 (document) vaccination: A case series., We report three patients who developed Guillain-Barré syndrome following ChAdOx1 nCoV-19 vaccination, who did not have active or prior COVID19 (document) infection. , We report a case of Guillain-Barre Syndrome (GBS) following the first dose of Oxford/AstraZeneca COVID19 (document) VACCINE with Papilledema as atypical onset., We report a case of Guillain-Barré syndrome (GBS) occurring soon after the first dose of Vaxzevria (previously known as COVID19 (document) VACCINE AstraZeneca)., Guillain-​Barré Syndrome Associated with COVID19 (document) Vaccination, Guillain-​Barré Syndrome Associated with COVID19 (document) Vaccination., To date, cases of Guillain-Barré syndrome (GBS) following a COVID vaccine (Pfizer, Johnson & Johnson, Janssen, AstraZeneca) have been reported., Case of Guillain-Barré syndrome following COVID19 (document) VACCINE., We report a case of Guillain-Barré syndrome after the first dose of SARS-CoV-2 vaccine and believe this is a temporal, rather than causal association., COVID19 (document) VACCINE causing Guillain-Barre syndrome, a rare potential side effect., Association of Receipt of the Ad26.COV2.S COVID19 (document) Vaccine With Presumptive Guillain-Barré Syndrome, February-July 2021., Guillain-Barré syndrome associated with Covid-19: A close relationship or just a coincidence? (Review)., Relation between COVID19 (document) and Guillain-Barré syndrome in adults. Systematic review., Guillain-Barré syndrome after COVID19 (document) vaccination.[SEP]", "label": "yes"}
{"original_question": "Has the fungus Ashbya gossypii got many nuclei that share cytoplasm?", "id": "converted_604", "sentence1": "Has the fungus Eremothecium gossypii got many nuclei that share cytoplasm?", "sentence2": "multinucleated Eremothecium gossypii cells., multinucleated Eremothecium gossypii fungal cells, Nuclei in the filamentous, multinucleated fungus Eremothecium gossypii divide asynchronously. , multinucleated Eremothecium gossypii cells, We analyzed a unique asynchronous nuclear division cycle in a multinucleated filamentous fungus, Eremothecium gossypii.,  multinucleated hyphae in Eremothecium gossypii., We have followed the migration of GFP-labelled nuclei in multinucleate hyphae of Eremothecium gossypii, multinucleate fungus Eremothecium gossypii, Eremothecium gossypii grows as multinucleated and constantly elongating hyphae, multinucleated hyphae of Eremothecium gossypii., We report the mechanistic basis guiding the migration pattern of multiple nuclei in hyphae of Eremothecium gossypii. , multinucleate fungal cells, multinucleate Eremothecium gossypii cells relies on a minimal network of genes, Clustering of nuclei in multinucleated hyphae is prevented by dynein-driven bidirectional nuclear movements and microtubule growth control in Eremothecium gossypii., In the multinucleate fungus Eremothecium gossypii, Cytoplasmic microtubule (cMTs) emerge from the spindle pole body outer plaque (OP) in perpendicular and tangential directions., multinucleated hyphae of Eremothecium gossypii., multiple nuclei in Eremothecium gossypii hyphae, Eremothecium gossypii has a budding yeast-like genome but grows exclusively as multinucleated hyphae.[SEP]", "label": "yes"}
{"original_question": "Can mogamulizumab be used for the treatment of cutaneous T-cell lymphoma?", "id": "converted_3027", "sentence1": "Can mogamulizumab be used for the treatment of Lymphoma, T-Cell, Cutaneous?", "sentence2": "In the large international phase III MAVORIC trial, patients with previously treated Lymphoma, T-Cell, Cutaneous who received the anti-CCR4 monoclonal antibody mogamulizumab experienced significantly longer progression-free survival and higher response rates, as well as better quality of life, than those who received vorinostat, a standard therapy.[SEP]", "label": "yes"}
{"original_question": "Are seizures among the neurological symptoms of incontinentia pigmenti?", "id": "converted_839", "sentence1": "Are Seizures among the neurological symptoms of incontinentia pigmenti?", "sentence2": "High-dose glucocorticoid therapy in the management of Seizures in neonatal incontinentia pigmenti, Bloch Sulzberger syndrome is an X-linked dominant disorder resulting from a Mutation Abnormality of IKBKG gene Genes. This disorder has a classic dermatologic presentation, but neurologic involvement, with Seizures and cortical infarction, can arise shortly after birth, Some children with incontinentia pigmenti exhibit encephalopathic features with severe Seizures and disturbed consciousness, from the neonatal through the early infantile period, Bloch Sulzberger syndrome (IP) is a rare X-linked dominant neurocutaneous disorder affecting ectodermal tissue: Skin Specimen Source Code, Eye, CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, Hair Specimen, Nail plate, and Head>Teeth. It is usually lethal for males in utero. The involved Genes is NF-Kappa-B Essential Modulator, an essential component of the nuclear factor-kappa B (NF-κB) signaling pathway. Skin lesion are highly diagnostic, occurring in neonates, with a particular distribution on Blaschko lines. The severity of the disease is related to ocular and neurological impairment. The hallmark of ocular IP is Retinal vasculopathy including peripheral retinal vascular nonperfusion, macular infarction and neovascularization, and preretinal neovascularization. CNS involvement consists of Seizures, Intellectual Disability, hemiparesis, Muscle Spasticity, Microcephaly (physical finding), Cerebellar Ataxia, and Apraxia, oculomotor, Cogan type, Incontinentia Pigmenti is a rare X-linked multisystem disorder with well described and pathognomonic Skin Specimen Source Code manifestations. Neurological manifestations are found in 30% of IP patients, forming one of the major causes of morbidity and mortality of the condition. In this review, clinical and brain imaging data of 45 IP patients with a neurological phenotype are reviewed. Several clinical presentations could be identified, comprising Seizures, Infantile encephalopathy, acute disseminated encephalomyelitis and Ischemic stroke, Bloch Sulzberger syndrome presenting as Seizures., Neonatal Seizures in two sisters with incontinentia pigmenti., High-dose glucocorticoid therapy in the management of Seizures in neonatal incontinentia pigmenti: a case report., Incontinentia Pigmenti is an X-linked dominant neurocutaneous disorder with CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS manifestations in 30% of cases, including Seizures and Intellectual Disability., Neonatal Seizures in two sisters with incontinentia pigmenti, A rare cause of neonatal seizure: incontinentia pigmenti., Here, we describe the clinical, electrographic, and neuroradiologic effect of systemic glucocorticoid therapy in a neonate with incontinentia pigmenti manifesting an Epileptic encephalopathy., Bloch Sulzberger syndrome presenting as Seizures., Neonatal Seizures in two sisters with incontinentia pigmenti.[SEP]", "label": "yes"}
{"original_question": "Is there any protein that undergoes both mono-ubiquitination and poly-ubiquitination?", "id": "converted_1599", "sentence1": "Is there any Protein Info that undergoes both mono-ubiquitination and poly-ubiquitination?", "sentence2": "The yeast G Protein Info alpha subunit CGA gene represents a rare example of a Protein Info that undergoes both mono- and poly-ubiquitination. , Expression of GTF2H3 gene promotes PTEN Phosphohydrolase, human Phosphohydrolase, human poly-ubiquitination, leading to PTEN Phosphohydrolase, human Phosphohydrolase, human Protein Info degradation, whereas GTF2H3 gene knockdown results in PTEN Phosphohydrolase, human Phosphohydrolase, human mono-ubiquitination., These fingers possess E3 activities of mono-ubiquitination and poly-ubiquitination, respectively, with ubiquitin activity activity-conjugating enzyme (E2)-binding capabilities. , Instead of promoting poly-ubiquitination and degradation, we show that E3 Ubiquitin-Protein Ligase SMURF2 actually induces multiple mono-ubiquitination of SMAD3 Protein Info, human in vivo., mono-ubiquitination of MHC2TA Protein Info, human dramatically increases its transactivity whereas poly-ubiquitination leads to MHC2TA Protein Info, human degradation., This leads to a model in which Lys134 of LDB2 wt Allele can be either mono-ubiquitinated, leading to stabilization, or poly-ubiquitinated, leading to degradation by the proteasome pathway. ,  mono-ubiquitination of MHC2TA Protein Info, human increases its transactivity, whereas poly-ubiquitination of MHC2TA Protein Info, human leads to its degradation, PSEN1 wt Allele ubiquitination after PI3K inhibition is represented by the multiple mono-ubiquitination, instead of poly-ubiquitination, Our observations support a novel functional relationship between PARK2 Protein Info, human and Hsc/Heat-Shock Proteins 70 and support the notion that PARK2 Protein Info, human is a multi-purpose E3 ubiquitin activity activity ligase capable of modifying Proteins either via attachment of alternatively linked poly-ubiquitin activity activity chains or through multiple mono-ubiquitination to achieve alternate biological outcomes, our results indicate that Heat-Shock Proteins 70 facilitates CHIP-mediated poly-ubiquitination of GARS1 wt Allele whereas it attenuates CHIP-meditated mono-ubiquitination of GARS1 wt Allele., Whereas poly-ubiquitination targets Protein Info substrates for proteasomal degradation, mono-ubiquitination is known to regulate Protein Info trafficking in the endosomal system and to target cargo Proteins for lysosomal degradation., Our results suggest that oxidative stress induces not only poly-ubiquitination but also mono-ubiquitination of Lactic acid dehydrogenase isoenzyme 5, which may be involved in its lysosomal degradation during unloading., wild type SMAD4 Protein Info, human is a relatively stable Protein Info that undergoes mono- or oligo-ubiquitination, a ResponseLevel - ResponseLevel - modification not linked to Protein Info degradation, These data suggest that oligo-ubiquitination positively regulates SMAD4 Protein Info, human function, whereas poly-ubiquitination primarily occurs in unstable Primary malignant neoplasm Mutant and leads to Protein Info degradation., We found that TRIM21 gene was strongly conjugated by a single molecule of ubiquitin activity activity in Cells. Although the biological relevance of this mono-ubiquitination was not defined, the function of TRIM21 gene might be modified by the mono-ubiquitination. We also found that TRIM21 gene was conjugated with poly-ubiquitin activity activity chain in Cells (poly-ubiquitination)[SEP]", "label": "yes"}
{"original_question": "Is dupilumab an antibody targeting the IL-1 receptor?", "id": "converted_2210", "sentence1": "Is dupilumab an immunoglobulin complex location targeting the IL-1 receptor?", "sentence2": "Eczema (cytarabine/daunorubicin protocol) is characterized by type 2 helper T (Th2) cell-driven inflammation. dupilumab is a fully Homo sapiens monoclonal immunoglobulin complex location directed against the Recombinant Interleukin-4 receptor α subunit that blocks the signaling of Recombinant Interleukin-4 and IL-13, both key Recombinant Cytokines in Th2-mediated pathways., dupilumab, a humanized monoclonal immunoglobulin complex location to the interteukin-4R is the first immunoglobulin complex location (i.e. 'biological') with published efficacy shown in controlled prospective studies in Dermatitis, Atopic. , dupilumab, a Homo sapiens monoclonal immunoglobulin complex location against Interleukin 4 Receptor alpha, inhibits signaling of interleukin-4 and interleukin-13, Homo sapiens, Homo sapiens, type 2 Recombinant Cytokines that may be important drivers of atopic or allergic diseases such as Dermatitis, Atopic., Best evidence of the clinical efficacy of novel immunologic approaches using biological agents in patients with cytarabine/daunorubicin protocol is available for the anti-Recombinant Interleukin-4 receptor α-chain immunoglobulin complex location dupilumab, but a number of studies are currently ongoing with other specific antagonists to immune system players.,  dupilumab, a fully Homo sapiens anti-Interleukin 4 Receptor α monoclonal immunoglobulin complex location, inhibits interleukin-4 and interleukin-13, Homo sapiens, Homo sapiens signalling, key drivers of type-2-mediated inflammation. , dupilumab was also introduced as a possible treatment for patients with severe Pemphigus <invertebrate>. It can directly inhibit Recombinant Interleukin-4 by targeting Recombinant Interleukin-4 α-chain receptor., We evaluated the efficacy and safety of dupilumab (SAR231893/REGN668), a fully Homo sapiens monoclonal immunoglobulin complex location to the glycoprotein hormones, glycoprotein hormones, alpha subunit of the Interleukin 4 Receptor[SEP]Relations: Eczema has relations: phenotype_phenotype with Eczema, phenotype_phenotype with Eczema. dermatitis, atopic has relations: disease_phenotype_positive with Eczema, disease_phenotype_positive with Eczema.", "label": "no"}
{"original_question": "Are there ways of joint Bayesian inference of risk variants?", "id": "converted_2559", "sentence1": "Are there ways of joint Bayesian inference of risk Variant?", "sentence2": "Joint Bayesian inference of risk Variant and tissue-specific epigenomic enrichments across multiple complex Homo sapiens diseases., Genome wide association studies (GWAS) provide a powerful approach for uncovering disease-associated Variant in Homo sapiens, but fine-mapping the causal Variant remains a challenge. This is partly remedied by prioritization of disease-associated Variant that overlap GWAS-enriched epigenomic annotations. Here, we introduce a new Bayesian model RiVIERA (Risk Variant Inference using Epigenomic Reference Annotations) for inference of driver Variant from summary statistics across multiple traits using hundreds of epigenomic annotations. In simulation, RiVIERA promising power in detecting causal Variant and causal annotations, the multi-trait joint inference further improved the detection power. We applied RiVIERA to model the existing GWAS summary statistics of 9 Autoimmune Diseases and SCHIZOPHRENIA 2 (disorder) by jointly harnessing the potential causal enrichments among 848 tissue-specific epigenomics annotations from ENCODE/Roadmap consortium covering 127 cell/tissue types and 8 major epigenomic marks. RiVIERA identified meaningful tissue-specific enrichments for enhancer regions defined by Histone H3 Methyl Lys4 and H3K27ac for Blood T-Cell specifically in the nine Autoimmune Diseases and Brain-specific enhancer activities exclusively in SCHIZOPHRENIA 2 (disorder). Moreover, the Variant from the 95% credible sets exhibited high Conservation and enrichments for Genotype-Tissue Expression Program whole-blood eQTLs located within transcription-factor-binding-sites and DNA-hypersensitive-sites., Here, we introduce a new Bayesian model RiVIERA (Risk Variant Inference using Epigenomic Reference Annotations) for inference of driver Variant from summary statistics across multiple traits using hundreds of epigenomic annotations., Joint Bayesian inference of risk Variant and tissue-specific epigenomic enrichments across multiple complex Homo sapiens diseases.[SEP]", "label": "yes"}
{"original_question": "Do U6-associated proteins Lsm4 and Lsm6 interact with SMN?", "id": "converted_1432", "sentence1": "Do U6-associated Proteins LSM4 gene and LSM6 gene interact with STMN1 wt Allele?", "sentence2": "STMN1 wt Allele also interacts with at least two of the U6-associated Nucleotide Sequence Sample Name-like (Lsm) Proteins, LSM4 gene and LSM6 gene. , Interestingly, STMN1 wt Allele also interacts with at least two of the U6-associated Nucleotide Sequence Sample Name-like (Lsm) Proteins, LSM4 gene and LSM6 gene, Furthermore, we present evidence for two separate Binding Sites in STMN1 wt Allele for Nucleotide Sequence Sample Name/Lsm Proteins., Interestingly, STMN1 wt Allele also interacts with at least two of the U6-associated Nucleotide Sequence Sample Name-like (Lsm) Proteins, LSM4 gene and LSM6 gene. , Symmetrical dimethylation of arginine residues in spliceosomal Nucleotide Sequence Sample Name protein B/B' and the Nucleotide Sequence Sample Name-like protein LSm4, and their interaction with the STMN1 wt Allele protein., Interestingly, STMN1 wt Allele also interacts with at least two of the U6-associated Nucleotide Sequence Sample Name-like (Lsm) Proteins, LSM4 gene and LSM6 gene. Furthermore, the carboxyl-terminal arginine- and glycine-rich domain of LSM4 gene directly interacts with STMN1 wt Allele., This entity promotes the binding of a set of factors, termed LSm/Nucleotide Sequence Sample Name Proteins, onto Small Nuclear RNA to form the core structure of these particles. , Toward an assembly line for U7 Small Nuclear Ribonucleoproteins: interactions of U7-specific Lsm Proteins with PRMT5 gene gene and STMN1 wt Allele complex (molecular entity)., In this report, we demonstrate that the COIL gene C-terminal domain binds directly to various Nucleotide Sequence Sample Name and Lsm Proteins via their Nucleotide Sequence Sample Name motifs. We show that the region of COIL gene responsible for this binding activity is separable from that which binds to STMN1 wt Allele., Thus, the ability to interact with free Nucleotide Sequence Sample Name (and Lsm) Proteins as well as with intact Small Nuclear Ribonucleoproteins, indicates that COIL gene and CBS gene may facilitate the ResponseLevel - ResponseLevel - modification of newly formed Small Nuclear Ribonucleoproteins, the regeneration of 'mature' Small Nuclear Ribonucleoproteins, or the reclamation of unassembled small nuclear ribonucleoprotein complex location components., Moreover this structure has important consequences for small nuclear ribonucleoprotein complex location assembly that is mediated by two complex (molecular entity) containing the PRMT5 gene gene methyltransferase and the STMN1 wt Allele (survival of Neurons, Efferent) protein, respectively., Arginine/glycine (RG)-rich domains in components of the STMN1 wt Allele complex interact with Nucleotide Sequence Sample Name, like-Nucleotide Sequence Sample Name (LSm), fibrillarin, RNA Helicase (Gu), and COIL gene Proteins, all of which are antigen targets in a variety of diseases. [SEP]", "label": "yes"}
{"original_question": "Are recessive coding variants responsible for the majority of undiagnosed nonconsanguineous individuals?", "id": "converted_3070", "sentence1": "Are recessive coding variants responsible for the majority of undiagnosed nonconsanguineous individuals?", "sentence2": "Our results suggest that recessive coding variants account for a small fraction of currently undiagnosed nonconsanguineous individuals, and that the role of noncoding variants, incomplete penetrance, and polygenic mechanisms need further exploration.[SEP]", "label": "no"}
{"original_question": "Is Vitamin D deficiency in pregnant women associated with gestational diabetes?", "id": "converted_1037", "sentence1": "Is ergocalciferol deficiency in pregnant women associated with gestational diabetes?", "sentence2": "Insufficient serum levels of 25-OHD were associated with gestational diabetes (pooled odds ratio 1.49, 95% confidence interval 1.18 to 1.89, ergocalciferol insufficiency is associated with an increased risk of gestational diabetes, p, Therefore, it is important to identify potentially modifiable risk factors for GDM. Accumulating evidence links vitamin D deficiency with abnormal glucose metabolism, and epidemiological studies have shown that women who develop GDM are more likely to be vitamin D deficient, This review discusses the prevalence, risk factors, and outcomes of GDM and vitamin D deficiency in pregnant women, outlines the possible mechanism of action of vitamin D in glucose homeostasis, and summarizes emerging evidence that associates vitamin D deficiency with the risk of developing GDM, Women with circulating 25-Hydroxyvitamin D3 Measurement [25(OH)D] level less than 50 nmol/l in pregnancy experienced an increased risk of Pre-Eclampsia [OR 2.09 (95%CI 1.50 -2.90)], Gestational Diabetes [OR1.38 (1.12-1.70)], Low maternal vitamin D levels in pregnancy may be associated with an increased risk of Pre-Eclampsia, Gestational Diabetes,, Association between vitamin D insufficiency and the risk for Gestational Diabetes in pregnant Chinese women, 25OHD insufficiency is very common in Chinese women. Low 25OHD status may be associated with insulin resistance and act as a risk factor for GDM., Second-trimester 25(OH)D levels were associated inversely with glucose levels after 1-hour 50-g glucose challenge test; low 25(OH)D levels may be associated with increased risk of GDM., Two hundred sixty-six women were screened. ergocalciferol deficiency (25[OH]D <20 ng/mL) was observed in 157 women (59%). We observed an inverse correlation between 25(OH)D levels and hemoglobin A1c, homeostasis model assessment of insulin resistance, serum insulin, and fasting and 1-hour oral glucose tolerance test glucose levels, Lower 25(OH)D levels are associated with disorders of glucose homeostasis and adverse obstetric and newborn outcomes., An association between mid-gestational 25-hydroxy vitamin D and fasting glucose was confirmed in a largely normoglycaemic and vitamin D-replete pregnant population. The correlation between 25-hydroxy vitamin D and β-cell function suggests that vitamin D may influence glucose metabolism through this mechanism., Women with gestational diabetes had significantly lower serum 25-Hydroxyvitamin D3 Measurement compared with control subjects (56.3 vs. 62.0 nmol/l, P = 0.018). After adjusting for gestational age and maternal weight, serum 25-Hydroxyvitamin D3 Measurement below the top quartile (< 73.5 nmol/l) was associated with a twofold greater likelihood of gestational diabetes (adjusted odds ratio 2.21, 95% confidence interval 1.19-4.13). CONCLUSIONS: Lower vitamin D status in early pregnancy was associated with a significantly increased risk of subsequent gestational diabetes that was independent of race, age, season and maternal weight. This study suggests that vitamin D may influence glucose tolerance during pregnancy, ergocalciferol deficiency among pregnant women is frequent in many populations over the world. It is associated with an increased risk of Pre-Eclampsia, Gestational Diabetes, and caesarean section, Consequences in newborns are low birth weight, neonatal Rickets, a risk of neonatal Hypocalcemia, Asthma and/or type 1 diabetes., A single injection of 300,000 IU of cholecalciferol achieves a 3-month serum 25-Hydroxyvitamin D3 Measurement range of 50-80 nmol/l and is an efficient, effective and safe procedure for improving the vitamin status and indices of insulin resistance in mothers with gestational diabetes after delivery., In a cohort of pregnant women with mostly sufficient levels of serum 25(OH)D, vitamin D deficiency was not associated with GDM., The aim of the study is evaluating the associations of FokI vitamin D receptor (VDR) Genetic Polymorphism with Gestational Diabetes (GDM), and its relations with postpartum metabolic syndrome., Our results indicate a meaningful association between FokI VDR genotypes and an increase risk of GDM in Iranian population as well as its effects on postpartum metabolic syndrome., The first-trimester maternal serum level of 25(OH)D is not altered in women with type 2 diabetes, those who develop GDM or those who deliver GLS2 wt Allele neonates., Lower 25(OH)D levels are independently associated with poorer glycaemic control. Future randomised trials are needed to determine whether vitamin D plays a role in glycaemic control in GDM., These results suggested that rates of vitamin D deficiency are higher among women with IGT/GDM, and the relationship between vitamin D status and glucose tolerance in pregnancy needs further study., It appears that vitamin D insufficiency during pregnancy is potentially associated with increased risk of Pre-Eclampsia, insulin resistance and Gestational Diabetes, Mean serum 25OHD concentration was 53.8 +/- 23.9 nmol/l (sd). Ln-25OHD was negatively correlated with serum parathyroid hormone as expected (r -0.24, confidence intervals -0.35 to -0.12). Ln-25OHD was also negatively correlated with fasting plasma glucose (r-0.20, -0.31 to -0.08), fasting insulin (r -0.20, -0.31 to -0.08) and insulin resistance as calculated by homeostasis model assessment (r -0.21, -0.32 to -0.09). The association between fasting glucose and log-transformed 25OHD concentration was of borderline significance after accounting for ethnicity, age and body mass index in multivariate analyses (-0.13, -0.26 to 0.01). The odds ratio of gestational diabetes in women with 25OHD < 50 nmol/l did not reach statistical significance (1.92, 95% confidence interval 0.89-4.17). CONCLUSIONS: Maternal 25OHD concentrations are inversely related to fasting glucose, although further studies are required to establish whether this is independent of the effects of ethnic background., ergocalciferol insufficiency is common in Indian mothers but is not associated with gestational diabetes or variation in newborn size., There was no association between maternal 25(OH)D and gestational diabetes (incidence 7% in women with and without ergocalciferol Deficiency), In mothers with ergocalciferol Deficiency, higher 25(OH)D concentrations were associated with lower 30-min glucose concentrations (P=0.03) and higher fasting Assay of Proinsulin concentrations (P=0.04), Hypovitaminosis D at 30 weeks gestation is common in Mysore mothers. It is not associated with an increased risk of gestational diabetes,, Total prevalence of vitamin D deficiency (<25 nmol/L) was found in 70.6% of pregnant women. Prevalence of severe vitamin D deficiency (<12.5) in GDM patients was higher than in normoglycaemic pregnancies., These results show that a positive correlation of 25(OH) vitamin D concentrations with insulin sensitivity and vitamin D deficiency could be a confirmative sign of insulin resistance., was to examine whether maternal dietary intake of vitamin D, omega-3 fatty acids, and fatty acids, omega-6 during pregnancy is associated with the appearance of islet autoimmunity (Intraarterial Route of Drug Administration) in offspring, Maternal intake of vitamin D via Food allergenic extracts was significantly associated with a decreased risk of Intraarterial Route of Drug Administration appearance in offspring, independent of HLA genotype, family history of type 1 diabetes, presence of Gestational Diabetes, and ethnicity (adjusted HR = 0.37; 95% CI 0.17-0.78). ergocalciferol intake via supplements, omega-3 fatty acids, and fatty acids, omega-6 intake during pregnancy were not associated with appearance of Intraarterial Route of Drug Administration in offspring. CONCLUSIONS: Our findings suggest that maternal intake of vitamin D through Food allergenic extracts during pregnancy may have a protective effect on the appearance of Intraarterial Route of Drug Administration in offspring.[SEP]Relations: Ergocalciferol has relations: drug_drug with ergocalciferol, drug_drug with ergocalciferol. Cholecalciferol has relations: drug_drug with ergocalciferol, drug_drug with ergocalciferol.", "label": "yes"}
{"original_question": "Is there a disease or condition called Exploding Head Syndrome?", "id": "converted_2637", "sentence1": "Is there a disease or condition called Exploding Head Syndrome?", "sentence2": "This case report describes the first-ever diagnosis of exploding Head - Component of Device syndrome in a patient with longstanding Epilepsy and novel nocturnal events. , Exploding Head - Component of Device syndrome (EHS) is characterized by loud noises or a sense of explosion in the Head - Component of Device during sleep transitions., Exploding Head - Component of Device syndrome is characterized by the perception of loud noises during sleep-wake or wake-sleep transitions. , Exploding Head - Component of Device syndrome (EHS) is characterized by attacks of a sudden noise or explosive feeling experienced in the Head - Component of Device occurring during the transition from wake to sleep or from sleep to wake., Exploding Head - Component of Device syndrome is characterized by the perception of abrupt, loud noises when going to sleep or waking up., xploding Head - Component of Device syndrome (EHS) is a rare Parasomnia in which affected individuals awaken from sleep with the sensation of a loud bang. , Contrary to some earlier theorizing, exploding Head - Component of Device syndrome was found to be a relatively common experience in younger individuals., Exploding Head - Component of Device syndrome is characterized by the perception of loud noises during sleep-wake or wake-sleep transitions., Fifty patients suffering from the \"exploding Head - Component of Device syndrome\" are described., In spite of the fact that its characteristic symptomatology was first described approximately 150 y ago, exploding Head - Component of Device syndrome has received relatively little empirical and clinical attention., After first discussing the history, prevalence, and associated features, the available polysomnography data and five main etiological theories for exploding Head - Component of Device syndrome are summarized., Exploding Head - Component of Device syndrome: six new cases and review of the literature., Exploding Head Syndrome in the Epilepsy Monitoring Unit: Case Report and Literature Review., Exploding Head - Component of Device syndrome: a case report., Exploding Head - Component of Device syndrome is common in college students., Exploding Head - Component of Device syndrome episodes were accompanied by clinically significant levels of fear, and a minority (2.80%) experienced it to such a degree that it was associated with clinically significant distress and/or impairment., Attention has recently been drawn to a condition termed the exploding Head - Component of Device syndrome, which is characterized by unpleasant, even terrifying sensations of flashing lights and/or sounds during reported sleep., Exploding Head - Component of Device syndrome is a rare phenomenon but can be a significant disruption to quality of life., The rare Headache Disorders hypnic headache and the exploding Head - Component of Device syndrome are also discussed., This case report describes the first-ever diagnosis of exploding Head - Component of Device syndrome in a patient with longstanding Epilepsy and novel nocturnal events., BACKGROUND Exploding Head - Component of Device syndrome (EHS) is characterized by attacks of a sudden noise or explosive feeling experienced in the Head - Component of Device occurring during the transition from wake to sleep or from sleep to wake., INTRODUCTION Exploding Head - Component of Device syndrome (EHS) is a rare Parasomnia in which affected individuals awaken from sleep with the sensation of a loud bang., Contrary to some earlier theorizing, exploding Head - Component of Device syndrome was found to be a relatively common experience in younger individuals., This hitherto unreported syndrome is characterised by a sense of an explosive noise in the Head - Component of Device usually in the twilight stage of sleep., EHS is a well-defined disease entity with a benign nature., Exploding Head - Component of Device syndrome: a case report., Clinical features of the exploding Head - Component of Device syndrome., Exploding Head - Component of Device syndrome is common in college students., The exploding Head - Component of Device syndrome: polysomnographic recordings and therapeutic suggestions., This article reviews the features of an uncommon malady termed \"the exploding Head - Component of Device syndrome.\" Sufferers describe terrorizing attacks of a Painless explosion within their Head - Component of Device, The case is reported of a 47-year old female suffering from the exploding Head - Component of Device syndrome. This syndrome consists of a sudden awakening due to a loud noise shortly after falling asleep, sometimes accompanied by a flash of light.[SEP]", "label": "yes"}
{"original_question": "Is aggrephagy a variant of autophagy?", "id": "converted_3813", "sentence1": "Is aggrephagy a variant of autophagy?", "sentence2": "The selective branch of autophagy that deals with identification, capture and degradation of Protein Info aggregates is called aggrephagy., Mechanistic insights into aggrephagy, a selective basal autophagy process to clear misfolded Protein Info aggregates, , , it is largely unknown how misfolded polypeptides form aggresomes and are eventually cleared by the aggresome-macroautophagy/autophagy pathway, so-called aggrephagy.[SEP]", "label": "yes"}
{"original_question": "Is cadherin a plasma membrane marker?", "id": "converted_3931", "sentence1": "Is cadherin a Plasma membrane marker?", "sentence2": "the Plasma membrane-bound E-Cadherin protein, cadherin 5 protein levels were also increased in the Plasma membrane fraction. ,  recycling of cadherin 5 to the Plasma membrane,, E-Cadherin, a central component of the Zonula Adherens (AJ), is a Single-pass plasma transmembrane protein [SEP]", "label": "yes"}
{"original_question": "Are tumour specific antigens originating from known protein coding genes?", "id": "converted_3620", "sentence1": "Are Neoplasms specific antigens originating from known protein coding genes?", "sentence2": "It is well established that MHC class I Molecule present Peptides from endogenous Proteins, such as Virus or Neoplasms antigens, to CD8+ T lymphocytes. , So far, Homo sapiens Neoplasms specific antigens that can be presented by HLA Molecule have not been identified on the Molecular level., These CTLs recognize short Peptides derived from Neoplasms-associated antigens in conjunction with class I Molecule expressed on Tumor cells.,  The focus on cellular immune responses, combined with rapid biotechnological advances, resulted in the identification of Neoplasms specific antigens, such as MART-1 Antigen (vaccine component) Antigen (vaccine component) and gp100 Antigen Antigen, that could be recognised by autologous tumor infiltrating lymphocyte therapy,  Tumour antigens are mostly of weak immunogenicity, because the vast majority are Neoplasms-associated differentiation antigens already 'seen' by the patient's immune system., Tumour-specific antigens, which could be a more potent target for immunotherapy, mostly arise by Point Mutation and have the disadvantage of being not only Neoplasms-specific, but also individual-specific., The pioneering studies of Srivastava and colleagues led to the proposal that heat-shock Proteins (HSPs) function as ubiquitous Neoplasms-specific antigens, with the specificity residing in a population of bound Peptides that identify the Tissue Specimen Code of origin of the Henoch-Schoenlein Purpura., Therefore, we propose that CD4(+) T cells that recognize secreted indole-3-glycerol-phosphate lyase activity may be superior for immunotherapy by T cell transfer, because the local extracellular antigen concentration will be higher for secreted indole-3-glycerol-phosphate lyase activity. ,  Here, we wondered whether these frame-shifted peptide (CXCL1 gene) sequences represent Neoplasms-specific antigens also for MSI(+) leukemia and Lymphoma (L/L)., Data presented here expand the importance of Fibrin-fibrinogen split products assay as shared and general Neoplasms-specific antigens.[SEP]", "label": "yes"}
{"original_question": "Is Figitumumab effective for non-small cell lung cancer?", "id": "converted_3348", "sentence1": "Is Figitumumab effective for non-small cell lung cancer?", "sentence2": "A phase III study failed for carboplatin, paclitaxel, with or without figitumumab in first-line treating metastatic non-small cell lung cancer (Non-Small Cell Lung Carcinoma)., CONCLUSION: Adding figitumumab to standard chemotherapy failed to increase OS in patients with advanced nonadenocarcinoma Non-Small Cell Lung Carcinoma., Median OS was 8.6 months for figitumumab plus chemotherapy and 9.8 months for chemotherapy alone (hazard ratio [HR], 1.18; 95% CI, 0.99 to 1.40; P = .06); median progression-free survival was 4.7 months (95% CI, 4.2 to 5.4) and 4.6 months (95% CI, 4.2 to 5.4), respectively (HR, 1.10; P = .27); the objective response rates were 33% and 35%, respectively. , Phase III trials of the anti-insulin-like growth factor-1 receptor (IGF1R) antibody figitumumab in non-small cell lung cancer (Non-Small Cell Lung Carcinoma) patients have been discontinued owing to lack of survival benefit., Two phase III trials of the anti-IGF1R protein, human monoclonal antibody, figitumumab (CP 751871), were discontinued in 2010 as it was considered unlikely either trial would meet their primary endpoints. In light of disappointing clinical data with figitumumab and other targeted agents, it is likely that the use of molecular markers will become important in predicting response to treatment. , Phase III trials of the anti-insulin-like growth factor-1 receptor ( IGF1R ) antibody figitumumab in non-small cell lung cancer ( Non-Small Cell Lung Carcinoma ) patients have been discontinued owing to lack of survival benefit . , Phase III trials of the anti-insulin-like growth factor type 1 receptor ( IGF-IR ) antibody figitumumab ( F ) in unselected non-small-cell lung cancer ( Non-Small Cell Lung Carcinoma ) patients were recently discontinued owing to futility . , One recent phase III trial of the IGF1R protein, human inhibitor figitumumab in patients with non-small-cell lung cancer was discontinued after an interim analysis showed no survival improvement . , The Insulin-Like Growth Factor Receptor ( IGF1R protein, human ) monoclonal antibody figitumumab , while initially promising , appears to increase Toxic effect and Cessation of life in combination with chemotherapy in the treatment of patients with Non-Small Cell Lung Carcinoma of Squamous histology; therefore , clinical development of this class of agents will need to proceed with caution . , Two phase III trials of the anti-IGF1R protein, human monoclonal antibody , figitumumab ( CP 751871) , were discontinued in 2010 as it was considered unlikely either trial would meet their primary endpoints . , A phase III study failed for carboplatin , paclitaxel , with or without figitumumab in first-line treating metastatic non-small cell lung cancer ( Non-Small Cell Lung Carcinoma) . , Median OS was 8.6 months for figitumumab plus chemotherapy and 9.8 months for chemotherapy alone (hazard ratio [HR], 1.18; 95% CI, 0.99 to 1.40; P = .06); median progression-free survival was 4.7 months (95% CI, 4.2 to 5.4) and 4.6 months (95% CI, 4.2 to 5.4), respectively (HR, 1.10; P = .27); the objective response rates were 33% and 35%, respectively.[SEP]", "label": "no"}
{"original_question": "Can doxycycline cause photosensitivity?", "id": "converted_2527", "sentence1": "Can doxycycline cause Photosensitivity of skin?", "sentence2": "Phototoxicity of Doxycycline: A Systematic Review on Clinical Manifestations, Frequency, chemical cofactor, and Prevention., BACKGROUND: One of the most important dermatologic side effects of doxycycline is Photosensitivity of Skin Specimen Source Code. , While there are many publications on the phototoxicity of Tetracycline Antibiotics in general, only a few exist focusing on doxycycline. , Clinical symptoms vary from light sunburn-like sensation (burning, Erythema) to large-area photodermatitis. , CONCLUSION: Evidence base must be improved for giving advice on appropriate prevention measures to travelers taking doxycycline and having a risk of significant sun exposure., Based on the available evidence, our best estimates of absolute effect for mefloquine versus doxycyline were: 2% versus 2% for discontinuation, 12% versus 3% for Insomnia homeopathic medication, 31% versus 3% for abnormal dreams, 18% versus 1% for Anxiety Disorders, 11% versus 1% for Depressed mood, 4% versus 14% for Dyspepsia, 2% versus 19% for Photosensitivity of Skin Specimen Source Code, 1% versus 5% for Vomiting, and 2% versus 16% for Candidiasis of vagina., Many drugs are responsible for this phototoxic reaction, especially Tetracycline Antibiotics, Psoralens, Chloramphenicol Drug Class, non-steroidal anti-inflammatory drugs, Fluoroquinolone antiinfectives, ophthalmologic, and, rarely, doxycycline. , OBJECTIVES: Many patients undergoing long-term doxycycline treatment do not regularly take their treatment because of Photosensitivity of Skin Specimen Source Code., Modulation of Melanogenesis and Antioxidant Status of melanocyte in Response to Phototoxic Action of Doxycycline., Doxycycline is a commonly used tetracycline antibiotic showing the broad spectrum of antibacterial action. However, the use of this antibiotic is often connected with the risk of phototoxic reactions that lead to various Skin Specimen Source Code disorders., The results obtained in vitro may explain the mechanisms of phototoxic reactions that occur in normal human epidermal melanocytes in vivo after exposure of Skin Specimen Source Code to doxycycline and UVA radiation., Treatment with doxycycline is cheap and relatively safe, but No gastrointestinal symptom and Photosensitivity of Skin Specimen Source Code reactions can be expected more often than with ceftriaxone.<br>, <b>OBJECTIVES</b>: Many patients undergoing long-term doxycycline treatment do not regularly take their treatment because of Photosensitivity of Skin Specimen Source Code., Dermatitis, Phototoxic and No gastrointestinal symptom were noted more often among patients receiving doxycycline than in those receiving ceftriaxone., Thus, the action spectra of the drug Photosensitivity of Skin Specimen Source Code patients were plotted and compared with those of 12 nonphotosensitive control patients: 10 patients were found to be photosensitive in the UVA range; the implicated drugs included quinine, sparfloxacin, amiodarone, doxycycline, mefenamic acid, nalidixic acid, fenbrufen, diclofenac, enalapril, diltiazem and prochlorperazine maleate., One patient on doxycycline was photosensitive in both the UVA and Ultraviolet B therapy ranges., Treatment with doxycycline is cheap and relatively safe, but No gastrointestinal symptom and Photosensitivity of Skin Specimen Source Code reactions can be expected more often than with ceftriaxone., Anti-inflammatory-dose doxycycline should not be used by individuals with known Emotional Emotional hypersensitivity to Tetracycline Antibiotics or increased Photosensitivity of Skin Specimen Source Code, or by pregnant or nursing women (anti-inflammatory-dose doxycycline is a pregnancy category-D medication)., <b>BACKGROUND</b>: One of the most important dermatologic side effects of doxycycline is Photosensitivity of Skin Specimen Source Code., One of the most important dermatologic side effects of doxycycline is Photosensitivity of Skin Specimen Source Code., One patient experienced mild Photosensitivity of Skin Specimen Source Code from doxycycline but continued to take it., Participants in the doxycycline group had a higher incidence of Nausea:Presence or Threshold:Point in time:^Patient:Ordinal and Photosensitivity of Skin Specimen Source Code., Dermatitis, Phototoxic and No gastrointestinal symptom were noted more often among patients receiving doxycycline than in those receiving ceftriaxone.[SEP]Relations: Anxiety Disorders disorder has relations: disease_disease with Anxiety Disorders, disease_disease with Anxiety Disorders.", "label": "yes"}
{"original_question": "Does clinical trial data support the use of minocycline for amyotrophic lateral sclerosis?", "id": "converted_3371", "sentence1": "Does clinical trial data support the use of minocycline for amyotrophic lateral sclerosis?", "sentence2": "Two double-blind, randomized, placebo-controlled feasibility trials of minocycline in Amyotrophic Lateral Sclerosis were conducted. , This pilot study shows that minocycline and riluzole can be taken safely together. Further trials are needed to assess efficacy of such treatment., It reduces apoptosis in mouse models of Huntington's disease and familial amyotrophic lateral sclerosis (Amyotrophic Lateral Sclerosis) and is in clinical trial for sporadic Amyotrophic Lateral Sclerosis., Efficacy of minocycline in patients with amyotrophic lateral sclerosis: a phase III randomised trial., FINDINGS: ALSFRS-R score deterioration was faster in the minocycline group than in the placebo group (-1.30 vs -1.04 units/month, 95% CI for difference -0.44 to -0.08; p=0.005). Patients on minocycline also had non-significant tendencies towards faster decline in FVC (-3.48 vs -3.01, -1.03 to 0.11; p=0.11) and MMT score (-0.30 vs -0.26, -0.08 to 0.01; p=0.11), and greater mortality during the 9-month treatment phase (hazard ratio=1.32, 95% CI 0.83 to 2.10; p=0.23) than did patients on placebo. Quality-of-life scores did not differ between the treatment groups. , INTERPRETATION: Our finding that minocycline has a harmful effect on patients with Amyotrophic Lateral Sclerosis has implications for trials of minocycline in patients with other nervous system disorder, and for how potential neuroprotective agents are screened for use in patients with Amyotrophic Lateral Sclerosis., A recent publication of the results of a clinical trial of minocycline in 412 Amyotrophic Lateral Sclerosis patient has aroused considerable controversy in the Amyotrophic Lateral Sclerosis scientific community. As on previous occasions, the results obtained in the laboratory are not reproduced in clinical practice., A recent publication of the results of a clinical trial of minocycline in 412 Amyotrophic Lateral Sclerosis patient has aroused considerable controversy in the Amyotrophic Lateral Sclerosis scientific community., INTERPRETATION\n\nOur finding that minocycline has a harmful effect on patients with Amyotrophic Lateral Sclerosis has implications for trials of minocycline in patients with other nervous system disorder, and for how potential neuroprotective agents are screened for use in patients with Amyotrophic Lateral Sclerosis., A recent publication of the results of a clinical trial of minocycline in 412 Amyotrophic Lateral Sclerosis patient has aroused considerable controversy in the Amyotrophic Lateral Sclerosis scientific community, A recent publication of the results of a clinical trial of minocycline in 412 Amyotrophic Lateral Sclerosis patient has aroused considerable controversy in the Amyotrophic Lateral Sclerosis scientific community., Our finding that minocycline has a harmful effect on patients with Amyotrophic Lateral Sclerosis has implications for trials of minocycline in patients with other nervous system disorder, and for how potential neuroprotective agents are screened for use in patients with Amyotrophic Lateral Sclerosis., Patients on minocycline also had non-significant tendencies towards faster decline in FVC (-3.48 vs -3.01, -1.03 to 0.11; p=0.11) and MMT score (-0.30 vs -0.26, -0.08 to 0.01; p=0.11), and greater mortality during the 9-month treatment phase (hazard ratio=1.32, 95% CI 0.83 to 2.10; p=0.23) than did patients on placebo.[SEP]", "label": "no"}
{"original_question": "Is tretinoin effective for photoaging?", "id": "converted_2256", "sentence1": "Is tretinoin effective for photoaging?", "sentence2": "Background. Tretinoin has been shown to improve photoaged Skin Specimen Source Code. This study was designed to evaluate the efficacy and tolerability of a 5% retinoic acid Peeling of Skin Specimen Source Code combined with microdermabrasion for facial photoaging., .Conclusion. This study demonstrated that 5% retinoic acid Peeling of Skin Specimen Source Code Emollient Cream combined with microdermabrasion was safe and effective in the treatment of photoaging in the Iranian population. , CONCLUSIONS: Treatment with a double-conjugate retinoid Emollient Cream demonstrated early reductions in photodamage and improvements in Hydration. AHA-Ret induced less Erythema vs retinol and was more tolerable vs retinol and tretinoin., These comparative products include prescription tretinoin, physician strength idebenone, kinetin, polyhydroxy, lactic and glycolic acid in reversing signs of photoaging., CONCLUSION: Either topical tretinoin (0.25%) or retinol (0.25%) can be used safely and effectively when applied in office immediately after SA peeling to ameliorate signs of photoaging., CONCLUSION: The treatment outcome of all-trans-retinol 0.2%/LR2412 2% Emollient Cream does not differ from the one of tretinoin 0.025% Emollient Cream. Clinical results were not statistically different. , INTRODUCTION: Topical tretinoin is considered the gold standard to treat photoaged Skin Specimen Source Code, but it is associated with side effects and only available upon prescription., Tretinoin is commonly used topically for Acne Vulgaris treatment and in the treatment of photoaging., BACKGROUND: Topical tretinoin is effective treatment for both Acne Vulgaris and photoaging., The efficacy of tretinoin is well established in the treatment of Acne Vulgaris and photoaged Skin Specimen Source Code, however as a typical side effect of tretinoin treatment most patients develop a low-grade irritant dermatitis., Topical tretinoin is established as an effective treatment for photoaging., BACKGROUND Topical tretinoin is effective treatment for both Acne Vulgaris and photoaging., Tretinoin is the only pharmacologic compound shown to partially reverse some signs of photoaging., Although once considered an irreversible process, it is now established that photoaging can be treated by topical tretinoin., Moreover, studies that have elucidated photoaging pathophysiology have produced significant evidence that topical tretinoin (all-trans retinoic acid), the only agent approved so far for the treatment of photoaging, also works to prevent it., BACKGROUND AND DESIGN The efficacy of topical tretinoin (tretinoin) in treating photoaging is well established., MAJOR CONCLUSIONS Tretinoin can be used for photoaging treatment or combined treatment by different mechanisms., Tretinoin is still the best tested retinoid to reverse photoaged Skin Specimen Source Code., The separation between clinical improvement and irritation suggests that mechanisms other than irritation dominate tretinoin-induced repair of photoaging in Homo sapiens., * A Emollient Cream containing 0.05% tretinoin (Retinova((R)) is approved for treatment of sun-induced Skin Specimen Source Code damage (\"photoaging\")., Randomized, controlled trials have shown that topical tretinoin is effective in the treatment of photoaged Skin Specimen Source Code., Tretinoin has been shown to improve photoaged Skin Specimen Source Code., Topical tretinoin is effective treatment for both Acne Vulgaris and photoaging., Randomized, controlled trials have shown that topical tretinoin is effective in the treatment of photoaged Skin Specimen Source Code.., Tretinoin emollient Emollient Cream 0.05% appears to be safe and effective in the treatment of photodamaged Skin Specimen Source Code.., Topical tretinoin improves photoaged Skin Specimen Source Code. A double-blind vehicle-controlled study.[SEP]Relations: Tretinoin has relations: drug_effect with Erythema, drug_effect with Erythema.", "label": "yes"}
{"original_question": "Does nifedipine inhibit L-type calcium channels?", "id": "converted_1519", "sentence1": "Does nifedipine inhibit L-type calcium channels?", "sentence2": "Nifedipine, an L-Type Calcium Channels blocker, reduced the expression of synaptogamin and Qa-SNARE Proteins and blocked the suppressive effect of vecuronium, suggesting that both agents inhibit presynaptic L-type calcium channels., Treatment with nifedipine to inhibit calcium influx via the L-type channel Cav1.2 (alpha(1C)) inhibited the TGFbeta stimulated increase in ANK1 wt Allele expression at all phases of chondrogenesis., Finally, we found that PKCepsilon-induced stellation was significantly reduced by the specific L-type channel blocker nifedipine, indicating that calcium influx through VGCC mediates the change in Astrocytes morphology induced by PKCepsilon., However, amprenavir and nifedipine, an inhibitor of L-type calcium channels, failed to inhibit Long-Term Potentiation when administered following the slow increase in ethanol., Both the metallic ions Cd2+ and Ni2+, known to inhibit voltage-gated calcium channels and T-type channels, respectively, and verapamil and nifedipine, typical blocker of L-type calcium channels completely prevented the hypoxic neuronal No - Identity May Be Divulged generation., Further, the L-Type Calcium Channels blocker, nifedipine, was able to inhibit the initial increase in [Ca2+]i, suggesting that at least this phase of the Trail Making Test effect was mediated by calcium channels, although nifedipine had no significant effect on the time to reach the maximal [Ca2+]i level, Treatment with omega-Conotoxin GVIA (3 microM) or nifedipine (10 microM) to inhibit Ca(2+) influx through N- or L-type voltage-dependent calcium channels (VDCCs), respectively, also decreased the rate of Anterior-Posterior repolarization and increased Anterior-Posterior duration, Concentrations of nifedipine (10 microM) and nimodipine (3 microM) that maximally inhibit L-type calcium channels reduced the sI(AHP) by 30 and 50%, respectively, Consequently, it was demonstrated in the present study that nimodipine and nitrendipine inhibit both L- and N-type calcium channels and thus seem to be unique among the Dihydropyridines examined in their effects on calcium channels in dibutyryl cAMP-differentiated Neuroblastoma x glioma hybrid NG 108-15 Cells, whereas nifedipine and niguldipine appear to block mainly L-type calcium channels, However, amprenavir and nifedipine, an inhibitor of L-type calcium channels, failed to inhibit Long-Term Potentiation when administered following the slow increase in ethanol, Calcium-channel antagonists, omega-Conotoxin GVIA (omega-CgTx GVIA; N-type), nifedipine (L-type), and omega-conotoxin-MVIIC (omega-CmTx MVIIC; P/Q type), were used to characterize the voltage-operated Ca(2+) channels (VOCCs) involved in this release, The T- and L-Type Calcium Channels blocker (CCB) mibefradil attenuates leg edema induced by the L-type CCB nifedipine in the spontaneously Hypertensive (finding) Rattus norvegicus: a novel differentiating assay., L-Type Calcium Channels antagonist nifedipine reduces neurofilament restitution following Optic Nerve Injuries., Nifedipine, an L-Type Calcium Channels blocker, restores the hypnotic response in rats made tolerant to the alpha-2 adrenergic agonist dexmedetomidine., Comparison of L-Type Calcium Channels blockade by nifedipine and/or cadmium in Cavia porcellus ventricular myocytes., Nifedipine inhibits picrotoxin-induced seizure activity: further evidence on the involvement of L-Type Calcium Channels blockers in Epilepsy.[SEP]", "label": "yes"}
{"original_question": "Is pseudouridine a RNA modification?", "id": "converted_1942", "sentence1": "Is pseudouridine a RNA modification?", "sentence2": "Pseudouridine (Ψ) is the most abundant of>150 nucleoside modifications in RNA. , The number and Positioning Attribute of the pseudouridines of Haloarcula marismortui and Deinococcus radiodurans large subunit RNA have been determined by a combination of total nucleoside analysis by HPLC-mass spectrometry and pseudouridine sequencing by the reverse transcriptase method and by LC/MS/MS., Pseudouridine is the most abundant of more than 100 Chemicals distinct natural ribonucleotide modifications.[SEP]Relations: pseudouridine synthesis has relations: bioprocess_bioprocess with RNA modification, bioprocess_bioprocess with RNA modification.", "label": "yes"}
{"original_question": "Are retroviruses used for gene therapy?", "id": "converted_690", "sentence1": "Are retroviruses used for gene therapy?", "sentence2": "Several Immunologic Deficiency Syndromes have been treated successfully by stem cell-targeted, retroviral-mediated gene transfer with reconstitution of the immune system following infusion of the transduced Cells., In this work we have developed and tested a self-inactivating (Sinhalese language) gammaretroviral vector (SINfes.gp91s) containing a codon-optimized transgene (gp91(phox)) under the transcriptional control of a myeloid promoter for the gene therapy of the X-linked form of Peroxisome Biogenesis Disorder, Complementation Group D (X-Peroxisome Biogenesis Disorder, Complementation Group D).,  We used a lentiviral vector encoding functional Wiskott-Aldrich Syndrome wt Allele to genetically correct HSPCs from three Wiskott-Aldrich Syndrome patients and reinfused the Cells after a reduced-intensity conditioning regimen, We used a lentiviral vector to transfer a functional ARSA gene into hematopoietic stem Cells (Hematopoietic stem Cells) from three presymptomatic patients who showed Genetic, biochemical, and neurophysiological evidence of late infantile Leukodystrophy, Metachromatic. , We assessed lentiviral vectors (LVs) targeted to the EC surface marker CD105 for in vivo gene delivery., Guanine Nucleotide Exchange Factors and apoptin genes were cloned into a doxycycline-regulated retrovirus-mediated gene expression system.[SEP]Relations: Wiskott-Aldrich syndrome has relations: disease_protein with Wiskott-Aldrich Syndrome, disease_protein with Wiskott-Aldrich Syndrome.", "label": "yes"}
{"original_question": "Can ATAC-Seq be employed in single-cell mode?", "id": "converted_3849", "sentence1": "Can XCL1 wt Allele-Seq be employed in single-cell mode?", "sentence2": "Single-cell XCL1 wt Allele-Seq: strength in numbers., Assembly, and Single-Cell XCL1 wt Allele-Seq., Single cell RNA-seq and XCL1 wt Allele-Seq analysis of cardiac progenitor cell transition states and lineage settlement.,  Here, we comprehensively characterize Mus sp. cardiac progenitor cells (CPCs) marked by Nkx2-5 and Isl1 expression from E7.5 to E9.5 using single-cell RNA sequencing and Transposase-accessible chromatin location location profiling (XCL1 wt Allele-Seq)., Classifying cells with Scasat, a single-cell XCL1 wt Allele-Seq analysis tool., When done at single-cell resolution, XCL1 wt Allele-Seq provides an insight into the cell-to-cell variability that emerges from otherwise identical DNA Sequence by identifying the variability in the genomic location of open chromatin location location sites in each of the cells., Single-cell XCL1 wt Allele-Seq in Homo sapiens pancreatic islets and deep learning upscaling of rare cells reveals cell-specific type 2 diabetes regulatory signatures., THODS: We present genome-wide single-cell chromatin location location accessibility profiles in >1,600 cells derived from a Homo sapiens pancreatic islet sample using single-cell combinatorial indexing XCL1 wt Allele-Seq (sci-XCL1 wt Allele-Seq). W, Contiguity-Preserving Transposition Sequencing (CPT-Seq) for Genome-Wide Haplotyping, Assembly, and Single-Cell XCL1 wt Allele-Seq., SCALE method for single-cell XCL1 wt Allele-Seq analysis via latent feature extraction., Single-cell XCL1 wt Allele-Seq (scATAC-seq) profiles the chromatin location location accessibility landscape at single cell level, thus revealing cell-to-cell variability in gene regulation., The recently developed low-input and single-cell regulome mapping technologies such as XCL1 wt Allele-Seq and single-cell XCL1 wt Allele-Seq (scATAC-seq) allow analyses of small-cell-number and single-cell samples, but their signals remain highly discrete or noisy., This paper presents Scasat (single-cell XCL1 wt Allele-Seq analysis tool), a complete pipeline to process scATAC-seq data with simple steps., Here, we comprehensively characterize Mus sp. cardiac progenitor cells (CPCs) marked by Nkx2-5 and Isl1 expression from E7.5 to E9.5 using single-cell RNA sequencing and Transposase-accessible chromatin location location profiling (XCL1 wt Allele-Seq)., Single-cell XCL1 wt Allele-Seq (scATAC-seq) technology has also been developed to study cell type-specific chromatin location location accessibility in tissue samples containing a heterogeneous Cells population., Here we combined sequencing of the transcription-coupled nucleotide-excision repair-encoding genes with assay for Transposase-accessible chromatin location location with sequencing (XCL1 wt Allele-Seq) analysis at the single-cell level to provide information on the transcription-coupled nucleotide-excision repair specificity and epigenomic state of individual Therapeutic gamma delta T-lymphocytes., Substantial advances of this work include the optimization of a single-cell combinatorial indexing assay for Transposase accessible chromatin location location (sci-XCL1 wt Allele-Seq); a software suite,, The accessible chromatin location location landscape of the Mus hippocampus at single-cell resolution., Here we present a comprehensive map of the accessible chromatin location location landscape of the Mus sp. hippocampus at single-cell resolution., We expect this review will provide a guideline for successful data generation and analysis methods using appropriate software tools and databases for the study of chromatin location location accessibility at single-cell resolution., Single-cell sequencing assay for Transposase-accessible chromatin location location (scATAC-seq) is the state-of-the-art technology for analyzing genome-wide regulatory landscapes in single cells., Single-cell XCL1 wt Allele-Seq data are sparse and noisy, and analyzing such data is challenging., Here, we introduce a method for analyzing scATAC-seq data, called Single-Cell XCL1 wt Allele-Seq analysis via Latent feature Extraction (SCALE)., Single-cell XCL1 wt Allele-Seq signal extraction and enhancement with SCATE., Single-cell XCL1 wt Allele-Seq detects open chromatin location location in individual cells., Currently data are sparse, but combining information from many single cells can identify determinants of cell-to-cell chromatin location location variation., Predictions based on single-cell RNA-seq (Single-Cell RNA-Seq) can more accurately reconstruct bulk chromatin location location accessibility than using scATAC-seq., Global prediction of chromatin location location accessibility using small-cell-number and single-cell RNA-seq., Single-cell XCL1 wt Allele-Seq (scATAC-seq) maps from hundreds of single cells in aggregate closely resemble accessibility profiles from tens of millions of cells and provide insights into cell-to-cell variation., However, very few studies have been performed at the single cell level (scATAC-seq) due to technical challenges., Here, we present Perturb-XCL1 wt Allele, a method that combines multiplexed CRISPR interference or knockout with genome-wide chromatin location location accessibility profiling in single cells based on the simultaneous detection of CRISPR guide RNA and open chromatin location location sites by assay of Transposase-accessible chromatin location location with sequencing (XCL1 wt Allele-Seq)., Additionally, the same workflow can be used to aid de novo assembly (Adey et al., Genome Res 24(12):2041-2049, 2014), detect structural variants, and perform single cell XCL1 wt Allele-Seq analysis (Cusanovich et al., Science 348(6237):910-914, 2015)., ChromA can analyze single cell XCL1 wt Allele-Seq data, correcting many biases generated by the sparse sampling inherent in single cell technologies.,  circuits. Existing chromatin location location profiling methods such as XCL1 wt Allele-Seq and DNase-seq, applied to islets in bulk, produce aggregate profiles that mask important Cells and regulatory heterogeneity.METHODS: We present genome-wide single-cell chromatin location location accessibility profiles in >1,600 cells derived from a Homo sapiens pancreatic islet sample using single-cell combinatorial indexing XCL1 wt Allele, XCL1 wt Allele-Seq has become a leading technology for probing the chromatin location location landscape of single and aggregated cells.[SEP]", "label": "yes"}
{"original_question": "Are thyroid hormone receptor alpha1 mutations implicated in thyroid hormone resistance syndrome?", "id": "converted_191", "sentence1": "Are thyroid hormone receptor alpha1 mutations implicated in thyroid hormone resistance syndrome?", "sentence2": "This study reports the consequences of levothyroxine treatment over a prolonged period of time in 2 of the first patients with a heterozygous Mutation Abnormality in TRα1., Here we show that the dysregulation of the pituitary-thyroid axis was worsened by the lack of Tricuspid Valve Insufficiency alpha1 in Tricuspid Valve Insufficiency betaPV CASP14 gene, and severe impairment of postnatal growth was manifested in Tricuspid Valve Insufficiency betaPV CASP14 gene deficient in Tricuspid Valve Insufficiency alpha1., Heterozygous 2- to 3-week- old CASP14 gene exhibit a severe retardation of post-natal development and growth, but only a minor reduction in serum thyroxine levels. , The data demonstrate a novel array of effects mediated by a dominant negative TRalpha1, and may provide important clues for identification of a potentially unrecognized human disorder and its treatment., No mutations in DNA- and hormone-binding-domains of TRbeta1 and TRalpha1 genes were found in proband, suggesting that the defect could be due to an unknown Mutation Abnormality in either the Tricuspid Valve Insufficiency gene or a post receptor abnormality, These results demonstrate that the lack of Tricuspid Valve Insufficiency alpha1 exacerbates the manifestation of RTH in Tricuspid Valve Insufficiency betaPV CASP14 gene. Therefore, Tricuspid Valve Insufficiency alpha1 could play a compensatory role in mediating the functions of T3 thoracic segmental innervation thoracic segmental innervation in heterozygous patients with RTH. [SEP]", "label": "yes"}
{"original_question": "Does the human lncRNA LINC-PINT promote tumorigenesis?", "id": "converted_2454", "sentence1": "Does the human lncRNA LINC-PINT promote tumorigenesis?", "sentence2": "The human lncRNA LINC-PINT inhibits Specimen Source Codes - Specimen Source Codes - tumor cell invasion through a highly conserved Sequence - ParameterizedDataType element., Here we characterize the function of the p53-regulated human lncRNA LINC-PINT in Primary malignant neoplasm. We find that LINC-PINT is downregulated in multiple types of Primary malignant neoplasm and acts as a Specimen Source Codes - Specimen Source Codes - tumor suppressor lncRNA by reducing the invasive phenotype of Primary malignant neoplasm cells. A cross-species analysis identifies a highly conserved Sequence - ParameterizedDataType element in LINC-PINT that is essential for its function. This Sequence - ParameterizedDataType mediates a specific interaction with Polycomb Repressive Complex 2, necessary for the LINC-PINT-dependent repression of a pro-invasion signature of Genes regulated by the transcription factor EGR1 gene gene., We find that LINC-PINT is downregulated in multiple types of Primary malignant neoplasm and acts as a Specimen Source Codes - Specimen Source Codes - tumor suppressor lncRNA by reducing the invasive phenotype of Primary malignant neoplasm cells., These results thus indicate that low plasma LINC-PINT gene expression could serve as a minimally invasive biomarker for early Patient-Controlled Analgesia detection, and that low LINC-PINT gene levels in Patient-Controlled Analgesia tumors could be used for predicting patient prognosis., Our data demonstrate that LINC-PINT gene expression is lower in plasma samples from Patient-Controlled Analgesia patients than from healthy individuals, and indicate that plasma LINC-PINT gene levels are more sensitive than CA-19-9 Antigen for detecting Patient-Controlled Analgesia., Low plasma LINC-PINT gene levels correlate with Specimen Source Codes - Specimen Source Codes - tumor recurrence, while low Specimen Source Codes - Specimen Source Codes - tumor LINC-PINT gene levels correlate with poor prognosis for Patient-Controlled Analgesia patients after pancreatectomy., We find that LINC-PINT is downregulated in multiple types of Primary malignant neoplasm and acts as a Specimen Source Codes - Specimen Source Codes - tumor suppressor lncRNA by reducing the invasive phenotype of Primary malignant neoplasm cells., We find that LINC-PINT is downregulated in multiple types of Primary malignant neoplasm and acts as a Specimen Source Codes - Specimen Source Codes - tumor suppressor lncRNA by reducing the invasive phenotype of Primary malignant neoplasm cells., These results thus indicate that low plasma LINC-PINT gene expression could serve as a minimally invasive biomarker for early Patient-Controlled Analgesia detection, and that low LINC-PINT gene levels in Patient-Controlled Analgesia tumors could be used for predicting patient prognosis.<br>, The human lncRNA LINC-PINT inhibits Specimen Source Codes - Specimen Source Codes - tumor cell invasion through a highly conserved Sequence - ParameterizedDataType element.[SEP]Relations: malignant giant cell Specimen Source Codes - tumor has relations: disease_disease with Primary malignant neoplasm, disease_disease with Primary malignant neoplasm.", "label": "no"}
{"original_question": "Can the Micro-C XL method achieve mononucleosome resolution?", "id": "converted_1845", "sentence1": "Can the Micro-C XL method achieve mononucleosome resolution?", "sentence2": "We present Micro-C XL, an improved method for analysis of chromosome folding at mononucleosome resolution, We present Micro-C XL, an improved method for analysis of chromosome folding at mononucleosome resolution., Micro-C XL: assaying chromosome conformation from the nucleosome location location to the entire Genome - anatomical entity., Micro-C XL provides a single assay to interrogate chromosome folding at length scales from the nucleosome location location to the full Genome - anatomical entity.[SEP]", "label": "yes"}
{"original_question": "Is depression associated with poor prognosis of brain tumor patients?", "id": "converted_1497", "sentence1": "Is Depressive disorder associated with poor prognosis of brain tumor patients?", "sentence2": "Before surgery 27 patients (35%) had BDI scores indicating the presence of Depressive disorder. These scores were significantly higher in patients with a history of Depressive disorder (p = 0.017) and in those with a lower functional outcome (p = 0.015)., A lower functional status (KPS score < or = 70) in patients was significantly associated with high Depressive disorder scores at the 3-month (p = 0.000) and 1-year (p = 0.005) assessments., At all follow-ups, depressed low-grade glioma patients had a significantly shorter survival time, 3.3-5.8 years, compared to non-depressed low-grade glioma patients, 10.0-11.7 years., The results suggest that Depressive disorder and decreased QOL among low-grade glioma patients is related to shorter survival at long-term follow-up., The adverse impact of Depressive disorder in relation to survival among Primary malignant neoplasm patients is currently a subject of great interest in research., In the subgroup of patients with low-grade Glioma, depressive patients had a significantly shorter survival time compared with nondepressive subjects (P = 0.031, Kaplan-Meier survival analysis)., Preoperative Depressive disorder seemed to be a significant prognostic factor for worse survival in low-grade glioma patients., Major depressive disorder was marginally associated with outcomes, while surgical interventions and radiotherapy did not show strong associations with test performances.[SEP]", "label": "yes"}
{"original_question": "Is AZD9668 a VEGF mRNA drug?", "id": "converted_4283", "sentence1": "Is AZD9668 a VEGF mRNA drug?", "sentence2": "AZD9668, a ELANE gene inhibitor, plus ongoing budesonide / formoterol in patients with Chronic Obstructive Airway Disease., AZD9668 is a reversible and selective inhibitor of No evidence of, well tolerated at doses of 60 mg Twice a day during Phase I/IIa development.[SEP]", "label": "no"}
{"original_question": "Was golimumab tested for diabetes?", "id": "converted_4031", "sentence1": "Was golimumab tested for diabetes?", "sentence2": "CONCLUSIONS: Among children and young adults with newly diagnosed overt type 1 diabetes, golimumab resulted in better endogenous Therapeutic Insulin production and less exogenous Therapeutic Insulin use than placebo. , Golimumab and Beta-Cell Function in Youth with New-Onset Type 1 Diabetes., lticenter, placebo-controlled, double-blind, parallel-group trial, we randomly assigned, in a 2:1 ratio, children and young adults (age range, 6 to 21 years) with newly diagnosed overt type 1 diabetes to receive subcutaneous golimumab or placebo for 52 weeks. The primary end point was e, Golimumab and Beta-Cell Function in Youth with New-Onset Type 1 Diabetes[SEP]", "label": "yes"}
{"original_question": "Is there evidence that tomato juice lowers cholesterol levels?", "id": "converted_418", "sentence1": "Is there evidence that Lycopersicon esculentum juice lowers cholesterol levels?", "sentence2": "The hypocholesterolemic effect of Lycopersicon esculentum juice has been investigated in an intervention study with Rattus norvegicus, along with the possible inhibition effect of bioactive Lycopersicon esculentum compounds binding to the HMGCR protein, human protein, human Enzyme [APC]., The molecular modelling showed that components of Lycopersicon esculentum can bind to the Active Site of the Enzyme [APC] and compete with the ligand HMGCoA. Lycopene, from Lycopersicon esculentum juice, accumulates in the Abdomen>Liver and can inhibit the activity of the rate-limiting Enzyme [APC] of cholesterol biosynthesis, HMGCR protein, human protein, human.,  Juice consumption significantly improved resistance of Low-Density Lipoproteins+VLDL-C to Cu(2+)-mediated oxidation (P = 0.039), High Density Lipoproteins-C (47.3 ± 15.8 to 51.7 ± 14.8 mg/dL, P<0.001), and the ratio of total-C/High Density Lipoproteins-C (4.25 ± 1.59 to 3.63 ± 1.16, P<0.001) at 8 wk., RESULTS: Intervention with the enriched juice had no effect on the lipid profile, and serum levels of Triglycerides and cholesterol (total, Low-Density Lipoproteins, and High Density Lipoproteins) remained unchanged. , Women consuming ≥10 compared with<1.5 servings/wk of Lycopersicon esculentum-based food products had significant but clinically modest improvements in total cholesterol (CD55 wt Allele) (5.38 vs. 5.51 mmol/L; P = 0.029), the CD55 wt Allele:High Density Lipoproteins cholesterol ratio (4.08 vs. 4.22; P = 0.046), and Glycosylated hemoglobin A (5.02 vs. 5.13%; P<0.001) in multivariable models. Considering clinical cutpoints, women consuming ≥10 compared with<1.5 servings/wk were 31% (95% CI = 6%, 50%), 40% (95% CI = 13%, 59%), and 66% (95% CI = 20%, 86%) less likely to have elevated CD55 wt Allele (≥6.21 mmol/L), Low-Density Lipoproteins cholesterol (≥4.14 mmol/L), and Glycosylated hemoglobin A (≥6%), respectively. , In conclusion, women consuming ≥10 compared with<1.5 servings/wk of Lycopersicon esculentum-based food products had clinically modest but significant improvements in CD55 wt Allele, the CD55 wt Allele:High Density Lipoproteins cholesterol ratio, and Glycosylated hemoglobin A but not other coronary biomarkers., Tomato juice decreases Low-Density Lipoproteins cholesterol levels and increases Low-Density Lipoproteins resistance to oxidation., Total cholesterol concentration was reduced by 5.9 (sd 10) % (P = 0.002) and Low-Density Lipoproteins cholesterol concentration by 12.9 (sd 17.0) % (P = 0.0002) with the high Lycopersicon esculentum diet compared to the low Lycopersicon esculentum diet., In conclusion, a high dietary intake of Lycopersicon esculentum products had atheroprotective effects, it significantly reduced Low-Density Lipoproteins cholesterol levels, and increased Low-Density Lipoproteins resistance to oxidation in healthy normocholesterolaemic adults., Total, Low-Density Lipoproteins and High Density Lipoproteins cholesterol were significantly lower in the intervention group after the intake of Lycopersicon esculentum juice, Total cholesterol concentration was reduced by 5.9 (sd 10) % (P = 0.002) and Low-Density Lipoproteins cholesterol concentration by 12.9 (sd 17.0) % (P = 0.0002) with the high Lycopersicon esculentum diet compared to the low Lycopersicon esculentum diet. [SEP]", "label": "yes"}
{"original_question": "Is there a sequence bias in MNase digestion patterns?", "id": "converted_2245", "sentence1": "Is there a sequence bias in MNase digestion patterns?", "sentence2": "In addition, unlike MNase, MPE-Fe(II) cleaves Nuclear deoxyribonucleic acid with little sequence bias., These findings collectively indicate that MPE-seq provides a unique and straightforward means for the genome-wide analysis of chromatin structure with minimal DNA sequence bias., Micrococcal Nuclease does not substantially bias nucleosome location location mapping., MNase has hitherto been very widely used to map Nucleosomes, although concerns have been raised over its potential to introduce bias., These results indicate that biases in nucleosome location location positioning data collected using MNase are, under our conditions, not significant., Signal variation in these simulations reveals an important DNA sampling bias that results from a neighborhood effect of MNase digestion techniques., Standardized collection of MNase-seq experiments enables unbiased dataset comparisons., Here, we show that the cutting preference of MNase in combination with size selection generates a sequence-dependent bias in the resulting fragments., We propose that combined MNase/exoIII digestion can be applied to in situ chromatin for unbiased genome-wide mapping of nucleosome location location positions that is not influenced by DNA Sequence at the core/linker junctions., Signal variation in these simulations reveals an important DNA sampling bias that results from a neighborhood effect of MNase digestion techniques., Signal variation in these simulations reveals an important DNA sampling bias that results from a neighborhood effect of MNase digestion techniques., These results indicate that biases in nucleosome location location positioning data collected using MNase are, under our conditions, not significant.., Micrococcal Nuclease does not substantially bias nucleosome location location mapping., We find that maize MNase-hypersensitive (MNase HS) regions localize around active genes and within recombination hotspots, focusing biased gene conversion at their flanks.[SEP]", "label": "yes"}
{"original_question": "Has LB-100 been tested in clinical trials?", "id": "converted_3566", "sentence1": "Has LB-100 been tested in clinical trials?", "sentence2": "To determine the MTD and to assess the safety, tolerability, and potential activity of LB-100, a first-in-class small-molecule inhibitor of protein phosphatase 2A activity activity (Protein Phosphatase 2A) in adult patients with progressive Solid Neoplasm., Safety, Tolerability, and Preliminary Activity of LB-100, an Inhibitor of Protein Phosphatase 2A, in Patients with Relapsing course Solid Tumors: An Open-Label, Dose Escalation, First-in-Human, Phase I Trial.[SEP]", "label": "yes"}
{"original_question": "Can saponins be used as adjuvant?", "id": "converted_3898", "sentence1": "Can saponins be used as adjuvant?", "sentence2": "We report the design, synthesis, immunological evaluation, and conformational analysis of new Saponinum, Saponinum, saponin, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation variants as promising vaccine adjuvants, The purified active fraction of Albizia julibrissin Saponinum, Saponinum, saponin, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation (AJSAF) is an ideal adjuvant candidate, BALB/c mice immunized with subcutaneous injections of the Recombinant Proteins with or without liposome/Saponinum, Saponinum, saponin, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation (Lip/Sap) as an adjuvant.,  a Saponinum, Saponinum, saponin, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation-based Matrix-M™ adjuvant, . These results confirm that Momordica saponins are a viable natural source to provide potent Saponinum, Saponinum, saponin, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation, glucosidal found in Quillaya, Yucca and Senega, Homeopathic preparation adjuvants[SEP]", "label": "yes"}
{"original_question": "Are mucin overexpression associated with disease?", "id": "converted_3996", "sentence1": "Are Homo sapiens MUC1 protein overexpression associated with disease?", "sentence2": "The pathological mechanism underlying Liver calculus is closely related to bacterial infections of the Intrahepatic bile duct, followed by chronic inflammation and the overexpression of Homo sapiens MUC1 wt Allele protein 5AC (MUC5AC protein, human protein, Homo sapiens)., MUC1 wt Allele wt Allele is a Membrane Glycoproteins, which in adenocarninomas is overexpressed and exhibits truncated O-glycosylation. , Mucin 13 (MUC13 gene gene) is reportedly overexpressed in Homo sapiens malignancies., Inflammation causes MUC1 wt Allele wt Allele overexpression and hypoglycosylation. [SEP]", "label": "yes"}
{"original_question": "Does verubecestat activate BACE?", "id": "converted_2605", "sentence1": "Does verubecestat activate BACE?", "sentence2": "Verubecestat is a potent BACE1 protein, human protein, human enzyme inhibitor currently being investigated in Phase III trials for the treatment of mild-to-moderate and prodromal ALZHEIMER DISEASE, FAMILIAL, 1. [SEP]", "label": "no"}
{"original_question": "Are there small molecule CGRPs under development for the treatment of migraine?", "id": "converted_4011", "sentence1": "Are there small molecule CGRPs under development for the treatment of Migraine Disorders?", "sentence2": "Meanwhile, 1 small-molecule Calcitonin Gene-Related Peptide Receptor Antagonists (ubrogepant, MK-1602) is currently in phase 3 studies for the acute treatment of Migraine Disorders., Several other small-molecular CGRP receptor antagonists are in earlier stages of development for acute Migraine Disorders treatment or prevention. [SEP]", "label": "yes"}
{"original_question": "Is progesterone effective for treatment of patients with traumatic brain injury based on clinical trial data?", "id": "converted_436", "sentence1": "Is progesterone effective for treatment of patients with Traumatic Brain Injury based on clinical trial data?", "sentence2": "BACKGROUND: Progesterone [EPC] [EPC] has been associated with robust positive effects in animal models of Traumatic Brain Injury (TBI) and with clinical benefits in two phase 2 randomized, controlled trials. , The proportion of patients with a favorable outcome on the Glasgow Outcome Scale (good recovery or moderate Disability:Type:Pt:^Patient:Nom) was 50.4% with progesterone, as compared with 50.5% with placebo. Mortality was similar in the two groups. No relevant safety differences were noted between progesterone and placebo. CONCLUSIONS: True primary (qualifier value) and secondary efficacy analyses showed no clinical benefit of progesterone in patients with severe TBI. These data stand in contrast to the robust preclinical data and results of early single-center trials that provided the impetus to initiate phase 3 trials., BACKGROUND: Traumatic Brain Injuries (TBI) is a major cause of death and Disability:Type:Pt:^Patient:Nom worldwide. Progesterone [EPC] [EPC] has been shown to improve neurologic outcome in multiple experimental models and two early-phase trials involving patients with TBI. , There was no significant difference between the progesterone group and the placebo group in the proportion of patients with a favorable outcome (relative benefit of progesterone, 0.95; 95% confidence interval [NDUFB6 gene], 0.85 to 1.06; P=0.35). Phlebitis or Thrombophlebitis was more frequent in the progesterone group than in the placebo group (relative risk, 3.03; NDUFB6 gene, 1.96 to 4.66). , CONCLUSIONS: This clinical trial did not show a benefit of progesterone over placebo in the improvement of outcomes in patients with acute TBI. , Numerous studies, however, show that progesterone has substantial pleiotropic properties as a neuroprotective agent in both animal models and Homo sapiens., RESULTS: There was a better recovery rate and Genomics Outcome Scale score for the patients who were given progesterone than for those in the control group in a 3-months follow-up period (50% vs. 21%); subgroup analysis showed a significant difference in the percentage of favorable outcome between the two groups with GCS of 5-8 (p=0.03). CONCLUSION: The use of progesterone may significantly improve neurologic outcome of patients suffering severe TBI up to 3 months after injury, especially those with 5≤GCS≤8, providing a potential benefit to the treatment of acute severe TBI patients. Considering this Pharmacologic Substance had no significant side effects, so progesterone could be used in patients with severe TBI as a neuro-protective Pharmacologic Substance., While progesterone and cyclosporine have shown promise in phase II studies, success in larger phase III, randomized, multicentre, clinical trials is pending.,  All three studies reported the effects of progesterone on mortality. The pooled risk ratio (RR) for mortality at end of follow-up was 0.61, 95% confidence interval (NDUFB6 gene) 0.40 to 0.93. Three studies measured Disability:Type:Pt:^Patient:Nom and found the RR of death or severe Disability:Type:Pt:^Patient:Nom in patients treated with progesterone to be 0.77, 95% NDUFB6 gene 0.62 to 0.96., AUTHORS' CONCLUSIONS: Current clinical evidence from three small RCTs indicates progesterone may improve the neurologic outcome of patients suffering TBI. This evidence is still insufficient and further multicentre randomised controlled trials are required., Genomics Outcome Scale was classified to 2 main categories of favorable and unfavorable recovery, of which, favorable recovery in placebo, progesterone, and progesterone-ergocalciferol was 25%, 45%, and 60%, respectively which showed a statistical significant difference among the groups (P-value = 0.03). CONCLUSION: The results showed that recovery rate in patients with severe brain trauma in the group receiving progesterone and ergocalciferol together was significantly higher than that of progesterone group, which was in turn higher than that of placebo group.,  The pooled relative risk (RR) for mortality at end of follow-up is 0.61, 95% confidence interval (NDUFB6 gene) 0.40 to 0.93. Three studies measured Disability:Type:Pt:^Patient:Nom and found the RR of death or severe Disability:Type:Pt:^Patient:Nom in patients treated with progesterone was 0.77, 95% confidence interval (NDUFB6 gene) 0.62 to 0.96., AUTHORS' CONCLUSIONS: Current clinical evidence from three small RCTs indicates progesterone may improve the neurologic outcome of patients suffering TBI. This evidence is still insufficient and further multicentre randomised controlled trials are required., Clinical trials have shown that short-and long-term progesterone treatment induces a significant improvement in the level of Disability:Type:Pt:^Patient:Nom among patients with Brain Injuries. , Improved outcomes from the administration of progesterone for patients with acute severe Traumatic Brain Injury: a randomized controlled trial., CONCLUSION: Our data suggest that acute severe TBI patients with administration of progesterone hold improved neurologic outcomes for up to 6 months. These results provide information important for further large and multicenter clinical trials on progesterone as a promising neuroprotective Pharmacologic Substance. , The modified Functional Independence Measure scores in the progesterone group were higher than those in the placebo group at both 3-month and 6-month follow-up (P < 0.05 and P < 0.01). The mortality rate of the progesterone group was significantly lower than that of the placebo group at 6-month follow-up (P < 0.05). , CONCLUSION: Our data suggest that acute severe TBI patients with administration of progesterone hold improved neurologic outcomes for up to 6 months. These results provide information important for further large and multicenter clinical trials on progesterone as a promising neuroprotective Pharmacologic Substance. , These data, combined with the results of the previously published ProTECT trial, show progesterone to be safe and potentially efficacious in the treatment of TBI. Larger phase III trials will be necessary to verify results prior to clinical implementation., CONCLUSION: It indicated that successive early application of PEPSINOGEN GENE will benefit the patients with acute severe head injury by improving the recovery and reducing the Disability:Type:Pt:^Patient:Nom, which may be related to its alleviating inflammatory and Lipid Peroxidation response., Adverse and serious adverse event rates were similar in both groups, except that patients randomized to progesterone had a lower 30-day mortality rate than controls (rate ratio 0.43; 95% confidence interval 0.18 to 0.99). , However, moderate Traumatic Brain Injury survivors who received progesterone were more likely to have a moderate to good outcome than those randomized to placebo. CONCLUSION: In this small study, progesterone caused no discernible harm and showed possible signs of benefit., After more than 30 years of research and 30 failed clinical trials with as many different treatments, progesterone is the first agent to demonstrate robust clinical efficacy as a treatment for traumatic brain injuries., After more than 30 years of research and 30 failed clinical trials with as many different treatments, progesterone is the first agent to demonstrate robust clinical efficacy as a treatment for traumatic brain injuries, A US National Institutes of Health-sponsored, nationwide Phase III clinical trial is now evaluating progesterone for moderate-to-severe TBI in 1200 patients, An industry-sponsored Phase III international trial is also under way, and planning for a trial using progesterone to treat pediatric Brain Injuries has begun, More than two decades of pre-clinical research and two recent clinical trials have shown that progesterone (PROG) and its Metabolite exert beneficial effects after Traumatic Brain Injury (TBI) through a number of metabolic and physiological pathways that can reduce damage in many different Body tissue and organ systems, After more than 30 years of research and 30 failed clinical trials with as many different treatments, progesterone is the first agent to demonstrate robust clinical efficacy as a treatment for traumatic brain injuries, RESULTS: Analysis of these reviews yielded meanfuling observations: (1) The effectiveness of most ordinary treatments in TBI is inconclusive except that Corticosteroid ophthalmologic and otologic preparations are likely to be ineffective or harmful, and tranexamic acid, nimodipine and progesterone show a promising effect in bleeding trauma, Traumatic spinal subarachnoid hemorrhage, TBI or severe TBI., Laboratory data strongly show that progesterone treatment after TBI reduces Edema:Finding:Point in time:^Patient:Ordinal, improves outcomes, and restores blood-brain barrier function. Clinical studies to date agree with these data, and there are ongoing human trials for progesterone treatment after TBI.[SEP]Relations: Progesterone [EPC] has relations: contraindication with Thrombophlebitis, contraindication with Thrombophlebitis. Tranexamic acid has relations: contraindication with Thrombophlebitis, drug_drug with Progesterone [EPC], contraindication with Thrombophlebitis, drug_drug with Progesterone [EPC]. Cyclosporine has relations: drug_drug with Progesterone [EPC], drug_drug with Progesterone [EPC]. Thrombophlebitis has relations: drug_effect with Progesterone [EPC], drug_effect with Progesterone [EPC]. phlebitis has relations: disease_disease with Thrombophlebitis, disease_disease with Thrombophlebitis.", "label": "no"}
{"original_question": "Is sonidegib effective for basal cell carcinoma?", "id": "converted_2236", "sentence1": "Is sonidegib effective for Skin Basal Cell Carcinoma?", "sentence2": "This review of the literature aims to describe previous and current treatment options for oral therapy in locally advanced and metastatic NMSC otherwise unamenable to standard treatment. Oral SMO protein, human (Smo) inhibitors Vismodegib, sonidegib, and Taladegib have shown to be effective in several trials. , sonidegib is a new smoothened PPP1R1A gene currently under investigation for treatment of laBCC, which demonstrates a comparable safety profile to vismodegib. , The recent development of novel hedgehog pathway inhibitors for high-risk Basal cell carcinoma (including oral vismodegib and sonidegib) may represent a paradigm shift towards medical management of NMSC., sonidegib (Odomzo®), an oral smoothened (SMO) antagonist, is indicated for the treatment of adults with locally advanced Skin Basal Cell Carcinoma (laBCC) who are not candidates for surgery or radiation therapy, or adults with recurrent laBCC following surgery or radiation therapy. , The acceptable benefit-risk profile of sonidegib, along with a paucity of treatment options and the seriousness of the condition, makes sonidegib an emerging option for the treatment of adults with laBCC that has recurred following surgery or radiation therapy, or in those who are not candidates for surgery or radiation therapy., sonidegib phosphate: new approval for Skin Basal Cell Carcinoma., sonidegib, a novel smoothened PPP1R1A gene for the treatment of advanced Skin Basal Cell Carcinoma., Serious adverse events occurred in 11 (14%) of 79 patients in the 200 mg group and 45 (30%) of 150 patients in the 800 mg group.The benefit-to-risk profile of 200 mg sonidegib might offer a new treatment option for patients with advanced Skin Basal Cell Carcinoma, a population that is difficult to treat.Novartis Pharmacologic Substance Corporation.<CopyrightInformation>Copyright © 2015 Elsevier Ltd. All rights reserved.</, However, to date, Hh inhibitors, specifically those targeting SMO protein, human [such as vismodegib, BMS-833923, Patidegib (IPI-926), sonidegib/erismodegib (SMO protein, human Antagonist Smoothened Antagonist LDE225), PF-04449913, LY2940680, LEQ 506, and TAK-441], have demonstrated good efficacy as monotherapy in patients with Skin Basal Cell Carcinoma and Medulloblastoma, but have shown limited activity in other tumor types., The hedgehog pathway PPP1R1A gene sonidegib demonstrated meaningful tumor shrinkage in more than 90% of patients with locally advanced Skin Basal Cell Carcinoma (Basal cell carcinoma) or metastatic Basal cell carcinoma in the Basal cell carcinoma Outcomes with SMO protein, human Antagonist Smoothened Antagonist LDE225 Treatment study.This report provides long-term follow-up data collected up to 12 months after the last patient was randomized.In this multicenter, randomized, double-blind phase II study, patients were randomized 1:2 to sonidegib 200 or 800 mg. The primary end point was objective response rate assessed by central review.Objective response rates in the 200- and 800-mg arms were 57.6% and 43.8% in locally advanced B, Serious adverse events occurred in 11 (14%) of 79 patients in the 200 mg group and 45 (30%) of 150 patients in the 800 mg group.The benefit-to-risk profile of 200 mg sonidegib might offer a new treatment option for patients with advanced Skin Basal Cell Carcinoma, a population that is difficult to treat.Novartis Pharmacologic Substance Corporation.<CopyrightInformation>Copyright © 2015 Elsevier Ltd. All rights reserved.</C, Oral sonidegib is approved in Switzerland for the treatment of adult patients with advanced Skin Basal Cell Carcinoma (Basal cell carcinoma) and in the US and EU for the treatment of adult patients with locally advanced Basal cell carcinoma that has recurred following surgery or radiation therapy, or those who are not candidates for surgery or radiation therapy., sonidegib phosphate: new approval for Skin Basal Cell Carcinoma.[SEP]Relations: Medulloblastoma has relations: disease_phenotype_positive with Medulloblastoma, disease_phenotype_positive with Medulloblastoma.", "label": "yes"}
{"original_question": "Is Impetigo a viral infection that affects the skin?", "id": "converted_3660", "sentence1": "Is Impetigo a viral infection that affects the Skin Specimen Source Code?", "sentence2": "Importance: ozenoxacin, a novel topical antibacterial agent with potent bactericidal activity against gram-positive bacteria, has been developed as a cream with 1% active drug for the treatment of impetigo, a highly contagious Bacterial Infection of Skin Specimen Source Code and/or subcutaneous tissue, : To compare the in vitro activity of the anti-impetigo agent, ozenoxacin, and other Microbicides against Gram-positive clinical isolates from Skin Specimen Source Code and soft tissue infections, Streptococcus pyogenes is responsible for a wide variety of Recurrent Skin Diseases, Infectious ranging from Superficial impetigo to fulminant invasive necrotizing fasciitis., Impetigo is a highly contagious Bacterial Infection of Skin Specimen Source Code and/or subcutaneous tissue and is one of the most common Skin Specimen Source Code infections in children, Impetigo is a Superficial Bacterial Infections that most commonly affects the face and All All extremities of children., Impetigo is the most common Bacterial Infection of Skin Specimen Source Code and/or subcutaneous tissue of children., Impetigo is the most common Bacterial Infection of Skin Specimen Source Code and/or subcutaneous tissue in children two to five years of age., BACKGROUND Impetigo can result from Staphylococcus aureus (Staphylococcus aureus)., Impetigo , Cellulitis , and Specimen Source Codes - Abscess comprise the majority of childhood Bacterial Skin Specimen Source Code infections and are treated with topical or systemic Antifungal Antibiotics, Topical that cover group A Streptococcus and Staphylococcus aureus . , BACKGROUND\nImpetigo can result from Staphylococcus aureus (Staphylococcus aureus)., Impetigo is a Superficial Bacterial Infections that most commonly affects the face and All All extremities of children., Impetigo is a Superficial, but contagious, Bacterial Infections of the Skin Specimen Source Code that predominantly affects children and is common in primary care., Impetigo is a common, Superficial, Bacterial Infections of the Skin Specimen Source Code characterized by an inflamed and infected Epidermal cells., Impetigo, a Bacterial Infection of Skin Specimen Source Code and/or subcutaneous tissue that involves the Superficial layers of the Skin Specimen Source Code, is one of the most common Skin Specimen Source Code infections in children ages 2 to 5 but can occur in individuals across the lifespan., Impetigo contagiosa is a common, Superficial, Bacterial Infections of the Skin Specimen Source Code characterised by an inflamed and infected Epidermal cells caused by Staphylococcus aureus, Streptococcus pyogenes or both.[SEP]Relations: impetigo has relations: disease_disease with Infection of Skin Specimen Source Code and/or subcutaneous tissue, disease_disease with Infection of Skin Specimen Source Code and/or subcutaneous tissue.", "label": "no"}
{"original_question": "Are patients with marfan syndrome at increased risk of arrhythmias?", "id": "converted_933", "sentence1": "Are patients with marfan syndrome at increased risk of arrhythmias?", "sentence2": "FBN1 gene (Marfan Syndrome) is a variable, autosomal-dominant disorder of the Connective Tissue. In Marfan Syndrome serious Ventricular arrhythmia and Sudden Cardiac Death (SCD) can occur., Marfan's patients carry increased risk for cardiac arrhythmias. , Ventricular arrhythmias were present in 21% and were associated with increased left ventricular size, Mitral Valve Prolapse Syndrome, and abnormalities of repolarization., Cardiac complication are rare in young patients with FBN1 gene receiving medical therapy and close clinical follow-up. Sudden death still occurs, and appears more common in patients with a dilated left ventricle. Left ventricular dilation may predispose to alterations of repolarization and fatal Ventricular arrhythmia.[SEP]Relations: Sudden cardiac death has relations: phenotype_phenotype with Sudden death, phenotype_phenotype with Sudden death.", "label": "yes"}
{"original_question": "Has MLE4901 been tested in phase III clinical trials?", "id": "converted_3707", "sentence1": "Has MLE4901 been tested in phase III clinical trials?", "sentence2": "METHODS\n\nThis phase 2, randomised, double-blind, placebo-controlled, single-centre, crossover trial assessed the effectiveness of an oral neurokinin 3 receptor antagonist (MLE4901) on menopausal hot flushes., Neuromedin K Receptor antagonism as a novel treatment for menopausal hot flushes: a phase 2, randomised, double-blind, placebo-controlled trial.[SEP]", "label": "no"}
{"original_question": "Does vesatolimod inhibit TLR7?", "id": "converted_2796", "sentence1": "Does vesatolimod inhibit TLR7?", "sentence2": "vesatolimod (GS-9620) is an oral agonist of TLR7 gene, an activator of innate and adaptive immune responses. [SEP]", "label": "no"}
{"original_question": "Has single guide RNA been used on human cells?", "id": "converted_999", "sentence1": "Has single guide RNA been used on Human cells?", "sentence2": "We used a library containing 73,000 sgRNAs to generate knockout collections and performed screens in two human cell lines., Here we engineer this system to enable RNA-guided genome regulation in Human cells by tethering transcriptional activation domains either directly to a nuclease-null CRISPR-Associated Protein 9 or to an aptamer-modified single guide RNA (sgRNA)., The type II CRISPR/Cas system from Streptococcus pyogenes and its simplified derivative, the Cas9/single guide RNA (sgRNA) system, have emerged as potent new tools for targeted gene knockout in Bacteria, Saccharomyces cerevisiae, Drosophila <Drosophila <fruit fly, genus>, genus>, Zebrafish and Human cells., Here we engineer this system to enable RNA-guided genome regulation in Human cells by tethering transcriptional activation domains either directly to a nuclease-null CRISPR-Associated Protein 9 or to an aptamer-modified single guide RNA (sgRNA). , Using synthetic single RNA guides, Cas9 can be reprogrammed to create specific double-stranded DNA breaks in the Genome of a variety of Organism, ranging from Human cells to Bacteria, and thus constitutes a powerful tool for genetic engineering. , Here we engineer this system to enable RNA-guided genome regulation in Human cells by tethering transcriptional activation domains either directly to a nuclease-null CRISPR-Associated Protein 9 or to an aptamer-modified single guide RNA (sgRNA).[SEP]", "label": "yes"}
{"original_question": "Can ferric carboxymaltose be used to treat anemia in inflammatory bowel disease patients?", "id": "converted_1219", "sentence1": "Can ferric carboxymaltose be used to treat Genus Anemia in INFLAMMATORY BOWEL DISEASE 2 patients?", "sentence2": "Intravenous Ferrum metallicum, Homeopathic preparation should be preferred where oral Ferrum metallicum, Homeopathic preparation is poorly tolerated or where it has failed in moderate to severe Genus Anemia, and in combination with Recombinant Erythropoietin, ferric carboxymaltose is much more convenient, and has been shown to be more effective than Ferrum metallicum, Homeopathic preparation sucrose in a large randomized tria, Nemia and Ferrum metallicum, Homeopathic preparation deficiency Genus Anemia are very common in INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome, ferric carboxymaltose was associated with cost savings of 30-44 % per patient per treatment cycle compared to Ferrum metallicum, Homeopathic preparation sucrose. , Iron deficiency is common in pregnancy, postpartum, INFLAMMATORY BOWEL DISEASE 2, chronic kidney disease, Chronic heart failure, heavy uterine bleeding, Primary malignant neoplasm and following surgery. We estimate the budget impact (BI) on the Swiss mandatory health insurance associated with substituting Ferrum metallicum, Homeopathic preparation sucrose (standard) with ferric carboxymaltose (new treatment) using real-life data., reating Ferrum metallicum, Homeopathic preparation deficiency involves substantial costs to the Swiss MHI which may be reduced by substituting Ferrum metallicum, Homeopathic preparation sucrose with ferric carboxymaltose., e aim of this study was to observe, in a non-interventional way, how Swedish gastroenterologists adhere to guidelines in Irritable Bowel Syndrome outpatients treated with intravenous ferric carboxymaltose (MYOCLONUS, FAMILIAL CORTICAL), and the result of treatment, MYOCLONUS, FAMILIAL CORTICAL lowers platelet counts and platelet activation in patients with Irritable Bowel Syndrome-associated Reactive thrombocytosis., We performed a randomized, single-blinded placebo-controlled trial testing the effect of ferric carboxymaltose (MYOCLONUS, FAMILIAL CORTICAL) in patients with Irritable Bowel Syndrome with Reactive thrombocytosis (Blood Platelets > 450 G/L), e performed a randomized, placebo-controlled trial to determine if administration of ferric carboxymaltose (MYOCLONUS, FAMILIAL CORTICAL) prevents Genus Anemia in patients with Irritable Bowel Syndrome and low levels of Serum ferritin measurement, MYOCLONUS, FAMILIAL CORTICAL prevents recurrence of Genus Anemia in patients with Irritable Bowel Syndrome, compared with placebo. ,  A subgroup was analyzed regarding efficacy and side effects of Ferrum metallicum, Homeopathic preparation supplementation with ferric carboxymaltose., Iron deficiency and Genus Anemia are frequent in Irritable Bowel Syndrome patients. Treatment with ferric carboxymaltose is efficious, safe and well tolerated in Ferrum metallicum, Homeopathic preparation-deficient Irritable Bowel Syndrome patients.,  Intravenous Ferrum metallicum, Homeopathic preparation avoids these concerns, especially with the development of ferric carboxymaltose, which allow up to 1000mg to be given rapidly., What is the optimal treatment for Genus Anemia in INFLAMMATORY BOWEL DISEASE 2?, We compared the efficacy and safety of a novel fixed-dose ferric carboxymaltose regimen (MYOCLONUS, FAMILIAL CORTICAL) with individually calculated Ferrum metallicum, Homeopathic preparation sucrose (IS) doses in patients with INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome) and Inosine Dialdehyde, Study drugs were well tolerated and drug-related adverse events were in line with drug-specific clinical experience,  The simpler MYOCLONUS, FAMILIAL CORTICAL-based dosing regimen showed better efficacy and compliance, as well as a good safety profile, compared with the Ganzoni-calculated IS dose regimen., ferric carboxymaltose can be rapidly administered in doses of 15 mg/kg body weight, up to a ceiling dose of 1000 mg. A test dose is not required, and it can be used more widely across a spectrum of Ferrum metallicum, Homeopathic preparation deficiency and Ferrum metallicum, Homeopathic preparation deficiency Genus Anemia indication,  Intravenous Ferrum metallicum, Homeopathic preparation offers a rapid means of Ferrum metallicum, Homeopathic preparation repletion and is superior to oral Ferrum metallicum, Homeopathic preparation in many circumstances, especially in the presence of Genus Anemia of Chronic disease, where it appears to overcome the block to absorption of Ferrum metallicum, Homeopathic preparation from the Abdomen+Pelvis>Gastrointestinal tract and immobilization of stored Ferrum metallicum, Homeopathic preparation. The clinical situations where high doses of Ferrum metallicum, Homeopathic preparation are commonly required are reviewed. These include nondialysis-dependent chronic kidney disease, INFLAMMATORY BOWEL DISEASE 2, obstetrics, Menorrhagia, and Genus Anemia associated with Primary malignant neoplasm and its treatment. , ferric carboxymaltose can be administered at 15 mg/kg body weight to a maximum dose of 1000 mg, whereas Ferrum metallicum, Homeopathic preparation isomaltoside 1000 can be administered at 20 mg/kg body weight. The ability to give high doses of Ferrum metallicum, Homeopathic preparation is important in the context of managing Ferrum metallicum, Homeopathic preparation deficiency Genus Anemia in a number of clinical conditions where demands for Ferrum metallicum, Homeopathic preparation are high (including chronic blood loss associated with INFLAMMATORY BOWEL DISEASE 2, Menorrhagia, and chronic kidney disease), erric carboxymaltose (MYOCLONUS, FAMILIAL CORTICAL, Ferinject) was effective and well tolerated in the treatment of Ferrum metallicum, Homeopathic preparation-deficiency Genus Anemia (Inosine Dialdehyde) in nine, Phase III, randomized, controlled, multicenter trials in a diverse range of indications, including patients with INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome), post-partum Genus Anemia (phenylpropanolamine) or Abnormal uterine bleeding (AUB), Chronic heart failure (Congestive heart failure), non-dialysis-dependent chronic kidney disease (Chronic Kidney Diseases) and those undergoing hemodialysis (Hodgkin Disease, In patients with Irritable Bowel Syndrome or phenylpropanolamine, improvements in Hemoglobin levels were more rapid with MYOCLONUS, FAMILIAL CORTICAL than with FeSulf. , Caudomedial auditory cortex improved patient quality of life to an equivalent extent to oral FeSulf in patients with Irritable Bowel Syndrome or phenylpropanolamine, and to a greater extent than oral FeSulf in women with AUB, Four different products are principally used in clinical practice, which differ in their pharmacokinetic properties and safety profiles: Ferrum metallicum, Homeopathic preparation gluconate and Ferrum metallicum, Homeopathic preparation sucrose (lower single doses), and Ferrum metallicum, Homeopathic preparation dextran and ferric carboxymaltose (higher single doses)., he prevalence of Genus Anemia across studies on patients with INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome) is high (30%).,  novel intravenous Ferrum metallicum, Homeopathic preparation formulation for treatment of Genus Anemia in INFLAMMATORY BOWEL DISEASE 2: the ferric carboxymaltose (FERINJECT) randomized controlled trial., FeCarb is effective and safe in Irritable Bowel Syndrome-associated Genus Anemia. It is noninferior to FeSulf in terms of Hemoglobin change over 12 wk, and provides a fast Hemoglobin increase and a sufficient refill of Ferrum metallicum, Homeopathic preparation stores., Treatment-related adverse events (Scanning Auger Spectrometer (device)) occurred in 28.5% of the FeCarb and 22.2% of the FeSulf groups, with discontinuation of study medication due to Scanning Auger Spectrometer (device) in 1.5% and 7.9%, respectively., The median Hemoglobin improved from 8.7 to 12.3 g/dL in the FeCarb group and from 9.1 to 12.1 g/dL in the FeSulf group, demonstrating noninferiority (P= 0.6967). , ferric carboxymaltose prevents recurrence of Genus Anemia in patients with INFLAMMATORY BOWEL DISEASE 2., ferric carboxymaltose (MYOCLONUS, FAMILIAL CORTICAL, Ferinject) was effective and well tolerated in the treatment of Ferrum metallicum, Homeopathic preparation-deficiency Genus Anemia (Inosine Dialdehyde) in nine, Phase III, randomized, controlled, multicenter trials in a diverse range of indications, including patients with INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome), post-partum Genus Anemia (phenylpropanolamine) or Abnormal uterine bleeding (AUB), Chronic heart failure (Congestive heart failure), non-dialysis-dependent chronic kidney disease (Chronic Kidney Diseases) and those undergoing hemodialysis (Hodgkin Disease)., ferric carboxymaltose (MYOCLONUS, FAMILIAL CORTICAL, Ferinject) was effective and well tolerated in the treatment of Ferrum metallicum, Homeopathic preparation-deficiency Genus Anemia (Inosine Dialdehyde) in nine, Phase III, randomized, controlled, multicenter trials in a diverse range of indications, including patients with INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome), post-partum Genus Anemia (phenylpropanolamine) or Abnormal uterine bleeding (AUB), Chronic heart failure (Congestive heart failure), non-dialysis-dependent chronic kidney disease (Chronic Kidney Diseases) and those undergoing hemodialysis (Hodgkin Disease)[SEP]Relations: Phenylpropanolamine has relations: contraindication with INFLAMMATORY BOWEL DISEASE 2, contraindication with INFLAMMATORY BOWEL DISEASE 2.", "label": "yes"}
{"original_question": "Is gastro esophageal reflux related to burning mouth syndrome?", "id": "converted_1510", "sentence1": "Is gastro esophageal reflux related to burning mouth syndrome?", "sentence2": "Our results suggest that there is no causal connection between Local Pathology Review episodes and the occurrence of Intraoral approach burning sensations in the examined patients., As reported below, although this symptom may well be diagnostically misleading, careful diagnosis based on clinical signs may distinguish patients with BMS from those with reflux disease, and successful management of burning mouth is often enables.[SEP]", "label": "no"}
{"original_question": "Do mutations of AKT1 occur in meningiomas?", "id": "converted_34", "sentence1": "Do Gene Mutation of AKT1 protein, human occur in Meningioma?", "sentence2": "The recent identification of somatic Gene Mutation in components of the SHH-GLI1 and AKT1 protein, human protein, human-MTOR signaling pathways indicates the potential for cross talk of these pathways in the development of Meningioma., A Mutation Abnormality in PIK3CA gene gene or AKT1 protein, human protein, human was found in around 9 % of the cases., AKT1E17K Gene Mutation cluster with meningothelial and transitional Meningioma and can be detected by SFRP1 gene gene immunohistochemistry., AKT1E17K Gene Mutation were exclusively seen in Meningioma and occurred in 65 of 958 of these Neoplasms. A strong preponderance was seen in the Variant of Meningothelial Benign Meningioma WHO grade I of basal and spinal localization. In contrast, AKT1E17K Gene Mutation were rare in WHO grade II and absent in WHO grade III Meningioma. , We observed strong up-regulation of SFRP1 gene gene expression in all Meningioma with AKT1E17K Mutation Abnormality and in HEK293 Cells after transfection with Mutant AKT1E17K, but not in Meningioma and HEK293 Cells lacking this Mutation Abnormality., Samoan language and AKT1 protein, human protein, human Gene Mutation occur in non-Neurofibromatosis 2 Meningioma., Recurrent Gene Mutation in Samoan language and AKT1 protein, human protein, human are mutually exclusive with Neurofibromatosis 2 loss in Benign Meningioma., Genomic sequencing of Meningioma identifies oncogenic Samoan language and AKT1 protein, human protein, human Gene Mutation.,  A subset of Meningioma lacking Neurofibromatosis 2 alterations harbored recurrent oncogenic Gene Mutation in AKT1 protein, human protein, human (p.Glu17Lys) and Samoan language (p.Trp535Leu) and exhibited immunohistochemical evidence of activation of these pathways., Genomic analysis of non-Neurofibromatosis 2 Meningioma reveals Gene Mutation in TRAF7 gene gene, KLF4 protein, human protein, human, AKT1 protein, human protein, human, and Samoan language., A subset of Meningioma lacking Neurofibromatosis 2 alterations harbored recurrent oncogenic Gene Mutation in AKT1 protein, human protein, human (p.Glu17Lys) and Samoan language (p.Trp535Leu) and exhibited immunohistochemical evidence of activation of these pathways., Samoan language and AKT1 protein, human protein, human Gene Mutation occur in non-Neurofibromatosis 2 Meningioma, The recent identification of somatic Gene Mutation in components of the SHH-GLI1 and AKT1 protein, human protein, human-MTOR signaling pathways indicates the potential for cross talk of these pathways in the development of Meningioma, A subset of Meningioma lacking Neurofibromatosis 2 alterations harbored recurrent oncogenic Gene Mutation in AKT1 protein, human protein, human (p.Glu17Lys) and Samoan language (p.Trp535Leu) and exhibited immunohistochemical evidence of activation of these pathways, Genomic analysis of non-Neurofibromatosis 2 Meningioma reveals Gene Mutation in TRAF7 gene gene, KLF4 protein, human protein, human, AKT1 protein, human protein, human, and Samoan language, Genomic sequencing of Meningioma identifies oncogenic Samoan language and AKT1 protein, human protein, human Gene Mutation, Recurrent Gene Mutation in Samoan language and AKT1 protein, human protein, human are mutually exclusive with Neurofibromatosis 2 loss in Benign Meningioma, A subset of Meningioma lacking Neurofibromatosis 2 alterations harbored recurrent oncogenic Gene Mutation in AKT1 protein, human protein, human (p.Glu17Lys) and Samoan language (p.Trp535Leu) and exhibited immunohistochemical evidence of activation of these pathways. These Gene Mutation were present in therapeutically challenging Neoplasms of the Base of skull structure and higher grade. , A subset of Meningioma lacking Neurofibromatosis 2 alterations harbored recurrent oncogenic Gene Mutation in AKT1 protein, human protein, human (p.Glu17Lys) and Samoan language (p.Trp535Leu) and exhibited immunohistochemical evidence of activation of these pathways. [SEP]Relations: Meningothelial Benign Meningioma has relations: disease_protein with Neurofibromatosis 2, disease_protein with AKT1 protein, human, disease_protein with Neurofibromatosis 2, disease_protein with AKT1 protein, human. benign Benign Meningioma has relations: disease_protein with AKT1 protein, human, disease_protein with Neurofibromatosis 2, disease_protein with AKT1 protein, human, disease_protein with Neurofibromatosis 2. neurofibromatosis has relations: disease_protein with Neurofibromatosis 2, disease_protein with Neurofibromatosis 2.", "label": "yes"}
{"original_question": "Do selenoproteins and selenium play a role in prostate cancer prevention?", "id": "converted_941", "sentence1": "Do Selenoproteins and selenium play a role in Pelvis>Prostate Primary malignant neoplasm prevention?", "sentence2": "The selenoprotein-deficient mice exhibited accelerated development of Lesion associated with Pelvis>Prostate Primary malignant neoplasm progression, implicating Selenoproteins in Primary malignant neoplasm risk and development and raising the possibility that selenium prevents Primary malignant neoplasm by modulating the levels of these Selenoproteins, Notably and in contrast to previous studies, RWPE-1 cells were significantly more sensitive to selenite than either of the Pelvis>Prostate Primary malignant neoplasm cell lines. These results demonstrate that Selenoproteins and selenium metabolism are regulated at multiple levels in Pelvis>Prostate cells, In a low-selenium population, SOD2-Ala16+ men homozygous for SEPP1-Ala234 are at an increased risk of Pelvis>Prostate Primary malignant neoplasm/aggressive Pelvis>Prostate Primary malignant neoplasm especially if ever-smokers, because they are likely to produce more Mitochondrial Inheritance H(2)O(2) that they cannot remove, thereby promoting Pelvis>Prostate tumor cell proliferation and migration., Our results support a role of selenium and Genetic Polymorphism in selenoenzymes in Pelvis>Prostate Primary malignant neoplasm etiology, which warrants confirmation in future studies., This study provides evidence that SELENOF gene genetic variation may influence Patient-Controlled Analgesia mortality. Additionally, the association of selenium with Patient-Controlled Analgesia mortality was modified by a Variant, suggesting the possibility that some men with Patient-Controlled Analgesia may benefit more from selenium than others, depending on their Genotype determination., We conclude that decreased SELENOP wt Allele concentration in serum might represent an additional valuable marker for Pelvis>Prostate Primary malignant neoplasm diagnostics., The recently completed Selenium supplement supplement and Vitamin E Cancer Prevention Trial (SELECT) was one of the largest Homo sapiens Primary malignant neoplasm prevention trials ever undertaken. Its purpose was to assess the role of selenium and Vitamin E Drug Class in Pelvis>Prostate Primary malignant neoplasm prevention, but SELECT found no decline in Pelvis>Prostate Primary malignant neoplasm., We studied FUT2 gene levels in whole blood, plasma and Pelvis>Prostate of 32 Pachyonychia Congenita and 40 benign Pelvis>Prostate hyperplasia (BPH) patients and in the control group composed of 39 healthy subjects. The selenoenzyme glutathione peroxidase (GSH-Px) was also measured in the patients' Erythrocytes, plasma and Pelvis>Prostate tissue. FUT2 gene concentration in whole blood and plasma in both groups of patients was lower as compared with controls, while in Pelvis>Prostate gland it was significantly higher in Pachyonychia Congenita than in BPH patients and controls. Red cell GSH-Px activity was the same in Pachyonychia Congenita patients and controls but significantly lower in BPH patients., Of particular interest was the positive correlation between tissue GPx activity and Gleason score, with this relationship achieving statistical significance among African-Americans (r = 0.67, P = 0.02)[SEP]Relations: SELENOP has relations: disease_protein with Pelvis>Prostate Primary malignant neoplasm, disease_protein with Pelvis>Prostate Primary malignant neoplasm. Pelvis>Prostate gland has relations: anatomy_protein_present with Pachyonychia Congenita, anatomy_protein_present with Pachyonychia Congenita.", "label": "no"}
{"original_question": "Does erenumab target the calcitonin gene-related peptide?", "id": "converted_3970", "sentence1": "Does erenumab target the Calcitonin Precursor, human?", "sentence2": "Four Monoclonal Antibodies have been developed: one targeting the CALCRL gene (erenumab) and three targeting the Calcitonin Precursor, human (eptinezumab, fremanezumab, and galcanezumab).[SEP]", "label": "no"}
{"original_question": "Is there a mouse model for Fanconi anemia?", "id": "converted_1543", "sentence1": "Is there a Mus sp. model for Fanconi anemia?", "sentence2": "cyclophosphamide promotes engraftment of gene-modified cells in a Mus sp. model of Fanconi anemia without causing cytogenetic abnormalities, We compared Controlling (action) preconditioning with fludarabine (ZMYND10 wt Allele) or cytarabine (AraC) or no conditioning as a control in FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) ( -/- ) mutant CASP14 gene receiving gene-modified bone marrow cells, We conclude that Controlling (action) is an effective and superior preparative regimen with respect to engraftment of lentivirus-transduced cells and functional correction in FANCONI ANEMIA, COMPLEMENTATION GROUP A (disorder) ( -/- ) CASP14 gene, To study whether there is a causal relationship between doxorubicin/fluorouracil protocol pathway defects and Neoplasms development, we have generated a Mus sp. model with a targeted disruption of the doxorubicin/fluorouracil protocol core complex gene FANCONI ANEMIA, COMPLEMENTATION GROUP F, FANCONI ANEMIA, COMPLEMENTATION GROUP F-deficient Mus sp. embryonic Specimen Source Codes - Fibroblasts displayed a phenotype typical for doxorubicin/fluorouracil protocol cells: they showed an aberrant response to DNA cross-linking agents as manifested by G(2) arrest, chromosomal aberrations, reduced survival, and an inability to monoubiquitinate FANCONI ANEMIA, COMPLEMENTATION GROUP D2, FANCONI ANEMIA, COMPLEMENTATION GROUP F homozygous CASP14 gene were viable, born following a normal Mendelian distribution, and showed no growth retardation or developmental abnormalities. The Gonadal structure of FANCONI ANEMIA, COMPLEMENTATION GROUP F mutant CASP14 gene functioned abnormally, showing compromised follicle development and Spermatogenesis as has been observed in other doxorubicin/fluorouracil protocol Mus sp. models and in doxorubicin/fluorouracil protocol patients, In a cohort of FANCONI ANEMIA, COMPLEMENTATION GROUP F-deficient CASP14 gene, we observed decreased overall survival and increased Neoplasms incidence, To provide further experimental access to the doxorubicin/fluorouracil protocol-M complementation group we have generated Fancm-deficient CASP14 gene by deleting exon 2, FANCM gene gene deficiency caused Hypogonadism in CASP14 gene and Emotional Emotional hypersensitivity to cross-linking agents in Mus sp. embryonic Specimen Source Codes - Fibroblasts (MEFs), thus phenocopying other doxorubicin/fluorouracil protocol Mus sp. models, Fancm(Delta2/Delta2) CASP14 gene also showed unique features atypical for doxorubicin/fluorouracil protocol CASP14 gene, including underrepresentation of female Fancm(Delta2/Delta2) CASP14 gene and decreased overall and tumor-free survival, Fancm-deficient CASP14 gene reveal unique features of Fanconi anemia complementation group M, FANCONI ANEMIA, COMPLEMENTATION GROUP F-deficient CASP14 gene are prone to develop ovarian neoplasm, In vivo proliferation advantage of genetically corrected hematopoietic stem cells in a Mus sp. model of Fanconi anemia doxorubicin/fluorouracil protocol-D1, Using an doxorubicin/fluorouracil protocol Mus sp. model with a marked hematopoietic phenotype, the doxorubicin/fluorouracil protocol-D1 (Brca2(Delta27/Delta27)) CASP14 gene, we demonstrate that the lentivirus-mediated gene therapy of doxorubicin/fluorouracil protocol Hematopoietic stem cells results in the progressive expansion of genetically corrected clones in mild-conditioned doxorubicin/fluorouracil protocol-D1 recipients, Consistent with these data, hematopoietic progenitors from doxorubicin/fluorouracil protocol recipients progressively became Mitomycins C resistant and their chromosomal instability was reverted, Hematopoietic dysfunction in a Mus sp. model for Fanconi anemia group D1, We have investigated the hematopoietic phenotype of CASP14 gene with a hypomorphic Mutation Abnormality in the Brca2/Fancd1 gene (Brca2(Delta27/Delta27) Mutation Abnormality), Conventional Defecation competition experiments showed a marked repopulation defect in Brca2(Delta27/Delta27) hematopoietic stem cells (Hematopoietic stem cells), compared to wild-type Hematopoietic stem cells, Moreover, we have observed for the first time in a DNA repair disease model a very significant proliferation defect in Brca2(Delta27/Delta27) Hematopoietic stem cells maintained in their natural physiological environment, The hematopoietic phenotype associated with the Brca2(Delta27/Delta27) Mutation Abnormality suggests that this doxorubicin/fluorouracil protocol-D1 Mus sp. model will constitute an important tool for the development of new therapies for doxorubicin/fluorouracil protocol, including gene therapy, In vitro phenotypic correction of hematopoietic progenitors from Fanconi anemia group A knockout CASP14 gene, In this study we characterized the hematopoietic phenotype of a Fanca knockout Mus sp. model and corrected the main phenotypic characteristics of the bone marrow (Defecation) progenitors using Retroviral Vector, The hematopoiesis of these animal allergen extracts was characterized by a modest though significant thrombocytopenia, consistent with reduced numbers of Defecation Megakaryocytes progenitors, As observed in other doxorubicin/fluorouracil protocol models, the hematopoietic progenitors from Fanca(-/-) CASP14 gene were highly sensitive to Mitomycins C (Mitomycins), Aiming to correct the phenotype of Fanca(-/-) progenitors, purified Lin(-)Sca-1(+) cells were transduced with Retroviral Vector encoding the enhanced Green Fluorescent Proteins (EGFP) gene and human FANCA Genes. Lin(-)Sca-1(+) cells from Fanca(-/-) CASP14 gene were transduced with an efficiency similar to that of samples from wild-type CASP14 gene. More significantly, transductions with FANCA vectors corrected both the Mitomycins Emotional Emotional hypersensitivity as well as the impaired ex vivo expansion ability that characterized the Defecation progenitors of Fanca(-/-) CASP14 gene,  The Structure-Specific Endonuclease Subunit Structure-Specific Endonuclease Subunit SLX4 wt Allele knockout Mus sp. therefore establishes a disease model for Fanconi anemia and genetically links a regulator of nuclease incision complexes to the Fanconi anemia DNA crosslink repair pathway., Hematopoietic dysfunction in a Mus sp. model for Fanconi anemia group D1., Bone marrow hypocellularity in the Fanconi anemia group C Mus sp. model after DNA damage., In vivo proliferation advantage of genetically corrected hematopoietic stem cells in a Mus sp. model of Fanconi anemia doxorubicin/fluorouracil protocol-D1., Assessment of the flexed-tail Mus sp. as a possible model for Fanconi anemia: analysis of Mitomycins C-induced micronuclei., The Structure-Specific Endonuclease Subunit Structure-Specific Endonuclease Subunit SLX4 wt Allele knockout Mus sp. therefore establishes a disease model for Fanconi anemia and genetically links a regulator of nuclease incision complexes to the Fanconi anemia DNA crosslink repair pathway., cyclophosphamide promotes engraftment of gene-modified cells in a Mus sp. model of Fanconi anemia without causing cytogenetic abnormalities., Mouse models of Fanconi anemia., Five of these Genes have been deleted or mutated in the Mus sp., as well as a sixth key Genes, Regulator, to create Mus sp. models of Fanconi anemia., This review summarizes the phenotype of each of the Fanconi anemia Mus sp. models and highlights how Genetic and interventional studies using the strains have yielded novel insight into therapeutic strategies for Fanconi anemia and into how the Fanconi anemia pathway protects against genomic instability., To study doxorubicin/fluorouracil protocol complementation group A using the Mus sp. as a model system, we cloned and characterized the Mus sp. homolog of the human FANCA cDNA., Here we describe the phenotype of the Structure-Specific Endonuclease Subunit Structure-Specific Endonuclease Subunit SLX4 wt Allele knockout Mus sp., the Mus sp. ortholog of Structure-Specific Endonuclease Subunit Structure-Specific Endonuclease Subunit SLX4, which recapitulates many key features of the human Genetic illness Fanconi anemia., Five of these Genes have been deleted or mutated in the Mus sp., as well as a sixth key Genes, Regulator, to create Mus sp. models of Fanconi anemia, In contrast to observations made in other Fanconi anemia (doxorubicin/fluorouracil protocol) Mus sp. models, low numbers of hematopoietic colony-forming cells (Cardio-facio-cutaneous syndrome) were noted in Brca2(Delta27/Delta27) CASP14 gene, either young or adult, Fanconi anemia group A and C double-mutant CASP14 gene: functional evidence for a multi-protein Fanconi anemia complex., In addition, Mus sp. models are also useful for testing treatments for doxorubicin/fluorouracil protocol., Development and characterization of immortalized fibroblastoid cell lines from an doxorubicin/fluorouracil protocol(C) Mus sp. model., These Mus sp. models display the characteristic doxorubicin/fluorouracil protocol feature of cellular Emotional Emotional hypersensitivity to DNA cross-linking agents[SEP]Relations: Cytarabine has relations: drug_drug with cyclophosphamide, drug_drug with cyclophosphamide. Fanconi anemia complementation group has relations: disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_disease with Fanconi anemia, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_disease with Fanconi anemia, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_disease with Fanconi anemia, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_disease with Fanconi anemia, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_disease with Fanconi anemia, disease_protein with FANCONI ANEMIA, COMPLEMENTATION GROUP D2, disease_disease with Fanconi anemia. Mitomycin has relations: drug_drug with cyclophosphamide, drug_drug with cyclophosphamide, drug_drug with cyclophosphamide, drug_drug with cyclophosphamide. Hypogonadism has relations: disease_phenotype_positive with Fanconi anemia, disease_phenotype_positive with Fanconi anemia.", "label": "yes"}
{"original_question": "Is AZD5153 active in prostate cancer?", "id": "converted_3555", "sentence1": "Is AZD5153 active in Malignant neoplasm of prostate?", "sentence2": "AZD5153 Inhibits Prostate Cancer Cell Growth in Vitro and in Vivo., BRD4 protein, human gene (BRD4 protein, human protein, human) overexpression participates in Malignant neoplasm of prostate progression by enhancing the transcriptional activity and expression of several key oncogenes. AZD5153 is a novel BRD4 protein, human protein, human inhibitor.METHODS: Prostate cancer cells were treated with AZD5153. Cell survival was tested by MTT assay and clonogenicity assay. Cell proliferation was tested by [H3] DNA incorporation assay. Cell apoptosis was tested by caspase-3/-9 activity assay, Histone DNA ELISA assay, ANXA5 gene Fluorescence-Activated Cell Sorting assay and TUNEL staining assay. Cell cycle progression was tested by Propidium Iodide (Pulmonary Valve Insufficiency) Fluorescence-Activated Cell Sorting assay. Signal Transduction was tested by Western blotting assay. The nude mice PC-3 cell line cell line xenograft model was applied to test AZD5153's activity in vivo.RESULTS: AZD5153 inhibited proliferation and survival of established and primary Malignant neoplasm of prostate cells. AZD5153 induced apoptosis activation and cell cycle arrest in Malignant neoplasm of prostate cells. AZD5153 was non-cytotoxic to the prostate epithelial cells. AZD5153 downregulated BRD4 protein, human protein, human targets (Cyclin D1, MYC protein, human, BCL2 gene, FOSL1 wt Allele wt Allele and Cyclin-Dependent Kinase 4) in PC-3 cell line cell line and primary Malignant neoplasm of prostate cells. Further studies show that Proto-Oncogene Proteins c-akt could be the primary resistance factor of AZD5153. Pharmacological inhibition or genetic depletion of Proto-Oncogene Proteins c-akt induced BRD4 protein, human protein, human downregulation, sensitizing AZD5153-induced cytotoxicity in PC-3 cell line cell line cells. In vivo, AZD5153 oral administration inhibited PC-3 cell line cell line xenograft tumor growth in nude mice. Its anti-tumor activity was further enhanced with co-treatment of the Proto-Oncogene Proteins c-akt specific inhibitor MK-2206.CONCLUSION: Together, our results indicate a promising therapeutic value of the novel BRD4 protein, human protein, human inhibitor AZD5153 against Malignant neoplasm of prostate cells., AZD5153 induced apoptosis activation and cell cycle arrest in Malignant neoplasm of prostate cells., CONCLUSION\n\nTogether, our results indicate a promising therapeutic value of the novel BRD4 protein, human protein, human inhibitor AZD5153 against Malignant neoplasm of prostate cells., AZD5153 downregulated BRD4 protein, human protein, human targets (Cyclin D1, MYC protein, human, BCL2 gene, FOSL1 wt Allele wt Allele and Cyclin-Dependent Kinase 4) in PC-3 cell line cell line and primary Malignant neoplasm of prostate cells., RESULTS\n\nAZD5153 inhibited proliferation and survival of established and primary Malignant neoplasm of prostate cells., RESULTS AZD5153 inhibited proliferation and survival of established and primary Malignant neoplasm of prostate cells., AZD5153 induced apoptosis activation and cell cycle arrest in Malignant neoplasm of prostate cells., AZD5153 downregulated BRD4 protein, human protein, human targets (Cyclin D1, MYC protein, human, BCL2 gene, FOSL1 wt Allele wt Allele and Cyclin-Dependent Kinase 4) in PC-3 cell line cell line and primary Malignant neoplasm of prostate cells., CONCLUSION Together, our results indicate a promising therapeutic value of the novel BRD4 protein, human protein, human inhibitor AZD5153 against Malignant neoplasm of prostate cells., AZD5153 Inhibits Prostate Cancer Cell Growth in Vitro and in Vivo, AZD5153 induced apoptosis activation and cell cycle arrest in Malignant neoplasm of prostate cells.[SEP]Relations: signal transduction has relations: bioprocess_protein with Cyclin-Dependent Kinase 4, bioprocess_protein with Cyclin-Dependent Kinase 4.", "label": "yes"}
{"original_question": "Should dacomitinib be used for treatment of glioblastoma patients?", "id": "converted_2903", "sentence1": "Should dacomitinib be used for treatment of glioblastoma patients?", "sentence2": "Expert opinion: Despite the poor global results of dacomitinib in recurrent GB shown in a phase II trial, some patients had a significant benefit. , Conclusions: dacomitinib has a limited single-agent activity in recurrent GB with EGFR amplification., Expert opinion: Despite the poor global results of dacomitinib in recurrent GB shown in a phase II trial, some patients had a significant benefit., Expert opinion: Despite the poor global results of dacomitinib in recurrent GB shown in a phase II trial, some patients had a significant benefit.[SEP]", "label": "no"}
{"original_question": "Is NOD1 activated in inflammation?", "id": "converted_891", "sentence1": "Is NOD1 activated in Inflammation?", "sentence2": "NOD1 gene and Nod2 control Bacterial infections and Inflammation, The Nod proteins NOD1 gene and Nod2 are two NLR family members that trigger immune defense in response to Bacterial Peptidoglycan, Nod proteins fight off Bacterial infections by stimulating proinflammatory signaling and cytokine networks and by inducing antimicrobial effectors, such as nitric oxide and antimicrobial Peptides., NOD1 gene is also critically implicated in shaping adaptive immune responses towards Bacterial-derived constituents., Together, NOD1 gene and Nod2 represent central players in the control of immune responses to Bacterial infections and Inflammation., The innate immune receptor NOD1 gene protects the intestine from Inflammation-induced tumorigenesis., we show that NOD1 gene deficiency results in the increased development of both Colitis-associated and Apc tumor suppressor-related colon tumors. In the absence of NOD1 gene signaling, there is a greater disruption of the Intestines epithelial cell barrier due to Chemicals induced injury as manifested by increased surface epithelial apoptosis early on during Chemicals induced Colitis and increased Intestines permeability., The increased Intestines permeability is associated with enhanced inflammatory cytokine production and epithelial cell proliferation in NOD1 gene-deficient CASP14 gene as compared with wild-type CASP14 gene., Depletion of the gut microbiota suppressed tumor development in NOD1 gene-deficient CASP14 gene, thus highlighting a link between the commensal bacteria within the intestine and the host innate immune NOD1 gene signaling pathway in the regulation Inflammation-mediated colon cancer development.,  NOD1 protein is expressed in the Eye Specimen Source Code and promotes ocular Inflammation in a dose- and time-dependent fashion. , NOD1 expression in the Eye Specimen Source Code and functional contribution to IL-1beta-dependent ocular Inflammation in CASP14 gene, Genetic Polymorphism in NOD1 are associated with autoinflammatory diseases characterized by Uveitis such as Crohn's disease of oral soft tissues of oral soft tissues and SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding), NOD1 is homologous to NOD2 gene gene, which is responsible for an autosomal dominant form of Uveitis. Nonetheless, the role of NOD1 in intraocular Inflammation has not been explored., NOD1 gene and Nod2 regulation of Inflammation in the Salmonella Colitis model, CASP14 gene deficient for both NOD1 gene and Nod2 had attenuated inflammatory pathology, reduced levels of inflammatory cytokines, and increased colonization of the Mucous Membrane, The present study has demonstrated an unexpected role of NOD1 gene in the development of site-specific vascular Inflammation, especially Coronary arteritis., NOD1 gene ligands induce site-specific vascular Inflammation, Phenotyping of NOD1 gene/2 double deficient CASP14 gene and characterization of NOD1 gene/2 in systemic Inflammation and associated Kidney Diseases, The present study analyzed NOD1 gene and Nod2 double deficient (NOD1 gene/2 DKO) CASP14 gene under physiological and inflammatory conditions, Several inflammatory disorders, such as Crohn's disease of oral soft tissues of oral soft tissues and Asthma, are linked to genetic changes in either NOD1 gene or Nod2., Systematic analysis of NOD1 gene/2 DKO CASP14 gene revealed a possible role of NOD1 gene/2 in the development of Kidney Diseases during systemic Inflammation., NOD1 and NOD2 gene gene Signaling in Communicable Diseases and Inflammation, NOD1 engagement generates an inflammatory response via activation of NFκB and Mitogen-Activated Protein Kinases pathways. , In addition we profile novel inhibitors of ARHGEF28 wt Allele and NOD1 itself, which specifically inhibit NOD1 ligand induced inflammatory signalling in the Vasculature. , This data supports the potential utility of NOD1 and ARHGEF28 wt Allele as therapeutic targets in Homo sapiens disease where vascular Inflammation is a clinical feature, such as in Sepsis (Invertebrate) and Septic Shock., NOD1 expression elicited by gamma-D-glutamyl-meso-diaminopimelic acid in first trimester Homo sapiens trophoblast cells and its potential role in infection-associated Inflammation, This study aimed to investigate the expression and function of NOD1 in first trimester trophoblast cells, and evaluate the potential role of trophoblast cells in infection-associated Inflammation, NOD1 may have a role in mediating infection-associated Inflammation. Once gamma-D-glutamyl-meso-diaminopimelic acid is recognized by NOD1, the inflammatory response may be induced via NOD1-RICK-NF-κB-mediated pathways., NOD1/2(-/-) CASP14 gene were protected from HFD-induced Inflammation, lipid accumulation, and peripheral Therapeutic Insulin intolerance., In contrast, NOD1 gene gene-deficient CASP14 gene developed enhanced joint Inflammation with concomitant elevated levels of proinflammatory cytokines and Cartilage damage, consistent with a model in which NOD1 gene controls the inflammatory reaction., These data indicate that the NLR family members NOD1 gene and Nod2 have different functions in controlling Inflammation, and that Protoplasm NOD1 gene-Nod2 interactions may determine the severity of Arthritis in this experimental model., Whereas the lymphotoxin pathway was critical for the induction of the B-Lymphocytes chemoattractant Chemokine Chemokine CXCL13 in response to NOD1 gene agonists, B-Lymphocytes accumulation within the Abdomen>Spleen following NOD1 gene-induced systemic Inflammation was independent of the lymphotoxin pathway., The effect of NOD1 and NOD2 gene gene activation on Inflammation and the Therapeutic Insulin signalling pathway was also assessed., Nonetheless, the role of NOD1 in intraocular Inflammation has not been explored., A key role for the Endothelium in NOD1 mediated vascular Inflammation: comparison to TLR4 wt Allele wt Allele responses., We previously demonstrated that Homo sapiens first-trimester trophoblasts express NOD1 gene and Nod2, which trigger Inflammation upon stimulation., In addition, recent studies have revealed a role for Protoplasm NOD1 receptors in the regulation of vascular Inflammation and metabolism., In conclusion, the present findings describe an important role for NOD1 in the development of Therapeutic Insulin resistance and Inflammation in pregnancies complicated by Gestational Diabetes., Phenotyping of NOD1 gene/2 double deficient CASP14 gene and characterization of NOD1 gene/2 in systemic Inflammation and associated Kidney Diseases., NOD1 gene activation by Bacterial gamma-D-glutamyl-meso-diaminopimelic acid induces maternal-fetal Inflammation and Premature Obstetric Labor., The nucleotide-binding oligomerisation domain (Dentatorubral-Pallidoluysian Atrophy) Protoplasm molecules recognise a wide range of microbial products, as well as other Protoplasm danger signals, thereby initiating Inflammation through activation of NFI Transcription Factors (NFκB). , NOD1 gene ligands induce site-specific vascular Inflammation., The nucleotide oligomerization domain (Dentatorubral-Pallidoluysian Atrophy) Protoplasm molecules recognize a wide range of microbial products as well as other Protoplasm danger signals, thereby initiating Inflammation through activation of nuclear factor KB (NF-kappa B), a central regulator of the terminal processes of Homo sapiens labor and delivery. , CONCLUSIONS: We identify Dentatorubral-Pallidoluysian Atrophy proteins as innate immune components that are involved in diet-induced Inflammation and Therapeutic Insulin intolerance. , NOD1 gene and Nod2 regulation of Inflammation in the Salmonella Colitis model., In particular, muramyl Peptides trigger Inflammation, contribute to host defense against microbial infections, and modulate the adaptive immune response to antigens. , Systemic and tissue-specific Inflammation was assessed using enzyme-linked immunosorbent assays in Dentatorubral-Pallidoluysian Atrophy ligand-injected CASP14 gene. , CONCLUSIONS: We identify Dentatorubral-Pallidoluysian Atrophy proteins as innate immune components that are involved in diet-induced Inflammation and Therapeutic Insulin intolerance. Acute activation of Dentatorubral-Pallidoluysian Atrophy proteins by mimetics of Bacterial PGNs causes whole-body Therapeutic Insulin resistance, bolstering the concept that innate immune responses to distinctive Bacterial cues directly lead to Therapeutic Insulin resistance. , Interferon-gamma (IFN gamma), which is a potent pro-inflammatory cytokine in Intestines mucosal Inflammation, activates CARD4/NOD1 mRNA transcription in a time- and dose-dependent manner and results in augmentation of CARD4/NOD1 protein in SW480 cells., These studies suggest that the NELFCD wt Allele cytokine, IFN gamma, activates CARD4/NOD1 transcription and regulate innate immune mechanisms in the condition of Intestines mucosal Inflammation., NOD1 activation triggers Inflammation,, In contrast to enhanced leptin mRNA by Van der Woude syndrome and TNFα, NOD1 activation suppressed leptin mRNA in Adipocytes, suggesting the differential effects of NOD1 activation in Adipocytes.  Overall, our results suggest that NOD1 represents a novel target for adipose Inflammation in BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20., NOD1 activation triggers Inflammation, antimicrobial mechanisms and autophagy in both Epithelial Cells and murine macrophages., NOD1 is an Protoplasm immune receptor that senses Peptidoglycan from Gram-negative bacteria and responds by inducing autophagy and activating NF-κB, leading to Inflammation-mediated Bacterial clearance; however chronic pathogens can evade NOD1-mediated clearance by altering Peptidoglycan structure., Bacterial NOD1 activation is positioned as a component of metabolic endotoxemia that can contribute to Hyperlipidemia, systemic Inflammation and Therapeutic Insulin resistance by acting directly on Adipocytes., NOD1 ligand also caused Inflammation and Therapeutic Insulin resistance directly in primary Hepatocyte from Wild Type Unspecified - zebrafish, but not NOD1(-/-), CASP14 gene., We conclude that NOD1 activation reduced aromatic hydrocarbon receptor in allergen-induced lung Inflammation, which was accompanied by a reduction of allergen-specific T-cell proliferation., The effect of NOD1 and NOD2 gene gene activation on Inflammation and the Therapeutic Insulin signalling pathway was also assessed., Interferon-gamma (IFN gamma), which is a potent pro-inflammatory cytokine in Intestines mucosal Inflammation, activates CARD4/NOD1 mRNA transcription in a time- and dose-dependent manner and results in augmentation of CARD4/NOD1 protein in SW480 cells.[SEP]Relations: SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding), susceptibility to has relations: disease_disease with SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding), disease_disease with SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding). aryl hydrocarbon receptor complex has relations: cellcomp_protein with aromatic hydrocarbon receptor, cellcomp_protein with aromatic hydrocarbon receptor. intestine has relations: anatomy_protein_present with aromatic hydrocarbon receptor, anatomy_protein_present with aromatic hydrocarbon receptor. Inflammatory abnormality of the Eye Specimen Source Code has relations: disease_phenotype_positive with Uveitis, disease_phenotype_positive with Uveitis. coronary artery has relations: anatomy_protein_present with aromatic hydrocarbon receptor, anatomy_protein_present with aromatic hydrocarbon receptor.", "label": "yes"}
{"original_question": "Could divalent metal transporter 1 deficiency lead to anemia?", "id": "converted_1980", "sentence1": "Could divalent metal transporter 1 deficiency lead to Genus Anemia?", "sentence2": "The divalent metal transporter 1 (SLC11A2 gene) is a major iron transporter required for iron absorption and erythropoiesis. Loss of SLC11A2 gene function results in Microcytic Genus Anemia. , Dysfunction of human SLC11A2 gene is associated with several pathologies such as iron deficiency Genus Anemia hemochromatosis, Parkinson Disease and ALZHEIMER DISEASE, FAMILIAL, 1, as well as Malignant neoplasm of colon and/or rectum and Adenocarcinoma Of Esophagus, making SLC11A2 gene an attractive target for drug discovery., Deficiency of the divalent metal transporter 1 (SLC11A2 gene) leads to Microcytic hypochromic Genus Anemia (disorder). We have previously shown that SLC11A2 gene deficiency impairs Erythroid differentiation and induces apoptosis of Erythroid Cells. , We propose that SLC11A2 gene deficiency negatively affects metabolism and life span of mature Specimen Source Codes - Erythrocytes; two other aspects of defective erythropoiesis which contribute to the pathophysiology of the disease., Hypochromic Microcytic Genus Anemia associated with ineffective erythropoiesis caused by recessive mutations in divalent metal transporter 1 (SLC11A2 gene) can be improved with high-dose Recombinant Erythropoietin supplementation. , Belgrade rats exhibit microcytic, hypochromic Genus Anemia and systemic iron deficiency due to a glycine-to-arginine Mutation Abnormality at residue 185 in a metal ion transporter of a divalent metal transporter/divalent cation transporter/solute carrier 11 group A member 2 or 3 (SLC11A2 gene/DCT1/SLC11A2), a member of the natural-resistance-associated macrophage protein (Nramp) family., Deficiency of the divalent metal transporter 1 (SLC11A2 gene) leads to Microcytic hypochromic Genus Anemia (disorder), Belgrade rats exhibit microcytic, hypochromic Genus Anemia and systemic iron deficiency due to a glycine-to-arginine Mutation Abnormality at residue 185 in a metal ion transporter of a divalent metal transporter/divalent cation transporter/solute carrier 11 group A member 2 or 3 (SLC11A2 gene/DCT1/SLC11A2), a member of the natural-resistance-associated macrophage protein (Nramp) family, BACKGROUND/AIMS: Deficiency of the divalent metal transporter 1 (SLC11A2 gene) leads to Microcytic hypochromic Genus Anemia (disorder). , Microcytic Genus Anemia (mk/mk) CASP14 gene defective in SLC11A2 gene and wild-type CASP14 gene were exposed to either bleomycin or Saline Solution via intratracheal instillation and the resultant lung injury was compared. , Deficiency of the divalent metal transporter 1 (SLC11A2 gene) leads to Microcytic hypochromic Genus Anemia (disorder)., The divalent metal transporter 1 (SLC11A2 gene) is a major iron transporter required for iron absorption and erythropoiesis., This Mutation Abnormality severely impairs the iron transport capability of SLC11A2 gene, leading to systemic iron deficiency and Genus Anemia.[SEP]Relations: SLC11A2 has relations: disease_protein with Malignant neoplasm of colon and/or rectum, disease_protein with Microcytic Genus Anemia, disease_protein with Malignant neoplasm of colon and/or rectum, disease_protein with Microcytic Genus Anemia. Normochromic Microcytic Genus Anemia has relations: disease_phenotype_positive with Microcytic Genus Anemia, disease_phenotype_positive with Microcytic Genus Anemia. malignant colon neoplasm has relations: disease_disease with Malignant neoplasm of colon and/or rectum, disease_disease with Malignant neoplasm of colon and/or rectum.", "label": "yes"}
{"original_question": "Is peripheral neuroepithelioma related to Ewing sarcoma?", "id": "converted_51", "sentence1": "Is Peripheral Primitive Neuroectodermal Tumor of Bone related to Ewings sarcoma?", "sentence2": "The term \"small round-cell tumor\" describes a group of highly aggressive malignant tumors composed of relatively small and monotonous undifferentiated cells with high Nuclear (incident type) to cytoplasmic ratios. This group includes Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone (ES), Peripheral Primitive Neuroectodermal Tumor of Bone (aka, primitive neuroectodermal tumor or extraskeletal ES), Peripheral neuroblastoma (\"classic-type\"), Anal Rhabdomyosarcoma, Desmoplastic Small Round Cell Tumor, Lymphoma, leukemia, small-cell osteosarcoma, small-cell carcinoma (either undifferentiated or Neurosecretory Systems), Rat Olfactory Neuroblastoma, cutaneous Neurosecretory Systems carcinoma (aka, Merkel-cell carcinoma), small-cell melanoma, and Mesenchymal Chondrosarcoma. Their clinical presentations often overlap, thus making a definitive diagnosis problematic in some cases, AIMS: To retrospectively study the DNA content in a series of childhood Ewing Family Tumors (EFT), and to investigate its prognostic value. METHODS: The study was performed on a series of 27 EFTs (osseous Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone, 18 cases; extraosseous Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone, 2; Peripheral Primitive Neuroectodermal Tumor of Bone, 4; Askin Rosai tumors, 3, To improve the prognosis of patients with poor-risk Peripheral primitive neuroectodermal tumors (pPNETs; including Peripheral Primitive Neuroectodermal Tumor of Bone and Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone), Large group of small-round-cell tumours of soft tissue and Specimen Type - Bone represents a complex diagnostic problem for the pathologists. neuronal nature of many tumours from this group is proven by means of new methods--immunophenotypic analysis, tissue culture, cytogenetics. Peripheral Neuroectodermal Tumor, Primitive, Ewing Neoplasms, primitive Neuroectodermal Tumors (Ewings sarcoma-primitive neuroectodermal tumor (Ewings sarcoma-primitive neuroectodermal tumor (PNET))), Askin's tumor belong to these neoplasms, Comparison of Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone of Specimen Type - Bone and Peripheral Primitive Neuroectodermal Tumor of Bone. An immunocytochemical and ultrastructural analysis of two primitive neuroectodermal neoplasms, Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone of Specimen Type - Bone (carboxylesterase) and Peripheral Primitive Neuroectodermal Tumor of Bone (Peripheral Nervous System) are frequently considered to be different tumors. Some researchers have suggested that Peripheral Nervous System is morphologically a neuroectodermal Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone. We sought to determine the extent of neuroectodermal features in conventional carboxylesterase on direct patient material (25 cases) and to compare these tumors with a similar group of readily diagnosed Peripheral Nerve Stimulation (10 cases), Neuroectodermal antigens (Gamma-Enolase, Leu-7 [CD57 Antigens], Neurofilament Medium Polypeptide 200 kd, and S100A1 wt Allele) were found in nine of 10 cases of Peripheral Nervous System and in 17 of 25 cases of carboxylesterase, These data support the concept that carboxylesterase and Peripheral Nervous System are both Peripheral primitive neuroectodermal neoplasms, differing only in extent of neuroectodermal phenotype and morphological differentiation, Besides these antigenic features, Ewings sarcoma cells are characterized by a specific t(11;22)(q24;q12) translocation also observed in Neuroectodermal Tumor, Primitive, a neuroectodermal tumor, suggesting a possible evolutionary related origin., Ewings sarcoma (ES) and Peripheral Primitive Neuroectodermal Tumor of Bone (Peripheral Nervous System) are closely related tumors, and it can be difficult to distinguish them from other small-round-cell tumors (SRCTs)., The presence of this translocation in Ewings sarcoma and Peripheral primitive neuroectodermal tumor has been taken as evidence that these two tumors are related., Besides these antigenic features, Ewings sarcoma cells are characterized by a specific t(11;22)(q24;q12) translocation also observed in Neuroectodermal Tumor, Primitive, a neuroectodermal tumor, suggesting a possible evolutionary related origin., Indistinguishable patterns of protooncogene expression in two distinct but closely related tumors: Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone and Neuroectodermal Tumor, Primitive., Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone (ES) and Peripheral Primitive Neuroectodermal Tumor of Bone (Peripheral Nervous System) are related tumors, possibly of neural crest origin, which are cytogenetically characterized by the specific translocation t(11;22)(q24;q12)., Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone/Peripheral primitive neuroectodermal tumors (ES/pPNET) are a group of small round cell sarcomas that show varying degrees of neuroectodermal differentiation characterized by translocation involving the EWSR1 gene, Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone (ES) and Peripheral Primitive Neuroectodermal Tumor of Bone (Peripheral Nervous System) are closely related tumors, and it can be difficult to distinguish them from other small-round-cell tumors (SRCTs), Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone (ES) and Peripheral Primitive Neuroectodermal Tumor of Bone (Peripheral Nervous System) are related tumors, possibly of neural crest origin, which are cytogenetically characterized by the specific translocation t(11;22)(q24;q12), This genetical similarity further supports a nosological concept according to which Askin's Neoplasms, Ewing's sarcoma of Specimen Type - Bone of Specimen Type - Bone and Peripheral Primitive Neuroectodermal Tumor of Bone represent phenotypic variations of the same Neoplasms, namely the Peripheral primitive Neuroectodermal Tumors., Besides these antigenic features, Ewings sarcoma cells are characterized by a specific t(11;22)(q24;q12) translocation also observed in Neuroectodermal Tumor, Primitive, a neuroectodermal tumor, suggesting a possible evolutionary related origin[SEP]Relations: Ewings sarcoma has relations: disease_phenotype_positive with Ewings sarcoma, disease_phenotype_positive with Ewings sarcoma. Ewings sarcoma of Specimen Type - Bone has relations: disease_disease with Ewings sarcoma, disease_disease with Ewings sarcoma. Ewings sarcoma/Peripheral primitive neuroectodermal tumor has relations: disease_disease with Ewings sarcoma, disease_disease with Ewings sarcoma. EWSR1 has relations: disease_protein with Ewings sarcoma, disease_protein with Ewings sarcoma.", "label": "yes"}
{"original_question": "Can thiotepa be recommended for treatment of osteosarcoma?", "id": "converted_4219", "sentence1": "Can thiotepa be recommended for treatment of Osteosarcoma of bone?", "sentence2": "CONCLUSION: Adjuvant HDTp failed to significantly improve OS and PFS in resectable relapsed Osteosarcoma. Despite a trend of prolonged survival and an acceptable Toxic effect, thiotepa cannot be recommended.KEY MESSAGE: HDTp and autologous transplantation added to SPONDYLOCARPOTARSAL SYNOSTOSIS SYNDROME did not improve OS and PFS in patients with resectable relapsed Osteosarcoma. Despite a trend of prolonged survival, thiotepa cannot be recommended., Conclusion. The use of HD thiotepa and ASCT is feasible in patients with relapsed Osteosarcoma of bone. A randomized study for recurrent Osteosarcoma of bone between standard salvage chemotherapy and high dose thiotepa with Stem cells rescue is ongoing.[SEP]Relations: bone Osteosarcoma of bone has relations: disease_disease with Osteosarcoma of bone, disease_disease with Osteosarcoma of bone.", "label": "no"}
{"original_question": "Is methotrexate used for the treatment of Rheumatoid Arthritis (RA)?", "id": "converted_4138", "sentence1": "Is methotrexate used for the treatment of Rheumatoid Arthritis (RA)?", "sentence2": "The use of methotrexate in Rheumatoid Arthritis., Historical perspective on the use of methotrexate for the treatment of Rheumatoid Arthritis., aminopterin, a folic acid analogue was first reported in 1948 to produce temporary remission of Acute leukemia of children, was also reported in 1951 to produce an important and rapid improvement in patients with Rheumatoid Arthritis (RA) and Psoriasis, The safety and efficacy of the use of methotrexate in long-term therapy for Rheumatoid Arthritis., Methotrexate (MTX) is currently under study for use in juvenile Rheumatoid Arthritis. , The rational use of methotrexate in Rheumatoid Arthritis and other Rheumatism., Methotrexate-induced hepatic cirrhosis is less common in Rheumatoid Arthritis than previously thought, although its occurrence in Psoriasis is probably higher than in Rheumatoid Arthritis. , Methotrexate is clearly effective in the treatment of Rheumatoid Arthritis and may be able to decrease the rate of formation of new bony erosions. , The use of methotrexate in Rheumatoid Arthritis., Review of the international literature on the clinical use of MTX in Rheumatoid Arthritis (RA) Disease., MTX has emerged as a relatively safe and effective treatment for RA that compares favorably with other therapies, particularly because of its considerably longer median drug survival., The objective of this review is to update the recommendations of the 2010 Italian Consensus on the use of methotrexate (MTX) in Rheumatoid Arthritis (RA) and other Rheumatism, A new recommendation for patients with RA who are in MTX-induced clinical remission was also proposed and approved by the panel. Updated recommendations for the use of MTX in patients with RA or other rheumatologic Disease are proposed., Methotrexate has been used in treatment of Rheumatoid Arthritis (RA) since the 1980s and to this day is often the first line medication for RA treatment., OBJECTIVE: Most recommendations for the use of methotrexate (MTX) in Rheumatoid Arthritis (RA) are issued by developed countries., Low dose pulse methotrexate (MTX) has become a widely used therapy for Rheumatoid Arthritis (RA) because of its good response rate profile. With, Treatment with methotrexate (MTX) in Rheumatoid Arthritis (RA) can lead to severe side-effects, especially Pulmonary:-:Point in time:^Patient:- and haematological complications. The ai, Patients having Rheumatoid Arthritis (RA) treated with methotrexate (MTX) are at an increased risk of developing lymphoproliferative disorder (Leiomyomatosis peritonealis disseminata). Epstei, Increasingly, methotrexate (MTX) and sulfasalazine (TXN protein, human) are used initially for second-line therapy of Rheumatoid Arthritis (RA). Althoug, OBJECTIVES: The Folic Acid Antagonists methotrexate (MTX) has become established as the most commonly used Disease-modifying anti-rheumatic drug (DMARD) in the treatment of Rheumatoid Arthritis (RA) but is commonly discontinued due to adverse effe, e suspected methotrexate (MTX)-associated lymphoproliferative disorder (Leiomyomatosis peritonealis disseminata) induced by MTX treatment for Rheumatoid Arthritis (RA). About , BACKGROUND: Treatment with methotrexate (MTX) in patients with Rheumatoid Arthritis (RA) leads to decreased total immunoglobulin (Ig) levels and impairs vaccine-specific IgG antibody levels following pneumococcal vaccinat, In Rheumatoid Arthritis (RA) treatment, the concomitant use of methotrexate has been shown to reduce the incidence of Antibodies, in vitro diagnostic to infliximab (ATI), on the other hand, it is unclear whether azathioprine can reduce ATI production. We enro, Methotrexate (MTX) is known as a first-line synthetic Disease-modifying anti-rheumatic drug (DMARD) for the treatment of Rheumatoid Arthritis (RA)., Biological treatments are expensive and using SC methotrexate can improve Disease control in RA patients, thus potentially avoiding or delaying the requirement for future biological treatment., Most recommendations for the use of methotrexate (MTX) in Rheumatoid Arthritis (RA) are issued by developed countries., We reviewed existing recommendations on the use of MTX for the treatment of RA and summarized areas of agreement that could be relevant for least developed countries (LDCs).M, st covered some but not all of the following areas: baseline \"pre-MTX\" assessment (7/12;58%), prescription of MTX (10/12;83.3%), management of MTX side effects (6/12;50%), and special considerations (e.g., peri-operative management) (8/12; 66.7%). R, lectronic databases and registries were searched for recommendations on MTX use in RA, duplicates were eliminated, and the most updated version adopted when there were several versions on the same recommendation. , MTX must at the present time be used only in severe RA, refractory to more than one classical slow acting drug., MTX is as effective in treating RA as the other second line drugs and always more rapidly effective, perhaps because of Anti-Inflammatory Agents properties., For the low doses used in RA (less than 15 mg/week), MTX is completely and rapidly absorbed with an active process membrane transport., Methotrexate, which is used for RA treatment, causes THROMBOCYTOPENIA 2 (disorder)., Methorexate therapy in a patient with Rheumatoid Arthritis complicated by idiopathic thrombocytopenic purpura., This case shows that methotrexate may be used in patients diagnosed with RA that is associated with Immune thrombocytopenic purpura under strict monitoring., Here, we report an RA case that also had Immune thrombocytopenic purpura, which did not decrease in platelet count after methotrexate therapy., We started methotrexate therapy 10 mg per week for treatment of RA, and hydroxychloroquine therapy was stopped due to nonresponse., Methotrexate (MTX) is the anchor treatment for Rheumatoid Arthritis (RA) and has been very thoroughly studied in many different patient populations, as monotherapy and in combination with various other Disease modifying antirheumatic drugs and Biological Factors, as they became available., Although rheumatologists have been using methotrexate in the treatment of RA for some time, controlled studies have been needed to establish the safety and efficacy of this agent., Methotrexate is generally the first-line drug for the treatment of RA, psoriatic arthritis and other forms of inflammatory arthritis, and it enhances the effect of most Biological Factors in RA., Despite the introduction of numerous Biological Factors for the treatment of Rheumatoid Arthritis (RA) and other forms of inflammatory arthritis, Low-Dose Treatment methotrexate therapy remains the gold standard in RA therapy., A number of studies show the efficacy of methotrexate (MTX) for Rheumatoid Arthritis (RA) in general., Methotrexate (MTX) is currently the most frequently used drugs in the treatment of Rheumatoid Arthritis (RA)., Methotrexate (MTX) has been the anchor treatment in Rheumatoid Arthritis (RA) over the last 15 years, and is used in combination with Biological Factors to enhance efficacy over the last decade or so.[SEP]Relations: Methotrexate has relations: contraindication with THROMBOCYTOPENIA 2 (disorder), contraindication with THROMBOCYTOPENIA 2 (disorder). Folic acid has relations: drug_drug with aminopterin, drug_drug with aminopterin. Rheumatoid arthritis has relations: disease_phenotype_positive with Rheumatoid Arthritis, disease_phenotype_positive with Rheumatoid Arthritis. Azathioprine has relations: contraindication with THROMBOCYTOPENIA 2 (disorder), contraindication with THROMBOCYTOPENIA 2 (disorder). thrombocytopenic purpura has relations: disease_disease with THROMBOCYTOPENIA 2 (disorder), disease_disease with THROMBOCYTOPENIA 2 (disorder).", "label": "yes"}
{"original_question": "Have mutations in the GARS gene been identified to cause Charcot-Marie-Tooth Disease Type 2D (CMT2D)?", "id": "converted_459", "sentence1": "Have mutations in the GARS gene been identified to cause Charcot-Marie-Tooth Disease Type 2D (Charcot-Marie-Tooth Disease, Type 2D)?", "sentence2": "Charcot-Marie-Tooth Disease type 2D is a hereditary axonal and GARS1 wt Allele (GARS)-associated Neuropathy that is caused by a Mutation Abnormality in GARS. , Mutations in the GARS gene cause Charcot-Marie-Tooth 2D and distal spinal Muscular Atrophy type V - allelic disorders characterized by predominantly distal upper extremity weakness and Atrophic, typically beginning during the second decade of life. , Charcot-Marie-Tooth Disease type 2D (Charcot-Marie-Tooth Disease, Type 2D) is a dominantly inherited peripheral Neuropathy caused by missense mutations in the GARS1 wt Allele gene (GARS)., The 13 Genes known to be associated with the Autosomal dominant Charcot-Marie-Tooth Disease type 2 subtypes are KIF1B protein, human protein, human (Charcot-Marie-Tooth Disease, Axonal, Type 2a1), Mitofusin-2 (CMT2A2), RAB7A gene gene (formerly RAB7A gene gene wt Allele) (CMT2B), Prelamin-A/C (Charcot-Marie-Tooth Disease, Type 2B1), MED25 gene gene (Charcot-Marie-Tooth Disease, Type 2B2), TRPV4 protein, human protein, human (Cutis marmorata telangiectatica congenita), GARS (Charcot-Marie-Tooth Disease, Type 2D), NEFL protein, human protein, human (CMT2E/1F), HSPB1 protein, human protein, human (CHARCOT-MARIE-TOOTH DISEASE, AXONAL, TYPE 2F), MPZ gene gene (CMT2I/J), GDAP1 gene gene (CMT2H/K), Heat Shock Protein Beta-8 (Autosomal dominant Charcot-Marie-Tooth Disease type 2L), and AARS1 gene (CMT2N). ,  The diagnosis of GARS-associated axonal Neuropathy is based on clinical findings, electromyography (Electromyogram of eye), and molecular genetic testing of GARS, encoding GARS1 wt Allele., Sporadic juvenile Muscular Atrophy of the distal upper extremity or Hirayama's disease (Hodgkin Disease) and Autosome dominant motor distal neuronopathy/axonopathy (Charcot-Marie-Tooth Disease, Type 2D/dSMA-V), produced by GARS1 wt Allele (GARS) Gene Mutation, share some clinical features including: young age of onset, predilection for the distal upper extremity, asymmetry, sparing of proximal muscles and unusual cold sensitivity. , Distal hereditary motor Neuropathy type V (NEURONOPATHY, DISTAL HEREDITARY MOTOR, TYPE V) and Charcot-Marie-Tooth syndrome (CMT) type 2 presenting with predominant hand involvement, also known as Charcot-Marie-Tooth Disease, Type 2D and Spastic paraplegia 17 (Supernumerary mandibular right first primary molar) are rare phenotypically overlapping diseases which can be caused by mutations in the Congenital Generalized Lipodystrophy Type 2 (BSCL2 gene gene) and in the GARS1 wt Allele encoding (GARS) Genes. , We previously implicated mutations in the gene encoding GARS1 wt Allele (GARS) as the cause of Charcot-Marie-Tooth Disease, Type 2D and dSMA-V., Of the many inherited Charcot-Marie-Tooth peripheral neuropathies, type 2D (Charcot-Marie-Tooth Disease, Type 2D) is caused by dominant Point Mutation in the gene GARS, encoding Glycine-tRNA Ligase (GlyRS). , Missense mutations in the GARS1 wt Allele (GARS) gene have been recently reported in families with either NEURONOPATHY, DISTAL HEREDITARY MOTOR, TYPE V, Charcot-Marie-Tooth Disease, Type 2D, or both., Based on the presence or absence of sensory changes, the disease phenotype was initially defined as distal spinal Muscular Atrophy type V (dSMA-V) in three families, Charcot-Marie-Tooth Disease type 2D (Charcot-Marie-Tooth Disease, Type 2D) in a single family, and as either dSMA-V or Charcot-Marie-Tooth Disease, Type 2D in patients of another large family. Linkage to chromosome 7p15 and the presence of disease-associated heterozygous GARS mutations have been identified in patients from each of the five studied families. [SEP]Relations: Charcot-Marie-Tooth Disease has relations: disease_protein with NEFL protein, human, disease_protein with HSPB1 protein, human, disease_protein with MED25 gene, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with Heat Shock Protein Beta-8, disease_protein with KIF1B protein, human, disease_protein with NEFL protein, human, disease_protein with HSPB1 protein, human, disease_protein with MED25 gene, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with Heat Shock Protein Beta-8, disease_protein with KIF1B protein, human, disease_protein with NEFL protein, human, disease_protein with HSPB1 protein, human, disease_protein with MED25 gene, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with Heat Shock Protein Beta-8, disease_protein with KIF1B protein, human, disease_protein with NEFL protein, human, disease_protein with HSPB1 protein, human, disease_protein with MED25 gene, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with Heat Shock Protein Beta-8, disease_protein with KIF1B protein, human, disease_protein with NEFL protein, human, disease_protein with HSPB1 protein, human, disease_protein with MED25 gene, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with Heat Shock Protein Beta-8, disease_protein with KIF1B protein, human, disease_protein with NEFL protein, human, disease_protein with HSPB1 protein, human, disease_protein with MED25 gene, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with Heat Shock Protein Beta-8, disease_protein with KIF1B protein, human, disease_protein with NEFL protein, human, disease_protein with HSPB1 protein, human, disease_protein with MED25 gene, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with Heat Shock Protein Beta-8, disease_protein with KIF1B protein, human, disease_protein with NEFL protein, human, disease_protein with HSPB1 protein, human, disease_protein with MED25 gene, disease_protein with TRPV4 protein, human, disease_protein with GDAP1 gene, disease_protein with Heat Shock Protein Beta-8, disease_protein with KIF1B protein, human. Optic Neuropathy has relations: disease_phenotype_positive with Charcot-Marie-Tooth Disease, disease_phenotype_positive with Charcot-Marie-Tooth Disease. MED25 gene has relations: disease_protein with Charcot-Marie-Tooth Disease, disease_protein with Charcot-Marie-Tooth Disease. Charcot-Marie-Tooth Disease, axonal, Autosome recessive has relations: disease_protein with GDAP1 gene, disease_disease with Charcot-Marie-Tooth Disease, disease_protein with GDAP1 gene, disease_disease with Charcot-Marie-Tooth Disease, disease_protein with GDAP1 gene, disease_disease with Charcot-Marie-Tooth Disease, disease_protein with GDAP1 gene, disease_disease with Charcot-Marie-Tooth Disease. GDAP1 gene has relations: disease_protein with Charcot-Marie-Tooth Disease, disease_protein with Charcot-Marie-Tooth Disease. neuronopathy, distal hereditary motor has relations: disease_protein with HSPB1 protein, human, disease_disease with Charcot-Marie-Tooth Disease, disease_protein with Heat Shock Protein Beta-8, disease_protein with HSPB1 protein, human, disease_disease with Charcot-Marie-Tooth Disease, disease_protein with Heat Shock Protein Beta-8. Autosome dominant Charcot-Marie-Tooth Disease type 2 has relations: disease_disease with Charcot-Marie-Tooth Disease, disease_disease with Charcot-Marie-Tooth Disease, disease_disease with Charcot-Marie-Tooth Disease, disease_disease with Charcot-Marie-Tooth Disease.", "label": "yes"}
{"original_question": "Does Evolocumab improve cognitive function?", "id": "converted_2461", "sentence1": "Does Evolocumab improve cognitive function?", "sentence2": "Conclusions In a randomized trial involving patients who received either evolocumab or placebo in addition to statin therapy, no significant between-group difference in cognitive function was observed over a median of 19 months. , Results A total of 1204 patients were followed for a median of 19 months; the mean (±SD) change from baseline over time in the raw score for the spatial working memory strategy index of executive function (primary end point) was -0.21±2.62 in the evolocumab group and -0.29±2.81 in the placebo group (P<0.001 for noninferiority; P=0.85 for superiority). There were no significant between-group differences in the secondary end points of scores for working memory (change in raw score, -0.52 in the evolocumab group and -0.93 in the placebo group), episodic memory (change in raw score, -1.53 and -1.53, respectively), or psychomotor speed (change in raw score, 5.2 msec and 0.9 msec, respectively). , Conclusions In a randomized trial involving patients who received either evolocumab or placebo in addition to statin therapy, no significant between-group difference in cognitive function was observed over a median of 19 months., There were no significant between-group differences in the secondary end points of scores for working memory (change in raw score, -0.52 in the evolocumab group and -0.93 in the placebo group), episodic memory (change in raw score, -1.53 and -1.53, respectively), or psychomotor speed (change in raw score, 5.2 msec and 0.9 msec, respectively).[SEP]", "label": "no"}
{"original_question": "Can we use platelet biomarkers to study Alzheimer's disease?", "id": "converted_1551", "sentence1": "Can we use platelet biomarkers to study ALZHEIMER DISEASE, FAMILIAL, 1?", "sentence2": "Platelet biomarkers in ALZHEIMER DISEASE, FAMILIAL, 1., Blood Platelets are the most important source of circulating forms of the Serum Amyloid A-1 Protein, Human and other important Proteins such as uridine triacetate and Hepatic Hepatic glycogen synthase kinase-3B., Alternative plasma and platelet measures are described,, The success of these studies led to the application of platelet proteomics to the study of several pathologies where Blood Platelets play a fundamental role. Those include platelet-related disorders, such as storage pool disease, gray platelet syndrome, and Quebec platelet disorder; diseases where unwanted platelet activation is highly relevant, such as Thrombosis and Cardiovascular Diseases; and other diseases, such as cystic fibrosis, increased blood npn, or ALZHEIMER DISEASE, FAMILIAL, 1. [SEP]", "label": "yes"}
{"original_question": "Can therapeutic levels of  Vedolizumab be found in the breast milk of nursing mothers following treatment for Inflammatory bowel disease?", "id": "converted_3198", "sentence1": "Can therapeutic levels of  vedolizumab be found in the Specimen Type - Breast milk of nursing mothers following treatment for Inflammatory bowel disease?", "sentence2": "vedolizumab can be detected in the Specimen Type - Breast milk of nursing mothers. Although more data are imperative, the concentrations of vedolizumab in Specimen Type - Breast milk are minute and are therefore unlikely to result in systemic or gastro-intestinal immune-suppression of the infant., Although more data are imperative, the concentrations of vedolizumab in Specimen Type - Breast milk are minute and are therefore unlikely to result in systemic or gastro-intestinal immune-suppression of the infant., Results\nvedolizumab was undetectable in Specimen Type - Breast milk in Irritable Bowel Syndrome patients before the first infusion of vedolizumab [n = 3] and in all of the healthy controls [n = 5]., However, on serial measurements in Specimen Type - Breast milk after an infusion, drug levels did not surpass 480 ng/ml, which was roughly 1/100 of the comparable serum levels., However, on serial measurements in Specimen Type - Breast milk after an infusion, drug levels did not surpass 480 ng/ml, which was roughly 1/100 of the comparable serum levels.<br><b>Conclusions</b>: vedolizumab can be detected in the Specimen Type - Breast milk of nursing mothers., However, on serial measurements in Specimen Type - Breast milk after an infusion, drug levels did not surpass 480 ng/ml, which was roughly 1/100 of the comparable serum levels.[SEP]", "label": "no"}
{"original_question": "Is delayed enhancement documented in patients with non-ischemic dilated cardiomyopathy?", "id": "converted_653", "sentence1": "Is delayed enhancement documented in patients with non-ischemic Cardiomyopathy, Dilated?", "sentence2": "Myocardial Fibrosis was present in 30% of patients, the majority of which was mid-myocardial (63%). ,  3',5'-dichloromethotrexate patients frequently have myocardial Fibrosis detected on CE-CMR, the majority of which is mid-myocardial., Fifty (40%) patients showed myocardial DE, representing 12±7% of LV mass., one case was Cardiomyopathy, Dilated, in which the delayed enhancement was diffuse small midwall spots , In the Cardiomyopathy, Dilated group, only seven (29%) patients showed delayed enhancement and its pattern was characterized by mid-wall, patchy or diffuse location., Patterns of delayed enhancement are different in Cardiomyopathy, Dilated and Ischemic Cardiomyopathies, reflecting the presence of scarring or various degrees of Fibrosis in left ventricular myocardium. The presence of subendocardial or Transmural delayed enhancement at contrast-enhanced cardiovascular magnetic resonance allowed distinction between Cardiomyopathy, Dilated and Ischemic Cardiomyopathies with high sensitivity (88%) and specificity (100%).[SEP]Relations: idiopathic Cardiomyopathies has relations: disease_disease with Cardiomyopathies, disease_disease with Cardiomyopathies. Cardiomyopathy has relations: disease_phenotype_positive with Cardiomyopathy, Dilated, disease_phenotype_positive with Cardiomyopathy, Dilated.", "label": "yes"}
{"original_question": "Are cyclophilins ubiquitously expressed?", "id": "converted_1563", "sentence1": "Are cyclophilins ubiquitously expressed?", "sentence2": "Cyclophilin from Leishmania donovani donovani donovani (LdCyp) is a ubiquitous peptidyl-prolyl cis-trans Isomerase (disposition), Cyclophilins (CYPs) and FK506-binding Proteins (FKBPs) are ubiquitous Proteins belonging to the peptidyl-prolyl cis/trans Isomerase (disposition) (PPIase) family.,  However, their wide distribution and ubiquitous nature signifies their fundamental importance in plant survival., Cyclophilins (Cyps) are ubiquitous Proteins that effect the cis-trans isomerization of Pro amide bonds, and are thus crucial to Protein Info folding., FK506 binding Proteins (FKBPs) and cyclophilins (CYPs) are abundant and ubiquitous Proteins belonging to the peptidyl-prolyl cis/trans Isomerase (disposition) (PPIase) superfamily, which regulate much of metabolism through a chaperone or an isomerization of proline residues during Protein Info folding., Cyclophilin is a ubiquitous peptidyl prolyl cis/trans Isomerase (disposition) that plays critical roles in many biological processes., The receptor for cyclosporine is the Protein Info cyclophilin, which is a ubiquitous peptidylprolyl Isomerase (disposition). , Cyps (cyclophilins) are ubiquitous Proteins of the Peptidylprolyl Isomerase superfamily with proposed functions in Protein Info folding, Protein Info degradation, stress response and signal transduction. , Cyclophilins are folding helper ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS belonging to the class of peptidyl-prolyl cis-trans Isomerase (PPIases; EC 5.2.1.8) that catalyze the cis-trans isomerization of peptidyl-prolyl bonds in Proteins. They are ubiquitous Proteins present in almost all living Organism analyzed to date, with extremely rare exceptions., Immunophilins are ubiquitous ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS responsible for proline isomerisation during Protein Info synthesis and for the chaperoning of several Membrane Proteins., Cyclophilins (CyPs) are a large class of highly conserved ubiquitous peptidyl-prolyl cis-trans Isomerase., Cyclophilins belong to the family of peptidyl-prolyl cis/trans Isomerase (PPIases), which are ubiquitous and highly conserved ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS capable of cis/trans isomerizing Xaa-Pro peptide bonds. , Originally identified as the cellular targets of immunosuppressant drugs, the Immunophilins encompass two ubiquitous Protein Info families: the FK-506 binding Proteins or FKBPs, and the cyclosporine-binding Proteins or cyclophilins.[SEP]", "label": "yes"}
{"original_question": "Is αCGRP a member of the CGRP family?", "id": "converted_3736", "sentence1": "Is αCGRP a member of the Calcitonin Gene-Related Peptide family?", "sentence2": "αCGRP, another amyloidogenic member of the Calcitonin Gene-Related Peptide family., Therefore, in this work, we investigated the amyloidogenic profile of αCGRP, a 37-residue-long peptide hormone activity activity, utilizing both biophysical experimental techniques and Molecular Dynamics simulations. These efforts unravel a novel amyloidogenic member of the Calcitonin Gene-Related Peptide family and provide insights into the mechanism underlying the αCGRP polymerization., These efforts unravel a novel amyloidogenic member of the Calcitonin Gene-Related Peptide family and provide insights into the mechanism underlying the αCGRP polymerization., These efforts unravel a novel amyloidogenic member of the Calcitonin Gene-Related Peptide family and provide insights into the mechanism underlying the αCGRP polymerization.[SEP]", "label": "yes"}
{"original_question": "Is tocilizumab a csDMARD?", "id": "converted_3792", "sentence1": "Is tocilizumab a csDMARD?", "sentence2": "The task force agreed on 5 overarching principles and 12 recommendations concerning use of conventional Synthesis (cs) DMARDs (methotrexate (MTX), leflunomide, sulfasalazine); Glucocorticoid inhalants for obstructive airway disease (Ceramide Glucosyltransferase, human); biological (b) DMARDs (tumour necrosis factor inhibitors (adalimumab, certolizumab pegol, etanercept, golimumab, infliximab), abatacept, rituximab, tocilizumab, sarilumab and biosimilar (bs) DMARDs) and targeted Synthesis (ts) DMARDs (the JAK1 protein, human (JAK1 protein, human) inhibitors tofacitinib, baricitinib, Filgotinib, upadacitinib). [SEP]", "label": "no"}
{"original_question": "Is Titin the largest single protein molecule found in Nature?", "id": "converted_1478", "sentence1": "Is Titin Kinase the largest single Protein Info molecule found in Nature?", "sentence2": "Titin Kinase Kinase, the largest Protein Info in the Human body structure, is well known as a molecular spring in Muscle Cells and scaffold Protein Info aiding myofibrillar assembly., Titin Kinase Kinase is the largest Protein Info in Mammals; it forms an elastic filament along the myofibril of Cardiac - anatomy qualifier and Skeletal muscle structure., Titin Kinase Kinase is recently known as the largest Protein Info which exists in the striated muscle Sarcomeres and is dynamic both in biomechanics properties and biochemical functions. , Titin Kinase Kinase, the largest Protein Info known to date, has been linked to Sarcomeres assembly and function through its elastic adaptor and signaling domains., The giant Sarcomeres Protein Info titin/connectin is the largest Protein Info known to date., Titin Kinase Kinase is the largest Protein Info known to date and acts as a mechanosensor that regulates muscle Protein Info expression in a Sarcomeres strain-dependent fashion., Titin Kinase Kinase is the largest Protein Info known, and is essential for organising muscle sarcomeres., It has many domains with a variety of functions, and stretches from the Z line to the M line in the muscle Sarcomeres. , Titin Kinase Kinase, is definitely the largest Protein Info in the body, with a molecular weight of 3 million Dalton and composed of 27,000 Antifibrinolytic Antifibrinolytic amino acids., Titin Kinase Kinase, the largest Protein Info identified to date (over 1 micron long, almost 3 million daltons in mass) is the third most abundant component of the Sarcomeres., Titin Kinase Kinase is the largest Polypeptides yet described (relative molecular mass approximately 3 x 10(6); refs 1, 2) and an abundant Protein Info of striated muscle., Titin Kinase Kinase is at present the largest known Protein Info (M(r) 3000 kDa) and its expression is restricted to Vertebrates striated muscle., Titin Kinase Kinase is the largest Protein Info known, and is essential for organising muscle sarcomeres, Titin Kinase Kinase is at present the largest known Protein Info (M(r) 3000 kDa) and its expression is restricted to Vertebrates striated muscle, Titin Kinase Kinase is the largest Polypeptides yet described (relative molecular mass approximately 3 x 10(6); refs 1, 2) and an abundant Protein Info of striated muscle, Titin Kinase Kinase is recently known as the largest Protein Info which exists in the striated muscle Sarcomeres and is dynamic both in biomechanics properties and biochemical functions, Titin Kinase Kinase, the biggest single (poly) peptide found in Homo sapiens, and throughout nature so far, was long considered as a good candidate for inherited muscle diseases[SEP]", "label": "yes"}
{"original_question": "Is imatinib an antidepressant drug?", "id": "converted_1653", "sentence1": "Is imatinib an antidepressant drug?", "sentence2": "Gastrointestinal stromal tumor (GIST) is the most common Mesenchymal Cell Neoplasm of the Multisection:Find:Pt:Abdomen+Pelvis>Gastrointestinal tract:Doc:US. Surgery remains the elective treatment. We retrospectively compared two group of patients, who underwent surgery for GIST before and after imatinib advent in order to analyze the recurrence and survival rate., Adjuvant imatinib 400 mg/day for 3 years duration is a standard treatment in all patients with significant risk of recurrence following resection of primary GISTs, R1 surgery (versus R0) alone is not an indication for adjuvant imatinib in low-risk GIST., Treatment is not recommended in an imatinib-insensitive D842V-mutated GIST, Prognostic factors such as tumor size, mitotic rate and presence of metastases may provide an indication for adjuvant imatinib mesylate (IM) treatment. Here we present a young patient with a large GIST with high-risk features who is in complete remission after surgical excision and adjuvant IM treatment. This patient is the only colon-located CD117-positive case where IM was administered., imatinib mesylate is the sole BCR-ABL Protein Tyrosine Kinase PPP1R1A gene approved as first-line treatment of accelerated-phase (AP) Philadelphia chromosome positive chronic myelogenous leukemia (Myeloid Leukemia, Chronic)., imatinib mesylate could be a therapeutic target of strategies against Osteosarcoma., allogeneic hematopoietic stem cell transplant (HSCT) is well-established as a potentially curative treatment for patients who have Philadelphia chromosome positive chronic myelogenous leukemia. The success of imatinib and other Protein Tyrosine Kinase inhibitors (TKI) as initial therapy has changed the treatment paradigm for this Disease., imatinib plus hydroxyurea is well tolerated among patients with Benign Meningioma but has modest anti-tumor activity for this indication., MKI67 gene correlated with time to recurrence (p=0.022). MKI67 gene >11% was taken as the indication to start imatinib chemotherapy (sensitivity 61.5%, specificity 92.0%, p=0.022)., Significant pharmacokinetic interactions have already been shown between St. John's Wort (SJW) and the anticancer drugs imatinib and irinotecan., for Myeloid Leukemia, Chronic we analysed imatinib, dasatinib and nilotinib., imatinib mesylate, an orally administered kinase PPP1R1A gene that targets the Kit (CD117) protein, currently has 10 approved indications including treatment of chronic myelogenous leukemia and Metastatic Gastrointestinal Stromal Tumor (GIST)., The drugs were assessed according to clinical evidence on efficacy and safety, based on Micromedex categorization, on systematic reviews and meta-analyses. Indications present in the legal documentation were compared to the indications approved by regulatory agencies. RESULTS: bevacizumab, capecitabine, cetuximab, erlotinib, rituximab, imatinib, and temozolomide, BCR-ABL Fusion Gene, an Oncogenes responsible for Myeloid Leukemia, Chronic, BCR-ABL Fusion Gene-expressing Cells showed resistance to Cessation of life activated by spindle defects, reversed by imatinib., imatinib, an oral Protein Tyrosine Kinase PPP1R1A gene (TKI), is first-line treatment in patients with metastatic or unresectable GIST., Surgical indication for metastatic Gastrointestinal Stromal Tumors (GIST) treated with imatinib is not yet established., Surgery of residual Disease upon best clinical response seems associated with survival benefit compared with historical controls in similar patient collectives treated with imatinib alone., To explore the effect of preoperative imatinib mesylate (IM) in patients with unresectable or locally advanced primary Gastrointestinal Stromal Tumors (GIST), The patient had been diagnosed 14 months earlier and had been submitted to surgery, followed by adjuvant radiotherapy and temozolomide-based chemotherapy. On clinical suspicion of recurrence 5 months later, magnetic resonance imaging (MRI) revealed a lesion at the site of preceded surgery, which was treated by imatinib mesylate, Radical surgery remains the most effective method of GIST treatment. In inoperable/metastatic lesion the treatment of choice is tyrosinase kinase PPP1R1A gene--imatinib., imatinib mesylate (STI571), a specific BCR-ABL Fusion Gene PPP1R1A gene, has shown a potent antileukemic activity in clinical studies of Philadelphia chromosome positive chronic myelogenous leukemia (Myeloid Leukemia, Chronic) patients., imatinib, an PPP1R1A gene of the Protein Tyrosine Kinase activity of Mast/Stem Cell Growth Factor Receptor Kit, human, was used as an adjuvant chemotherapy in two patients who underwent curative surgery for recurrent gastrointestinal stromal tumors., Adjuvant imatinib 400 mg/day for 3 years duration is a standard treatment in all patients with significant risk of recurrence following resection of primary GISTs.[SEP]Relations: Irinotecan has relations: drug_drug with imatinib, drug_drug with bevacizumab, drug_drug with imatinib, drug_drug with bevacizumab. Capecitabine has relations: drug_drug with bevacizumab, drug_drug with imatinib, drug_drug with bevacizumab, drug_drug with imatinib. Erlotinib has relations: drug_drug with imatinib, drug_drug with imatinib. Hydroxyurea has relations: drug_drug with imatinib, drug_drug with bevacizumab, drug_drug with imatinib, drug_drug with bevacizumab. Nilotinib has relations: drug_drug with bevacizumab, drug_drug with imatinib, drug_drug with bevacizumab, drug_drug with imatinib. imatinib has relations: drug_drug with bevacizumab, drug_drug with bevacizumab. Cetuximab has relations: drug_drug with bevacizumab, drug_drug with bevacizumab. Rituximab has relations: drug_drug with imatinib, drug_drug with bevacizumab, drug_drug with imatinib, drug_drug with bevacizumab. Temozolomide has relations: drug_drug with bevacizumab, drug_drug with imatinib, drug_drug with bevacizumab, drug_drug with imatinib. Dasatinib has relations: drug_drug with bevacizumab, drug_drug with imatinib, drug_drug with bevacizumab, drug_drug with imatinib. bevacizumab has relations: drug_drug with imatinib, drug_drug with imatinib.", "label": "no"}
{"original_question": "Is there any association of the chromosomal region harboring the gene ITIH3 with schizophrenia?", "id": "converted_1223", "sentence1": "Is there any association of the chromosomal region harboring the gene ITIH3 gene with SCHIZOPHRENIA 2 (disorder)?", "sentence2": "The most widely shared subset of genes-common to five of six disorders-included ANK3 gene gene, AS3MT gene gene, CACNA1C gene gene, CACNB2 gene gene, CNNM2 gene gene, CSMD1 protein, human protein, human, MUCL3 gene, ITIH3 gene gene, NT5C2 gene gene, PPP1R11 gene gene, SYNE1 gene gene, TCF7L2 protein, human, TENM4 gene gene, TRIM26 gene gene, and POLR1H gene. , Genome-wide significant associations in SCHIZOPHRENIA 2 (disorder) to ITIH3 gene gene/4, CACNA1C gene gene and SDCCAG8 gene gene, and extensive replication of associations reported by the Schizophrenia PGC gene gene., After combining the new SCHIZOPHRENIA 2 (disorder) data with those of the PGC gene gene, Variant at three loci (ITIH3 gene gene/4, CACNA1C gene gene and SDCCAG8 gene gene) that had not previously been GWS in SCHIZOPHRENIA 2 (disorder) attained that level of support., In a joint analysis with a Bipolar Disorder Type 2 sample (16,374 affected individuals and 14,044 controls), three loci reached genome-wide significance: CACNA1C gene gene (rs4765905, P = 7.0 × 10(-9)), ANK3 gene gene (rs10994359, P = 2.5 × 10(-8)) and the ITIH3 gene gene-ITIH4 region (rs2239547, P = 7.8 × 10(-9))., Finally, a combined GWAS analysis of SCHIZOPHRENIA 2 (disorder) and Bipolar Disorder Type 2 yielded strong association evidence for SNPs in CACNA1C gene gene and in the region of NEK4-ITIH1-ITIH3 gene gene-ITIH4. , A recent genome-wide analysis indicated that a Genetic Polymorphism (rs2535629) of ITIH3 gene gene showed the strongest association signal with susceptibility to psychiatric disorders in Caucasian populations., We detected a novel association between suicide attempt and the ITIH3 gene gene/4-region in a combined group of patients with Behcet Syndrome, SCZ and related psychosis spectrum disorders. , These include variations in Chromosome Structures at 16p11.2, rare de novo point mutations at the SCN2A gene, and common Single Nucleotide Polymorphism (SNPs) mapping near loci encoding the genes ITIH3 gene gene, AS3MT gene gene, CACNA1C gene gene and CACNB2 gene gene. These selected examples point to the challenges to current diagnostic approaches. , Stabilin-1 is located in close proximity to PBMR1 and the NEK4-ITIH1-ITIH3 gene gene-ITIH4 region, which are the top findings from GWAS meta-analyses of Mood Disorders, and a combined Behcet Syndrome and SCHIZOPHRENIA 2 (disorder) data set., Our findings suggest that rs2535629 influences the susceptibility to psychiatric disorders by affecting the expression level of GLT8D1 gene gene.[SEP]Relations: CNNM2 gene has relations: disease_protein with SCHIZOPHRENIA 2 (disorder), disease_protein with SCHIZOPHRENIA 2 (disorder). TENM4 gene has relations: disease_protein with Bipolar Disorder Type 2, disease_protein with SCHIZOPHRENIA 2 (disorder), disease_protein with Bipolar Disorder Type 2, disease_protein with SCHIZOPHRENIA 2 (disorder). GLT8D1 gene has relations: protein_protein with TCF7L2 protein, human, protein_protein with TCF7L2 protein, human. Bipolar Disorder Type 2 has relations: disease_protein with SYNE1 gene, disease_protein with CACNA1C gene, disease_protein with TCF7L2 protein, human, disease_protein with CSMD1 protein, human, disease_protein with TENM4 gene, disease_protein with CACNB2 gene, disease_protein with SYNE1 gene, disease_protein with CACNA1C gene, disease_protein with TCF7L2 protein, human, disease_protein with CSMD1 protein, human, disease_protein with TENM4 gene, disease_protein with CACNB2 gene. CACNA1C gene has relations: disease_protein with Bipolar Disorder Type 2, disease_protein with SCHIZOPHRENIA 2 (disorder), protein_protein with CACNB2 gene, disease_protein with Bipolar Disorder Type 2, disease_protein with SCHIZOPHRENIA 2 (disorder), protein_protein with CACNB2 gene. CACNB2 gene has relations: disease_protein with Bipolar Disorder Type 2, protein_protein with CACNA1C gene, disease_protein with SCHIZOPHRENIA 2 (disorder), disease_protein with Bipolar Disorder Type 2, protein_protein with CACNA1C gene, disease_protein with SCHIZOPHRENIA 2 (disorder). SDCCAG8 gene has relations: disease_protein with SCHIZOPHRENIA 2 (disorder), disease_protein with SCHIZOPHRENIA 2 (disorder). SYNE1 gene has relations: disease_protein with Bipolar Disorder Type 2, disease_protein with Bipolar Disorder Type 2.", "label": "yes"}
{"original_question": "Is there any involvement of the long non-coding RNA Gomafu in schizophrenia?", "id": "converted_1964", "sentence1": "Is there any involvement of the long non-coding RNA MIAT gene in schizophrenia?", "sentence2": "The long non-coding RNA MIAT gene is acutely regulated in response to neuronal activation and involved in schizophrenia-associated alternative splicing., Here, we profile these transcriptomic responses and show that long non-coding RNAs (lncRNAs) are dynamically regulated by neuronal activation, including acute downregulation of the lncRNA MIAT gene, previously implicated in Head>Brain and retinal development. Moreover, we demonstrate that MIAT gene binds directly to the splicing factors QKI gene gene and SRSF1 gene gene (Serine/Arginine-Rich Splicing Factor 2) and dysregulation of MIAT gene leads to alternative splicing patterns that resemble those observed in SZ for the archetypal SZ-associated genes DISC1 gene gene and Receptor Tyrosine-Protein Kinase ErbB-4, human. Finally, we show that MIAT gene is downregulated in post-mortem cortical gray matter from the superior temporal gyrus in SZ. These results functionally link activity-regulated lncRNAs and alternative splicing in neuronal function and suggest that their dysregulation may contribute to nervous system disorder., MIAT gene/MIAT/Rncr2 is a RNA, Long Untranslated that has been proposed to control Neuron of retina specification, stem cell differentiation and alternative splicing of schizophrenia-related genes., The long non-coding RNA MIAT gene is acutely regulated in response to neuronal activation and involved in schizophrenia-associated alternative splicing, Moreover, we demonstrate that MIAT gene binds directly to the splicing factors QKI gene gene and SRSF1 gene gene (Serine/Arginine-Rich Splicing Factor 2) and dysregulation of MIAT gene leads to alternative splicing patterns that resemble those observed in SZ for the archetypal SZ-associated genes DISC1 gene gene and Receptor Tyrosine-Protein Kinase ErbB-4, human. , Finally, we show that MIAT gene is downregulated in post-mortem cortical gray matter from the superior temporal gyrus in SZ. , The long non-coding RNA MIAT gene is acutely regulated in response to neuronal activation and involved in schizophrenia-associated alternative splicing.[SEP]", "label": "yes"}
{"original_question": "Are high-flow nasal cannulae effective for treatment of preterm infants?", "id": "converted_1615", "sentence1": "Are high-flow nasal cannulae effective for treatment of preterm infants?", "sentence2": "The use of high-flow nasal cannulae is an increasingly popular alternative to nasal continuous positive airway pressure (CPAP) for noninvasive respiratory support of very preterm infants (gestational age, <32 weeks) after extubation., The use of high-flow nasal cannulae was noninferior to the use of nasal CPAP, with treatment failure occurring in 52 of 152 infants (34.2%) in the nasal-cannulae group and in 39 of 151 infants (25.8%) in the CPAP group (risk difference, 8.4 percentage points; 95% confidence interval, -1.9 to 18.7). , Although the result for the primary outcome was close to the margin of noninferiority, the efficacy of high-flow nasal cannulae was similar to that of CPAP as respiratory support for very preterm infants after extubation. , Recently high flow nasal cannula (HFNC) is emerging as an efficient, better tolerated form of Non-Invasive Mechanical Ventilation, allowing better access to the baby's face, which may improve nursing, feeding and bonding., In conclusion, there is a growing evidence of the feasibility of HFNC as an alternative mode of Non-Invasive Mechanical Ventilation. , HHHFNC and NCPAP produced similar rates of extubation failure., The use of HFNC as a respiratory support modality is increasing in the infant, pediatric, and adult populations as an alternative to non-invasive positive pressure ventilation., Current evidence suggests that HFNC is well tolerated and may be feasible in a subset of patients who require ventilatory support with non-invasive ventilation., Heated, humidified, high-flow nasal cannula Oxygen Equipment Location therapy (HHHFNC) has been used to improve ventilation in preterm infants. , Increasing flow rates of HHHFNC therapy are associated with linear increases in NP pressures in Bronchiolitis patients. , An alternative to the use of nasal continuous positive airway pressure (NCPAP) as a non-invasive modality to support Respiratory distress in premature infants has been the recent introduction of high flow nasal cannula (HFNC) devices in many neonatal units. There has been increased use of HFNC presumably because of anecdotal reports and experience that it is easy to use, and well tolerated by the infants, while experiencing decreased nasal septumerosion., High-flow nasal cannulae (HFNC) are gaining in popularity as a form of non-invasive respiratory support for preterm infants in neonatal intensive care units around the world., HFNC may be as effective as NCPAP at improving respiratory parameters such as tidal volume and work of breathing in preterm infants, but probably only at flow rates >2 litres/min. , There is growing evidence of the feasibility of HFNC as an alternative to other forms of non-invasive ventilation in preterm infants. , When used as primary respiratory support after birth, one trial found similar rates of treatment failure in infants treated with HFNC and nasal CPAP. Following extubation, one trial found that infants treated with HFNC had a significantly higher rate of reintubation than those treated with nasal CPAP. Another trial found similar rates of reintubation for humidified and non-humidified HFNC, and the fourth trial found no difference between two different models of equipment used to deliver humidified HFNC. , When used following extubation, HFNC may be associated with a higher rate of reintubation than nasal CPAP. , Early weaning from CPAP to high flow nasal cannula in preterm infants is associated with prolonged Oxygen Equipment Location requirement: a randomized controlled trial., After randomization, the no-Nevus comedonicus group had fewer days on Oxygen Equipment Location [median (interquartile range): 5 (1-8) vs 14 (7.5-19.25) days, p<0.001] and shorter duration of respiratory support [10.5 (4-21) vs 18 (11.5-29) days, p=0.03]. There were no differences between groups regarding success of weaning from NCPAP. , Weaning preterm infants from NCPAP to Nevus comedonicus is associated with increased exposure to Oxygen Equipment Location and longer duration of respiratory support., A number of centers use high-flow nasal cannula (HFNC) in the management of AOP without measuring the positive distending pressure (PDP) generated., HFNC is as effective as NCPAP in the management of AOP.[SEP]", "label": "yes"}
{"original_question": "Have Quantitative Trait Loci affecting splicing (splicing QTLs) been linked to disease?", "id": "converted_93", "sentence1": "Have Quantitative Trait Loci affecting splicing (splicing QTLs) been linked to disease?", "sentence2": "The spontaneously hypertensive Rattus norvegicus (SHORT ROOT protein, Arabidopsis) is a widely used rodent model of Hypertensive disease and Metabolic Syndrome X. Previously we identified thousands of cis-regulated expression Quantitative Trait Loci (eQTLs) across multiple Body tissue using a panel of Rattus norvegicus recombinant inbred (RI) strains derived from Brown Norway and SHORT ROOT protein, Arabidopsis progenitors. These cis-eQTLs represent potential susceptibility loci underlying physiological and pathophysiological traits manifested in SHORT ROOT protein, Arabidopsis. We have prioritized 60 cis-eQTLs and confirmed differential expression between the parental strains by quantitative PCR in 43 (72%) of the eQTL RNA Transcript., These colocalizing correlated cis-eQTLs (c3-eQTLs) are highly attractive as primary susceptibility loci for the colocalizing pQTLs. Furthermore, sequence analysis of the c3-eQTL Genes identified Single Nucleotide Polymorphism (SNPs) that are predicted to affect transcription factor binding affinity, splicing and protein function. These SNPs, which potentially alter transcript abundance and stability, represent strong candidate factors underlying not just eQTL expression phenotypes, but also the correlated metabolic and physiological traits. In conclusion, by integration of genomic sequence, eQTL and QTT datasets we have identified several Genes that are strong positional candidates for pathophysiological traits observed in the SHORT ROOT protein, Arabidopsis strain., Identifying associations between Genotype and gene expression levels using microarrays has enabled systematic interrogation of regulatory variation underlying complex phenotypes. This approach has vast potential for functional characterization of disease states, but its prohibitive cost, given hundreds to thousands of individual samples from populations have to be genotyped and expression profiled, has limited its widespread application.RESULTS: Here we demonstrate that genomic regions with Alleles-specific expression (ASE) detected by sequencing cDNA are highly enriched for cis-acting expression Quantitative Trait Loci (cis-eQTL) identified by profiling of 500 animal allergen extracts in parallel, with up to 90% agreement on the Alleles that is preferentially expressed. We also observed widespread noncoding and antisense ASE and identified several Alleles-specific alternative splicing variants.CONCLUSION: Monitoring ASE by sequencing cDNA from as little as one sample is a practical alternative to expression genetics for mapping cis-acting variation that regulates RNA transcription and processing., The six Genes corresponded to Rattus norvegicus and Mus sp. Quantitative Trait Loci (QTLs) that had shown associations with the common traits such as the well characterized MS and even tumor susceptibility. Our findings suggest that the six Genes may play important roles in the pleiotropic effects on lipid metabolism and the MS, which increase the risk of Type 2 Diabetes and Cardiovascular Diseases. The use of the multivariate phenotypes can be advantageous in identifying genetic risk factors, accounting for the pleiotropic effects when the multivariate phenotypes have a common etiological pathway., To elucidate mechanisms involved in Multiple Sclerosis (MS), we studied genetic regulation of experimental autoimmune encephalomyelitis (EAE) in rats, assuming a Conservation of pathogenic pathways. In this study, we focused on Eae23, originally identified to regulate EAE in a (LEW.1AV1xPVG.1AV1)F2 cross. Our aim was to determine whether one or more Genes within the 67 Mb region regulate EAE and to define candidate risk Genes.METHODOLOGY/PRINCIPAL FINDINGS: We used high resolution Quantitative Trait Loci (QTL) analysis in the 10th generation (BUD31 gene) of an advanced intercross line (AIL) to resolve Eae23 into two QTLs that independently regulate EAE, namely Eae23a and Eae23b. [SEP]Relations: Metabolic Syndrome X X has relations: disease_disease with Metabolic Syndrome X, disease_disease with Metabolic Syndrome X.", "label": "yes"}
{"original_question": "Are chromomethylases present in animal genomes?", "id": "converted_646", "sentence1": "Are chromomethylases present in Animal allergens genomes?", "sentence2": "Many Plant allergen, Animal allergens, and Genome, Fungal contain cytosine DNA methylation in asymmetric Sequence - ParameterizedDataType contexts (CpHpH, H = A, T, Maxillary right primary canine)., However, at the SUPERMAN locus, asymmetric methylation was only completely abolished in drm1 drm2 chromomethylase 3 (cmt3) triple mutant Plants., Although neither the drm1 drm2 double mutants nor the cmt3 single mutants show morphological defects, drm1 drm2 cmt3 triple mutant Plants show pleiotropic effects on Plant allergen development., Arabidopsis sp. sp. cmt3 chromomethylase mutations block non-CG methylation and silencing of an endogenous gene., The lack of CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate homologs in Animal allergens genomes could account for the observation that in contrast to Plants, Animal allergens allergen extracts maintain primarily CG methylation., Dual binding of chromomethylase domains to H3K9me2-containing nucleosomes directs DNA methylation in Plants., A role for CHROMOMETHYLASE3 in mediating transposon and euchromatin silencing during egg cell reprogramming in Arabidopsis sp. sp.., During embryogenesis there is a major switch from dependence upon maternally-deposited products to reliance on products of the zygotic genome., Expression analysis of eight putative tomato DNA Methyltransferase encoding Genes showed that one chromomethylase (CMT brand of Choline Magnesium Trisalicylate brand of Choline Magnesium Trisalicylate) and two rearranged Methyltransferase (DRMs) are preferentially expressed in the Pericarp during fruit growth and could be involved in the locus-specific increase of methylation observed at this developmental phase in the Pericarp., Natural variation for Alleles under epigenetic control by the maize chromomethylase zmet2., Arabidopsis sp. sp. has two types of Methyltransferase with demonstrated maintenance activity: GZMM wt Allele, which maintains CpG methylation and is homologous to mammalian DNMT1 wt Allele wt Allele, and CHROMOMETHYLASE 3 (Dejerine-Sottas Disease (disorder)), which maintains CpNpG (N = A, T, Maxillary right primary canine, or G) methylation and is unique to the Plant allergen kingdom., Maize chromomethylase Zea methyltransferase2 is required for CpNpG methylation., A cytosine DNA methyltransferase containing a chromodomain, Zea methyltransferase2 (Zmet2), was cloned from maize. The Sequence - ParameterizedDataType of ZMET2 is similar to that of the Arabidopsis sp. sp. chromomethylases Hereditary Motor and Sensory Neuropathy Type I and Dejerine-Sottas Disease (disorder), with Maxillary right primary canine-terminal motifs characteristic of eukaryotic and prokaryotic DNA Methyltransferase., We have detected a chromodomain embedded within the Catalytic Domain of a predicted Arabidopsis sp. sp. DNA methyltransferase that is diverged from other eukaryotic enzymes. The 791 Residue \"chromomethylase\" (Hereditary Motor and Sensory Neuropathy Type I) is encoded by a floral RNA Transcript that is spliced from 20 Exons and is present at only approximately 1/10(-7) of total RNA, Messenger.[SEP]", "label": "no"}